USMLE STEP | REVIEW STUDY GUIDE 2015 EDITION DOCTORS IN TRAINING BETTER DOCTORS. BETTER WORLD. BRIAN Jenkins, MDDoctors In Training.com: USMLE Step 1 Review, 2015 elton Author: Brian Jenkins, MD. Copyright © 2015 Doctors In Training.com, LLC swortrdoctorsintraininggcom Doctors In Trainingcom, LLC 1704 River Run, Suite #750 Fort Worth. TX 76107 ahhisResaval Ts testepeatecty ony No p Inte asap se ie tone ten gr ts bon ay beeen ay ba UY aR GES eb NED evant DIscLAMER 118 AUTIEAELNSEX ANS Abe AT: Hass uy, Ang INCU AS ONL QUEICEBEC TO OIL TE Ha eee Ana) MMNICATIOH OH AY OL 188 COSICHT AND MAW RIA. CONTARAM TGC 7, ALIHGUGIL FE STOFSADE RL Peete iiAs ny He At etry VE VAD FO ORT HS THE ADT CASNET ACCT AGI RESPORGSAUTY Fo ARLES Pesipoe unisiaray HAL THE AUTHOR FIAPES PRO WARDANI LMPRISRORIFGAILD Ay TE (UE CLELE TEES. CRATES eee eee A TI CORI EIS OF IHS lace IEE BROORSATH ON ONTABI IN Te XT SUR DBIOT OCONEE AS SPU asin hose vom aba IAL PATRITS, PARA AG AG RSPRCQICA IAFCMTIATIRUARDD EAC Cte LIS SERS KE VE WA> IRaCUDINNS COE HA ATIONS, DOMAR ES AND HFCATIION FoRCUR NT NECA sos eon pzatne orang run orn mther a errr 11216FOUNDATIONS 1, Embryology. 2. Teratogencsis Cell Biology: Organeltes Cell Biology: Cytoplasm & Cytoskeleton ‘Cell Biology: Plasma Membrane Cellular Suffering and Death Taflammation Extracellular Environment (Cellular Adaptations EURO ‘Brain Embryology Nervous System Basics Cortex and*Brain Lesions Cranial Nerves part 4 (CranialiNerves part 2 Brainstem in Cross Section ‘Brainstem Lesions Limbie System and Hypothalamus CSP and ICP mo 10. Vascular Events 11. Seizures 12, Headache 13. Brain Tumors 14. Sleep 15, Anesthenies 16, Movement 47. Basal Ganglia’ 38. Spinal Cord and Lesions 19. Brachial Plexus and Upper Extremity Nerves|part 1 20. Brachial Plexus and Upper Extremity Nerves part 2 21, Lower Extremity nd Skeletal Muscle 22. Sensation 23. Bye 24, Ear 25. Delitiuim and Dementia PHARM BASICS 1. Parasympathetic Activation Parasympathetie ‘Sympathetic Activation G Protein Second Messengers Pharmacokinetics Pharmacodynamics Drug Metabotism 10. Drug 11. Drug Side Effects 12, Antidotes 10 12 16 18 20 2 28 33 36 39, 42 a7 50 52 54 7 eL 63 66 68 4 6 83 87 1 95 98 103, 106 108 110 112 us ug 123, 125 127 431 135 SLN3LNOD 40 aTevL‘TABLE OF CONTENTS v vi TABLE OF CONTENTS CARDIOVASCULAR 1. Embryology 2. Congenital Heart Defects 3. Cardiae Output 4, Heart Failure 5. Treatment of CHF 6. 7. 8. 9. : ic Heart Murmurs 9. Systolic Hare Murmurs 10. Electrophysiolo 11, Aatamuyeimie 12. Electrocardiography 13. Aerhyehimi 14. Regulation of BP 15. Hypertension 16. Antihypertensives 17, ‘Atherosclerosis 18. Antianginal Therapy and Lipid-Lowering Agents 19. Myocardial Tafaretion part 1 20. Myocardial Infarction part 2 21, Cardiomyopathies and Endocarditis 22. Other Cardiac Pathology 23, Nasculit RHEUM & DERM 1. Bone Formation and Bone Tumors 2. Bone Disorders 5. Musculoskeletal Injuries . is and Rheumatoid Arthritis 5. Other Types of Arthritis 5. Systemic Disorders Dermatology part 1 ‘Dermatology part 2 3. 4. 5 6 7 8 REPRODUCTION 1 2. 3. 4 S. 6 2. 8, Reproductive Anatomy . Genital Embryology Androgens 1. Testicular Pathok Penis and Prostate Patk@logy Female Reproductive Cycle ‘Menstruation and Menopause Vulva, Vagina and Cervix 9. Userine Pathology 10, Ovarian Pathology 11. Ovarian Neoplasms 12, Prognancy part 1 13. regaaney pare 2 14, Chromosomal Disorders 15. Genetie Disorders: AD and ‘Trinucléotide Repeats 16. Genetic Disorders: AR and X-Linked 17. Breast 139 142 aaa 146 148 150 153, 157 159 161 163, 165, 167 17 174 17% 179 182 184 187 189 191 193, 195 199 201 204 208, 210 22 24 217 221 223, 225 227 229, 232 235 238 240 242 244 2ar 249 251 255vu MICRO 1, BacterialBasics 2, Bacterial Toxins 3. Staphylococcus 4, Streptococcus 5. Other Gram-Positive Bacteria! 6. Gram-Negative Bacteria part 1 7. Gram=-Negative Bacteria part2 8. Spirochetes and Zoonoties 9, Mycobacteria 10, Nonstaining Bacteria 1. Penicillins 12. Cephalos 13. Other Cell Wall Tabibitors 14, Protein Synthesis Inhibitors 15. Other Antibiotics 16, Micro by Systems part 1 17. Mierolby Systems part 2 18, Viral Basics 19. DNA Virusesipart 2 20, DNA Viuses part 2 21, RNA Viruses part 1 22. RNA Viruses part 2 23. HIV. 24. HIV Drugs 25. Mycology part 26. Mycology part 2 27. Antifun 28. Protozoa 29, Helminths ani Betoparasites Haband eich TE Seem BA ‘Antigen Presentation ‘T Cells. B Cells and Antibodies ‘Immunization and Autoantibodies: Hypersensitivity and Complement ‘Macrophages, Granuloeytes/and Cytokines Immunosuppressants: Tmmunadefclencies 263 265 269 a7 223 275 27 279 281 283 285, 289 292 295 298 301 303 306 308 310 313, 315 318 320 322 325 328 333 335 337, 339 341 344, 345. 348, 350 SUNRINOD 40 378VL‘TABLE OF CONTENTS 1 xt cI 1. Oropharynx 2. Esophagus 3. Stomach 4. Upper GI Patholoy 5. Denise 6 Enterocytes and Absorption 7, Diseases of the Small Intestine 8. Large Intestine part 1 9. Large Latestine part 2 10, Large Intestine part 3 ML Panereat 12. Liver Basies 13. Alcoholic Liver Disease and Cirrhosi¢ 14. Liver Pathology 15, Hepatitis 16. Biliary Tract PULMONARY 1, ‘Anatomy and Physiology. Lung Volumes and Pulmonary Circulation Oxygen and Hemoglobin Osygenation tion and Perfusion Eas Ener PE, DVT and Pneumothorax COPD and Asthma Pulmonary Medications 10. Restrictive Lung Disease 2. Lung Cancer: 12, Lung Infections MEDICINE IN SOCIETY Research Study Designs Diagnostic Test Evaluation Interpretation of Study Data Study Validity Statistical Distribution and Error Biostatistics Disease Prevention and Public Health Healthcare System Ethics 357 361 64 366 368 370 372 374 376 378 380 382 384 386 388 390 395 397 400 402 404 406 409 a a3 as a8 420 425 427 429 432 434 436 438 442 448xi xi xiv BIOCHEM . DNA Basics DNA Replication, Mutation and Repair RNA Protein Synthesis Tnberitance Genetic Lab Techniques Clyeoljaia 3 Gluconeogenesis Glycogen Energy Metabolism Shunt and Other Sugars . Starvation and Malnutrition Lipids ‘Amino Acids and Nitrogen 45, Amino/Acid Disorders 46. Minerals 17, FarSolible Vitam 18, Water-Soluble Vi PSYCH 1. Psychology’ ‘Child Psych Eating Disorders Alcohol Abuse Substance Abuse Psychosis ‘Antipsychotics Bipolar Disorder ‘Depression 10. Antidepressants 1. Anxiety and Somatoform Disorders 12, Ego Defense Mechanisms and Personality Disorders RENAL 1. Renal Embryologyiand Anatomy, Glomerular Physiology ‘Nephron Physiology. Diuretics Electrolyte Disorders Acid-Base Disorders ‘Nephtitis Nephrosis Other Renal Pathology part Other Renal Pathology part 2 and Antioxidants Beene MAED 457 "460 464 465 46) 47 476 479 482 486 488 491 494 496 498 ‘502 507 509 Sut 513 516 513 522 524 525 528 530 535 537 539, 544 546 548 350 552. 554 556 SLNINOD 4O a78VLTABLE OF CONTENTS x s xv xvi PEDIATRICS 1. Pediatric Review ENDOCRINE Endocrine Overview Pituitary ‘Adrenal Steroid Synthesis Glucocorticoids and Cushing Syndrome Other Adrenal Pathology ‘Thyroid Basies and Hyperthyroidism Hyporhyfoidism and Thyroid Cancer Diabetes DKA and Diabetes Treatment 10. Obesity 11, Calcium Metabolism HEME Clotting Factors 2 icosgtant Bru RBC Basics 4. Exythropoi 5. Nonhemolytic Anemnias Hemolytic Anemias Platelet Function Platelet Disorders Lymphoma 10. Leukemia and Multiple Myeloma ONCOLOGY 1, Cancer Basics 2. Genetics of Cancer ‘Cancer Risk Factors Cancer Sercening and Prevention Cancer Drugs part 1 Cancer Drugs part 2 560 S67 69 573 576 578 580 582 S84 586 590 592 97 599 601 603 1605 607 10 612 6M 616 en 623 626 628 630 632KEY TO ABBREVIATIONS ‘This Study Guide contains page references to several medical educational resources. Below is a key to the abbreviations that accompany the various page number references appearing in this text. FAIS FAIA GG Le, T, Bhushan, V, etal. Fest id fr the USMLE Step 1 2015. New York, NY: McGraw-Flill; 2014, Le, T, Bhushan, V, etal. First Aid for the USMLE Step 1 2014. New York, NY: McGraw-Hill; 2013. Jenkins Ba al: Sop: Up te USMLE Sip 12015, Philadephia, PA: Lippincott Williams & Wilkins; 2014. Hall, JE. Guyton and Hall Texibook of Mes Philadelphia, PA: Saunders Elscvier; 20 Kumar, V, Abbas, AK, et al. Robbinsand Cotran Pathologie Bass of Disease 9th ed. Philadelphia, PA: Saunders Elsevier; 2015. Moore, KL, Dalley, AF, & Agur, AMR. Clinically Oriented Anatomy. 7th ed. Philadelphia, PA: Lippincott Williams 8 Wilkins; 2014, Longo, DL, Fauci, AS, Kasper, DL, Hauser, SL, Jameson, JL, Loscalzo, J, eds. Harrison's Principlesof Internal Medicine. 18th ed. New York, NY: McGraw-Hill 2012. Brunton LL, Chabnes BA, ¢Knollman, BC, os, Conan Gilman’ Toe Pharmacological Basis fs, 12th ed. New York, S¥eMecrw titeon wy Deven SBL0NNOTES Kara ‘Mary Beth Cox, M.D. Aaj Selzer, M.D. Jennifer Shuford, M.D. Katharina Hathaway, M.D. Hampton Richards, M.D. COURSE VIEWING OPTIONS Part 2 consists of 238 videos. Examples of 15, 18, 21, 24, and 30-day plans are provided below for maximum flexibility to meet your personal study needs. 15-day plan 18-day plan 2-day plan | 2a-day plan 30-day plan t No. of Videos/Day |Video Runtime/Day* 6 ‘Approx. 5.5hes 8B Approx. 45 hrs uo Approx. 4hies 10 | Approx. 35 hrs 8 Approx. 25 hes “Does not include study breaks oF time spent annotating and answering questions.| AXTHOUGH YOU HAVE THE FLEXOIITY TO VW THE VIDEOS IM ANY ORDER, WE STRONGLY RECOMMEND | “THAT YOU WATCH THE VIDEOS THE ORDER WHICH YOUR FERSONALIZED DASHBOAND PRESENTS THEM | RECAROAESS OF HOW MANY VIDEOS YOU VEW IN A DAY ‘WIQUO 3SYNOD G3GNIMWODIY ‘Neuro 4 ~ Cranial Nerves part 1 2B Neuro 5 - Cranial Nerves part 2 2C Neuro 6 - Brainstem in Cross Section 2D Neuro 7 - Brainstem Lesions 2E Neuro 8 - Limbic System and Hypothalamus, 2F — Neuro 9 - CSF and ICP 2G Neuro 10 - Vascular Events 2H Neuro 11 -Seizures 21 Neuro 12 - Headache 2 Neuro 13 - Brain Tumors 2K Neuro 14 -Sleep 2L__ Neuro 15 - Anesthetics A (edRECOMMENDED COURSE ORDER [x] Cardiovascular 1 - Embryology Cardiovascular2 - Congenital Heart Defects Cardiovascular3 ~ Cardiac Output Cardiovascular 4 ~ Heart Faitare Cardiovascular ~ ‘Treatment of CHF Cardiovascular 6 - Edema and Shock Cardiovascular 7 = Cardiae Cycle Cardiovascular ~ Diastolic Heart Murmurs. Cardiovascular9 - Systolic Heart Murmurs Cardiovascular 10 - Electrophysiology Cardiovascular 11 - Antiarshythmies Cardiovascular 12 - Electrocardiography oroductive Anatomy “Reptoduction 2- E Reproduction 4- Testicular Pathology. Reproduction 5- Penis and Prost Reproduction 6 - Female Reproductive Cycle Reproduction 7 - Menstruation and Menopause Reproduction 8 - Vulva, Vagina and Cervix Reproduction 9 - Uterine Pathology Reproduction 10 - Ovarian Pathology Reproduction 11 - Ovarian Neoplasms Reproduction 12 ~ Pregnancy part 1 Reproduction 13 - Pregnancy part 2 Reproduction 14 ~ Chromosomal Disorders Reproduction 15 ~ Genetic Disorders: AD and Trinucleotide Repeats Reproduction 16 - Genetic Disorders: AR and X-Linked Reproduction 17 ~ BreastWAQO 3SUNOD GEUNSHODIY 8A 8B Immunology 7 - Macrophages, Granulocytes and Cytokines 8C Immunology 8 ~ Immunosuppressants 8D Immunology 9 - Immunodeficiencies 85 SF 8G ‘Neuro 16 - Movement Neuro 17 - Basal Ganglia ‘Neuro 18 - Spinal Cord and Lesions 8H Neuro 19 - Brachial Plexus and Upper Extremity Nerves part 1 81 Neuro 20 - Brachial Plexus and Upper Extremity Nerves part 2 8} Neuro 21 - Lower Extremity and Skeletal Muscle 8K Neuro 22 - Sensation BL Neuro 23 - Eye Gli2 Cli3- Al ON Gl tx]RECOMMENDED COURSE ORDER Lx 0A, 108 GL 15 - Hepatitis G1 16- Biliary Tract Pulmonary 1 - Anatomy and Physiology Pulmonary 2~ Lung Volumes and Pulmonary Circulation Pulmonary 3 - Oxygen and Hemoglobin Palmonary 4 - Oxygenation Pulmonary 5 - Ventilation and Peefusion Pulmonary 6 Extreme Environments Palmonary 7 - PE, DVT, and Pneumothorax Pulmonary 8- COPD and Asthma Pulmonary 9 - Pulmonary Medications Pulmonary 10 - Restrictive Lung Disease Pulmonary 11 - Lung Cancer Pulmonary 12 - Lung Infections ‘Medicine in Society 4 - Seudy Validity ‘Medicine in Society 5 ~ Statistical Distribution and Error ‘Medicine in Society 6 ~ Biostatistics ‘Medicine in Society 7 ~ Disease Prevention and Public Health ‘Medicine in Society 8 - Healtheare System ‘Medicine in Society 9 - Ethies Micro 11 ~ Penicillins ‘Miceo 12 - Cephalosporins ‘Micro 13 - Other Cell Wall Inhibitors ‘Micro 14 - Protein Synthesis Inhibitors ‘Micco 15 - Other Antibiotics ‘Micro 16 - Micro by Systems par 1 Micro 17 - Micro by Systems part 2Paych 8 - Bipolar Disorder Paych 9 - Depression Paych 10 ~ Antidepressants Paych 11 - Anxiety and Somatoform Disorders Paych 12 - Ego Defense Mechanisms and Personality Disorders Renal 1- Renal Embryology and Anatomy Renal 2- Glomerular Physiology Renal 3 - Nephron Physiology Renal 4~ Diuretics Renal 5 ~ Electrolyte Disorders Renal 6~ Acid-Base Disorders Renal 7 - Nephritis Renal 8 Nephrosis YECYO 3SUNOD GIGNIKWODIYRECOMMENDED COURSE ORDER {xiv A 168 16C 16D 16E, 16F a7N 170 18B 8c 18D 18E, 18F 18G 18H 18h 19 18K 18L, 18M Biochem 17 Fat-Soluble Vitamins and Antioxidants Biochem 18 ~ Water-Soluble Vitamins Endocrine 1 = Endocrine Overview Endocrine 2 ~ Pituitary Endocrine 3 Adrenal Steroid Synthesis Endocrine 4 - Glucocorticoids and Cushing Syndrome Endocrine 5 - Other Adrenal Pathology Endocrine 6 - Thyroid Basics and Hyperthyroidism Endocrine 7 - Hypothyroidism and Thyroid Cancer Endocrine 8 - Diabetes Endocrine 9 - DKA and Diabetes Treatment Endocrine 10 - Obesity Endocrine 11 - Calcium Metabolism deme Te Micro 24- HIV Drugs ‘Micro 25 ~ Mycology part 1 sm 26 - Mycology part 2 ‘Micro 27 - Antifungals ‘Micro 28 - Protozoa Micro 29 - Helminths and Ectoparasites Oncology 1 - Cancer Basics Oncology 2 ~ Genetics of Cancer Oncology 3 ~ Cancer Risk Factors Oncology 4 ~ Cancer Sercening and Prevention Oncology 5 ~ Cancer Drugs part 1 Ontology 6 - Cancer Drugs part 2FOUNDATIONS 1 Embryology JE fel NTater | le) 2 Teratogenesis rae 3. Cell Biology: Organelles 4 Cell Biology: Cytoplasm & Cytoskeleton 5 Cell Biology: Plasma Membrane 6 Cellular Suffering and Death 7 Inflammation 8 Extracellular Environment 9 Cellular AdaptationsNeuron (FA valves (FAL ps esis (FAIA pS > Trephoblen——> spaces *tembyonte membrane 2. What neural crest structures are found in each of the following adult structures? Peripheral nervous system ‘Mouth Thyroid Heart Digestive system Adrenal gland Skin ADOTOAWENIE SNOLLVONNOdEMBRYOLOGY End of Session Quiz 3, What's the relationship between the notochord, the neural plate the neural tube, and the neural crest cells? 4. What is the embryologic origin of each the following adult structures? ‘Asmerir ploukary * Cornea, = Lens + Retina * Olfsctory epithelium = Mammary glands + Salivary glands + Swear glands 5. At what developmental age does each of the following events typically take place? + chamber heart begins to develop + Genitalia begin to take on visible sex-specific characteristics ‘+ Feral movement begins ‘+ Limb buds begin to formHlomeabeox (10%) g Genes of embyogeness (FA 3 Question Warm-Up 1. What embryonic structure (derived from the hypoblast) serves asa secondary ‘energy source? 2. What embryonie structure cerves asa reservoir of nonepecialized (undifferentiated) stem eels? 3, What are the three germ ayers that derive from the epiblast? I. Potentially teratogenic drugs: ACE inhibitors — ‘malformations Aminoglycosides Fluoroquinolones ‘Tetracyclines = ‘Cyclophosphamide ~ ear/facial anomalies, limb hypoplasia, absence of digits ‘Methotrexate ~ neural tube defects, abortion Carbamazepine ~ Valpeoic acid — - Phenytoin — fetal hydantoin syndrome Lichium = Statins — CNS and limb abnormalities ‘Warfarin ~facial/imb/CNS anomalies, spontaneous abortion Isotretinoin ~ Dicthyistlbestrol (DES) ~clear cell vaginal adenocarcinoma ‘Thalidomide - phocometia siIssNaDOLV¥aL, SNOLLWAONNOJ5, Homeobox (HOX) Genes © Blueprint for skeletal morphology ‘Code for transcription regulators © Mutation in Homeobox HOXD-13 — synpolydactyy (extra fused digit berwoen Sed and 4th finger) © Retinoic acid alters HOX gene expression End of Session Quiz 6. Which antibiotics are potentially teratogenic? 7. Which drugs have such high potential for teratogenicity that they are classified ‘5 pregnancy category X? 8 Examination of a fetus from a spontaneous abortion at 14 weeks gestation. reveals a vestigial par of legs that arse from the torso, just below the arms. A. ‘mutation in what family of genes is the mostlieely cause of this malformation? Rapip-Fire Facts ‘Most common cause of neural tube defers | ‘Most common preventable cause of | congenital malformations in the US.SaTIBNVOYO ADOTOIS THD 3 Question Warm-Up 1. Whats the embryologic origin ofthe tissue just proximal to the peetinae line? ‘What is the origin ofthe tissue just distal to the pectinate line? (FAt4 p553) (FAIS 559) (SUIS pli6) 2. What effect might each of the following teratogens have on a developing fetus? (ALA 5) (AIS p50) SUIS p37) + ACE inhibitors + Aminoglycosides © Diethylstilbestrol + Tetracyclines + Valproe ac 3. Which vitamin should not be supplemented in large amounts during pregnancy? (Al4 p55) (AIS p50) GUIS 312) 4, Nuclear localization signals © Amino acids sequences: 4-8 amino acids ich in proline, arginine, and lysine © Essential component of proteins bound for or residing in the nucleus (eg. histones) © Nuclear pores recognize these signals and transport proteins into the nucleus via ATPase * A muration ima single amino acid may prevene nuclear transportCELL BIOLOGY: ORGANELLES Cell cycle basics + Cyctins + cyclin-dependent kinases (CDK) phosphorylate target proteins to drive the eal gee © All eyelins are degraded by ——— ‘When ther cell-cycle specific jo is complete © p21, p27, and p57 bind to and inactivate cyelin-CDK complexes (p53 controls the setivation of 2) Gi-s © Cyclin D binds/activates CDK4 —> phosphorylation of Rb protein —> Rb protein is released from transcription factor E2F —+ with B2F unbound, the cel is ce to transribe/ synthesize components needed for progression through the S phase (cyclin E, DNA polymerase, thymidine kinase, dihydrofolate reductase) © Cyclin E binds/activates CDK2 —> the cells allowed to progress into S phase GM © Cyclin A~ CDK2 complex —+ mitotic prophase © Cyclin B- CDK1 complex is activated by cde25 —> breakdown of. and initiation of mitosis -cell disease + Deficiency in mannose phosphorylation No. secretion out of cel instead oF int lysosomes + Death by age 8 years + Comeal clouding, coarse faces, hepatosplenomegaly skeletal abnormalities, res joint movement + May have intellectual disability to target lysosomal proteins > cd Chaperones and heat shock proteins = Chaperones asist in the proper folding and transport of polypeptides in the ER, Gol, etc. Some chaperones ate synthesized constantly and are involved in normal intracellular protein trafficking. © Other chaperones are induced by stressors such as (heat shock proteins hsp70, and hsp), These chaperones “rescue” shock-stressed proteins from misfolding, = Ifthe folding process snot success the chaperones facitate degradation of the darraged protein. This degradative process often involves ubiquitin aso a heat shock protein), which added to the abnormal proten and marks it for degradation. 8. Peroxisomes dation of very long chain itty acids and branched chain fey acids fo portant phospholipids found "© Oridases and catalase for metabolizing ethanol (and other toxic substances)End of Session Quiz 9, What must be present on a protein inorder for that protein to gain entry into the nucleus? 10, Which cyelin-CDK complexes assist in the progression from G, phase to S phase? 11, Which cyclin-CDK complexes assist in the progression from G, phase to M phase? 412. What molecule does the Golgi spparstus add to proteins in order to direct the proteins o the lysosomes? 13. What are the different methods that a cell uses to break down protins? SATENVO¥O 2901019 THD SNOILWGNNO4‘CELL BIOLOGY: CYTOPLASM & CYTOSKELETON ‘Gytoskleton (FAM p78) (FAL AMeofiemens (FAl1 p79) (FMS pr Moot 3 Question Warm-Up 1, Which amino acids are found in nuclear localization signals? (2. What is the most common cause of intellectual disability in infants? (FAN p55) AIS p56) 3. How do Rb protein and p53 regulate the cell cycle? F414 p74) (415 p72) 4. Intermediate filament structures Intermediate Structural Stain used to Filaments ‘Component of: identify... Cytokeratin Epithelial cells (ke jn desmosomes and hemidesmosomes) Desmin ‘Muscle cells (smooth, skeletal, heart) Glial fibrillary acid Astrocytes, Schwann cells, proteins (GFAP) “other neuroglia | Neurofilaments ‘Axons within neurons (L, M, H molecular wt) Nuclear lamins(A, B,C) | Nuclear envelope and DNA within Vimentin Connective tissue + Support cellular (Fibroblasts, leukocytes, membranes endothelium) + Keep certain organelles fixed in eytopasmNOL31S¥SOAAD 8 WSVOLAD “ADOTOIE 1139. cudCELL BIOLOGY: PLASMA MEMBRANE 3 Question Warm-Up 1. Daring what weeks of fetal development does organogenesis take place? 4 152) (AIS )S58) 2. What molecules provide the structural framework: for DNA and the nuclear envelope? 3. What is deficient in I-cell disease? (414 p77) (FAIS 73) ‘Tyrosine kinase receptors © Transmembrane receptors that Bind an extracellularligand then intacelhulaly eranefora phosphate group (phosphorylate) from ATP to selected tyrosine side chains on specific cellular proteins induding self autophosphorylaion). The frst stp inthe signaling cascade thats initiated by tyrosine kinase receptcrsis autophosphoryltion. ¢ PDGF and other growth factor receptors: single-pass transmembrane protein © Insulin and IGF-1 receptors: 2.1 subunits (bound by csulide bonds) ~ bind extraelblarFgend 2B subunits— tyrosine nase actwity5. Receptor-mediated endocytosis Clathrin Dy wma A) Normal LDL receptor LDL binding site LoL clathrin coated pit, CYTOSOL 8B) Mutant LDL receptor LDL receptor protein with ‘abnormal coated pit binding site CYTOSOL, SNVUEW3N VHISYTd ADOTO!B 13D, Asmutant LDL receptor lacks the coated-pit binding site but retains a funetioning LDL- binding site. As a result, cells with ‘mutant receptors are able to bind LDL normally but are tunable to ingest it. Individuals with this mutation have @ higher risk of dying prematurely from a ‘myocardial infarction. SNOILVONNO4A a 6, List the steps outlining the derivatives of arachidonic acid. fe tUow 5 ANVUSHIH VHSV'd ADOTOIS 1139. (ayEnd of Session Quiz 7. Which arachidonic acid product causes each of the following effects? + Increased bronchial tone + Decreased bronchial tone + Tcreasd platelet aggregation * Decreased platelet aggregation + Increased uterine rove * Decreased uterine rone * Increased vascular tone + Decreased vascular tone Zz 8 = (e) vA 6 ANVEEHZN VASYId ADOION 12D 8 What are the two most abundant substances in plasma membranes? 9. What drugs act on the arachidonic acid product pathway? What enzymes do they affect?‘CELLULAR SUFFERING AND DEATH R Chapter | 15 (FAL4 220) (FAIS p22) Exenss peatray ocr (A422!) FANS 223) Reversible vz. reversible imry (FAV p22) (FAIS p224) ‘Mechanisms of cell mary Defects n membrane permet ity Real vs plenfacts (FAIS p22) (FAIS p24) 3 Question Warm-Up 1. What are the stages that an embryo goes through between conception and the development of an inner cell mass? ‘2. What drugs interfere with mieronihule fanctioniing® (FAl4 p78) (FAIS p74) 3. Which ceil types are constantly regenerating themselves due to an absence of the G, phase and a short G, phase? (FAl4 p76) (FAIS p72) 4, Intrinsic pathway of apoptosis ‘© Bul-2is the major anti-apoptotic regulator of mitochondrial permeability © DNA damage or apoptotic signal activates Bax (pro-apoptotic) ‘© Bax ereates channels in mitochondrial membrane © Cytochrome C moves from the mitochondria into the eytosol and aetirates caspases + Caspases are primary initiator of apoprosis 5S. Extrinsic pathways of apoptosis © Death receptor ~ TNF receptor and Fas receptor are located on cell membrane ~ TNF ctand Fas ligand actwate the receptors ~ Activated receptors wil lead to activation of caspases © Cytotoxic T lymphocyte (CTL) = Cytotoxic T cells recognize foreign or infected cell CTLs release perforin and granzyrne B Perforin punches hole in membrane = Granayme B enters and activates caspasesMechanisms of cel injury = ATP depletion: due to decreased oxygen/nutrients and toxin (cyan) Mitochondrial damage: impairs ATP production and can induce apoptosis + Influx of calcium: increases mitochondrial permeability and can activate phospholipases, proteases, endonucleases and ATPases © Accumulation of oxygen-derived fe radicals: cll damage through membrane lipid peroxidation, prin modification and DNA breakage. Multiple causes like radiation ‘exposure, metabolism of drugs, redox reaction, nitric oxide, transition metals, leukocyte ‘oxidative bust, iron overdose and reperfusion injury. 7. What cellular by-products might you detect in the serum when the following cell types are injured? Cardiac myocytes Hepatocytes Skeletal myocytes | Salivary gland cells Pancreatic exoerinc cells | RBCs End of Session Quiz 8. What histologic fearures are seen in apoptotic liver cells? 9, What substances do cytotoxic T cells and NK cells use to induce apoptosis in the cells infected with a virus? 30, What highly damaging events can cause ireversble cell injury? 1, What cellular enzymes are responsible for handling oxygen free radicals? Hiv ONY ONIWWINS YYTATAD SNOILVONNO4INFLAMMATION 3 Question Warm-Up 1. What are the characteristic fearutes of «cel undergoing apoprosis? (FAIA p220) AIS p222) 2. How do Bax and Bel-2 affect apoptosis? 3. What neural crest derivatives are found in each of the following adult structures? (FAl4 553) (FAIS p552) Peripheral nervous system Ear Eye ‘Adrenal gland Mouth Heart Digestive system ‘Thyroid Skin 4, Acute inflammation © Release of inflammatory mediators +» Vasodilation and increased vascular permeability —> fuid exudation Serotonin Bradykinin + Fibrosis Fiorotass lay down (equres —) + Tissue remodeling by metalloproteinases (which cortain, )6 Elevated ESR © Polymyalgia rheuratica © Temporal art © Discase activity in RA and SLE, © Infection, inflammation (e.g, osteomyelitis) © Malignancy C-reactive protein © Acute-phase eactant synthesized by the liver © Partof the innate immune response: opsonizes bacteria and activates complement © Canbe secreted from cells within atherosclerotic plaques to activate loa! endothelial calls to induce a prothrombotic state and increase the adhesiveness ofthe endothelium to Teukocytes © Elevations area strong predictor of MI, stroke, PAD, and sudden cardiac death © CRP can be lowered by smoking cessation, exercise, weightloss, and statins End of Session Quiz 7. Describe the process of leukocyte extravasation. 8, What cytokine is particuladly important in the formation of granulomas? 9. Whar cell type plays azole in inflammation by generating Aibrinogen and C-reactive protein? 410. What cell is most responsible for the acute phase of inflammation? NOWWWHYTANI on € Zz Ss Ea fe) Zz aS EXTRAC! 3 Question Warm-Up 2. What protein is involved in transporting endocytosed vesicles from the plasina ‘membrane to the endosome? (alt p77) (AIS p72) 2 Which metals are known to facilitate the generation of oxygen free radicals? 3. Which tumor suppressor proteins prevent the progression ofthe cell nto S phase? (PAIS prt) FAIS p72) |. Cutaneous wound healing 0-3 hours Hlemorshage and clotting 12-24 hours Acute inflammation (PMNs) 153 days. = Macrophage infiltration + Granulstion tissue (fibroblasts and vascular endothelial cells) «+ Epitheliaization ‘Wecks-months | Collagen production (type Tl then type)End of Session Quiz 5, What findiags are associated with Ehiler-Danlos syndrome? mn fe) eS Zz S zi fe) Zz Pa ANAWNOWANS HVT 6. What are the different types of collagen, and where can they be found? 7. Which amino acide are found in large encentrations in collagen? In elastin? 8, Whats the role of vitamin C in collagen production? Rapio-Fire FACTS. Hyperflexible joints, arachnodactyly, aortic dissection, lens dislocation Hereditary nephritis, cataracts, sensorineural hearing lostCELLULAR ADAPTATIONS “CELUULARADAPTATIONS = R: Choptor | Hiner he 3 Question Warm-Up 1. What developmental structure matches each ofthe following descriptions? The fetal placental strucrure that seretes hCG. * Maternal component ofthe placenta 2. How does having a high cholesterol content in the plasma membrane affect the function of the plasma membrane? 3. A patient presents with an agangtionic colon and other neural crest derivative deficiencies. What other findings would you expect to see? FAI4 p53) (FAIS 2559)End of Session Quiz: 4. Does the compensatnry growth of muscle fibers occur primarily as a result of hyperplasia or hypertrophy? 5. Does myometrial growth in pregnancy occur primarily as a result of hyperplasia or hypertrophy? 6. What can happento the cells ofthe lower esophagus in response to chronic acid wellux? 7. Whats actually occurring atthe cellular level during atrophy? 8, Whats a lipofuscin granule? SNOLWLAVOY WWIOT SNOLWONNO4NEUROLOGY Brain Embryology Nervous System Basics Cortex and Brain Lesions Cranial Nerves part 1 Cranial Nerves part 2 Brainstem in Cross Section Brainstem Lesions Limbic System and Hypothalamus CSF and ICP 10 Vascular Events wean aunr wre 11 Seizures 12 Headache 13 Brain Tumors 14 Sleep 15 Anesthetics 16 Movement 17 Basal Ganglia 18 Spinal Cord and Lesions 19 Brachial Plexus and UE Nerves part 1 20 Brachial Plexus and UE Nerves part 2 21 Lower Extremity and Skeletal Muscle 22 Sensation 23 Eye 24 Ear 25 Delirium and DementiaBRAIN EMBRYOLOGY {26} R: Cropter 28, Developing bran (FAIL p44) (FAIS p48) (SUIS p23) Newz tbe defects (AM fv445) (FAIS p40) (SUIS p21) (R p1256) Ferchrom anomalies FAV p445) (FAIS p14) (SUIS p24) ‘Cri malrmatins (FAL pit) (FAIS p49) (SUIS p24, Spergonyci (FAL pte) (AIS 150) (SUIS p39) (R p!258) (4 p3373) Bana Water syne (FAI4 prF85) (FAIS p49) (SUIS 924) rant apparatus (FA 9898) (FAIS p56) Branch eft dericnmes (FAI p55) (FAIS ps4) Branch pouch deities (FAI p60) (FAIS 1568) Branch ech derivates (FAI p59) (FAIS p505) (SUIS p226 227) _ 3 Question Warm-Uj : A. What adult cel arise from neural crest cells? (F 1 the Golgi apparatus? FA/47) (FlEnd of Session Quiz 4, What abnormalities are often found with a Chia malformation® 5, What are the classe presenting symptoms of syringomyelia? 6. What amniotic Hud lab abnormality might point you to a diagnosis of ancncephaly? 7. From whic’ branchial pouch are each ofthe following structures desived™ > Middle ear and eustachian tubes . ger : 1 pay oe ple won + Thymus ASO TOYS NIVES fe) [aE in|EM BASICS. NERVOUS SY (su 3 Question Warm-Up 1. What organelle becomes hypertrophied in hepatocytes with chronic phenobarbital use? (f p!2) 2. Wiatenzyme mitigates the aging effects of cellular division by maintaining chromosomal length? (8 pé7) 3. Whatis currently known as the most effective way of prolonging life span? WR p67) blocking these pathways? Major pathway 7) (FAIS ptS1 152) 5 153) (GG p76) (Phys p50) Result of blocking ‘What are the four major dopaminergic pathways, and what is the result of Mesocortical pathway ‘Mesolimbic pathway | Nigrostriatal pathway ‘Tuberoinfundibular pathway5. What disorder is thought to arise from reduced norepinephrine activity? Increased norepinephrine activity? 6. What disease is associated with the degeneration of the basal nucleus of Meynert and less CNS acetylcholine? End of Session Quiz 7. Which nervous system cell matches each of the following descriptions? + Look like fried exgs under histologic staining + Form multinucleated giant cells inthe CNS when infected with HIV. + Myslinares multiple CNS axons + Myelinates one FNS axon + Damaged in Guillain-Barré syndrome + Damaged in mukiple sclerosis + Macrophages of the CNS * Calls ofthe blood-brain barrier 8 Inwhich newological diseases is acetylcholine altered? 9. What's the main inhibitory neurotransmitter of the CNS? In which diseases are levels alrered? 10. What are the components of the blood-brain barrier ESAS SNOAYEN, OS Ya Wi fe) [aF IN|CORTEX AND BRAIN LESIONS Phys: Chapter 87 COR Chapter? Covel conto (F414 p45) (FAIS 460) (SUIS p31) muncuts (AI p55) ALS p63) Blood supply to the ban (PA pASB 459) (FAIS 162) (SUIS p28) ice of Wis CAL p58) (FAIS p482) (SUIS p26) ‘Arteria load supply othe cortex (FAIA 138) (FATS p62) (SUIS p28) ‘Apasios FAIA p57) (AIS pt60) ‘Bean Fess (AVA 158) (FAIS prt6l) (SUIS p31)NEURO. ‘CORTEX AND BRAIN LESIONS 4, Label the following diagram of the Circle ofSIONS CORTEX AND BRAIN Li 5. Dysprosody © Expresive dysprosody Inability to express emotion or election in speech 'Non-dominant cortical son corresponding o Brocas area © Receptive dysprosody = Inability to cormprehend emotion oriectionin speech "Non-dominant cortical lesion corresponding to Wernick’ area End of Session Quiz ‘6. A lesion to which area of the brain is responsible for each of the following clinical scenarios? 7. What typically isthe cause ofa lesion 16 the mamnmillary bodies? 8. What artery is damaged in each ofthe following presentations? + Brocas or Wernicke's aphasia + Unilateral lower extremity sensory and/or motor loss + Unilateral sensory and/or motor loss in the fice and arma3 Question Warm-Up 1. Whut regulates the progression of G, phase ofthe cell eyelet § phase? (FAIS p76) (FAIS p72) 2. What arachidonic acid product has actions that oppose that of prostacyclin? ANd pA) FAIS pg) 3, In what disorder is there an abnormal breakdown of elastin? (FA 4p) (FAIS p77). (Gus n296) Liiva S3MN WINES, fe}-[aF IN)CRANIAL NERVES PART I 4, Label the cranial nerves as they come off the brainstem:End of Session Quiz 5. Which cranial nerve nuclei are located in each of the following locations? © Medulla = Pons ° Midbrain 6. ‘Where isthe pathology located in each of the following scenarios? 7. When lights shone in a patients right eye, his right pupil fails to constrict but his left pupil constricts normally. When light is shone in the left eye, the left ‘pupil constricts but the right pupil does not. Where is the likely pathology? 1 Lud S3AW3N INVES, ONIN3 Question Warm-Up 2. What organelle and cytochrome are particuladly important in intrinsic apoptosis? (Als p220 (AIS $229) 2. Label the following diagram of the Circle of Willis: Fi4 p459) (FAIS p44p GUS pity 3. What prenatal testing is abnormal in a fecus with a neural tube defect? (FAIA p45) AIS 449)5. 7 ‘What conditions can result in facial nerve palsy? (Hint: Lovely Bella Had An STD) Lyme discase AIDS Sarcoidosis Tumors © Diabetes How do the symptoms of a facial nerve (or facial nerve nucleus) lesion from the symptoms of a facial motor cortex lesion? * Facial nerve/nucleus lesion ~ Paralysis of ipsilatcral side of face © Facial motor cortex lesion — Paralysis of contralateral side of face Why does a motor cortex stroke not affect the upper face? ‘© The facial motor nucleus receives motor fibers forthe lower face only from the contralateral ‘motor cortex, but it receives motor fibers forthe upper face from both left and right motor © Inaleft motor cortex stoke, ony the right lower face will be paralyzed because the right “upper fice stil receives innervation from the right motor cortex. If the right vagus nerve or nucleus is damaged, to which side will the uvula deviate? A patient's uvula deviates to the right when she says, “Ah.” What neurological structures might be damaged? Rightward deviation of uvula means that the muscles ofthe right palate arc raising the palate and the muscles of the let palate are not. This could be caused by damage to: eo Le © Left recsives input from: = Right cortcobutbar tract = Right motor cortex CAuva S3AYEN TWINYED. fo)-TaFINAL NERVES PART 2 9. Ifthe right hypoglossal nerve or nucleus is damaged, to which side will the tongue deviate when sticking out? End of Session Quiz. 10. What two nerves are tested with the gag reflex? 11. A19-year-old man presents with a furuncle on his philtrum, and the cavernous sinus becomes infected. What neurological deficits might you seein this patient? 12. How can a stroke of the ficial motor cortex he distinguished from Bell’ palsy?BRAINSTEM IN/GROSS SECTION | 3 Question Warm-Up 1. What effect might aminoglycosides have on a developing fetus? (Fas p54) (AIS p9eu) UIs 97) 2. What molecule rarges proreins inthe endoplasmic reticulum for lysosomes? EBC TIS 3, What birth defect can result from the following teratogenic agents? (A p554) (PAIS pS80) GUIS 1397) + ACE inhibitors + Folate anagonists ‘+ Tetracycline + Lid 5 Zz g z g fe)[aE IN|BRAINSTEM IN CROSS SECTION 4, Rostral midbrain ‘Scalomotor (CI nucleus Cerebral aqueduct 5. Pons | jue Abducens (CN VI) nucleus: | ‘Vestibular (CN Vit) nucleus oe Oat ee | Zs ee a ZR ~~ iS er | 5 cna “sre 1 6. Medulla Hypoglossal (XIN nucleus Dorsal motor nucleus /Muclous of solitary tract Vestibutar (CN VID nucet Inferior corebellar peduncle Spinal trigeminal tract ‘and nucleus ad ‘Nucleus ambiguus y bessrsomtnan Sy) toferor tivary nucleus oe.End of Session Quiz 7. What acterysupplics the medullary pyramids and the medial emriseus in the medulla? 8. What artery supplies the inferior cerebellar peduncle, nucleus ambiguus and lateral spincthalamic tract in the medulla? 9. Where does each ofthe following spinal tracts decussate? © Corticospinal sract + Dorsal colurnn-medial lemniscal pathway + Lateral spinothalamictract 10. What is the triad of Homer syndrome? NOILD3S SSOUD NI WBLSNIVY! OWNIANBRAINSTEM LESIONS. [2] He-chaprer 370 The rule of furs Bransiem sues (FAIS p60) (FAIS 464) (Hp 3268) tac pcm FAIA 102) AS 8H) US 8) (2 Locked in sydrome (FAIS p56) (H p22 Weber syndrome (H p3287)4, Whats the hallmark sign of a general brainctom lesion? Alternating syndromes: long tract symptoms on one side (.g., hemiparalysis) and cranial nerve symptoms on the other 5. The Rule of Fours 1. There are 4 medial/midline structures, beginning with M + Motor pathway (corticospinal tract) Deficits + Medial lemniscus Deficit: + Medial longitudinal fasccules Deficit: = Motor cranial nerve nucle Deficit 2, There are 4 “side” (lateral) structures, beginning with § © Spinocerebella tract, Deficit: = Spinothalamic tract Deficit: © Sensory nucleus of CNV Deficit + Sympathetic pathway Deficit: 3. cranial nerves o ate in the pons, 4 ori inate above the pons (2 in the midbrain). oiginat in the midbrain originate in the pos originate in the media 4, "The 4 motor cranial nerve nuclei in the midline are those that divide equally into 12 (except for CN T and CN TI) CN + CN + CNW +N te below the pons, and 4 oF SNOIS31 W31SNIVEEBRAINSTEM LESIONS ‘What are the symptoms of lateral medullary syndrome (Wallenberg. syndrome)? Loss of pain and temperature over contralateral body (spinothalamic tract damage) © Loss of pain and temperature over ipsilateral fare (spinal trigeminal nucleus damage) © Hoarseness, difficulty swallowing, loss of gag re‘icx (nucleus ambiguus: CN IX and X damage) © Ipsilateral Horner syndrome (descending sympathctic tract) = Vertigo, nystagmus, nausca/vomiting (vestibukar nuclei damage) + Ipsilateral cerebellar deficits (ic, ataxia, past pointing) (inferior cerebellar peduncle damage) ‘Which vessel is most likely occluded in a stroke of the lateral medulla? ‘What are the symptoms of medial medullary syndrome? © Contralateral spastic hemiparesis (pyramid/corticospinal tract damage) + Contralateral tactile and kinesthetic defects (medial lemniscus damage) + Tongue deviates toward side of the lesion (hypoglossal nucleus/nerve damage) ‘+ Note that pain and temperature sensation are generally preserved What are the symptoms of lateral inferior pontine syndrome? © Ipsilateral facial nerve paralysis (facil nucleus and nerve fbr damage) ‘Ipsilateral limb and gait ataxia damage to middle cercbellae peduncle) + Ipsilateral loss of pain and temperature sensation from the face (spinal trigemi 0 Eine fiecdimp) Cons genial mcs © Contralateral loss of pain and temperature sensation (damage to spinothalamic tract) © Ipsilateral Horner syndrome (amage to descending sympathetic tact) © No contralateral body paralysis or loss of ight touch/vibratory/proprioceptive sensation What are the symptoms of medial pontine syndrome! Contralateral spastic hemiparesis (ortcospinal tract damags) * Conta ln of igh touche proprioceptive sensation (med nists Ipilterlimermclea ophthalmoplegia Jamag o medal longi fuieuls) Gaze away from side oF lesion (damage to pontine gze center: PPRF) Ipsilateral paralysis of atral rectus muscle (damage to abducens nucleus) ‘Nowe that pain and temperature sensation are preserved12. What causes and what are the symptoms of Weber syndrome? Anterior midbrain infarction resulting from occlusion of the paramedian branches of the posterior cerebral artery: © Cerebral peduncle lesion = Dysphagia. dysphonia, dysarthria (cortcobulbar tract damage) Contralateral spastic hemiparess (corticobuibar tract damage) * Oculomoror nerve (CNM) palsy ~ ipsilateral ptoss, pupillary dilation, and lateral strabismus (eye looks down and out) SNOISHT W3LSNIVEE (o)-[a EINSIONS BRAINSTEM LE End of Session Quiz 13. A patient comes to the ER with double visio and left-sided weakness. On physical examination, she cannot abduct he right eye. In addition to motor ‘weakness ofthe left arm and leg she also as loss of fine touch, proprioception and vibration sense in the left arm and leg, Where isthe lesion and what vesel is most likely involved? 14, A patient presents with vertigo, nystagmus and slurred speech. Physical amination reveals right-sided ptosis and miosis, decreased gag reflex on the right, deviation of the uvula tothe lef, diminished pain/temperature sensation on the right side of his face, and diminished pain/temperature sensation on the left side of his body. Where i the lesion and what vessel is most likely involved? 15. A patient presents with double vision, slurred speech, hoarse voice and acute right-sided weakness. Physical examination shows weakness of the right arm ‘and leg, and the left eye is depressed and abducted. Where isthe lesion and. what vessel is most hikely involved?___UMBIC SYSTEMAND Pips Chapt 115 p38) 3 Question Warm-Up 1. Which cell types are derived from the neural crest? (FA/4 9553) (FAIS 1552) 2. Which amino acids are modified by the Golgi a FAH p77) (FAS 673) 3, Whatare the components of the blood brain barier® FAM p44” (FS 453 JASAS DAWN SAWYTVHLOdAH ONY Wi (o)-[aEINLIMBIC SYSTEM AND HYPOTHALAMUS 4, Hypothalamic nuclei NUCLEUS | FUNCTIONS [NOTES ANTERIOR HYPOTHALAMUS Anterior “Thermoregulation (cooling) | Damage causes Suprachiasmatic | Circadian rhythms “Master clock 1 Preopticarea | Secretes : Supraoptic | Seeretes Damage causes Secretes Paraventricular | Secretes GRA Sccretes TRH TUBERAL HYPOTHALAMUS Secretes GHRH eu Secretes dopamine Arcane —____ GnRH secretion Regulate appetite Regulates hunger Damage leads to aan Inhibited by Se Regulates satiety Damage leads Stimolatedby——__ | and savage behavior — ulation leads to obesiy Regulates hunger and savage behavior POSTERIOR HYPOTHALAMUS Posterior ‘Thermoregulation (warming) | Damage causes Mam Memory Damage causesEnd of Session Quiz 5. Which typothalamic muck fiteach ofthe following desciptions? > Savage behavior and obesity result from stimulation + Savage behavior and obesiy result from destruction + The “master clock” for setting circadian rhythms + Relesses hormones affecting the anecor pituitary + Responsible for sweating and cutaneous vasodilation in hot temperatures + Responsible for shivering and decreased cutancoas blood flow in the cold. + Produces antidiuretic hormone (ADH) to regulate water balance + Regulates the release of gonadotropic hormones (i. LH and FSH) + Destruction results in inability to say warm, + Receives input from the retina + Stimulation leads to cating and destruction leads to anorexia + Destruction results in diabetes insipidus 6. A patient is evaluated for behavior and personality changes. She used to be argumentative and aggressive, but has become fairly quiet and docile. She has also become socially disinhibited, and has been making inappropriate sexual advances toward fiends, relatives, and strangers. During the interview, you note the patient's tendency to chew on pens, her fingers, and her necklace. Damage to what neurological structure might account for these behaviors? SNWVIVHLOdAH ONV W3JSAS DIBWIT io} [a= IN}SF AND ICP 3 Question Warm-Up 1 Whiatis the main inhibitcry neurotransmitter of the CNS? In which discascs are levels alered® (14 pt) (a1s p53) 2, What conditions are associated with an clevated erythrocyte sedimentation rate (ESRY (4149379) (a p230) 3, Which cytokine is particularly important in maintaining granulomas? (AY p28 (AIS p20) ‘What are the characteristic features of idiopathic intracranial hypertension {AKA pseudotumor cerebri? Headaches —chily, pulseile, worse at night or carly AM, possible netroocular pain ‘worsened by eye movernent, possible N/V “Most worrisome sequalais vision loss CT scan: no ventricular dilstion, no rumor, no mass Intracranial pressure (ICP) — patients, > 250 mm HO in otese patients) 200mm H,Oin non-obese5. How is idiopathic intracranial hypertension managed? * Discontinue any inciting agents (eg, excess vitamin A, isotretinoin, tetracyclines, danazol) ° in obese patients . = firs-line pharmacotherapy Invasive tweatment options Serial Lumbar punctures ‘Optic nerve sheath decompression Lumboperitoneal shunting (CSF shunt) End of Session Quiz 6. Where is CSF generated? Where is CSF reabsorbed? 7. Whatis the difference between communicating and noncommunicating hydrocephalus? 8, What clinical features characterize normal pressure hydrocephalus? LNY 483) 3 re}: (aE IN|VASCULAR EVENTS. Re Chapter 28 ‘Aneuryams (FA pt (FAIS pts) (SUIS p79) Suborachnou esroreie (FAI 2) Epidral hematoma (FAM 462) (FAIS pe Seindra hematoma (FAY p62) {FAIS p66) (SUIS p2 nchymal hemorrhage (FAIS p62) PAIS p66) (Hp Ischeme stroke [FAI pt63) (AIS p17) (SUES p29) Wiarterstee ces (FAI p80) (FA frid2) SUIS p29 30) 30) (Hp3379) 3 Question Warm-Up 1. What the function ofthe lysosome? FAs (77) AIS P73} 2, A woman involved in an accident cannot turn her head to the left and has a ‘ight shoulder droop. What structure is damaged? (F'4 p474) (AS p47) (IS pl) 3. _Inwhich section of the brainstem is cach of the cranial nerve nuclei located? (PAYA pi72) (FAIS p74) 4. Intraventricular hemorrhage in the newborn © Hemorrhage into the ventricular system © Most common in premature/very low birth weight infants (« 32 wks, < 1500g) within the first 72 hours ofife © Originates from the germinal matrixin the subependymal, subventsicular zone that gives rise to neurons and glia during development © Allinfants born at younger than 30-32 ws gestational age should receive a sereening US todeteetEnd of Session Quiz ‘5, Whats the most common site of a berry aneurysm? What diseases are often associated with berry aneurysms? 6, An 85-year-old man with Alaheimer disease falls at home and presents three days later with severe hesduche and voriting. What isthe mos likely diagnosis and which strucrures were damaged? 7. Abcalthy 52 year old man presents to the ER with stoke symptoms that began two hours ago. What treatment should be considered immediately? What study must be ordered irameciately? Rapib-Fire FACTS [_ “Worst headache of my life” | Lucid interval following head trauma Bloody CSF on LP ‘Most common © subdural hematoma “Most common cause of ej jural hematoma SLNAAB BYTNDSVA lo) [aE|y|SEIZURES 4] "SEIZURES 5 : 4. Hi Chepter 389 Phys Chopra 59 ‘GG Chapter 21 Sozures (FAM p85) (FAIS p89) (SUIS pA3 Tube‘ous sderais (FAVA p187) (FANS p99) (Rp Sturge Webs syrtionne (FAL 187) (FAIS p49) fs noon (FAIA p92) (FAIS p96) (SUIS p44) (H p3261 3267) (GG p90. 606) (Phys p72) (6 p3251) ) 3 Question Warm-Up 1. What information is communicated at the nucleus solitarius? Nucleus ambiguus? Dorsal motor nucleus? (F4 p47) (AIS p76) 2. Which cranial nerve is responsible for each of the following actions? {FA14 9472) (FAIS p75) (SUIS 40°41) + Eyelid opening + Taste from anterior 23 of ngue + Head turning + Tongue movement Muscles of mastication + Balance ‘+ Monitored carotid body and sinus chemo and baroreceptors 3. What cranial nerve innervates the tongue in each of the following ways? (AIA p72 (FAIS p75) + Tasrein the aneroe 2/3 + Taste inthe posterior 13 (main innervation) + Moror + Sensation in the anterior 2/3 “+ Sensation in the posterior 1/3 Tuberous sclerosis © Autosomal dominant; 1/5,000 - 1/10,000 live Births © Incomplete penetrance and variable expressivity Most common mutations are in ehe TSC1 or TSC2 genes TSC: gene > hamartin protein = TSC2.gene ~ tuberin protein © Classic triad: setaures, mental retardation, angiofibromas| © Additional findings: hypometanotie macules (ash-leaf spots), retinal hamartomas, cortical tubers (glioncuronal hamartomas) © ‘Tumor associations: renal angiomyotipema, cardiac rhabdomyora, astrocytoma (ubependymal giant cll astrocytoma)2 Be ‘Trigeminal neuralgia (tic douloureux) «© “Lighening-like” pain, “clectreshocke," along a division of the trigeminal (usually maxillary) triggered by light touch (wind, bed sheets) © Treatment: carbamazepine or other anticonvulsant (phenytoin, gabapentin, opiramate) Drug of choice for absence seizures: Used to treat status epilepticus: Used to treat eclamp: ‘Additional SE of phenytoin: |. Which anti-epileptics are teratogens? What drugs cause Stevens-Johnson syndrome? What drugs are known to cause agranulocytosis? Hepatotoxic anti-epileptics: S3unZIBS fey [aE iN)14, What drugs induce the P450 system? SEIZURES End of Session Quiz 15. In regard to seizures, what do the tcums partial, simple, couples, and ‘generalized mean? 16. What are the most common causes of seizures in children? 17. A10-year-old child “spaces out” in class (stops talking midsentence and then Continues as ifnothing had happened). During the spells, there is slight quivering oflips, What is the diagnosis? 18, Whar drugs are known for causing Stevens-Johnson syndrome? 19, What are the tonic side effects of phenytoin Rapip-HRe FACTS ‘Treatment for absence seizures | ‘Treatment for tonic-clonic seizures3 Question Warm-Up 1. Which acca ofthe hypothalasmus regulate the autonomic nervous estem? (PAL p50 AS p59) 2. Which nucleus of the hypothalamas fits each ofthe following descriptions® TFA p50) FAS p45H) '* Considered the “master clock” for most of our circadian rhythms ‘+ Regulates the parasympathetic NS + Regulates the sympathetic NS + Produces antidiuretic hormone (ADH) to regulate water balance “+ Mediates oxytocin production + Regulates the release of gonadotropic hormones (.c., LH{ and FSH) 3. ‘What are the differences between oligodendroglia and Schwann cells? Al 447448) (AIS p51 452) BHOVOVaH 1e)- [AENHEADACH: 4 Patient Profile: Eddie's Exploding Eye Eddie is a 27-year‘old man who comes to the physician because of two weeks of recurrent headaches. The headache begins around 10:00 AM and lasts about 90 minutes before resolving spontaneously. The pins alway located bend the ight eye, ad fecls like a red hot poker is being jabbed into his eye. The headache docs nor throb During the headache, the right eye is red and watery, and the right side of his nose runs profusely. He denies any nausea or vomiting, The headache is not worsened by bright lights, loud noises, or physical activity. What therapy will treat this patient's headache most rapidly? Tension headache © Constant, non-throbbing pain (lasts 4-6 hours, up to 7 days) Occurs in the regions (most often bilateral) oF asa band around the bead = No associated symptoms such as: Migraine headache © Atleast attacks © Headache lacing 4-72 hours (2-48 hours in children) © Atleast2 ofthe flowing: location quailty ‘Moderate to severe intensity (inhitits or prohibits day activities) ‘Aggravated by routine physcal actwity © Atleast 1 of the following: ‘Nausea andor vomiting ‘Cluster headache © Strictly © Severe pietcin © Does not chrob like a migraine. No aura. © Duration of 15 minutes to 3 hours, occurs (often at the ‘same time), and continues for an interval of 4-8 wecks © Maybe associated with: ~ Partial Homer syndrome ( ) = Ipsilateral tearing, hinorthea, or nasal congestion region8. What is the most likely cause of headache based on each of the following descriptions? ‘Made worse by foods containing tyramine ‘Obese female with papilledema Jaw muscle pain when chewing Photophobia and/or phonophobia Bilateral frontal/occipital pressure Pati using topical retinoic acid for acne “Worst headache of my life” Headache + extraocular musele palsies ‘Scintllating scotomata prior to headache Headache occurring either before or after orgasm Responsive to 100% oxygen supplementation ‘Trauma to the head > headache begins days after the event, persists for over a week and does not go avay Severe headache + fever or neck stiffness 3HOVOV3H o}-[aE IN}HEADACHE [60}BRAINTUMORS | (14 pA8B) (FAIS p92) (SUIS Pechatn bin tumors (FAIA pi89) 93) (SUIS (91308) (6 93382) 3 Question Warm-Up 1. Which cranial nerve relays the following information? (Fl4 p472) (AIS 0475) + Hypoxia measured by the carotid body = Motor information for swallowing + Blood pressure from the aortic arch + Salvation from che sublingual glands + Salivation from the parotid gland + Blood pressure from the carotid 2, Which type of collagen is abnormal in Alpor« syndrome? (14 979) FA15 p75} 3. Which type of collagen is abnormal in Ehlers-Danlos syndrome? (414572) (15 975) SHOWNL Niv¥e e)-[a=lN|BRAIN TUMORS End of Session Quiz, 4. What are the three most common primary brain tumors in adults? What are ‘he three most common in children? 5. Which primary brain tumor fits each of the following descriptions? « Pscudopaisading necrosis + Polyeythemia + Neurofbromatosis type 2 + Associated with von Hippel- Lindau syndrome + Foamy cells, high vascularity + Hyperprolactinemia —> galactorthea, amenorthes, anovulation +» Psammoma bodies + Fried-egg appearance + Perivascular pseudorosetss + Bitemporal hemianopia + Worst prognosis of any primary brain tumor © Child with hydrocephalus + Homer: Weight pseudoroseresSLEEP 3 Questiun Warm-Up LA 43-year-old man presents with symptoms of dizziness and tinnitus. CT shows an enlarged intemal acoustic meatus, What is the diagnosis? 2. Which portions of the hypothalamus are inhibited by leptin? Which are stimulated by leptin? (FAl4 9/50) (FS p454) 3. What substances are utilized by natural killer cells to induce apoptosis in other ‘celle? (FA!4 p199) (IS p201) as loy-/aE ly!SLEEP 4, What medications are common in the treatment of insomnia? What makes each one unique? ‘Melatonin Non-addictive, OTC, vivid dreams, safe for < 3 months Valerian OTC herbal remedy, studies show no benefit ‘Antihistamines (Benadryl, | Commonly used by patients first-line, associated ‘Tylenol PM, doxylamine) with poor sleep quality, not for long-term use, anticholinengic side effects (avoid in the elderly) “Trazodone ‘Antidepressant, increases REM slecp, small risk ‘of priapism TCAs (amitriptyline, ‘Antidepressant, small risk of arrhythmias doxepin) (obtain EKG prior to use), anticholinergic side effects (avoid in the elderly) Longactngbenzdinspnes | Addi, soneexm only 35 dae) (emazepam, lorazepam, clonazepam, diazepam, chlordiazepoxide) Zolpidem (Ambien), zaleplon | Act at the benzo receptor, short-term only (Sonata) (< 35 days), rebound insomnia when discontinued Eszopiclone (Lunes ‘May be used long term Ramelteon (Rozerem) ‘Non-addictive because it works at melatonin receptors instead of GABA/benzo receptors; hepatic insufficiency; sm studies are lacking, 5, What is the treatment for narcolepsy? © Avoitdance of drugs that cause sleepiness * Scheduled naps (once or twice a day for 10-20 min) © Stimulants~ modafinil is first-Hine © Support group attendance © fcataplexy then use venlafaxine, fluoxetine, oF atomoxetine + Sodium oxybate (GHB) can assist in sleep and reduce caaplexyans (681ANESTHETICS Motignanthyperthe Daniolene FAM p Local anastreucs (FAI p95) (FAIS p99) 3 Question Warm-Up 1. Which intracranial tumor best fits cach of the following descriptions? (4 88-409 (a p92 499 GUIS p5D) + Polyeythemia + Newofibromatosi ype 2 « Hyperprolactinemia ~ galactonea, amenorchca, anovaltion| + Poammoma bodies + Peciascular pseudorostes + Bitemporal hemianopia + Worst prognosis of any primary bran tumor 2. What portion of the brain is supplied by the anterior cerebral artery? Middle cerebral artery? (FAl4 p458 459) (FAIS p42) SUIS p24) 3, What brain structure is responsible for extraocular moments dusing REM sleep?End of Session Quiz 4. Which anesthetic fits each ofthe following descriptions? + TV, associated with hallucinations and bad dreams + IV, most common drug used for conscious sedation + Tohaled,sde effec of hepatotoxicity + TV, used for rapid anesthesia induction and shore duration of action + IV, decreases cercbral blood flow (important in brain surgery) * Opioid tht does not induce histamine release * High tigheeride content, inreases the risk of pancreatitis with longterm use z 5. What is the mechanism of action of dantrolene? 6. Whit is the mechanism of action of local anesthetics? Which nerve fibers are blocked fist with local anesthesia? 7. What drug can be used to reverse neuromuscular blockade? for-[aEiyyMOVEMENT MOVEMENT Phys Chapters 54, 55, 56 Lote corticospinal rt (FAIA pi) (FAIS p70) (Phys ps ron sigs (FAIA 166) (FAIS p70) tum (FAIA p52) (FAIS p57) (SUIS p21) (Phys pt) pr) (FAIS p59) (H 3327) 3 Question Warm-Up 1. Whats the initial tearment for vertricular fibiltion? (AH 2) (AIS 124) 2. What organism is associated with each ofthe following clues? + Rabbit hunter » Pet prairie dog + Tavdes tick + Lymphadenopathy +a new kien + Dog bite 3. What bacterial structure has the following function? «+ Provides rigid support to the bacterial cell and protects against osmotic pressure differences + Space beoween the inner and outer cellular membranes in gram-negative bacteria + Mediates adherence of bacteria to the surface ofa cell © Protects against phagocytosis,4, Muscle spindle control Muscle spindle: monitors muscle length © Extrafusal muscle fibers: fanetional unit of muscle * Intrafusal muscle fibers: regulate length ‘Muscle stretch resuits in intrafusl stretch which stimulates la afferent ~> dorsal hom —> ‘motor neuron, causing reflex muscle contraction Hint: help you pick up a heavy suitease * Golgi tendons: monitor tension rather than length (perpendicular to intrafusal muscle fibers) Provide inhibitory Ib aflarent feedback Hint: cue you to drop a heavy suitcase Gamma loop: regulates sensitivity of reflex are © CNS the ¥ motor neuron — contracts intrafusal fiber (cntral part of spindle), increasing the sensitivity ofthe reflex are ALNIW3AOW (@)[aF ly)HOVEHENT What portions of the thalamus relay each of the following types of information: © Sensory signals from body (via medial lemniscus and spinothalamic tract) —> cortex + Trigeminothalamic and tase signals > somatosensory cortex © Retina (visual information) —> occipital bbe © Inferior colliculus (auditory information) > primary auditory cortex © Mammillochatamic tract cingulate gyrus (part of Paper ccc © Communications with prefrontal cortex; memory loss results i © Cerebdlum (dentate nucleus) and basal ganglia > motor cortex © Basal ganglia — prefrontal, premotor, and orbital cortices lestroyed Describe the general flow of information through the cerebellum. Inputs (mossy and climbing fibers) cerebellar cortex > Purkinje fiber — deep nucle! of cerebellum ~> output rargets List the deep nuclei of the cerebellum, from medial to lateral. ‘What structure provides the major output pathway from the cerebellum? ‘Superior cerebellar peduncle — contralateral ventral lateral nucleus (VL) of thalamus (On which side of the body (contralateral or ipsilateral) would motor control be affected by a lesion of the cerebellum? © Motor control ipsilateral to the side of the lesion would be affected © Output from the cerebellum > contralateral thalamus > cortex “> corticospinal tract ~ body contralateral to cortex10. What are the longitudi © Vermis * Intermediate (paravermal) zones (right and left) * Latzral hemispheres (Fight and lei) Spinocerebellum Vermis Intermediate hemisphere v co (igferal hemisphere) Dentate ucleus Tomotor Tolateral Tomedial and premotor descending descending ——‘To vestibular contices systems systems nuclel —[ - Motor Motor Balance planning execution andeye movernent ANSW3AOW @) EIN)MOVEMENT ‘What is the difference between resting tremor, intention tremor and essential tremor? © Resting tremor ‘Tremor occurs at rest, but disappears with voluntary movernents, Associated with Parkinson disease © Tntention tremor ‘Tremor appears only with voluntary movernents Associated with cerebellar damage © Essential tremor ‘Tremor occurs both with movement and at rest ‘Assodated with family history of tremor 12, What are the features of essential (AKA familial) tremor? © Ropid fine tremor of ead, hands, arms, and/or voice © Occurs both with movement and at rest + 5016 of patients have a Family history of tremor * ‘Treated with B-blocker (propranolo), primidone an anticonvulsant), clonazepam, or alcohol (patients often selfemedicate)| End of Session Quiz 13, What are the differences between the 1a afferent motor pathway and the 1b afferent motor pathway? ALNIW3AOW 4, Whatare the classic signs of an upper motor neuron lesion? What are the classic signs ofa lower motor neuron lesion? 15. What is the difference herween essential tremor, resting tremor, and intention ‘tremor? Rapip-Fire Facts “Toe extension upon stimulating the soe of the foot with a blunt instrument Hyperreflexia, increased musele tone, and __ positive Babinski sign Hyporeflexia, decreased muscle tone, znd muscle atrophyBASAL GANGLIA Phy 6 Re Chapter 28 Ht Chapter 372 4) (Phys po03) (H p3317) 3321) (6 6t4) 1) (GG porip ) (H 93230) 3 Question Warm-Up 1. What isthe inital treatment for ventricular tachycardia when there is no pulse?, 2. Whatis the function of catalase? (FA'4pi23) (FAIS pi32) 3. Whats the most common aerobic sin flora? (FAM pI70) (45 p79) Guurradsin | [ cmatatozce | lo (renee =]End of Session Quiz: 5, What are the cardinal features of Parkinson disease? 6. 28-year-old chemist presents with MPTP exposure. What neurotransmitter is Aepleed? 7, How do each of the following structures normally impact movement? = Globus pallidas interaa + Subthalamic nucleus 8, A.male patient presents with involuntary filing of one arm. Whereis te lesion? 9. What neurotransmitters are altered in Huntington disease? Rapin-Fire Facts ‘Depigmentation of the substantia nigra CChorea, dementia and atrophy of the eaudate and putamen in the cytoplasm of neurons ve WNONVO 1¥' fo} larly!SPINAL CORD AND LESIONS SPINAL CORD AND LESIONS Spun cord 3 Question Warm-Up 1, What infections are caused by Streptococrus pyogenes (group A strep)? (FA pi3)) ANS p29) (SUIS p323 2. Which Gram (¢) organism matches each of the following statements? (ats 9129-135) als p27 134) + Causes scalded skin syndrome * Gray-white membrane in the posterior pharynx ofan unvaccinated child + Pharyngitis —> glomerulonep! + Most common cause of meningitis + Most common eause of osteomyelitis + Serious newborn infections 3. What molecules are expressed on the surface of antigen presenting dendritic cells?End of Session Quiz 5. Which spinal tract conveys the following types of information? «+ Touch, vibration and pressure sensation «+ Valuntary motor command from motor cortex to body ‘+ Veuntary motor command from motor cortex to head/neck + Pain and temperature sensation (ORD AND LESIONS Importact for postural adjustments and head movements roprioceptive information forthe cerebellum SPINAL 6 What are the findings of Brown-Séquard syndrome? 7. What clinical presentation would lead you to suspect amyotrophic lateral sclerosis 1s a diagnosis? 8. Whatare some of the more classic presenting scenarios for multiple sclerosis? Rapip-Fire FACTS Conjugate at “and ipl Degeneration of the dorsal columns Demyelinating disease in a young woman Mixed upper and lower motor neuron disease| SUBRAGHIALPLEXUSAND UEN 3 Question Warm-Up 1. Which gram-positive organisin matches each of the folowing statements? (Alt p12 135) (AIS p27 13) + Tafant with poor muscle tone + Diarthea after using antibiotics « Respiratory distress ina postal worker + Otitis media in children + Collis 2, What is the classic presenting symptom in a patient with Lyme disease? {FAH pial (AIS pHO) (IS p333) 3. What is the function of macrophages in the spleen? (44 p97) (FAI5p199) RVES PART I! | 1d WIHV¥a 1 Auvd S3AW3N 3n ONY sNXx OundNTerminal Branches Cords | ig UO we 4, Label the following diagram of the brachial plexus: Divisions | Diva S3A¥3N 30 CNY SNX3Td WHOVE £80)pede ‘Session Quiz ; = & & : 2 é & a Zz a z asrrecperert | BRACHIAL PLEXUS AND UE NERVES PART | 1982) Rarib-Fire FACTS ‘Newborn with arm paralysis fellowing a diffcalthbor 7res (AM pla (F 3 Question Warm-Up 1, What patients are susceptible to Listeria monocytogenes? 2. What name is given to RBCs that have been partially digested by splenic macrophages? 3, Which nerve is being tested with each of the following reflexes? + Biceps reflex + Thiceps reflex + Patellar reflex * Achilles reflex 4, Radial nerve Motor ‘+ Triceps brachii (extends forearm) + Supinator(supinates) + Brachioradials (Rees forearm, supinates and pronstes) + Extensor earpi radials longus (extends wrist) + Extensor digitorum, extensor pollicis longus plus other extensors (extends wrist and digits) + Mnemonic: BEST Sensory + Posterior arm + Dorsal side ofthe hand Pathology + “Saturday night palsy” (wrist drop, difficulty straightening the fingers, numbness on back: of hand and posterior arm) Compression of radial nerve agains the spiral groove of the humerus + Damage associated with fracture ofthe shaft of the humerus 7 Luv S2AWBN 2/N GNY SNXa1d WIHDWYSBRACHIAL PLEXUS AND UE NERVES PART 2 5. Ulnar nerve Motor © Hypothenar muscles (controls hand and Sth digi) © Sr and 4th humbricals (Rexcs at MCP and extends a interphalangeal joints) © Interosscous abducts and adduets digits) * Adductor pollicis (adducts thumb) Sensation © Sth and ¥4 oF ath digit © Medial side of palm and dorsal hand Patholo © Proximal injury (los of exion ofthe wrist and digit) . ae claw" deformity (MCP joint hyperextension and IP joint flexion at 4th and Sth igi © Weak abduction and adduction of digits © Hypothenar wasting 6. Median nerve Motor © Pronator tres and pronator quacratus (pronatce hand) * Flexor pollicis longus (flexes thumt) + Astand 2nd lumbricals (exes MCP joints and extends IP joints) Sensation © Lateral palm © First 34 digits Pathology © “Ape hand” deformity (loss of thumb abduction) + “Hand of benediction” deformity (loss of flexion of 2nd and 3rd digits) © Carpal tunnel syndrome (numbness ofthe first 34 digits)z Musculocutaneous nerve Motor © Coracobrachialis, biceps, brachialis (exes and supinates forearm) Sensation © Lateral side of forearm, Pathology © Decreased flexion and supination of forearm, Axillary nerve Motor + Deloid fabduers shoulder) © Long head of triceps (extends forearm) © Teres minor (externally rotates arm) Sensation © Lateral shoulder Pathology © Occurs with dislocation of shoulder or fracture of surgical neck of humerus © Loss of abduction, weak flcxion and extension and rotation of shoulder © Loss of sensation to lateral shoulder © Posterior circumflex artery runs with nerve Long thoracic nerve Motor © Serratus anterior (hols scapula tothe thorax) Sensation © None Pathology + Winged scapula © Due to Blow to the neck or shoulder or after radical mastectomy 7 Luvd S3AY3N 30 CNY SAX3Td WIHOWYS fey [aEiNiRVES PART 2. Nel BRACHIAL PLEXUS AND U End of Session Quiz 10. What nerve is damaged when 2 patient presents with the following syrmptorn Copper extremity)? “= Unable to extend 4th and Sth fingers + Unable to flex index and middle finger + Wei drop + Scapular winging + Loss of sensation over fingers I-4 + Cannot abduct or adduct fingers + Loss of shoulder abduction + Los of elbow flexion and forearm supination + Loes of wet extension 11, What nerve is most at risk of injury with the following types offractures/injury? + Fracture of the shaft of the humerus « Fracture of the surgical neck of the humerus + Anterior shoulder dislocation + Injury to the carpal tunnel 12. A patient falls oa mororcyele and lands on his ight shoulder. On physical ‘exam you notice his shoulder has an abnormal configuration. X-rays indicate an anterior dislocation of his shoulder. What artery and nerve are most at risk of being damaged?3 Question Warm-Up 1. What pupillary sign might point you toa diagnosis of syphilis? (FAs pl) FAS) 2. Which type of hypersensitivity is responsible for each ofthe following clinical problems? (FA!4 209) (FAIS p22) * Poststreptococal glomerulonephritis + Rheumatse fever += Polyartertis nodosa Scrum sickness ~» Contact dermatitis 3. Whats the difference between essential tremor, resting tremor, and intention ‘tremor? (FAI p454) (FAIS p#59) + Essential tremor + Intention tremor + Resting tremor 4, Femoral nerve Motor * Psa, iliacus, pectineus, sartorius (hip flexion) © Vastus lateralis, vastus intermedius, vastus medialis, rectus femoris (knee extension) Sensation © Anterior thigh * Medial lower leg. Pathology © Pelvic facture IBS ONY ALIWFYLX3 Y3MOT S1DSNW TAIT: e}larly|LETAL MUSCLE LOWER EXTREMITY AND SK' 5. 1 Obturator nerve Motor © Adduetor magnus, adductor longus, adductor brevis (hip adduction) © Grails (knee flexion) Sensation © Medial thigh Pathology © Anterior dislocation Superior gluteal nerve Motor © Tensor fea lata, gluteus medius, gatcus minimus (hip abduction and medial rotation) Sensation © None Pathology © Posterior hip dislocation © Polio + Trendelenburg ge Inferior gluteal nerve Motor + Glutcus maximus (hip extension and lateral rotation) Sensation = None Pathology © Posterior hip dislocation replacement © Difficulty standing up or climbing stairs Sciatic nerve Motor © Biceps femoris (bial branch), semitendinosus, semimembranosus, adductor magnus (hip ‘extension and knee flexion) Sensation © Posterior thigh and gluteal regions © Entire lower leg except medial aspect Pathology © Intervertebral dise herniation © Spinal stenosis © Spondylolisthesis9, Tibial nerve Motor © Gastrocnemius, soleus, plantaris (plantar flexion) © Popliteus (unlocks knee) © Flexor hallucis longus. flexor digitorum longus (te flexion) Sensation ® Sole ofthe foot ® Back of the calf (sural nerve) Pathology © Knee injury 10. Common fibular nerve (common peroneal nerve) ‘Motor © Peroneus longus, peroncus brevis, short head of thebiceps femoris Sensation © Lateral ower leg © Dorsal side of foot Prthology ¢ Chronic compression © Habitual lg crossing © Fracture of neck of fibula © Foot drop SIDS TLTTENS ONY ALINAYLX3 YBANOT Il, Deep fibular nerve (deep peroneal nerve) Motor © Peroneus tetius (foot eversion) © Tibialis anterior, extensor hallucs longus, extensor digitorum longus (oot dorsiflexion) Sensation © Webbing between first and second digits Pathology © Trauma to lateral knee = Foot dropLOWER EXTREMITY AND SKELETAL MUSCLE 12, Label the sarcomere: End of Session Quiz 13, Which nerve would most likely be damaged with each of the following injuries? « Pelvic fracture * Anterior hip dislocation « Posterior hip dislocation * Vertebral disc hemiation + Knee injury + Hiabiual crossing of the legs 414. Which two muscle receptors are responsible for opening the sarcoplasmic reticulum in response to depolarization? 15. What drug prevents the release of calcium from the sarcophismic resculum of ‘skeletal muscle? 16. What are the differences herween type 1 and type 2 muscle fibers?3 Question Warm-Up 1. Which complement is responsible for neutrophil chemotaxi? (Fats p204 (FAIS 9206) 2. What are classic signs of an upper motor neuron lesion? Of a lower motor neuron lesion? (FAl4 p466) (FAIS p477) 3, What are tie differences between the 1a afferent motor pathway and the 1b afferent motor pathway? |. Sensory corpuscles [Adaptation Sensation Location/other Mertel Meissner Raffint Pacinian Free nerve ending SNaS Nolavs fo): (aE IN|SENSATION 5. What is the difference between the intrafusal muscle fiber and the Golgi tendon organt End of Session Quiz 6. Whatsensory receptor communicates the following types of information? +S Priding pala (ast enjtinancd) + Buming or dul pain and itch (ow, unmycinated) + Vibration and presure + Dysamic/changing Hight, dsciminatory euch + Sta/unchanging light touch + Proprioception information, muscle length monitoring + Proproception information, muscle tension monitoring, 7. What CSF changes are present in Guillain-Barré syndrome? 8, What are the classic manifestations of Guillain-Barré syndrome?4. COA: Chapter 7 FE Chapter 28 (FAI pt 5) (FANS p479) (COA p ATI) (FAIS p18) 3 Question Warm-Up ‘1. Which eytine, more than any other, should be Imown as the macrophage activating cyrokcne? (4 p37) (AS p36) U5 360) 2, What are the cardinal features of Parkinson diseasc? (FAl4 p453) (FAIS pt52) 3. What neurotransmitters are altered in Huntington disease? (FA14 p44) (FAIS 453) Describe the flow of aqueous humor. © Aqueous humor is constantly produced by the ciliary epithelium of the ciliary body (inflow) © Constant low of aqueous humor moves from the posterior chamber into the anterior chamber by passing through the pupil + Aqueous humor in the anterior chamber needs to ext the eye (outflow) + Aqueous humor exits the eye via the trabecular meshwork 3A e}laEly|EYE 5, Acute angle-closure glaucoma © Emergency © Abrupt onset of pain, headache (temporal, eyebrow), nausea, colored halos, rainbows around light + Red, cary eye with hazy comca and fixed, mid-dilted pupil (aot reactive to light) thats frm tw palpation ‘& Open-angle glaucoma © Common, insidious form usually bilateral * Risk factors older than 40, African American, family history of glaucoma, myopia, nd diabetes © Barlystage: asymptomatic, elevated intraocular pressure © Late stage gradual loss of peripheral vision, permanent blindnes if untreated 7. What is the classic presentation of a patient that has a cataract? © Usually bilateral, but sometimes unilateral + Progressive, painless decrease in vision manifested with diffculy driving at night, reading road signs, or reading fine print + Possible disabling glare or from oncoming headlights at night ¢ Near-sightednessis often an carly manifestation End of Session Quiz 8. Whatinitial type of vison loss is commonly seen in patients with open angle gaucoma? 9. What drug classes are used in the treatment of glaucoma? 10, Whats the treatment for dry age-related macular degeneration?SS ee af 4. HE Chop 21 COA: Chapter 7 Ausstory sensation (SUIS p34) lari testing Acute 0 a (COA p 978) Acute eis media (COA P978) Cholestectoma (H p219) (p74 Vertigo FAI p44) (FAIS 9190) 3 Question Warm-Up 4. Whatclinical presentation would lead you to suspect amyotrophic lateral sclerosis aga diagnosio (74 p47) (FAIS p71) GUI pt7) 2. Whatis the mechanism of action of thalidomide? 3. Which spinal tract conveys the following information? (F4 pte) FAIS p70) “+ Alternate routes for the mediation of voluntary movement + Pain and temperature sensation + Important for postural adjustments and head movement “+ Proprioceptve information forthe cerebellum Auditory pathway © ‘Tympanic membrane '* Middle ear ossicles (malleus > incus —> stapes) © Auditory has cells in the cochlea (Olivocochlear bundles send cholinergic signals to the cochlea, which causes contraction ofthe outer ha els stiffening tne bas lr membrane and sersitzng the ier hair cells to a particular frequency Amninoglycosides (eg, streptomycin, gentamicin) cause hearing loss by damaging the ‘outer hair cels Spiral (cochlea) ganglion © Cochlear nuclel * Superior olivary nucleus (contralateral) © Lateral lemniscus + Inferior colliculus © Medial geniculate body + Primary auditory cortex (temporal lbe) wa fe) [aE IN|EAR 5. Weber test ‘Normal —> midline ‘Conductive hearing loss ~ lateralizes to the side of the affected ear Sensorincural hearing loss ~ lateralizes to the side opposite the affected ear 6. Rinne test Normal — air conduction > bone conduction (AC > BC) Conductive hearing loss > BC > AC 7. Given the following exam findings, what is the diagnosis? Weber Rinne (left) 1 (right) [Diagnosis Patient A | Midline | AC > BC AC > BC Patient B Right AC> BC BC > AC Patient C Left AC> BC AC > BC PatientD | Midtine | BC > AC BC>AC ‘Acute otitis externa (swimmer’s ear) + Inflammation/infection of the ear eanal Pain with manipulation of the ear (pinna) or instrumentation ofthe canal © Most commonly caused by P. aeruginowt or. aureus «Treatment: irrigation and topical antibiotics 9. Acute otitis media (AOM) © Infection of the Middle ear effusion (opacity, afd level, pus) Exythema ‘TM immobility under positive pressure with a pneumatic otoscope ‘© Most common bacterial causes: S. pneumoniae, nontypable H. influemzac, M. catarrhalis = Treatment: = Antibiotics amonicilin, amoxclin plus davulac acid, cephalosporins) Tympanostomy tubes © Complications may include seute mastoidits (typical AOM symptoms plus pose-curicular swelling, redness, and mastoid tenderness) 10. Cholesteatoma © Overgrowth of desquamated keratin debris within che middle ea space that may ‘eventually erode the ossicular chain and the mastoid air cells © Causes: negative middle car pressure (chronic retraction pocket) from eustachian tube dysfunction or direct growth of epithelium through a'TM perforation © Commonly associated with chranie middie ear infection © Physical exam: grayish-white “pearly” lesion behind or involving the’TM, conductive hearing oss, vertigo © Treatment: surgical removal usually involving tympanomastoidectomy and reconstruction of the ossicular chainBenign ovals wih the vestibular apparatus. The Dix-Hallyke maneuver and the Epley -maneuver are used for diagnosis and treatment. Vestibular neuritis - Inflammation of vestibular nerve ‘© Méniérediscase (endolymphatic hydrops) ~ Imbalances of the fluid and electrolyte composition of the endolyrnph cause a triad of intermittent vertigo, tinnitus and hearing loss. ‘© Central vertigo - Brainstem and cerebellar lesions damaging the vestibular nuclei End of Session Quiz 12. A patient presents with vertigo, tinnitus, and hearing loss. What is the diagnosis? 13. Which organisms are most commonly responsible for acute otitis media? 14, What organism is most commonly responsible for otitis externa? 15. Chronic otitis media can sometimes result in a eystic lesion that is lined by keratinizing squamous epithelium, which can be metaplastic, that i filled with amorphous debris. What is the name of this condition? waDELIRIUM AND DEMENTIA 4, Alchoimer cu Dement with Lewy bodes (7 ( 5 ps8) (fk pL295) (6 2312) Fromotemoval demenca (FAM p43) (FAIS p82) (SUIS 48) (R p1292) (H p3310) aod Jasob disease FAI Deka (FAL ‘Onontanen FV p03) 3 Question Warm-Up 1, Which opinal tract conveys the following information? (414 p66) (45 +70) « Touch, vibration, and pressure sensation “* Voluntary motor command from motor cortex to body. * Voluntary motor command from motor cortex to head/neck. 2. What are the symptoms of a lesion to the C5 and Cé nerve roots? (FAIA pAl3) (FAIS ptt) 3. What are the symptoms of a lesion to the inferior trunk ofthe brachial plexus? (FAl4 pl3) (FAIS p19) Identify the neuronal pigment/inclusion that matches each of the following statements: © Intranuclear inclusions seen in herpes simplex encephali © Cytoplasmic inclusions pathognomonic of abies ‘= Neuronal inclusions characeristic of Parkinson disease Cytoplasmic inclusion bodics associated with aging © Dark cytoplasmic pigment in neurons of the substantia nigra and locus coeruleus, not seen inpatients with Parkinson Eosinophilic, rod-like inclusions in hippocampus of Alzheimer patients Diagnostic of Alzheimer disease iamensous inclusions that stain with silver, do not survive neuronal death Filamentous inclusions that stain with PAS and ubiquitin5. Delirium vs. Dementia Dementia Onset Daily cous Level of consciousness ‘Thought production Paychotic features Prognosis VILNaHa ONY HONG fe} [aE IN!LIRIUM AND DEMENTIA, o End of Session Quiz 6. What are the usual components of a dementia worleup? 7. Whyis Alzheimer disease more common in patients with Down syndrome? 8. Whit is the mechanism of action of the drugs used in the treatment of Alzheimer disease? 9. A 72-year-old woman is brought into the clini by her family because of strange behaviors over the past week. She has been very agitated, takes many naps uring the day, occasionally urinates on herself, and has had a poor appetite. She ‘will not focus her attention on the questions you ask her. What is the most likely agnosis Rapip-Mre [Acts ‘Most common cause of dementia ‘Second most common cause of dementia Extracellular amyloid deposits in che grey matter Intracellular deposits of hyperphosphorylated tau protein Intracellular spherical aggregates of tau protein seen om silver stainPHaRM Basics Parasympathetic Activation Parasympathetic Inhibition Sympathetic Activation Sympathetic Inhibition Neurotransmission G Protein Second Messengers Pharmacokinetics Pharmacodynamics > IN ORDER Drug Metabolism , Rexam. To Corn annewene 10 Drug Elimination 11 Drug Side Effects 12 AntidotesPARASYMPATHETIC ACTIVATION | 3 Question Warm-Up 1, Wharare the differen types of collagen, and where can they be found in dhe body? (FAl4 579) (FAIS p75) 2 A yearold mani ahisoryof Ex Dank ame ad hyperenion presents witha severe headache, A head CT is normal at, ae een eee eee cause ofthis man's headlache? (Fl4 pBl) (FAIS p77) 3, How does the presentation of a dominant parietal lobe lesion differ from that of 1 nondominant parietal lobe lesion? (Ald paSs (FAIS pi) NOLLWALLY DILZHLWAHASW Yd SOS CR ALh Aa!PARASYMPATHETIC ACTIVATION Patient Profile: Old MacDonald Gets Leaky ‘A.38.-year-old man presents to the emergency department with shortness of breath, diaphoresis and agitation. He has excessive urination and diarshea. He recently maved to the area and worksat a local farm. Physical exam shows he has constricted pupils, a heart rate of 55 bpm, mild inspiratory wheezes, excessive salivation and muscle twitching throughout his body. What is the mechanism of action of the medication most likely used to treat this patient's symptoms? Parasympathetic activation ‘Cholinergic excess + Gincreased digestion 'D © Bladder: wall contriction, relax sphincter ou. © Bye: miosis, ciliary muscle contraction 7M. © Lung: smooth muscle contraction oB © Heart: decrease heart rate/eontractility 7B cE © Lacrimal glands: stimulate tears ek © Salivary gland: watsry secretion °s a + Userus: contract © Ponis/Clitoris: eree-ion/engongement ‘Summary © Organophosphate poisoning — inactivation of. excess DUMBBELSS (Leaky) © Treatment: Goat decrease stimuation of excess acetylcholine on muscarinic receptors ‘Atropine blocks muscarinic receptors Praldoxime regenerates acetychotinesterase Myasthenia gravis © Antibodies to the acetylcholine receptor © Most common board question presentation: ‘worsens throughout the day © Tenslon test © Thymus pathology: 50% associated wth thymic 20% associated with thymic 15% assocated with thymic ® Myasthenic crisis: rapidly progressing weakness esp. Treatment: musclesEnd of Session Quiz 6. How does the parasympathetic nervous system affect the following body structures? + Heart 33 + Salivary glands + Bronchilar smooth muscle + Bladder + Male GU + Gliact 7. What drug regenerates acetylcholinesterases after organophosphate poisoning? 8, Whavis the antidote for organophosphate poisoning? 9. Which anticholinesterases are used in the treatment of Alzheimer disease? Rapip-Fire FACTS NOLWALLDW DUSHIVAWASY Hd SOISWa WYWHd Amyloid deposits in gray matter of the brain Drooling farmerPARASYMPATHETIC INHIBITION | PARASYMPATHETIC INHIBITION 3 Question Warm-Up 1. What are the endogenous agonists to the different opioid receptors? (F414 p190) (FAIS p94) 2. A patient comes to your office and before you notice any other symptoms, you see that the patients uvala deviates to the right when she says “Ah.” What neurological areas might be damaged in order for this abnormality to be seen? 3. What are the classic presenting symptoms of a syringomyelia? (FAM p48) AIS p50) 4. What are the symptoms of inhibiting parasympathetic activity?5. What anticholinergies are used in the treatment of urge type urinary incontinence? © Oxyburynin © Tolterodine ° Darifenacin and solifenacin © Trospium 6. In what patient populations is atropine contraindicated? 7. What other medications have anticholinergic side effects? ©. First generation Hi blockers diphenhydramine (Benadry)), doxylamine (Unisom), Awopine + Edrophonium = Donepeai + Tolterodine + Pralidoxime + Trospium + Bethanechol + Rivastigmine + Neostigmine + Homatropine + Darifenacin + Pysidostigmine + Ipratropium + Carbachol 9, Which of the muscarinic antagonists discussed could be used to improve FEV; in a patient with COPD? NOLLISIHN! SUSHLVEWASWH¥d SOISV WYVHdSYMPATHETIC ACTIVATION | /SYMPATHETICACTIVATION 3 Question Warm-Up 4. A patient cannot adduct her left eye on lateral gaze, but convergence is normal. ‘Whar structure is damaged? (F4l4 p482) (FAIS p44) (SUIS p35) 2. A smother brings in her 2-year-old child who has had multiple viral and fungal infections and is found to be hypocalcemic. Which ofthe three germ layers (cctoderm, endoderm, or mesoderm) gives rise to the missing structure in this, child? (F414 p212, 560) (FAIS p2I4, 56) 3, Describe the sensory innervation ofthe tongue. (Al4 p46) (Als 2450)End of Session Quiz 4. Which receptors are stimulated by each ofthe following syrmpathomimetics? + Clonidine ‘5. Which sympathomimetic matches each of the following statements? + Given as nebulizer for asthma + Drug of choice for anaphylaxis + Most corzmon firstine agent for patents in septic shock * Given sutQ for asthma + Used by ENT to vasoconstrict nasal vessels DUBHAvEWAS NOLVALOY Pd z > - 4 2 raSYMPATHETIC INHIBITION [10] GG Chapter 12 1 blockers (FAIA 250) (FAIS 9255) (SUIS p75 76) Bbtcckers (FA 251) (FAIS 1256) (SULS 977-78) ‘Gy avenge agonists (FAL p49) (FAIS p25) 1 474) (FAIS pA77)End of Session Quiz 4. Which selective a-blocker has less effect on blood pressure? 5. What are the common side effects of B-blockers? Which patient populations should use caution when taking B-blockers? 6. Whatare the various clinical applications of B blockers? Rapib-Fire Facts Medical treatment for pheochromocytoma Selective o, -antagonist used to treat BPH SOS EAE MacNEUROTRANSMISSION 5 26) (6 182) (Pigs 721) 5 p20) (SUIS p26) 3 Question Warm-Up 4. What are the three different mechanisms cells employ to break down proteins? (FAL p75) (FAIS prt), 2. Which medication fits each of the following descriptions? (414 p490) (AIS (494) + Opioid cough suppressant commonly used with the expectorant guaifenesin * Opioid use in the treatment of diarrhea * Opioid receptor antagonist + Non-additive weak opioid agonist + Partal opioid agonist thac causes les respiratory depression 3. Your patient has facial angiofibromas,ash-leaf spots of skin depigmentation, a history of scizures, and intellectual disability. What condition does this patient Ihave? What neoplasms is this patient at risk of developing? (4 p23) (AS p235)4, Fill in the diagram of acetylcholine synthesis and neurotransmission: Cholinergic 4 Fates of ACh 5. What enzymes and cofactors are required to convert phenylalanine to epinephrine? NOISSIMSNWWLONEN al 5 B 4 @ od 9 veNEUROTRANSMISSION ‘6. Fillin the diagram of norepinephrine synthesis and neurotransmission: End of Session Quiz L 10. ‘Which three enzymes are requured to convert phenylalanine to dopamane? ‘A patient develops paralysis after being bitten by a black widow spider. Is this a spastic or flaccid paralysis? What other autonomic symptoms might be seen? What substances inhibit the reuptake of norepinephrine? ‘What substances stimulate the release of norepinephrine from neurons?3 Question Warm-Up ‘L_ What artery is damaged (via hemorrhagic stroke or ischemic stroke) with each of the following presentations? (FA4 p60) (FNS p464) * Aneurysm causes the eye ro look down and out » Ancurysm may cause bilateral loss of lateral visual elds + Broca or Wernicke aphasia * Unilateral lower exremity sensory and/or motor loss * Unilateral facial and arm sensory and/or motor loss SYION3SSIW GNOD3S NIBLO¥d 9 2. Which diuretic is used in the treatment of pseudotumor cerebri? (AIA p57) (AIS p68) 3. Whea does implantation of the zygote take place? (FAl4 p552) (FAIS p558) = x BS 2 xs es Bs ia io} 7)IGERS G PROTEIN SECOND MESSEN 4, Signal transmission pathways hormone binds growth factor binds Zpass transmembrane receptor rine bnaze receptor seated phn seated pha senate adaptor poten ebunfofPeten——fobuntat@Protan > phophotpe c i faracianng ten actvendenfatecyiase oso uiponphateOPa}—“dlayaeol DAG) ‘ Inceted nrc eat i reread tls scsvaton ct proelnlnae tere AM oameemeen cvadonaf proteinase activation of protein ‘aivatinet ——_setiatonofprewein eal arias toners ctvaon of proteinase pace w—tegewony "> atc target proteins and/or gene regulator protins &~'SUIDNISSIW NODIS NIZLOW D ‘Outline the pathway by which ¢ 7]PHARMACOKINETICS, [18] 66: Chapter 24 Enzyme kinoties (AAI p238) (FAIS 242) (SUIS p9 10) Phurmcakinenes(FAL4 1.239) (FALS 1243) (SUIS pl2, 395) (GG p28) Buoavesebaay (FAL p239) (FAIS p243) ‘Mea io (FAI 7239) (PAIS p243) 3 Question Warm-Up 1 ac 3, What are the ptoms of inhibiting eer4, Label the following graphs of enzyme kinetics: Reaction Velocty (Vo) Substrate Concentration [$] SDUANDIOOWWWYHd SOISV WYVHdCOKINETICS PHARMAG '5. Label the following plots as either competitive or noncompetitive inhibition: 8. D Reaction Velocity (V}6. What four pharmacokinetics equations are most important to know for Step I? SOMANDIODWWYVHd SOISVa WYVHdPHARMACOKINETICS End of Session Quiz. -A.60-kg man with status asthmaticus is being given an IV infusion of drug X at 60 mg/h. The clearance of drug X is 2 L/h, and the volume of distribution is approximately 0.5 L/kg, 48 hours after administration has begun, the asthma attack is under control. At this time, the concentration of drug X in his plasma is 20 mg/L. 7. What is the halflife of drug X in this patient? 8. Wharloading dose could have been used to reach the target concentration of 20 mg/L? 9. Ifthe patient begins to show signs of taxicty, and the target dose is decreased to 10 mp/L, what would you do to get to this level? 10. Assuming 100% bioavailal ‘maintain the new target level? what oral dose of drug X would he necessary to 1. Ifthe patient has a kidney disease, and the clearance is reduced to 1 L/h, but Va js unchanged, what effect will this have on loading dose and maintenance dose?3 Question Warm-Up 4. Tn what disonderis there an abnormal breakdown of elastin? (FAl+4 p8!) (FAI5 p77) GIS p27) 2. Whatare the syrpeoms of normal pressure hydrocrphalu? (4 p46 a 465) 3. A 76-year-old man who recently suffered a stroke is brought tothe clinic by lis wife. She says that he now shaves only the le side of his fice, and he eats off only the lft half ofa plate, When asked to draw a clock, he draws just the [eft half ofthe clock face. A lesion in which area ofthe brain is most likely responsible for these findings? (FA p460) FAIS p44) (SUIS p31) 4. Partial vs. Full agonists 100 50 paténcy | Decreased potency (higher Kim) % of maximum effect Dose (log scale) SDINYNAOODVHYWHd BOTS EME MSCODYNAMIC: PHARMAC! End of Session Quiz 5S. An investigator has developed two new preparations of insulin. Both preparations can lower the blood glucose by a maximum of 100 mgfdL. It takes 16 units of insulin preparation A to lower the blood glucose by 100 mg/dL. It takes 12 units of preparation B to lower the blood glucose by 100 mg/dL. Which insulin preparation has the higher efficacy, and which has the higher potency? 6. What effect will a reversible competitive antagonist have on V._, and K,? 7. Your patient is taking experimental drug Z,1o lower his LDL cholesterol. When he is given the antagonist drug X, the potency of drug Z.is decreased, but efficacy is unchanged. Doubling the dose of drug Z is shown to overcome the inhibition by drug X- Does drug X inhitit drug Z competitively, or noncompetitively? 8, Drug A has a therapeutic index of 10:1, while Drug B has a therapeutic index of 2:1, Which drug would be considered safer?DI LISM 3 Question Warm-Up 1, What substances are known teratogens? List as many as you can recall. (F414 p54) (AIS 958) GUIS 6397) 2. Which regions of the brain are included in he limbic system? (Fats pASD AS pA50) GUIS p=) 3, When peeforming « himbar puncture for anesthesia administration, where isthe anesthesia dosed? Where is CSF found? Grapefruit juice ‘Omeprazole ‘Sulfonamides wsnosviaw ona SOISVd WHWHdDRUG METABOLISM j. PASO inducers: * Griscofulvin © Carbamacepine © Phenytoin © Barbiturates © Rifmpin © St John’s Wore © Chronic aloholism End of Session Quiz, 6. Which hepatic phase of metabolism is lost first by geriatric patients? Which phase is mediated by cytochrome P450? 7. What medication inhibits acetaldehyde dehydrogenase? 8. What medication inhibits alcohol dehydrogenase? 9. List 7 inducers and 11 inhibitors of cytochrome P450,"DRUG ELIMINATION) Drug eimstxiuon (FAIA 1240) (FAIS p44) (SUIS p 3 Question Warm-Up 1. Which agenss are often used in the treatment of urpe incontinence? 2. Outline the pathway by which stimulation of a G, receptor activates protein. Kinase C. (FAL4 1244) (FAIS 9246) (SUIS pI73) 3. 30-year-old schizophrenic man now has urinary rewention due to his ‘neuroleptic. What do you treat it with? (A p26) (als p30) NOUYNINI] ON¥G SOISVa WHVHdNATION o 2 a 4, Drug elimination and urinary pH ee A acidic drug anion BHY ~————— _H* +B basic drug uncharged base © pKa (acid dissociation constart) isthe pH at which the amount ofthe non-protonated form {A° of B)= the amount of protonated form (HA or BH") + TfpHis low (cidic environment) and less than pK, there will be more of the protonated form (HA or BH") > basic drugs (BH) get trapped © If pH is high (basic environment) and higher than pKa, there will be more of the snonprotonated form (Aor B) > acidic drugs (A) get trapped © Treat acidic drug OD (.e, salicylates) with NaHCO, ~ traps the acidic drugiin the basic + Treat basic drug OD (.c,, amphetamines) with NH Cl — traps basic dragin the a5. Drug suffixes | Suffix Drug Class Examples. | afl Phosphodiesterase inhibitor | Sildenafil, tadalafil ~azepam | Benzodiazepine Lorazepam, diazepam Chlorpromazine, thioridazine, ae promethazine sezolam Alprazolam, midazolam, triazolam barbital Phenobarbital, secobarbital | ~bendazole ‘Mebendazole, albendazole | “exine | Local anesthetics jocaine, tetracaine | =chol “Muscarinic agonist Bethanechol, carbachol | ~eillin Per Amoxicillin, methicillin ~conazole | Tmidazole (antifungal) Fluconazole, ketoconazole ceurium | Non-d:polarizing ‘Atracutium, mivacurium neuromuscular blocker jum | Non-depolarizing Vecuroniurm, rocuronium ccuronium | neuromuscular blocker -cycline | Protein synthesis inhibitor “Tetracycline, doxycycline cdipine | Dibyopyidine calcium dipine, amlodi ~dconate | Bisphosphonate ‘Alendronate, risedronate etine ‘SSRI Fluoxetine, paroxetine, sertraline -fiurane | Inhaled anesthetics Isoflurane, sevoflurane DPP-1V inhibitor Sitagliptin, saxagliptin idinedione Pioglitzzone, “ipramine_ | TCA Clomipramine, imipramine mab Monoclonal antibody Infliximab, rituximab =mustine | Nitrosourea (nitrogen mustard)_| Lomustine =navir Protease inl navir, saquinavir ola B-blocker ‘Atenolol, metoprolol operidol | Neuroleptic Haloperidol, droperidol Zz @ Ba 9) oeDRUG SIDE EFFECTS 4, What drugs have the following potential side effects? Flashing © Niacin © Adenosi + Dihydropyridine calcium channel blockers Coronary vasospasm * Cocaine = Amphetamines © Exgotamine Dilated cardiomyopathy © Doxorubicin © Daunorubicin Torsades de pointes © Potassium channel blockers (dass 111) © Sodium channel blockers (class 1A) ° Haloperido! © Chloroquine © Protease inhibitors ‘Thrombocytopenia ° Cimetidine Agranulocytosi © Carbamazepine © Colchicine © Propylthiouracil © Methimazole © Dapsone Aplastic anemia © Chloramphenicol © Benzene © NSAIDs © Propylthiouracit = Mathimazole Gray baby syndrome Hemolysis in G6PD deficiency © Isoniazid aqui © Aspirin © Ibuprofen © Nitrofurantoin © Dapsone © Favabeans © Naphthalene ‘Thrombosis © Oral contraceptives Pulmonary fibrosis + Bleomycin © Busulfan Cough = ACE inhibitors Pseudomembranous colit © Amoxicilin/ampicilin Hepatic necrosis © Halothane © Acetaminophen © Valproic acid + Amanita phalleides Hepatitis © Isoniazid ‘Tertiary adrenal insufficiency © Corticosteroid withdrawal Gynecomastia * Digoxin © Estrogens © Cimetidine ® Alcohol (chronic use) © Ketoconazole © Marijuana (THC)4. (continued) Hot flashes © Clomiphene Hypothyroidism © Lithium Sulfonamides Gout © Diuretics (loop and thiazide) © Tetracycline Stevens Johnson syndcome © Carbamazepine © Lamotrigine Drug-induced lupus Sulfonamides © Teoniazid © Procainamide * Phenytoin ‘Tendinitis/eartilage damage © Fluoroquinolones, © Demecloeyeline Fanconi syndrome + Tetracycline expired) Parkinson-like syndrome © Antipsychoties © Reserpine Cinchonism © Quinidine © Quinine Seizures © Imipeneméilasatin © Isoniazid © Tramadol © Metoclopramide © Benzodiazepine/alcohol withdrawal Tardive dyskinesia © Antipsychotics © Metoclopramide Disulfiram-like reaction > Certain cephalosporins Procarbazine © Fin generation sulfonylireas + Disulfiram sipadga gals snva SOISWa WVHd€ EFFECTS DAUG SIDI 4, (continued) © Cisplatin © Polymicins Nephrotoxicity + Ototoxicity = Aminoglycosides © Loop diuretics + Cisplatin End of Session Quiz Nephrotoxicity + Neurotoxicity Anticholinergic effects * Atropine + Tricyclic antidepressants ©, blockers © Low-poteney neuroleptics 5. What medication causes cardioraiciry and bone marrow suppression? 6. An Affican-American man who goes to Africa develops anemia after taking. prophylactic medicine for primary disease prevention. In what enzyme is this patient deficient? 7. 65-year-old male patient raking multiple medications presents with gynecomastia. Which medications could be responsible for this patient’ gynecomastia? 8. A paticnt presents with tinnitus, dizziness, headaches, and GI distress. What drugs causing these symptoms? 9. What medications are known for causing drug-induced lupus?GG. Chepter 4 Anudotes (FAl4 9252) (FAIS p2S7) (SUAS p398} SLOGILNY (35)ANTIDOTES End of Session Quiz 4, What ae the antidotes to each of the following toxin? ‘Acetaminophen Salicylates “Amphetamines “Anticholinesterases, ‘organophosphates ‘Antimuscarini anticholinergic agents Digoxia Tron’ Lead ‘Arsenic, mercury, gold Copper, arsenic, gold ‘Carbon monoxide Methemoglobin Cyanide Matianl etylene gol (antifreeze) cee Opioids Benzodi ‘Teieyelic antidepressants Heparin Warfarin EPA, stveptokinase “TheophyllineCARDIOVASCULAR Embryology Congenital Heart Defects Cardiac Output Heart Failure Treatment of CHF Edema and Shock Cardiac Cycle Diastolic Heart Murmurs Carn aunawne Systolic Heart Murmurs 10 Electrophysiology 11 Antiarrhythmics 12 Electrocardiography 13 Archythmias 14 Regulation of BP 15 Hypertension 16 Antihypertensives 17 Atherosclerosis 18 Antianginal Therapy and Lipid-Lowering Agents 19 Myocardial Infarction part 1 20 Myocardial Infarction part 2 21 Cardiomyopathies and Endocarditis 22 Other Cardiac Pathology 23 Vasculitis 24 Other Vascular Diseases3 Question Warm-Up 1. What marker of inflammation produced by the liver and within atherosclerotic: plaques isa strong predictor of MI risk? 2, Whats the classic presentation of a syringomyelia? What malformation is associated with syringomyelia? (Fal4 p446, 469) (FAIS p450, 483) (WUI5 p39) 3. A 28-year-old woman is involved in a motor vehicle accident, She initially feels fine, but minutes later she loses consciousness. CT scan reveals an intracranial hemorrhage that does not cross suture lines. Which bone and vessel were injured in the crash? (4 p02) (AIS pos) (SUIS p29) 4, Outline the pathway by which the heart tube forms the atria of the four-chambered heart, Tube grows, elongates, and folds into an S-shape —> atrial chamber lays posteriorly in S, ard ventricular chamber lays anteriotyin S Arial chamber grows and incorporates superior vena cava and pulmonary vein ‘Septum primum forms Septum secundum forms incompletely (leaving a hole called foramen ovale) Call death in septum primum forms hole called ostium secundurn 5. What divides the right and left atria? AOOTOAWANS, fal ba Es ie) Q S a a c a > 2BEMBRYOLOGY | | | fo. | How is blood shunted from the right atrium to the left atrium in the embryo? ‘Through the foramen ovale (of the septum secundum) and ostium secundum (of the septum primum) ‘What are the three possible causes of an atrial septal defect? What structure grows to close the openingicanal between the atrial chamber and ventricular chamber into two smaller openings? ‘What genetic abnormality is commonly aszociated with endocardial cushion defects? ‘Outline the pathway by which the ventricles and their outflow tracts are separated. © Ventricular chamber lays anteriorly in the S-shaped heart tube —> muscular ventricular septum forms which begins to divide the ventricles © Truncoconical swellings (ridges) of the truncus arteriosus meet, fuse, and zip (both ly and inferiorly) in a 180-degree turn to form the spiral seprum (AKA aorticopulmonary septum) * Inferior portion of spiral septum mects with muscular ventricular septum to divide the ventricles and form the aorta and pulmonary arteries Name six different truncoconical (spiral) septum defects. © Tetralogy of Fallot © Persistent truncus arteriosus © Transposition of the great vessels (RV —+ aorta, LV —+ PA} + Dextrocardia © Ventricular septal defect (VSD) © Fenestrae Describe how the ventricles are remodeled in order to form the atrioventricular valves. © Myocardium erodes —> ventricles enlarge asa result —> residual mesodermal tissue becomes and forms chordie tendineae + Formation of papitlary muscles and AV valvesEnd of Session Quiz 13. Which embryologic structure ofthe heart gives rise to each of the following adule structures? + Ascending sorta and pulmonary trunk + Coronary sinus + svc + Smooth parts ofthe left and right venercles + Smooth part ofthe right atrium + Trabeculated left and sight atria + Trabeculated parts of the left and right ventricles ADOTONAW 14, What structure divides the truncus arteriosus into the aortic and pulmonary trunks? What is the cellular origin of this structure? 15. Which feral vessel has the highest oxygenation? ce) ood = ie] fe) < aod = z = aoa = 16, What causes the ductus arteriosus to close? 17. What causes the foramen ovale to close?CONGENITAL HEART DEFECTS 4, HE Chapters 236, 238 ‘Ava septal def Coaretation ofthe arta (Al 283) (FAIS 92 Rg to lft shunts (FALS p28) (FAIS p266) (SU Trarsposnen ofthe iexspd ests logy ef Flot jemalous pulmorery venous return Condi fed with cade malformations (FAM p28) (FAIS p290) 3. Question Warm-Up 1. Which cell types are rich in smooth ER? (FA'¢ p76) (FAIS p72) 2, Whatare the treatments for overdose of heparin and warfarin Al 4p2309 (AIS 9257) 3. Outline the pathway forthe generation of norepinephrine from tyrosine, (FAI p10) (AIS pi07) Ebstein anomaly © Tricuspid leaflets ae displaced is vicuspid regurgitation o stenosis 80% have apatent foramen ovale with a right to-teft shunt Dilated right atrium causing increased risk of SVT and WPW Physical exam: widely sli S,, rics regurgitation Associated with maternal use 0 ight ventricle, hypoplastic right ventrck,| End of Session Quiz ‘5, Whatare the components of the tetrabgy of Fallot? 6, Explain how the great vesels are attached in transposition ofthe great vessels. 5193490 LUV3H WLIN3DNOD 7, 45-year-old man presents with a blood pressure of 160/90 mm Hg oa the right arm and 170/92 mm Hig on the left arm, There are no palpable pulses in the feet or ankles: What problem does this patient most ikely have? a) ES i} eS 8. What heart defectis associated with each of the following disorders? $s * Chromosome 22411 deletions 6 + Down syndrome © Congenital rubella Ehvalal { + Tumer syndrome Rapib-FiRe FACTS Continuous, machinery-like heart murmur “Boot-shaped heart™ Rib notching “Most common congenial cardiac anomaly Mest common congenital cause of early cyanosis,CARDIAC OUTPUT 78 (Phy SUIS 16) (1 ples) 3 Question Warm-Up 1. Which type of collagen is used in “slippery” tissues? Which is used in “bloody” | tissues? (Ala pm AIS OTS) OUI) 2. Whar enzymes are used inthe catsboism of norepinephrine? 3. Wharare the various clinical applications of atropine? (Id p27) (FAIS p25) 4 Cardiac Output or Stroke Volume5. Cardiac and vascular function curves te eleetetelata tr Inoented . cenvacty ¢ , : cardacoupet stating A ee ee een e- + ected Mean sptemic preste sem Hg (End-dastle volume) End of Session Quiz 6. Whatis the pulse pressure in a patient with systalic blood pressure of 150 mm He: and a mean arterial pressure (MAP) of 90 mm Hg? 7. What is the basic equation for cardiac output (CO)? What is the Fick principle? 8, How can the myocardial oxygen demand be decreased in circumstances where the heartis ischemic? 9. What can make the stroke volume (SV) increase fora given preload? 10. What factors affect stroke volume (SV)? 11 Whats the cardiac election fraction (EE? Andino Dvigyy> fe) bos ES 9g Q S a halalHEART FAILURE [146] Phys Chapter 22 Choque 14 FF Chayer 24 ‘Corde pressues (414 280) FAIS p26) CHE plysoiogy (AL p21) PAIS 277) (SUIS p83 85) (Rp528) Fenn cgetensn lsterone syste (ANH pS30) (ATS pS2H) (SUIS pas) (ys p260) “CH ges ena pnpoms (FAP P291) (FAIS 297) (SUIS p& ‘BNP 3 Question Warm-Up cho4. CHF compensation z g (fSympatheticl #lViContactity—r{FCardac| | activation (output z (Voariec i § | ol 2 " a ae) FSeene) pressure, Uipiceal \Puimenan]) > (JRVeUip} (Begg venous = ‘edema > [Paimonary ‘edema congestion ————___ End of Session Quiz. 5, What are the signs of rightsided heart flure? aQ zB is] eS A a Cc = oa eo 6. What ae the signs offside hear ilure? 7, How does poor cardiac output result in an inerease in aldosterone?TREATMENT OF CHF | 4, OF CHF == TREATMEN 26 ent ofcienic CHE (FAI p29) (FAIS p297) (SUIS p84) Eagan 307) (SUIS pr) 3 Question Warm-Up 1. What are the symptoms of organophosphate poisoning? What are the symptoms of atropine overdose? (FAl4 p247) (FAIS p25) (& p245, 227) 2. Outline the pathway by which stimulation ofa G, receptor activates protein kinase C. (FAs p24) (AIS 248) GUIS p173) ‘Wich what type of congenital heart defect would increasing afierload be beneficial (F44 p282 283) (AIS 268269) Patient Profile: The Anaerobic Bodybuilder ‘A 76-year cld Caucasian man who is a competitive bodybuilder comes to the physician complaining that he has started “getting anaerobic” very quickly when exercising, Upon farther questioning, you determine that he is experiencing shortness of breath after only 2-3 minutes of exercise. Physical examination shows mild pedal edema. His lings are clear. Aa echocardiogram shows an estimated left ventricular ejection fraction of 25% without valvular dysfunction. What are the mechanisms of action of the drug lasses proven to reduce mortality inthis patient5. Which classes of drugs are proven to improve survival and reduce | hospitalizations in chronic CHF! Which are used only for symptomatic relief? | Improved Survival = ‘Symptomatic Relief 4HO 4O AN3WLVIWL 6. Cardiac glycosides (digoxin) ton Exchange ATPase Ca Gt Nat Net Ke fa) Ba Es 9g fe) < 5 fa} fs i= BS ee) End of Session Quiz 7. Whar medications are used to treat chronic heart failure? ‘8. What medications are used to treat acute heart failure? 9, What s the mechanism of action ofthe cardiac glycosides («, digaxin)>-DEMA AND SHOCK EDEMA AND SHOCK 3 Question Warm-Up 1. What drugs have each of the following sie effects? A! p252255) (5 p257 240) (5159396) + Agrinulocytosis: Osteopores 2. What adult structures are derived from the 3rd, 4th and 6th aortic arches? (FAl4 558) (AIS p64) QUIS p62) 3. What agents stimulate the release of NE from the presynaptic bouton? ‘What agents potentiate the action of NE by inhibiting its reuptake into the presynaptic cell from the synaptic cleft (als p24) (415249)4. Iilustrate the Starling forces affecting capillaries. DOHS ONY HIGa each of the following types of shock? svR_ | Co Rx fa) Ba 2 Q cS a Hypovolemic halal Carciogenie Sepsis/anaphylaxis Neurogenic Locations of central lines: Pros: easiest site w'th the least risk Cons: cannot stay in place more than 5-7 days due ta risk ofinfection Pros: good landmarks for easy placement, can remain in place 3.4 weeks, less dliscomfort ‘Cons: highest risk of pneumothorax. Not great choce in patients with COPD (barrel- chested) or ung tumors, Pros: ood landmarks for easy placement, can remain in place 3-4 weeks Cons: more discomfort, risk of puncturing the carotid or causing pneumothorax | 5. How do systemic vascular resistance (SVR) and cardiac output (CO) change in | | | | | © Swan-Ganz catheter preferred sites right IJ > left SC > right SC > left IEDEMA AND SHOCK End of Session Quiz 7. How do the following circumstances impact the Starling forces of fluid movement though capillaries? + Heart flare + Liver failure + Oliguric renal flare * Infections and toxins + Nephrotic syndrome + Lymphatic bok + Diuretic administration + IV infusion of alburain or clotting factors + Venous insufficiency 8, How does the vascular resistance and stroke volume differ in hypovolemic shock: ‘compared to septic shock? Vascular resistance Stroke volume ‘Hypovolemic shock Septic shock 9, Whatare some of the causes of cantiogenic shock? 410, How is the skin of patient differen in cardiogenic chock compared to septic chock?CARDIAC CYCLE 31949 Dvigwy> 3 Question Warm-Up What drug eategory has each of the following endings? (FA p256) (FAIS p26!) + -plitazone > -dipine 2. Two drops of drug X are instilled into a patient’s left eye. In the dark, both. pupil ae dilated. In the light, the right pupil becomes miotic while the lft pupil remains mydriatic, What is drug X? (FAIA 9247) (FAIS p251) B34 ES iS] g i a S = Ea 3. What is the antidote for each of the following toxins? (14 p252)(F'5 p257) ‘+ Ansenic, mercury, gold + «PA, streptokinase een4, Pressure-volume loop (normal) CARDIAC CYCLE g Pressure (mmHg) 8 Volume (ml) 5. Pressure-volume loop (variations) 3 Pressure (mmHg) [isa]CARDIAC CYCLE Aone premire CARDIOVASCULAR 6. Cardiac cycleCARDIAC CYCLE End of Session Quiz 7. When does isovolumetric contraction take place? 8 How does an increase in afterload affect the stroke volume of the heart assuming contractility remains the same? 9, What impact does an increase in contractility have on stoke volume assuming preload and aftcrload remain constant? 10, What heart sound is associated with dilated congestive heart failure? What heart sound is associated with chronic hypertension? ‘UL, What gives ise tothe jugular venous a, and v waves? 12, Where does the ORS complex fallin relation to valvular dynamics?DIASTOLIC HEART MURMURS (FAL 9272.2 SUAWYNH LYv3H DNOLSvia 3 Question Warm-Up 1. What drug category has each of the following endings? (FAI p254) (FAIS p26!) + -azepam, acca oO > 2. How does hemicholinium inhibit the transport of choline into the nerve 3 terminal? g Q a fa 3. Which aortic arch develops into cach of the following structures? | = (ALA p55) (FAIS p564) (SUIS p62) | Bod + Common carotid artery al » Aortic rch “* Right subclavian + Pulmonary arteries 4. What heart sounds are considered benign when there is no evidence of disease? © Splits, * Split Son inspiration +S, heart sound ina patient « 40yo © Early, quiet systolic murmurDIASTOLIC HEART MURMURS 1158)f SYSTOLIC HEART MURMURS | SHNUAW LYV3H IMOSAS. 3 Question Warm-Up 1. Outline the pathway of converting phenylalanine to epinephrine, (FAM pli) 5 pio? 2. List eight different indirect cholinergic agonists and the use for each. E GAla pe) (Als 9250) fa) bs eo iw] fo) r > ca fa Cc ¢ > a 3. Outline the flow of fetal circulation. (FAl4 p265) (FAIS p27) (SUIS p43) 4. What are the mast common causes af aortic valvular stenosis?SYSTOLIC HEART MURMURS End of Session Quiz 5. Which heart murmar is associated with weak pulses? 16. Which pathology is associated with each of the following murmurs? ‘Crescondo- decrescendo systolic murmur best heard in the 2nd- rd right interepace close to the sternum Early diastolic decrescendo ‘murmur heard best along, the left || steal border, with BP of 160/55 Late diastolic decreseendo murmur heard best along the lower lefe sternal border Holosystolic murmur best heard at the apex and often radiates to the left axi preceded by a mid-systolic click Late systolic murmur usually Crescendo- decrescendo systolic murmur best heard in the 2nd- 3rd left interspaces close to the sternum Holosystotic murmur best heard along the left lower sternal border Rambling: lecdiasrelic auarmur Seine asopes inthe Sih intesp midaxillary lire Continuous machine fike murmur (insystole and diastole)3 Question Warm-Up 1. A gardener prosente with chortnese of breath salivation, miosis, and diarthoa. ‘What eaused this? What is the mechanism of action? (Ald p20) (FS 1250) 2. What is the mechanism of action of /V-aceryleysteine when given as an antidote for acetaminophen overdose? (FAl4 pi40) (FAIS pt44) 3, What is the equation for halFTife? (Fd p239) (Al5 p43) ADOTOISAHAO¥LIT Bo eI 9 fe) e > a fa) co 5 B= EEnd of Session Quiz phases 5 8 3 z é g__ANTIARRHYTHMICS | SOINHLAHYUVILNY 3 Question Warm-Up 1. What are the four important pharmacokinetic equations? (14 9239 (FAIS p23) fa) > Es 9 iS o> rs fa) os Cc os Ey 2. What G protein clas does each ofthe following receptors strmulae>(Pal4p244) casspaa) 3. What enzyme is inhibited by fornepizole? (14 p97) FAIS p95)ANTIARRHYTHMICS End of Session Quiz 4, Whatis the mechanism of action of each class of antiarrhythmic? 5. Which antiarchythmic has the side effect of éinchonism? 6. What are the potential side effects of amiodarone use? 7. Whats the mechanism of ation of adenosine as an antiarthythmic? 8, Towhich clas of antiarrhythmics does each ofthe following agents belong? * Sotalol + Bretylium = Quinine + Verapamil + Procainamide + Lidocaine + DiltiazemELECTROCARDIOGRAPHY. 3 Question Warm-Up 4. What typically cases lesion to the mamillary bodies? (414 p45) (415 pt) 2. What effect will a noncompetitive antagonist have on V.._ and K._? Fl p242) (Als pa4s) 3. What pathology is associated with each of the following murmurs? (Fl4 p272- 273) (AS £278279) + Cresoendo-decrescendo systolic murmur best heard in the 2nd-3rd right Jnterspace close to the sternum + Rumbling lte-diastolic murmur with an opesing 1 Paspcts AKASiapeal rae Se are ons a spaces, adjacent to the sternum * Continuous machine-like murmur (in systole nd diastole) ECG axis, ‘The net electrical signal (anda ans wl all within the shaded region in normal caediae physiology. AHeV¥DOIYYIONLIITA 9 Bs Es iw) g 5 A fal c 5 Bs eoELECTROCARDIOGRAPHY 5, Common conditions that result in axis deviation: © Leftaxcis deviation Inferior wall myocardal nfarction Left anterior fascicular block Left ventricular hypertrophy (ometimes) Left bundle branch block (888) © Right axis deviation Right ventricular hypertrophy ‘Acute night heart strain (eg, massve pulmonary embotsir) Left posterior fascicular block Right bundle branch block (RBBB) End of Session Quiz 6. How does the cause of a narrow QRS complex differ from the cause of a wide QRS complex? 7, Whatis the ECG axis given the QRS deflections in each of the following scenarios? ~ Positive in lead 1, postive in lead II « Positive in lead I, negative i lead IL « Negative in lead I, postive in lad 11 « Positive in lead I, negative in VR 8, How does hyperkalemia affect the shape of T waves? 9, What are the most common causes of left axis and right axis deviation?ARRHYTHMIAS | SVINHLARWUY 08 62) (H p89) re 2329) 3 Question Warm-Up 11. Whats the vasopressor of choice for anaphylactic shock? Cardiogenic shock? Septic shock? (E14 p248) (FAIS p253) 2. On auscultation ofa patient, you hear a pansystolic murmur atthe apex with radiation to the axilla. What is the most likely cause of this murmur? FA pZ70) Gals 2) S z 6 9 > z id e i= Pa Fs 3. What drug inhibits the cellular sodium-potassium ATPase? (F414 p79 (FS 075) 4, Atrial fibrillationARRHYTHMIAS9. Third degree AV block SVIMHLAHWYY [169]13, Ventricular escape rhythm 14, Junctional escape rhythm, 15. Monomorphic ventricular tachycardia : : | 16, Torsades de oointes (170)17. Drugs that prolong the QT interval Antisinfectives: macrolides, chloroquine Anti-psychotics: haloperidol, risperidone Methadone Anti-HIV protease inhibitors (navirs) ‘Antiarthythmics: class 1A (quinidine) and class 11 (K. channel blockers such as sotalol) 18. Ventricular fibrillation End of Session Quiz 19, Whatis the initial treatment for ventricular fibrillation? 20. What are the mjor characteristics of ail fibrillation? ‘21. What is the hallmark of a third degree AV block? 22. What drugs are known tn prolong the CUT interval, increasing the likelihood of torsades de pointes in those at risk? 23. What are the two different types of second degree AV block? How do they diffe? 24, Why is warfarin anticoagulation important in patents with chronic atrial fibrillation? SVIWHLAHWEY fa) bo FS Q fo) 2 > &REGULATION OF BP REGULATION OF BP Buoreceprrs (FAM 280) (1 cmorecepsors (FAL 280) (AS 286) Pdi eas pa) 0) (FAIS p25. 534) 3 Question Warm-Up 1, What isthe mechanism and time frame of acute transplant rejection? (a4 p2) (PANS 217) (SU 9385) 2. What GI problem is most closely associated with each of the fellowing? postive AMA Gl bleeding and buccal pigmentation 60yo woman, RA, no alcoho! history, fatigue and right abdominal pain; clevated ANA and ASMA, elevated serum IgG levels, no viral serologic markers 23yo woman, no alcohol history; elevated levels of LKM-1 antibodies, no viral serologic ‘markers, liver biopsy with infiltration of the portal and periportal area with lymphocytes Fatal disease of unconjugated bilirubin resulting from a complete lack of UDPGT activity 3, Avweightlifter undergoes emergency surgery for a life-threatening condition. Examination of a section of his small bowel reveals focal hemocthages. What is the process responsible for this?4. Physiology of vasoconstriction Sildenafil * bradykinin (Miagray Smooth muscle call Ach *alpha-2- agonist *hetamine 8 40 NOWWINDIY ‘Endothelial cell trates ; “*Carchannel _ * Epinephrine Gy Mas UPS blockers" + Prostaglandin €2 End of Session Quiz 5. Outline the mechanism by which the kidneys regulate blood pressure, Q s ay fa) Ss Ss a oo] 6, What substances act on smooth muscle myosin light chain kinase? How does this affect blood pressure? 7. Deseribe the chain of evens in which hypotension causes reflex tachycardia.HYPERTENSION 3 Question Warm-Up 4. Which immunosappressant marches each of the following statements? + Precunor of 6-meraptopurine + Antibody that binds to CD3 on T ells + Ansibody that binds IL-2 receptor on activated T cells «Inhibits inosine monophosphate dehydrogenase + Tohibits ealdneuria ~ loss of IL-2 production ~> blockage of T cell diferenation and activation + Metabolized by anthine ondase, therefore allopurinol increases is toxivity 2. What are the five 2s of a Mectcel diverticulum? (7414 p356) (FAIS 364) SU15 p16) 3. Whavis the ereatment for Zollinger-Elison syndrome? (AM p32) (AS p336 337) |. What causes secondary hypertension? eros common © Chronie kidney disease (CKD) or end stage renal disease (ESRD) © Medications , NSAIDs, antidepressants, glucocorticoids) © Tlliciedrugs (eg, cocaine, amphetamines) © Adrenal discase (hypercortisolism, hyperaldosteronism, pheochromocytoma) Hypercortisolsm (Cushing syndrome) Hyperdtdosteronism (Conn syndrome) Hypothyroidism Hyperparathyroidism CCoaretation of the aortaEnd of Session Quiz 5. Whatisthe blood pressure cutoff forthe dlagnods of hypertension? 6. What would you most suspect the cause of hypertension to bein a patient with cach ofthe following clinical ues? ~ Parcaysins of increased sympathetic tone: anxiety, palpitations, diaphoresis « Age of onset beeween 20 and 50 + Abdominal brit « Blood pressure in arms > legs + Family history of HTN + Tachycardia, heat incoleranc, diarrhea + Hyperkalemia + Hypokalemia + Central obesity, moon shaped fae, hirsutism + Young individual with acute onset tachycardia + Proteinuria 7, What chest ay finding isa possible sign for aortic dissection? 8. What category of blood pressure medications is preferred in the treatment of aortic dissection? NOISNALYRUAH re) oy e Q Q S a ral c i= > zsIVES ANTIHYPERTEN 6G Chapters 25,24 Pry Chopter 12 ACE intces (FAL Angotersn recep FA'S P9S8) blockers (FAL p23) (FAIS p30%) (SUIS p77 78) (FAL 9298) (FAIS 1304) (SUIS p77, 79) ramos (SUI p77, 79) {GG p28!) ‘Nites FAM p 299) (FAIS p ng on anuhyper 5 p55) (SUIS pr) (FAL p555) (SUIS pre) (SUIS pA ver (FAI 299) (FAIS p304) (GG p772 784) 3 Question Warm-Up ‘A patient with recent kicney transplant on cyclosporine for immunosuppression requires an antifungal agent for candidiasis, What antifungal agent would result in cyclosporine toxicity? (F< p255) (FAS p260) 2. What nerve is damaged when a patient presents with each of the following upper extremity symptoms? (FAM pl4) (FAIS p4l8) + Scapular winging + Los of forearm pronation + Cannot abiuet or adduct fingers + Weak extemal rotation of arm. “+ Unable to abduct arm beyond 10 degrees 3. What nerve damage causes carpal runnel syndrome? (AI4 pz, 414) (AIS pA? 418) 4, Calcium channel blockers (CCBs) ‘© Dihydropyridines: amledlipine,felodipine, nicardipine, nifedipine, nlsoldipine Mechanism act on vascular smooth muscle to cause vasodation Therapeutic use: hypertension, angina, vasospasm (Prinzmetals angina, Raynaud phenomenon} esophageal spasm, migraine prophyiaxs ‘Adverse effects: peripheral edema, fishing dizziness, constipation, reflex tachycarcka + Non-dinydropyridines diltizem, verapamil Mechanism tock calcium channels at pacemaker cells ‘Therapeutic use. hypertension, angina, arrhythmias Adverse effects: cardiac depression, AV block flushing dizziness, constipation5 6 2 Minoxidil © Mechanism: opens K* channels and hyperpolarizes smooth muscle, resulting in rlaxation ‘of vascular smooth muscle © Therapeutic use: severe hypertension, topical application for h © Adverse effects: hypertrichosis, hypotension, reflex tachyca What are the JNC-8 recommendations for initial antihypertensive pharmacotherapy in each of the following patient populations? Population Inicial pharmacotherapy CKD patients Black patients (without CKD) Non-black patients (without CKD) For each comorbid candition, which antibypertensives might be considered first, and which antihypertensives should be avoided (either used with caution, or absolutely contraindicated)? Hypertension plus... | Initial Therapy Options _|_Avoid ~ ACE inhibitor/ARB * CCB a + B-blocker + B-blocker (in acute decompensated CHF cr cardiogenic shock) © Aldosterone antagonist Da ‘ACE inhibitor/ARB B-blocker * Thiazide B-blocker ACE inhibitor/ARB CCB (as needed for angina) Nitrates (as needed for angina) Post-MI/CAD : B-blocker Atsial fibrillation 2 Ene verapamil = Beblocker Bradycardia + Diltiazem/verapamil BPH acblocker > Hydralazine ‘ACE inhibito/ARB 5 + Methyldopa *regnancy + Labetalol Dihydropyridine CCB ' * CCB Migeaines * B-blocker Essential tremor Propranolol S3ASN3LY3dAHUNY Bs Ea iS) Sg > a a cs S Bo efERTENSIVES ANTIHYP# End of Session Quiz 8. Which antihypertensive class or drug fits each of the following side effects? Hypertrichosis Cyanide toxicity Reflex tachycardia Cough Posible development of drug-induced kapas Possible angioedema 9. Which autlypertensives are pa Geulaily Leveliial w beat falar patients 410, Which antihypertensives are safe to use in pregnancy?ATHEROSCLEROSIS | 3 Question Warm-Up 1, Where do neurons of the lateral corticospinal tract synapse prior to exiting the spinal con to affect movement? (4/4 p46) (AS p#70) 2. Whar drugs and endogenous hormones regulate the secretion of gastric acid? {FAl4 p16) (FAIS 1354) 3. Whats the difference between direct bilirubin and indirect bilirubin? (4/4 p34%) (AIS 357), BHLV SISOURTOSOY: ba ea 9g iS > rv fa) = = B= eo4. Pathogenesis of atherosclerosis ‘* Endothelial dysfunction: leads to increased vascular permeabil thrombosis leukocyte adhesion and © Accumulation of lipoproteins: occurs in the vessel wall and is mostly LDL = Monocyte adhesion to the endothelium: migration of the monocytes into the intima and then transformation ofthese cells into macrophages and foam cells © Factor release: activated platelets, macrophages and inflammatory mediseors ‘© Smooth muscle cell proliferaion: migration of smoorh muscle cls into intiria © Lipedaccurmulstion: occurs extracellularly and within macrophages and smooth muscle cals ATHEROSCLEROSIS 3. Abdominal aortic aneurysm + Caused by atherosclerotic plaque compressing the underlying media © Nutrient and waste diffusion is compromised © Media deyenerates and necroses, eaing to arterial wall weakness “More common in men over 50 and in smokers Presents a a pulsating mass in the abdomen Consequences include: rupture leading to fatal hemorehage, embolism from atheroma, ‘obstruction of a branch vessel and impingement on an adjacent structure (ureter)4. Deadly causes of acute chest pain © Aortic dissection (or dissecting aortic aneurysm) © Unstable angina MI © Tension pneumothorax ° PE SisOWsTOSOWIHIY 7. What is the most likely cause of chest pain in each of the following scenarios? ST segment elevation only during brief episodes of chest pain Patients abe to point to localize the chest pain using one finger Chest wall tenderness on palpation Rapid onset sharp chest pain that radiates tothe scapula Rapid onsct sharp pain in a 20-year-old and associated with dyspnea Oceurs afer heavy meals and improved by antacids Sharp pain lasting hours-days and is somewhat relieved by sitting forward Pain made worse by deep breathing and/or motion ‘Chest pain in a dermatomal distribution ‘Most common cause of non-cardiac chest pain End of Session Quiz 8 A.68-year old man has an abdominal ultrasound performed to check on the status ‘oF his abdominal aortic aneurysm (AAA). His last ulerasound from 6 months ago showed 2 maximum dilation of 45 em. This most recent uasound reveals that this AAA has enlarged to 5.1 em. He is asymptomatic. What isthe best next stp in his management? 2 Fe fa) C = > ea 9. A patent with poody managed HTN has sew, sharp substeral pain that adits ‘to the back and progresses over a few hours. Death occurs in a few hours. What is the most likely diagnosis? 40. Whats the most likely cause of chest pain in each ofthe following scenarios? “+ Acute onset dyspnea, tachycardia, and confusion in the hospitalized patict + Rapid onset of sharp pain in the 20-yearold and associated with dyspnea + Pain began the day following an intensive new exercise program ‘ST segment elevation only during brief episodes of chest pain + Sharp pain lasting hours to days and is somewhat relieved by sitting forward + Chest wall tenderness on palpation| ANTIANGINALTHERAPYAND D-LOWERING AGENTS 3 Question Warm-Up 1L._Label the following diagram of hing volumes. 44 p55) (AS pe02) i E p i = on 2, Whar subssance is important for relaxing the lower esophageal sphincter? (Pal p35 (als 1388) 3. Whats the most common type of TE fismula?rai« p33, 353) (a5 nz 559)End of Session Quiz 4. Which lipid dowering agent matches cach ofthe folowing descriptions? + SE: facial Sushing + SE: dlevated LFTs, myositis «+ SE: Gl discomfort, bad tate + Best effect on HDL + Best effect on trighcerides/VLDL + Best effect on LDL/cholesterl + Binds ©, dif toxio HL TYNIDNVILNY, B > z 6 2 8 5. A50-year-old man starts on lipid Jowering medication. Upon his frst dose, he develops arash, pruritus, and diarshea. What drug is he taking? SANaDV ONIY: 6. How can the flushing reaction of niacin be prevented? fa) Ba oa 1S) fe) 5 ro fa) Cc = — EoMYOCARDIAL INFARCTION PART | MYOCARDIAL INFARCTION PART | 3 Question Warm-Up 1. Whatis the classic presentation of congenital pyloric stenods? 4 p24) AIS pa) 2, For what eype of information is each of the following thalamic nuclei a relay station? (FA p52) (FAIS 456) + Ventral posterior lateral © Lateral geniculate + Ventral posterior medial + Ventral anterior 3, How does fetal hemoglobin differ from adult hemoglobin? (Al p597 (FAS p03)4. Evolution of an MI Timeframe | Gross Features | Microscopic Risks and Other Features Findings O-4 hes 42 bes 12-24 hes | Lud NOLLO¥VSNI TWId¥¥DOAH 153 days 3-14 days > 2weeks 5. ECG evolution of an MI STelevated | Twavelnvers | sTaormal ST normal wave decreases [wave deepent | Twavelnverted Twavenotml ‘aware appears ECG changes with MI (always obtain a previous ECG for comparison!) ‘© ST segment clevation ofa east 1 mm in 2 contiguous leads +» Twave inversion, + New LBBB © New Quaves (atleast 1 block wide or 1/3 height ofthe tts! QRS complex) a bs ra S] I a fa)MYOCARDIAL INFARCTION PART | End of Session Quiz 7. Which serum lab markers are commonly used to make the diagneeie of MI? 8, Which coronary artery is most commonly occluded in an MIP 9. What's the mast common lethal complication after a myocardial infarction? Rapip-Fire FACTS | Chest pain, pericardial friction | rab, and persistent fever occurring several weeks after an MIaxomy and Mls complcatians FAN p289) (FAIS p29S) (SUIS p62) 3 Question Warm-Up 1, Which hereditary hypesbilirubinemia matches each ofthe following statement? (4149369 6915 p37) = Mildly decreased UDPGT + Completely absent UDPGT + Grosly black iver + Responds to phenobasbital + Treatment includes plasmapheresis and phototherapy + Asymptomatic unless under physical stress alcohol, infection) 2, What infectious complication may arise from pulmonary silicosis? FAM p04) (AIS p12) 3, What are the pathological characteristics of the arteries in pulmonary hypertension? FA p599, 606) (EAS pe05, 64) |. Arteries ~ Walls - ECG Leads Artery Wall perfused | ECG leads Lefi anterior descending | Anterior wall Vi-Va, VS Lefi circumflex Lateral wall aVL, V5, V6 Right coronary Inferior wall” TT aVF, Right coronary Posterior wall__|R precordial EKG: V4 Always obtain a ight-sided ECG (VI-V6 on segment elevation in V4, then posterior right ve sided MI = fluids and avoid nitroglycerin chest) in inferior wall MI if ST. ele ulsy affected. This indicates right- 7.LW¥d NOILDWVJNI TYIG’Y2OAH fa) > ES iw) 2 > i fa} c = > eSMYOCARDIAL INFARCTION PART 2 5. Myocardial infarction treatment * ABCs » MONA: IV morphine Suprlemertal O, Nearoghcenn Aspain © Beblocker: oral metoprolol if no signs of heart failure or severe asthma © Sutin: atorvastatin, preferably before percutaneous intervention (PCI) © Antiplatelet therapy to all patients: clopidogrel or ticagrelor © Anticoagulant therapy to all patients: Unractionated heparin toa patents undergoing PCL Enoxaparn for patients not maraged wth POL + Ponassium and magnesium © IfST elevation myocardial infarction (STEMI): PCr |F PCs unavaable: lrinahss within 90-120 mites © Ifnon-ST elevation myocardial infarction (NSTEMI): Avoid fibrinolysis Pct If sigificane coronary artery disease on PCI: stenting or coronary artery bypass graft End of Session Quiz 66. What would cause each ofthe following findings afteran MIP «+ Cardiac tamponade «© Severe mitral regung + New VSD_ + Stroke 7. Which ECG leads will show evidence of ischemia in an anterior wall MI? 8, Tow would you usage patient presenting with an acute myocardial infarction?Canomyopathies = Fypertropi cardi thy PA p20) (A 1 Hit p20) AS pe (p59 1 (SUIS p37} 3 Question Warm-Up 1. Atwhat age should patients begin receiving screening colonoscopies? 2. What is the triad of Kartagener syndrome? What is the underlying defect? (PALA p78, 6) (AIS p74, 64) SUIS 02) 3, What are the classi symptoms of carcinoid syndrome? (4/4 p29) (FAIS p334) (SJI5 pid) Myocarditis © Generalized inflammation of the myocardium (not resulting from * Most common cause (in the U.S): © Hist: diffuse interstitial infiltrate of, ch What are the typical signs and symptoms of endocarditis? © Fever chills, weakness, anorexia © New regurgitation heart murmur or heat failure Mitral valve is most common “Tricuspid is most common in IV drug users —> septic pulmonary infarcts Splinter hemorrhages in fingernails * Osler nodes (painful red nodules on finger and toe pads) ‘Janeway lesions (erythematous macules on palme and sole) ‘Roth spots (retinal hemorshages with clear central areas) © Signs of embolism: brain infarct ~ focal neuro defeets, renal infuret “> hematuria, splenic infaret > abdominal or shoulder pain Systemic immune reaction: glomerulonephrits, arthritis ONY SaIHLvsOANOIaWY> siua¥y30aN fa) b= eS Q 9 ee 5 ra fa) om ‘ Minor criteria: Arthralgia Fever Elevated ESR or CRP Prolonged PR interval on ECG. ADOTOHLWs D¥IG¥VD WHO oO oa 2 g fe) SS re fay C¢ i= Pod EsARDIAC PATHOLOGY OTHER 5. Kussmaul’s sign vs. Pulsus paradoxus: Kussmaul’s sign Pulsus paradoxus Event IVD during inspiration Decreased SBP by more than 10 mm Hg during inspiration ‘Mechanism | Decreased capacity of RV Decreased capacity of LV Disease ___| Constrctve pericartiis > tamponade | Cardiac tamponade » Pericarditis End of Session Quiz 66. Under what circumstances might you se pulsus paradanus? 7. Whatare the Jones criteria for the diagnosis of acute sheumatic fever? 8, What heart pathology fits each ofthe folowing statements? ‘Focal myocardial inflammation with tnultinaleate giant cells Chest pain and course rubbing heart sounds in patient with Cr of 5.0 “Tree-barking of the aorta Child with fever, joint pain, cutaneous nodules four weeks after a throat infection ‘ST elevation in all ECG leads ECG shows electrical alternans Rapio-Fire FACTS Granulomatous nodules in the heart ‘Most common primary cardiae tumor in | adults “Most common primary cardiae tumor in child _ Most common cause of constrictive pericarditis3 Question Warm-Up 4. What isthe difference between primary biliary circhosis and primary serosing cholangitis? (14 360) (a15 374 G5 p35) 2. Apatient develops ARDS from an occupational inbialation of nitrogen dioxide, What histologic change is seen in a patient recovering from ARDS? 3. Whatis Reynolds pentad for cholangitis? SUIS ps) SILIINDS¥A fe) b= Ea iS] a > ra EalalVASCULITIS End of Session Quiz 4. Which type of vasculitis its each ofthe folowing high-yield characteristics? ‘Weak pulses in upper extremities Granulomas of lung, glomerulonephritis, | ANCA positive "Necrotizing immune complex inflammation of viceral/renal vessels | 2-year-old East Asian female 20-year-old East Asian female ‘Young male smokers ‘Young asthmatics coronary arteries ‘Most common vasculitis | | | Infants and young children; inyolves the | ‘Associated with hepatitis B infection j Occlusion of ophthalmic artery can Tead | to blindness Perforation of nasal septum Unilateral headache, jaw claudication Rapip-Fire Facts ANCA | p-ANCA| Treatm: or thromboangitis obit “Treatment for giant coll arteritisber dscase (FA: 3 Question Warm-Up 4. An IV drug user presents with chest pain, dyspnea, tachycardia, and tachypnea. ‘Whaat is the most likely cause? 2. A patient ina motor vehicle accident presents with chest pain, dyspnea, tachycardia, and tachypnea. What isthe most likely cause? 3. A post-op patient presents with chest pain, dyspnea, tachycardia, and tachypnea. What is the most likely cause? Patient Profile: The Shivering Scoutmaster A volunteer leader in a local youth organization comes to the physician complaining thae when he is camping in the winter months, his ight middle finger becomes quite cold and turns first white then dusky blue. This discoloration often spreads to other fingers on both hands. After about 15 minutes of warming his hands, the fingers ‘become quite red before returning to their normal color. What is the most likely diagnosis, and how can this disorder be treated? ‘S35¥3SI0 WW'INDSKA WHLO fa) bs ra 1S) ro} 4 Pa fa) c = > es‘OTHER VASCULAR DISEASES End of Session Quiz 5, Which disorders are commonly discovered in patients with Raynaud phenomenon? ‘6. Which vacular tumor fits each of the following desc:ptions? Benign, raised, red lesion about the size of a mok in older patients Raised, red area present at birth, inereases in size initially then regresses ‘over months to years Lesion caused by lymphoangiogenic rowth factorsin an FAV patient Polypoid red lesion found in pregnancy or after trauma Benign, painful, red blue tumor under fingernails Cavernous lymphangioma associated with ‘Turner syndrome ‘Skin papule in AIDS patient caused by Bartonella spp. fnRHEUM AND DERM 1 Bone Formation and Bone Tumors 2 Bone Disorders 3 Musculoskeletal Injuries 4 Osteoarthritis and Rheumatoid Arthritis 5S Other Types of Arthritis 6 Systemic Disorders 7 Dermatology part 1 8 Dermatology part 2 C CORRECTLY. ISCIPLINESBONE FORMATION/AND BONE TUMORS) 3 Question Warm-Up 1 What drug caregory has each of the following endings? (4 p250 (AIS p26) -olol SYOHIAL 3NO8 ONY NOILYH¥Od 3NO: ° -oxin ° pail aren © tropin, 2. Which a-adrenergic antagonists are used in the treatment of pheochromocytorma? (FAl4 p250) (FAIS p255) 3. Why do the kidneys retain Buid in heart failure patients? es) a nm Cc 4 os ra G Go inal 2) 4FORMATION AND BONE TUMOR: BON End of Session Quiz 4, Where does new bone formation take place in growing long bones? 5. Which primary bone tumor fits each ofthe following descriptions? ‘+ Most common malignant primary bone rumor of children “+ Most common benign bone tumor + 1;22 translocation + *Sunburst” pattern on x-ray + *Soap- bubble” appearance on ray += *Onion-skin” appearance of bone + May actualy bea hamartoma + Codman’ triangle on x-ray 6. What mutation lead to achondroplasia?3NO@ suaayosia 3 Question Warm-Up 1. Name five drugs that inhibit acetylholinesterase. Whats the clinical application fo each? (Fs p2s) lS p250) 2. When placing a femoral venous catheter, while palpating the pulsatile femoral artery, where ie the femoral catheter placed in relation tothe artery? (Al4p342) (ANS 9350) 3. What ae the different mechanisms by which heart contractility can be Smcreased? (FA4 p26?) (FAIS 9273) ] a C 4 > va GS 9 a ey <4BONE DISORDERS Osteoporosis treatment ‘© Stop smoking, stop alcohol consumption, stop steroids (if able), avoid PPIs and H, blockers (if possible) © Exercise (aerobic, resstance, and weight bearing) Falls assessment at home Vitamin D supplementation (Calcium supplementation Bisphosphonates (inhibit osteoclastic resorption, reduce fracture risk by 40-50%) ‘Teriparatide (rocombinant PTH analogue that stimulates osteoblasts) decreases hip fracture rate by 53%. Duration of therapy not ro exceed two years. Must use bisphosphonate afer stopping teriparatide to maintain bon mineral density. Other treatments worth knowing: + Conjugated estrogen (WHI tial ~ hip fracture reduction of 33%): USPSTF recommends not using estrogen for the sole purpose for fracture reduction risk duc to risk of ather side effects (MT and CVA). @ SERM (caloifene) decreases vertebral facture by 40% in women with osteoporosis, no effect on rsk of non-vertebral fracture risk, reduces risk of breast cancer. Calcitonin (Miacalen) inhibits osteoclasts, given nasally or SC/IM not as effective as bisphosphonates in fact, overall effectivencssis questionable © Denosumats: RANK-L inhibitor, inhibits osteoclast activity Osteitis fibrosa cystica (AKA von Recklinghausen disease of bone) © Abony manifestation ofan endocrine disorder * Can be caused by: Hyperparathyroidm High PTH — high serum caldum, low serum phosphate, high akatne Phosphatase “Type IA pseudohypoparathyroidsm (AKA Albright hereditary osteodystrophy) + PTH redstance at the renal tubules ~? low serum calcium and high phosphate + Low cau hygh PIHL © High PTH — exces osteoclastic activity > “brown tumors” in bone which are eystie spaces lined by osteoclasts filled with fibrous stroma and blood * DEXA scanrevealslow bone mineral density, but the mechanism of bone losis different from osteoporosis6. Bone disorder labs Serum Ca" | Serum Phos | AlkPhos [PTH Osteoporosis Osteopetrosis Paget disease Rickots/osteomalacia Renal insufficiency | Vitamin D intoxication Primary hyperparathyroidism Osteitis fibrosa cystica End of Session Quiz 7. What cell type is most similar to osteoclasts? ‘8. Which bony disease fits each of the following descriptions? + Reversible when vitamin D is replaced + Excess osteoclastic activity results in disorganized bony archireccure + Bone is replaced by fibroblasts, collagen, and iregular bony trabeculae + Soft bones due to defective mineralization of osteoid + Failure of bone resorption ~ thickened and danse bones » Genetic deficiency of carbonic anhydrase I 9. What measures can be taken to prevent osteoporosis? 10. Fillin the following table ‘Scrum Ca’ _| Serum Phos | Alk Phos | PTH Paget disease ‘Ostsomalacia/vickets Osteitis fbrosa cystica Osteoporosis Rapib-Fire FACTS. Bi ‘bone pain, arthritis pression fracture — S¥qNOSIG NOG Ele Asia latslMUSCULOSKELETAL INJURIES ration (SUIS p22) 3 Question Warm-Up 1, What drug category has each of the following endings? (Fl4 p258) (15 p26)) + -dronate + cho > -mstine + statin + “bendazale 2. What are the side effects of arniodarone? (FA!4 p203) (FAIS p30%) SUIS p05) 3. What are the conditions that cause diastolic murmurs? (FA\4 p273) (FAIS p27) (U5 par)4. Whatis the most common type of hip dislocation? What structures can be damaged with this type of dislocation? © Most common type: © Structures injured: Medial and lateral crcurflex femoral erteres : ven ___ verve 5. Patellofemoral syndrome Leading cause of knee pain in patients under age 45 © Typically presents with anterior knee pain that is exacerbated by activity © Treatment: Strengthening the — © Stretching exercises (hamstrings, cakes, hip, and ilotbial band) _______attwvities that put excessive stress on the knee: ‘waking and other low impact exercise Knee bursitis © Prepatellar bursitis (Chousemaid’s knee") ~ pressure anterior to the patella * Infrapatllar bursitis clergyman's knee”) ~ pressure on the tibial tuberosity How should an ankle sprain be treated? Ro ei] °C. cE NSAIDs Range of motion exercises 8, Plantar fasciitis © Characteristic features: Pain beneath the calcaneus orn the medial arch, worse withthe first steps in the ‘moming and after weight bearing - at the medal tubercle of the calcaneus #/-heel spur on xray © Treatment: NSAIDs Dorsitlexion wit right spits = Stretching the plantar fascia and Achiles tendon + OTC heel inserts Local steroid injections Surgcal release ofthe plantar fascia in severe cases sanuniNi wLaTaNsoINOsNH a nm cont = Bs Zz 5 ie] im & <JURIES MUSCULOSKELETAL ‘Whaat is the difference between a dislocated shoulder and a separated shoulder? + Dislocated head of humerus rotates out of glenoid cavity © Separated clavicle separates from acromion and coracoid process ofthe scapula 10, What structures can be damaged in an anterior shoulder dislocation? ® Axillary nerve and posterior circumflex artery © Supraspinatus tendon © Anterior glenohumeral ligaments and glenoid labrum separation from the articular surface of che anterior glenoid neck (AKA Banka lesion) © Posterolaceral humeral head defect (duc to abrasion against the anterior i {AKA Hill-Sachs lesion) of the glenoid) 1, Adhesive capsulitis © Severe shoulder adhesions that lock the shoulder in place; seen with disuse of the shoulder duc to pain or prolonged immobilization, + Presentation Resvicted use ofthe shoulder Plain says ‘Arthrogram shows constriction ofthe joint capsule and loss of axilary and subscapularis spaces, © Treatment ‘Glenohumeral cnt injection ‘Subacromial ont injection Heat and analgesia toincrease range of mction Break the adhesions under anes hesia 12, Epicondylitis > Lateral epicondylitis (‘tenniselbow") + Medial epicondylitis (goers elbow")End of Session Quiz 13. What ligamens are typically injured during an ankle sprain? 14, Whar the leading cause of knee pain in patents younger than 45? 15. Whats the other name for housemnaid’s knee? 16, Which muscles of the rotator cuff are responsible for each of the following actions? «= Initial 15 degrees of arm abduction 17. Which antibiotic clase is known to increase the rik of tendon rupeure in adults? Rapio-Fire FACTS [_ Pore ansir drome sgn IUNINI WLIIaNSOTNISAN PAMELOR IN Aa IaF ats| (OSTEOARTHRITIS AND RHEUMATOID ARTHRITIS E g “OARTHRI 3 Question Warm-Up 1. What effect will a noncompe (FANS p246) IS pio) antagonist have on V,., and K,? (al4 p24, oO 2, What effect will a competitive antagonist have on efficacy and porency? (A421 GS pote) SUIS pI) 3, An 80-year-old man presents with a systolic crescendo-decrescendo murmur. ‘Whatis the mos likely cause? (Al4 (273) FAIS 279) SUIS p85)1S End of Session Quiz 4, Whatis the classic earure of osteoarthritis? 5. What two antibodies are most useful in diagnosing cheumatoid arthritis? 8 & 3 z 2 6 s 5 2 5 z 3 z 6. By what mechanism do NSAIDs cause renal disease? Rapib-Fire Facts Swollen, hard, painful finger joints Swollen, boggy, painful finger joints | Cartilage erosion with polished bone [_bencat = = x4 oo ra io] iv] ™ 2 xdER TYPES OF ARTHR oTHe OTHER TYPES OF ARTHRITIS 1441) (AIS pt 11 p26) (PALS po 3 Question Warm-Up 1. Whatis the competitive antagonist used in cases of benzodiazepine overdose? {FAIA 252) (FAIS p257) 2. Place the following agents in the appropriate categories: (PAA p24e 25) FAIS p250 256) norepinephrine, metoprolol, uma), scopolamine, phenoxybenzomine, bethanechol, (opatenotdonepeal prema oropne, etl) cto erbucie, dopamine, pilocarpine, carbachol, edrophonium, phenylephrine, Bh eroate: ‘phentolamine, neostigmine, benztropine, terazosin, prakdaxime, echothiophate, Ipratropum, epinephrine, esmolol, oxybutyrin, doxazosn Dicer Neer ic gone Indirect cholinergic agonists (Cholinergic antagonists: ‘Cholineserare regenersior ‘adrenergic antagonists (blocker) Sympathomimetics: 2, 6B Bago 2.0, Bagoniet D,=0,> 8,» @agoniat B-advenergic antagonist (B-blocker) B= 8, agit BB, agonist re > 6 agit 3, What s the mechanism of action of the bisphosphonates? (A p140) FAS pt45)4, Juvenile idiopathic arthritis (JIA) © Affects children (onset before age 10) © Persistent joint swelling (synovial thickening, accumulation of synovial Aud) © Subtypes - severe symmetrical arthritis, dactylts ~typicaly involves large pints 20-25% have welts 5 (Gtis disease) - begins with systemic Sampions (ever rath, eleated WAC, anemia, hepatosplenomegayerphadenopainy) End of Session Quiz 5. What medications are used in the treatment of an acute gout exacerbation? ‘6. What drugs can be used in the treatment of chronic gout? 7. X-rays of a patient’ fingers show pencil-in-cup deformities. What is the most Tikely diagnosis? 8, A sexually active 19-year-old man presents with pink eye, arthritis of the right ‘knee, and dysuria. Whats the most likely diagnosis? Rapip-Fike FACTS Swollen, red, acutely painful great toe joine Positively bis crystals fringent rhomboid-shaped. Negatively birefringent needle-shaped crystals Bamboo spine on x-ray HLA-B27, SLLIVHAWY 4 S31 WBHLO Wad GNV WAJH¥| SYSTEMIC DISORDERS _ a 3 Question Warm-Up 1. What bone disorder results from excess PTH? 2. What are the clinical uses for each ofthe following antimuscarinic drugs? (Ala pot AIS 9251) * Ipratropium + Atropine, homatropine, tropicamide + Benctropine + Scopolamine 3. Which receptors use a G, protein? ((Al4 p24) FAS p218) 4. Systemic lupus erythematosus = 4/11 | © Skin disorders | Malar rash | Dscoid rash | = Photosensitvity | ~ Painless oral ulcers | Inflammatory disorders | ‘Arthritis (Pon-erosive, 2 joints) Serostis (pleut, pericartits) () ANA © Ongan system disorders = Renal (proteinuria, cellular casts) ‘Neuro (seizures, psychosis) Heme (hemolytic anemia, leukopenia lymphopenia thrombocytopenia) {immune (antiphospholipid antibodies, anti-dsONA, anti-Smith, false-positive VDRL)5. Fibromyalgia 4 © Excess muscular tenderness in 11 of 18 particular sites 4 * Chronic generalized pain, fatigue, slep disturbances, HAA, cognitive difficulty, mood 2 disuinaces 5 © 30% also have depression and/or anxiety 3B * Pharmacological treatment 2 FDA approvedt pregabat, mihacipran 2 “Traditional (non FDA-approved): amitnptyine low-dose analgesic, Nuoxetine ° Non-pharmacological treatment | ~ Reassurance tht itis areal disease and that tis beng, exercise and stretching, seep, relaxation techniques, stress reduction End of Session Quiz 6. A patient presents with photosensitivity, arthritis, hemolytic anemia and recurrent ‘oral ulcers. What isthe most likely diagnosis? 7. What drugs are known for causing drug-induced Iupas? 8, What are some of the characteristics of polymyositis that distinguish it from polymyalyia theurnatic? 2 a iS i b= Zz is] ie} fat = Rapi-Fire Facts Anti-Smith and anti-dsDNA antibodies: Anti-histone antibodies { A -centromere antibodies Anti-topoisomerase antibodies Anti-Jo-1 antibodies Anti-Ro antibodies Arthritis, dry mouth, and dry eyes ‘Most common cause of death in SLEDERMATOLOGY PART DERMATOLOGY PAI ig 3 Question Warm-Up 1. How does the drug dose responce curve change with the addition of a ‘competitive antagonist compared to a noncompetitive antagonist? (FA/4 p242) (FAIS p24) 2. What are the various clinical uses for the following sympathomimetic? (Patt 216) AIS 9253) = Dopamine © Clonidine + Amphetamine © Tesbataline © Epinephrine 3. What are the risk factors for osteoporosis? F414 p#l9 (FAIS p43) |. Fibroblasts © Synthesize extracellular matrix Provide structural integrity Important role in wound healing Produce collagen, glycosaminoglycans, reticular and clastic fibers, glycoproteins ‘Stimulated by tissue damage 5. Melanocytes © Melanin-producing cells ‘© Located in the stratum basale (bottom layer) of the epidermis © Responsible for skin color6. Atopic dermatitis (eczema) treatment: © Formild cases, switch to.a moisturizing soap and add an emollient © Calcincurin inhibitors tacrolimus or pimecrolimus) © Topical steroids Antibiotics for open lesions (cover S. aureus and Sérep. spp.) © Antihistamines © Leukotriene inhibitors © UVlight therapy © For severe cases, consider systemic ster © Forvery severe cases, consider methotrexate, cyclosporin, azathioprine 7. Acne Pathophysiology _ ‘Treatment Hyperkeratosis ‘Scbum overproduction Prop mibacterium aenes proliferation Inflammation | Lvvd ADOTOLWLNG. ERG NV ANOE lat}DERMATOLOGY PART | End of Session Quiz, 8. List the layers of the epidermis, ‘9. Which structure connects epithelial cells to the basement membrane? 10, What are the four primary causes of acne? 111, Which skin disorder matches the following statement? + Prurivus associated with asthma + Allergy to nickel + Parakeratoric sealing + Caused by HPV types 2 and 4DERMATOLOGY PART 2 3 Question Warm-Up 41, Whatare norinal blood pressures in the right and let ventricles? (PAE p280) (FAIS p23) 2. What medication inhibite the callular codium potassium ATPase? What is ito clinical application? (414 p°0) (FAIS p307) 3. Which primary bone tumor fits each of the following descriptions? als p22-425 (NS pg ‘+ Most common malignant primary bote tumor of children ‘+ Most common benign bone tumor + 11;22 translocation + *Soap bubble” appearance on x-ray + Onion-skin” appearance of bone + Codmans triangle on x-ay a ZLWVd ADOTOLYHY zp a mn a <4 5 rm G Go aa B =DERMATOLOGY PART 2 End of Session Quiz 4, What are some of the hallmark features of necrotizing fasciitis? What organism ‘causes this infection? 5, Whar pathogen causes painless white patches on the tongue that cannot be scraped off 6. Which skin disorder matches each of the following statements? + Prati, purple, polygonal papules + Pruritic vesicles associated with celiac disease + Antibodies against hemidesmosomes ‘+ Antibodies against desmosomes + Keratin-illed eyes + Sand:-paper; predisposition to squamous cell cancer ‘Honey crusting lesions common zbout the nose and lips + Histology shows palisading nuclei Rapip-Fire FACTSREPRODUCTION 1 Reproductive Anatomy 2 Genital Embryology 3 Androgens 4 Testicular Pathology 5 Penis and Prostate Pathology 6 Female Reproductive Cycle 7 Menstruation and Menopause 8 Vulva, Vagina, and Cervix 9 Uterine Pathology 10 Ovarian Pathology 11 Ovarian Neoplasms 12 Pregnancy part 1 13 Pregnancy part 2 14 Chromosomal Disorders 15 Genetic Disorders: AD and Trinucleotide Repeats 16 Genetic Disorders: AR and X-Linked 17 BreastAWOIWNY 3ALLINGOWEY 3 Question Warm-Up | 4. Where can you fiad nicotine acetylcholine receptors in the body? (PA14 p43) (FAS p24?) 2. What drug category has each ofthe following endings? (ls 259 (15 p26) = -operidol += -phylline + terol © -triptyline + sin 3. What are the systolic heart murmurs? (Als p273 (FAIS 279) GUIS pe9) ra faa 3 es (o} g ia) 4. Types of urinary incontinence = Cause Symptoms ‘Treatment ‘ Weakening of : Stress | pelvie floor scaey Lifestyle modifications Urge (ea, oxybuty darifenacin, solifenacin) Inability to void . Overflow | Bormally > 1 eandeing caer overdistention ; Bes of bladder myRODUCTIVE ANATOMY EPI End of Session Quiz 5. A professional cyclise develops erectile dysfunction and perinedl pain and numbness. Which nerve was most likely injured? 6. A6/-year-old man with prostate cancer develops erectile dysfunction after tundeiguinyg« adical prostatectomy. What nerves were mos likely injured? 7. Describe the autonomic control of erection, emission, and ejaculation. 8. To where does testicular cancer first merastasize? 9. What sructures make up Heselbach’s triangle? 10, Which type of urinary incontinence matches each ofthe following descriptions? + ‘Treated with antimuscarinics (e.g, oxybutynin) + Occurs with coughing and sneezing + Present ass continuous leakage of urine Rapip-FirE FACTS Main artery of the pelvis, | Main nerve of the pelvis “Bag of worms” scrotum15 p56?) (SUI p196 198) 68) 3 Question Warm-Up 4. What are the common side effects of B-blockers? F425! (FAIS 3258) SUIS p72) 2, Describe how the murmur of mitral regurgitation is different from the murmur ‘of aortic regurpitation. (F414 pZ73) (AIS p279) (SUIS p89) 3. In which order of elimination (zero or firs) would you see linear decrease in the plasma concentration of a substance when ploted against time? (FAld 9240) (FAIS p244) (SUIS pia) 1. Exstrophy of the bladder ~ congenital gap in the anterior bladder wall and abdominal wall in front of it > exposure of the bladder interior to the outside world ADOTOAYAHA TWLINED NOILDNGOWdIYNITAL EMBRYOLO End of Session Quiz 5, Wharstructures develop fiom the mesonephric duct system? 6. Whatis the male homolog to each of the following female structures? + Vestibular bulbs * Labia minora = Bartholin glands + Urethral and paraurethral glands 7. What gene product comes from the SRY gene that underlies male genital development? 8. What structure anchors the testes to the scrotum?3 Question Warm-Up 1, What medications are known for having anticholinergic side effects? 2. What drug category has each ofthe following endings? (7/4 p25 (AIS p26) + ane © -barbital + -cillin 3,_A 21-year-old man presents with five days of fever, chills, and an enlarged, painful nee. What organism is most likely sponsible for his symptoms? GUIS p25) SN3DONANV iNiolthefatelo}:FE}](226) ANDROGENS3 Question Warm-Up 1. What elbow injury is common in tennis players? What elbow injury is common in golfers? 15 242) 2, What isthe general by-product of phase I metabolism? What is the general by-product of phase II metabolism? What reactions take place in phase 1 ‘metabolism? What reactions take place in phase I metabolism? (PALA p40) (FAIS p44) SUIS lA) 3. _Which three enzymes are required to convert phenylalanine to dopamine? {FAIA plo (EAS pi07) 4. Epididymitis © Inflammation of the epididymis © Diagnosis: support ofthe testes - some relief © Treatment < 35yo = GC/Chlamydia CCefiraxone IM then doxycycline x 10 days © Treatment » 35y0 or history of anal intercourse = Enterobacteriaceae Fluoroquinokone x 10-H4 days L ADOIOHIVe WY INSILS: z fad ae] Ps fe) G Ss fa) fe) raICULAR PATHOLOGY 7 5. Testicular torsion «Twisting ofthe spermatic cord —> ischemia © Diagnosis: support of testis no relief, US © Treatment: surgical detorson with bilateral orchiopexy wi 6. Cryptorchidism + ailure of testis to descend into scrotum © Usually unidaeral ‘© Descent usually complete in first year of fe © 35x increased risk of malignant tumor in the undescended testicle (usually a germ cell tumor) End of Session Quiz 7. A2-yearold patient presents with one testicle, For what i this patient at risk? 8. What testicular rumor is described by each of the following statements? + Composed of eywtrophoblasts and syneytiotrophoblasts + May presen initially with gynecomastia, + Elevated AFP + Elevated BhCG + Most common testicular tumor + Most common testicular tumor in infants and children up to 3 years of age + Most common testicular tumor in men overage 60 + Histologic appearance similar to koilocytes (cytoplasmic clearing) + Histologically may have alveolar or tubular appearance sometimes with papillary convolutions| * Composed of multiple tissue types + Histologic endodermal sinus structures chiller-Duval bodies) + 25% have cytoplasmic rod-shaped crystalloid of Reinke + Androgen: producing and associated with precocious puberty3 Question Warm-Up 1 Wat the fio ofthe point absent in Duchenne mula scopy? (PALA BP (ALS p5) SUIS pa 2, Explain why methanol is sucha txic substance. 3. Which skin disorder matches each of the following statements? (A/4 p43/-438) (AIS pA39-443) (SUIS p25 + Pruritic, purple, polygonal papules + Pruritic vesicles associated with celiac disease + Thickened scar especially around face/chest + Paraleratotc sealing, + Kerati-filled cysts + Skin rash and proximal muscle weakness «Hloney-crusting lesions common about the noe and lips + Hyperkeratosis and kilocytosis 4. Erectile dysfunction (ED) © Failure to initiate (psychogenic, endoctinologic or ncurogenic) © Failure to fill atherosclerosis) © Failure to store adequate blood volume within the lacunar nerwork © Diabetic, atherosclerotic and drug-related causes account for > 80% of cases of ED in older men XOOTOHIVd 3LV1SO¥d ONY SINIEPATHOLOGY PENIS AND PROSTAT! ‘What are the different types of Bowen disease? Bowen disease + Gray, solitary, rusty plaque on the penile shaft or the serotum © Can occasionally progress to invasive squamous cell carcinoma Exythroplasia of Queyrat + Red, velvety plaque usually involving the glans Bowenoid papulosis ‘+ Multiple papular lesions, which do not become invasive «Typically affects younger individuals 6, Condyloma acuminatum © Benign genital wars © Caused by HPV types Gand 11 7. Benign prostatic hyperplasia (BPH) © Present in 80% of men over age 80 © Diagnosis based on the following symptoms: ‘Sensation of incomplete voxing Increnced urinary freewency (es than every 2 hours) Staining to void Intermittent or weak urine stream Urgency Noctura (at cast 23 times a night) © Palpable prostace size may not corrlate with degree of obstruction or symptom severity + Medical intervention Nonselecive of, blockers doxazosin prazosin, terazosin © Decrease prostate smooth muscle tone > immedbate improvement in urine flow + Side effects dizziness postural hypotension. fatigue. asthenia Selective 0.9 blocker: tamsulosin + Fewerside effects than non-selective, has no antihypertensive elects Sat reductase inhibitors: finasteride, dutasteride © Slowly reduces dhydrotestosterone levels > 20% decrease in prostate vokane ‘over 3.6 months + Side effects decreased ibido, gjaruatory disorder, impotence © Surgical interventionEnd of Session Quiz 8. Wharis the mechanism of action of sildenafil? 9. What arc the side effects of sildenafil? 10. What organism is commonly implicated in balanitis? 11. How does the mechanism of action and clinical use of futarmide differ from, Finasteride? 12. A.55-year-old man undergoing treatment for BPH has increased testosterone and decreased dihydrotestosterone (DHT) as well as gynecomastia and edema. ‘With what medication is he being treated? 49. What are the diagnostic symmproms of BPH? Rapib-Fire Facts Most common cancer in men Most common cause of urinary obstruction in men ‘Most common treatment of erectile dysfunction SOUd ONY SINId AOOTOHLYa 3. NOMONdOwdsYFEMALE REPRODUCTIVE CYCLE FEMALE REPRODUCTIVE CYCLE 3 Question Warm-Up 1. What are some examples of substances climinated at a constant rate (2er0- order climination)? (FAl4 p240) (FAIS p244) SUIS pit) 2, What enzymes are used to metabolize alcohol? 4/4 p97 FAIS p25) SUIS p04 305) 3, A30-yearold woman presents with a low-grade fever, arash across her nose. that gets worse when she is out in the sun, and widespread edema. What blood. ‘test would you order to confirm your clinical suspicion? (Fal4 127) (FAIS p33) (GUIS p235.234)4, Two-cell theory of estradiol production oO Chotesterot Granulosa coll Estrogen | Desmolase Aromatase Androstenedione ~ Androsteredione Basementmembrane 5. Female reproductive cycle Degenerative Follicle Maturing Folikte oation Corpus Luteum Degeneratl MENSTRUATION Follicular =e" Luteal © Follicle maturation > © Produetion of estradiol -> © Production of LH surge > © Ovulation and production of progesterone (along with estradiol) —> + Inhibition of FST and LH production > © Decline of corpus luteum —> © No production of estradiol and progesterone —> © Loss of FSH inhibition > © Increase in FSH (repeat step 1) 31243 BNLONGOWRY 3TH Fa 3 PI fe) Q c 6 gS fe) PaFEMALE REPRODUCTIVE CYCLE End of Session Quiz 7, During whar stage of meioss i the primary oocyte arrested? The secondary oocyte? 8. Which hormone (estrogen or progesterone) is responsible foreach ofthe following ‘staternents? ‘+ Production of thick mucus that inhibits entry of sperm into the uterus +» Tnduces LH surge + Relaxes uterine smooth muscle «+ Stimulates endometrial proliferation «+ Tnhibits endometrial proliferation 9. Outline the steps that occur during the feral reproductive cycle. 10, Human chorionic gonadotropin has an alpha subunit identical to what other ‘hormones? 11. What hormonal changes facilitate lactation?a MENSTRUATION AND MENOPAUSE | ]ON3H ONY NOLLYAYLSN 3 Question Warm-Up 1. A patient falls off motorcycle and lands on his right shoulder. On physical ‘examination you notice his shoulder has an abnormal configuration. X-rays indicarean anterior dislocation of his shoulder. What artery and nerve are most at risk of being damaged? 2. A 75-year-old man presents with acute knee pain and swelling. An x-ray reveals absence of erosion ofthe joint space, but thece are calcum deposits inthe ‘menisci. What is the diagnosis, and what would you find on aspiration ofthe Goi 14 p475) FAIS pt) (LIS 239 3. Whatare some of the inducers of eytochrome PASO® (4 p255) (As 260) Eo} mm BS fe} S < fa) i} fe) ZzMENSTRUATION AND MENOPAUSE Methods of contraception Class Examples Notes > Condom Barrer + Diaphragm + Sponge: + Pill COCPF") ‘im Combined : HIN estrogen-progestin | * vasinal tng + Ml and stroke ~ Pall CMinipill”) ~ Irregular bleeding © DMPA injection — | + ight gain, mood meaty | ETB | agestin-only |» Exonogestel implant (Nexplanon) + Lovonorgesteel 1UD (Mirena) Other Copper UD feat Menopausal hot flashes © Occur in 75% of menopausal women Presentation: starts in face/chest then generalizes, associated with diaphoresis and palpiations, followed by chills and shivering; lasts 2-4 minutes, ‘May cause sleep disturbances “Treatment: > SSRI, SNRI, gabapentin Herbal treatment: soy isoflavonest, red cloverf, black cobosh, vitamin ‘tporential estrogenic effect on the breast, much like estrogen replacement Hormone replacement therapy for menopause © Uscestrogen + progesterone if uterus present Unopposed estrogen increases risk of © Forrelief of menopausal symptoms, not to prevent chronic disease © Use for only shortest amount of time and at lowest dose needed. Avid if = Coronary heart dsease Active liver disease = History of,End of Session Quiz 7. Whatis a common cause of iregular bleeding in the first few years after menarche? What is the treatment? aSNVJONSH ONY NOLLWMULSN3H 8, A 23-yearold woman who uses OCPs for contraception has a positive screening tes for TB. She is arte on the appmpriate therapy for ltent’TR. Despite good compliance with all her medications, she becomes pregnant. What isthe most likely cause? "9. What hormonal changes are seen during menopause? 40. Why is progesterone used in combination with estrogen during hormone replacement therapy? ER] z 6 oO ‘Ss [et fo) Zz Rapip-Fire FactsINA, AND CERVIX VA, VAC UI 3 Question Warm-Up 1. What are the by-products of MAO and COMT enzymatic activity on dopamine, norepinephrine, and epinephrine? 2, What are the common locations for tophi in gout patients? (684 p25) (FAIS 30) 3. What structures are a isk for injury with an anterior shoulder dislocation? 4. Lichen sclerosus + Inflammatory condition of vulva characterized by thinning of thee + Produces smooth white plaques © Can lead to shrinking of introitus and fusion of labia mgjora and minora © Symptoms: pain, dyspareunia © Diagnosis: biopsy © Treatment: topical corticosteroids © Associated with increased risk ofRapiD-Fire FACTS “Grape-like” vaginal tumor Koilocytes XIAWID ONY 'WNIDWA 'WATINA (239)UTERINE PATHOLOGY (UTERINEPATHOLOGY™ 3 Question Warm-Up 1. What are some medications that are known for having a low therapeutic index? (PALA pte (NS p48) 2. Describe how the murmus of mitral regurgitation is different from the murmur of aortic regurgitation. (FAl4 p27?) FAIS p279) (SUIS p89) 3, What are the layers ofthe epidermis? (14 p40 (AIS p436) SUIS p25) 4, What are the layers of the endometrium? Which layers are shed during menstruation?5. Leiomyosarcoma > Rare malignant tumor that arises de novo from the myornetsiur. » Suspect in woman with a rapidly enlarging uterus 6. Uses of leuprolide + Letomyomas oct term to shrink tumors pric to surgery) XSOTOHL¥d 3NIILA © Central precocious puberty © Advanced prostate eancer © Infertiliey Given continous to suppress intrinsic hormane production during VF Given once to induce ovulation End of Session Quiz 7, What causes endometial hyperplasia? 8 What uterine pathology matches each of the following descriptions? + Excess unopposed estrogen is the main risk factor “+ Characterized by plasma cells inthe endometrium + Causes cyclic pelvic pain +/ bowel and bladder symproms + Menorthagia + nontender, enlarged uterus with irregular contours * Menorthagia + tender, enlarged, globular uterus + Malignant rumor that arises de nove fro the smooth muscle ofthe uterus 9. Whats the mechanism of action of leuprolide? a m at] zB fe) is} fat fal G re) a RapiD-FiRe FACTS ‘Most common benign tumor in women “Chocolate eyst” ofthe ovary “Powder burn? lesionOVARIAN PATHOLOGY OVARIAN PATHOLOGY 3 Question Warm-Up 1. What are the symptoms of inhibiting parssympathetic activity? (FALE p247 AIS p25} 2. Aman presents with exquisite pain and Jn the metatarsophalangeal joineo as ogi grea te. syrah crystals, What is the ‘diagnosis? (FAi4 ees TAS po0 uis 7233) 3. Which structure connects epithelial cells wo the basement membrane? Which. structure connects adjacent epithelial cells to each other? (Ald p40) iS p47) 4. Ovarian torsion © Twisting of supportive ligaments —> impaired vascular supply ~> ischemia and necrosis © Risk increases with + Presentation: acute onset of severe pelvic pain (sharp, stabbing) with possible radiation, +/+ nausea and vomiting, © Diagnosis clinical, pelvic ultrasound5. What hormonal abnormalities are seen in polycystic ovarian syndromet 6. Evidence of ovulatory cycles: © Cyclic menses . mideycle pelvic pain associated with ovulation © LE surge: tested for by OTC ovulation prediction kts © Biphasic basal body temperature End of Session Quiz 7. Which typeof ovarian st matches each of the flowing description’? + Forms from an unruprured Graafian follicle + Formsif the corpus lateum fails to involute + Associated with high hCG levels = Contains tissue from multiple germ cell layers * *Chocolae est” of the ovary 8, What are the clinical manifestations of polycystic ovarian syndrome? 9. A patient with polyeystic ovarian syndrome isa increased rik for developing: which type of cancer? 10. Whats the mechanism of action of clomiphene? Rapib-Fire FACTS ‘Most common cause of infertility in women Mideyele pelvic pain associated with ovulation ADOTOH.¥d NWIYYAO iNelthejateloy ER]OVARIAN NEOPLASMS 3 Question Warm-Up 1. Whats the clinical use of clomiphene? How does this drug work? (14 p590) (ANS p596) SUIS p20%) 2. What drugs can be used to reverse neuromuscular blockade? (FAl4 p246) (FAS p25) 3. What psychiatric disorder arises from increased norepinephrine? (Al4p449) (Pats AS GUIS p55) 4. What are the four main categories of ovarian tumors?5. Ovarian neoplasms Epithelial Germ Cell ‘Sex Cord-Stromal jumors Tumors Tumors ~ Scrous © Teratoma * Granulosa cell + Mucinous + Dysgerminoma + Scrtoli-Leydig Subtypes |» Endometvioid * Yolk sae + Fibroma © Clear cell * Choriocarcinoma |» Thecoma + Brenner Age Unilateral! Bilateral * Serous eystadenoma © Fibroma * Mucinous + Thecoma Benign cystadenoma © Serous ystadenccarcinoma _|+ Dysgerminoma + Mucinous » Yolk sac Malignant | cystadenocareinoma |» Choriocarcinoma Prognosis SMSY1dO3N NVIYWAO 2 ia a 2 fe) =) 5 a fe} raDPLASMS OVARIAN NE End of Session Quiz 6. What are the risk factors for ovarian cancer? 7. Which ovarian neoplasm is associated with each of the following statements? + Estrogen: producing + precocious puberty or postmenopausal bleeding “+ Androgen-producing > viriization + Contains fallopian tube-like epithelium Contains urinary trace-like epithelium + Historically associated with pseudomyxoma peritonei 8. Which ovarian neoplasm is associated with each of the following histological findings? + Schiller Duval body + Call Exner body + Psammoma body + “Fried egg” clls 9, Which ovarian neoplasm is associated with each of the following tumor ‘markers? + AFP hCG + LDH Rapib-Fire FACTS Ovarian tumor + ascites + hydrothorax “Teratoma —> hyperthyroidismHe Chapter iwnang (FAM p85) (FAIS ps Ecione 79) AIS p 0k 3 Question Warm-Up 1. Whatis the result of blocking the following dopaminergic pathways? ‘+ Mesocortical + Mesolimbic + Nigrostiatal + Tuberoinfundibular 2. What stage of tleep is associated with the following EEG findings? (14 pA) (AIS B55) GUIS pi3) Alpha waves + Beta waves © Delea waves + Theta waves 3. Whacocher severe problems often coexist with septic shock in ICU patients? Gestational trophoblastic disease + Hydatidiform mole © Invasive mole © Chorioearcinoma Partial Mole. Complete Mole Karyotype Feral parts Chorionic villi Uterine size hCG Risk of invasive mole Risk of choriocarcinoma | dvd ADNYNO Sd Xio}Hheya lato}: (E}*]PREGNANCY PART | 5. 6 Rh alloimmunization © Rh(D)-negative woman develops IgG antibodies against Rh(D)-postive fetus «In subsequent pregnancies, anti-D antibodies cross placenca and attack fetal RBCs hemolytic disease of the fetus and newborn (erythroblasts fetalis) + Provent by adminisering ant-D immune globulin (eg, Rhogam) when risk of feromaternal hemorthage Physiologic changes in pregnancy Basal metabolic rate increases 10-20% + Phisma volume inereases 30-50%, RBC volume increases 20-20% © Cardiac output increases 30-50% © Blood pressure decreases in easy pregnancy — nadir at 24-26 weeks, return to pre- pregnancy levels by erm. © Increased GFR — decreased BUN and Cr * Increased procoagulation fietors -> hypercoagulable state End of Session Quiz 7. What are the tisk factors for e:topie pregnancy? 8. Which ype of ovarian cystis associated with molar pregnancies? 9. What's the most common location for metastasis in choriocarcinoma? 10. Filed involution of what embryological structure is associated with each of the following statements? + Drainage of urine from the umbilicus + Drainage of meconium from the umbilicus 11, Whatcondition is suggested by each of the following abnormaiities on second. trimester maternal serum screening? + TAEP + | AFP, | estriol, J hCG + LABP, | estriol, | hCG RaPID-Fire FACTS ““Snwstorm” appearance on ultrasound3 Question Warm-Up L_ What effect wil stimulating the following receptors have on heart rate? (Als p244) FAIS 248) °B B oM, 2, Whatare the primary mechanisms of action ofthe different classes of antiarrhythmies? °Al4 p302.304) N15 p206 310) + Class 1 + Class It + Class 1 + ChssIV 3, A patient comes tothe clinic complaining of anterior shoulder pain that radiates dow into the forearm. On examination, you notice a swelling ofthe biceps muscle. What is the most likely diagnosis? What are the causes of postpartum hemorrhage? © amost common cause) Enlarged, soft, boggy utervs + _ Risk factors overdstended uterus (age fetus, multfetal gestation), induced or augmented labor, prolonged labor © Retained placental tissue © Genital lacerations © Aboormal placentation (placenta accreta/inereta/percreta) © Uterine rupture © Coagulation defects Z.Luvd ADNYND3¥d m bas] Bp fe) is) Ee ia) 4 fe)PREGNANCY PART 2 5, Diabetes in pregnancy © Gestational iaheres Daabetes that develops during pregnancy butresoives postparturn Screen with oral guucose tolerance test between 24-28 weeks gestation Management: diet +/insuin ‘Complications hypoglycemia + Pregestational diabetes Patient has dlabetes prior to pregnancy Management: nsul ‘Complications: macrosomia, hypoghceria, congenital anomalies ee. ),stibith End of Session Quiz 6. Which placental abnormality marches each ofthe following descriptions? + Placenta covers internal cervical 03 + Premature separation of placenta + Abnormal adherence of placenta to myometrium + Invasion of placenta into myometrium + Invasion of placenta through myometrium and serosa + Presents as painless vaginal bleeding late in pregnancy + Presens as painful vaginal bleeding late in pregnancy 7. Whatis the most common cause of postpartum hemorrhage? 8. What condition is best described by each of the following statements? + Patient with PMH of HTN becomes pregnant + New-onser HTTN during pregnancy with no proteinaria, + New onset HTTN during pregnancy + proteinuria or end-organ dysfunction + Patient with preeclampsia has a seizure + Patient with preeclampsia has low hemoglobin, low platelet count, and high AST. ‘9. What isthe mechanism of action of mifepristone? What is the mechanism of action of terbutaline?£202 203) (R plt-167) R pl63) 3 Question Warm-Up 4. What changes in sleep partes and sexval anaromy are seen in the elderly? (Ald p43) FAL poo) 2, What psychiatric disorcer arises from decreased norepinephrine? (FH p44} (5 pss) 3, What other neurcloge pathology ae pains who have migraine with aur a SW3QWOSIO TYHOSOWO¥HCHROMOSOMAL DISORDERS End of Session Quiz 4, 6. 7 ‘What prenatal ultrasound finding isa clue that the fetus may have Down. syndrome? ‘What is the most common event that causes Down syndrome: meiotic nondisjunction, mosaicism, or Robertsonian translocation? What are the clinical features of Williams syndrome? ‘What are the possible defects in cases of chromosome 22q11 deletion? ‘What are the distinguishing characteristics of Klinefeiter syndrome compared t0 ‘Turner syndrome? RapiD-FiRe FACTS Most common genetic cause of intellectual disability Second most common genetic cause of intellectval disability Horseshoe kkincy, congenital heart defeets, streak ovaries, and cystic hygroma Rocker-bouon fe clenched hands, microcephaly ‘prominent occiput and small jawGENETIC DISORDERS: | __ADAND TRINUCLEOTIDE REPEATS _ QYOSIO DLBN: 3 Question Warm-Up 1. What eerum lab marker is helpful in assessing the appropriate ceypenation of tissue? 2, What are the five branches ofthe Facial nerve? (4i4p472) FAS pf78) UISp41) SLV343¥ JGLOTTIONNIUL GNY OV SY 3. What would you suspect asa cause of headache in a patient using topical retinoic acid for acne? (45 p46) SUIS p312) ee) fal al el) le) g ont fa) 9 raREPEATS. AD AND TRINU! NETIC DISORDER End of Session Quix 4, What genetic defect is responsible for achondroplasia? 55. A genetic defect in which proteins results in hereditary spherocytosis? 6. What autosomal dominant disease fits each of the following statements? ‘+ Associated with floppy mitral valve, dissecting zortic aneurysm, berry aneurysm ‘Associated with mitral vale prolapse, liver disease, berry aneurysms "Neural tumors and pigmented irs hamartomas ‘Very strong association with colon cancer Ml before age 20 Hemangjoblastomas of retina/eerebelum/medulla + Increased MCHC, hemolytic anemia + Bilateral moustic neuromas + Facial lesions, seizure disorder, cance isk CCaudate atrophy, dementia (Cystic matial necrosis ofthe aorta Defect of fibroblast growrh factor (FGF) receptor 3 7. What are some of the disorders resulting from trinucleotide repeats?3 Question Warm-Up 1. What are the defects in tetralogy of Fllot (ls p282) (lS p86) U5 po4p 2. Whatiis the defect in Ebstein anomaly? (F414 263 FAIS p269) 3, Which antibiotic css is known to increase the risk of tendon ruprure in adults? (PALA p16) (AIS p16?) CUISp341) 4. Cystic fibrosis Blood sOYOSIO D1L3N39 DINIX ONY BY SY IN\ejHbejatale}: (=):ERS: AR AND X-LINKE GENET! End of Session Quiz 5. What gene is defective in cystic fibrosis? 6. Whatis the traditional test used to diagnose cystic fibrosis? 7. Classify the following disorders as either autosomal dominant, autosomal recessive, or X-linked recessive. + Glycogen storage diseases + Wiskott-Aldsich syndrome + Adu polycystic Kidney disease (PKD) + von Recklinghausen disease + Infantike polycystic kidney disease (PKD) + von Hippel-Lindau discase + Phenyltetonuria (PKU) + Hemophilia A and B + Hereditary spherocytosis + Fabry disease + Duchesne muscular dystrophy (DMD) + Mucopolysaccharidosis + Familial adenomarous polyposis (FAP) + Familial hypercholesterolemia + Lesch-Nyhan syndrome eH) + Brutonagammaglobulinemia + Marfan syndrome + Huntington disease (HD) + Cystic fibrosis (CF) + Thalassemias + Hemochromatosis, + Sickle cell anemia + GOPD deficiency ‘Autosomal dominant_[ Autosomal recessive3 Question Warm-Up 1. Describe what changes you would see in serum calcium, serum phosphate, alkaline phosphatase, and PTH with each ofthe following diseases: (PALA 2) (AS p27) ‘Serum Ca** ‘Alk Phos | PTH Primary hyperparathyroidism| Paget disease of bone Vitamin D toxicity 2, What are the roles of Sertoli cells and Leydig cells in male spermatogenesis? (FAM pee) (5 572) 3. What is the mechanism of action of sildenafil FAl4 9572 (FAIS 596) SUIS pas) rs} fas} fae] ed ie} is} (iS a = fe) aBREAST 4. 5. Benign epithelial lesions Non-protiferative breast (ibrocystic) changes © Fibrosis = Cysts Proliferative broast disease without atypia © Sclerosing adenosis ~ © Epithelial hyperplasia © Complex sclerosing lesion (radial sear) © Fibroadenoma Breast carcinoma in situ (15-30%) Ductal carcinoma in situ (DCIS, intraductal carcinoma) + Comedoearcinoma = + Solid © Cribriform © Papillary + Micropapillary Lobular carcinoma in situ (LCIS) Invasive breast cancer (70-85%) © Invasive ductal carcinoma (75-B0%)= © Invasive lobular carcinoma ~ © Medullary carcinoma ~ © Tubular/cribriform carcinoma © Mucinous carcinoma + Papillary carcinoma © Metaplastic earcinoma © Inflammatory carcinoma = signs of inflammatory breast eancer may include:End of Session Quiz 7, What are some of the causes of gynccomastia? Asvaua ‘8. What organism is most commonly responsible for acute mastitis? classic presenting complaint in a patient with intraductal papilloma? 10. What breast pathology fits each of the following descriptions? * Most common breast tumor in women under 25 ‘+ Most common breast mas in postmenopausal women ‘* Most common breast mass in premenopausil women = Most common form of bresst cancer > Small, mobile, firm mass with sharp edges in 24-year-old woman + Histological “leaFlike projections” + Signet ring cells + Loss of e-cadherin cell adhesion gene on chromosome 16 + Always ER() and PR) + Commonly presents with nipple discharge + Eczernatous patches on nipple + Multiple bilateral fuid-filed lesions with diffuse breast pain + Firm, fibrous mass in a 55-year-old woman 11. A58-year-old postmenopausal woman is on tamoxifen. What is she at increased risk of acquiring? NOILDNGOwdITY Rapio-Fire FACTS Most common cancer in women in the U.S. ‘Most common benign breast tumor ‘Most common malignant breast tumor Blue dome cyst in the breast [Treatment for ER(.) breist cancer Red, itchy, swollen rach on the areola and nippleMicro ae Bacterial Basics Bacterial Toxins Staphylococcus Streptococcus Other Gram-Positive Bacteria Gram-Negative Bacteria part 1 Gram-Negative Bacteria part 2 Spirochetes and Zoonotics CONAN ONE Mycobacteria 10 Nonstaining Bacteria 11 Penicillins 12 Cephalosporins 13 Other Cell Wall Inhibitors 14 Protein Synthesis Inhibitors 15 Other Antibiotics 16 Micro by Systems part 1 17 Micro by Systems part 2 18 Viral Basics 19 DNA Viruses part 1 20 DNA Viruses part 2 21 RNA Viruses part 1 22 RNA Viruses part 2 23 HIV 24 HIV Drugs 25 Mycology part 1 26 Mycology part 2 27 Antifungals 28 Protozoa 29 Helminths and EctoparasitesBACTERIAL BASICS 3 Question Warm-Up 1. Which medication averdose can be treated with sodium biearbonste? (4 £252) pais pas7) 2. A paticnt presents with tinnitus, dizziness headaches, and Gl distress, What drug: 4s causing these symptoms? FAl4 p554) (AIS p259) 3, What testicular tumor is described by the following statement? (414 (582) AIS p53) (GUIS p25) + Composed of eytotrophoblass and syncytiotrophoblasts “+ May present initially with gynecomastia « Elevated AFP + Elevated B-hCG_ + Histologic appearance similar to kolocytes (cytoplasmic cewing) Isva TWiyaL Ive {e}:)8)1)\)BACTERIAL BASICS End of Session Quiz 4, What bacterial structures have the following functions? + Mediates adherence of bacteria tothe surface ofa cell + Protects against phagocytosis ~ Provides rigid support fart cella pret asin ono pene « Space between the inner and outer cellular membranes in gram-negative bacteria + Motility + Bacterial form which provides resistance to dehydration, heat, and chemicals, «Forms attachment between two bacteria during transfer of DNA material (AKA conjugation) + Independent pieces of genetic material within bacteria that may contain genes for antibiotic resistance ‘What stain is required ro see the following organism (or substance)? + Cryptococcus neoformans + Pacunsecystsjirovecii (PCP) + Cama 6 Which organisms are not well visualized with Gram stain? 7. Which bacteria are encapsulated? 8. Bywhat method are slasmids exchanged between bacteria?3 Question Warm-Up 1 ‘Whats the antidore wo each ofthe folowing rains? (4 252 (5 p257) LIS p19 What testicular tumor is described by each ofthe following statements? (FV4 p588) (ais 59g UIs 6219) + Histologically may have an alveolar or tubular appearance, sometimes with papillary convolutions * Composed of multiple tissue types + Histologic endodermal sinus structures Schille-Duval bockes) * 2506 have cytoplasmic rod shaped crystalloids of Reinke + Androgen producing and associated with precocious puberty, ‘What onanism is commonly implicated in balanitis? _ BACTERIAL TOXINS SNIXOL TwniaLove fo} toxic ro leukocytes, hemolysin —+ hemolysis) © Schemolysin®-toxin —> toxic wo erythrocytes and other cells ‘© Pantor-Valentineleukocidin —+ tissue destruction with MRSA, affects both neutrophils and macrophages © Enterotaxins —» food poisoning —> vomiting and diarthea * Toxic shock syndrome toxin-1 (TSST-1) —+ release of cytokines > toxic shock syndrome (high fever, hypotension, diffuse rash) What known toxins are secreted by Streptococcus pyogenes (group A strep)? ‘Whaat is the action of each? © Strepeolysin © hemolysis (Oxygen labs) © Streprolysin Sr hemolysis oxygen Stable) + Strepeococeal pprogenie exotoxins type A, B, Clerythrogenic toxins > red rach (erythto-) ‘and fever (pyto- of scarlet fever wae of Session Quiz, ‘What exotoxin matches each of the following characteristics? + Inibts ACh release — flaccid paralysis + Phospholipase that eauses gas gangrene «Inhibits the inhibitor of adenylate cyclase —> whooping cough + Stimulates adenylate cyclase —> chloride and water into gut —> diarchea + Destroys leukocytes + Composed of edema factor, lethal factor, and protective antigen + Enterotorin causing rice-water diarthea © Causes scarlet fever Causes taxic shock syndrome + Tnactivates EF-2 —> pecudomembranous pharyogitis + Blocks the release ofthe inhibitory neurotransmitter glyeine 7. What seven bacteria secrete enterotoxins (exotoxin that causes water and electrolyte imbalances of intestinal epithelium resulting in diarrhea)?3 Question Warm-Up During what deep stage would a man have vaiable Blood pressure, penile ‘tumescence, and variable EEG? (4 p51) AIS D455) 2, Whatis the twocell theory of estradiol production? 3. What drug would you give to inhibi prolactin secretion? P4210) A'S p36) 4, Gram-positive algorithm oN <= SNODODOTAHAYLS OUDdIW.STAPHYLOCOCCU End of Session Quiz 5. Label the following gram-positive algorithm: Gram (+)—> ee 6, Whats the function of catalase? 7. One hour after eating potato salad at a picnic, an entire family began to vorit. ‘After ten hours, they were bettes. What is the organism? 8. What very common aerobic skin colonizer is responsible for many indwelling, foreign device infections?He Chapter 138 Gram positive algo FAN p29) (FAIS pi 1 (FAH 130) (FAIS p29) (SU (FALA p24) (FAIS pl23) pia ANS ps (FAIS pl29) SUIS p25 (AIS pI29 (SUIS p: (AIS p20) (SUIS p3 ococcus bows (FAM p32) FAIS pl.) (SUI 3 Question Warm-Up 1. Which medication overdose can be treated with ammonium chloride? (Fs p252 415 p257) 2. What are the target cells of luteinizing hormone (LH)? 3, What ovarian tumor matches each ofthe following statements? (FAl4 S82 583) (FAIS p586-587) SUIS p2l4) + Estrogen secreting, precocios pubery + Produces AFP + Psammoma bodies » Intraperitoneal accumulation of mucinous material ++ Testosterone secreting, virilization ‘What are the different viridans group streptococci? © S. mutans = Most prominent organism in dental plague © S.salivarins S.anginosus © Smits © S.sanguinis ‘May enter circulation during dental procedures and cause subacute endocarditis in those ‘ath turbulent flow heart problems (pre-existing endothelial damage) fa patient has a turbulent flow heart problem, then use prophylaxis with amoxiciin, nor to dental procedures $N930301d31S oe)