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Anti Hypertensive Drugs Diuretics - DOC x HTN monotherapy

plasma volume ECFV VR CO MAP/BP TPR (Reflex) PRA CO a maintained lowered TPR; 1) intravascular volume and 2) vascula responsiveness by Na and Ca++
Name MOA Pharmacology Toxicities/SDFX
Sexual Dysfunction, hypovolemia, Hypokalemia/alkalosis, Hypomanesemia, Hypercalcemia, Hyperuricemia, Hyperlipidemia, Hyperglycemia

Reflex

Drug Drug Interactions

Contraindications

Administration

Misc

Work on Distal Thiazides convoluted Tubule (Hydrochlorothiazide/Hy (descending loop of droDiuril/H2TZ) Henle?)

Brain

w Quinidine=Torsade de Pointes; w Digoxin= Dig Elderly or dehydrated or Toxicity; w other RxRx interactions; Cotricosteroids= Na DM, Hypokakemia Retention; w Li= Plasma [Li]; w Warfarin= effectiveness; w NSAIDS=HTN DM, Hypokalemia

Along w tx HTN Diuretics (in may need K general) are good supplements; in K for Edema, BP and Dyspnea; Thiazides arrythmias are good x Severe Renal Impairment w HTN

Thiazide-like (Chlorthalidone/Hygroto n) blocks Na/2Cl-/K on Ascending Loop of Henle so they stay in lumen Aldosterone receptor antagonist; Reduce aldosterone levels? Hearing Loss (just like aminoglycosides), Hypocalcemia Estrogenid SDFX/Gynecomastia b/c of steroid like sx of drug; NSAIDS, blockers and ACE inhibitors Hyperkalemia; may lead to cardiac arrest

Loop (Furosemide/Lasix)

DM, Hypokalemia

good x tx of HTN w Renal Impairment even morese than Thiazides good x tx of HTN w Hypkalemia

K-Sparring (Spironolactone, Eplerenone/inspra)

RAAS Ihibiting Drugs


Name MOA Pharmacology Toxicities/SDFX Reflex Drug Drug Interactions Contraindications Administration Misc

ACE Inibitors (end in pril eg Captopril)

Block A I: A II conversion in lung endothelial cells; Bradykinin

Captorpril causes rash; hpotension, Na depletion; Dry cough A-II prodx TPR compliance, and aldosterone and Hyperkalemia bc K not Na excretion; ACE excreted bc aldosterone breaks down bradykinin, is inhibited; Angioedema so if it's blocked the (esp if black); Renal bradykinin can stick Failure due to GFR, around longer Proteinuria, rashes (captopril) fever, pancytopenia, BM depression

w NSAIDS = HTN

Great Results If Used w Thiazides

Little sex dysfx SDFX; help manage DM; mortality if prior MI; only antihypertensive mx w/o sexual dysfx

Angiotensin II Receptor Blockers/ARB's (end in "- Block AII type I sartan"; Losartan, receptors Valsartan, Irbersartan, aldosterone relaease Candesartan, and vaeesel relaxation Telmisartan, Eprosartan) Aldosterone Receptor Blocker (Spironolactone, Eplerenone)

bradykinin angioedema

Sympathoplegic Agents

CNS 2 Agonists; Ganglionic Blockers; Neurotransmitter Depletors; , , Blockers


Name MOA Pharmacology Toxicities/SDFX
some orthostatic hypotension; Dry Mouth, Drowsiness, Depression; Sexual Dysfx; Withdrawl Supersensitivity; Pseudotolerance Orthostatic Hypotension; Sexual Dysfx; Paralytic Ileus, Urinary Retention (esp old men) Reserpine: Suicide, depression, sypmathetic action. Guanethidine: Retrograde Ejaculation. Orthostatic Hypotension, Fluid Retention, Sexual Dysx; Parasympathetic Predominace (Nasal Stuffiness, GI acid secretion, Diarrhea, Bradycardia); Supersensitivity

Reflex

Drug Drug Interactions

Contraindications

Administration

Misc

2 Agonists (Clonidine, Guanabenz)

Ganglionic Blockers (Trimthapham Camsylate)

HR, VR, TPR, CF

none :)

Vasodilation w/o reflexes (cool)

Sympatholytic Agents (Reserpine, Guanethidine, Guanadrel)

Deplete adrenergic neurotransmitters

HR, VR, TPR, CF

OTC decongestants; pts w hypokalemia (b/c diarrhea causes K loss); Reserpine depression

Reserpine is cheap and effective but as HORRIBBLE SDFX

blockers (Doxazosin, end in "-sin") Bronchospasm (esp nonselective), Hrt Failr; Bradycardia; AV block; response TPR Peripheral Vascular Diss and VR; Atenolol TPR esp in Raynauds: (reflex) Depression (not as bad as Reserpine); Vivd Dreams; Sex Dysfx TPR, HR, CO, VR (basically sympathetics) Orthostatic Hypotension, Bradycardia, Heart no reflex tachycardia block, CF Hydralazine SLE esp in slow acetylators 200mg/day, Rapid Drop in TPR angina; Minoxidil Hair growth K channel efflux excitability arterial reactivity/constriction; blood volume, in venous capcitance; TPR, HR, contractility

pts using Doxazosin were 25% more likely to have hrt falu Esp good in white ppl w hyperkinetic hearts; Esp good for Ventricular Ectopies, Angina, Sinus Tachycardia and Dissecting Aneurysm

Blockers (end in "-ol", Nadolol, Propranolol, Timolol, Atenolol, Bisoprolol, Metoprolol, Labetalol)

CO via HR and CF; CNS; RAAS (no compensatory volume expansion

NonSelective blockers Asthma, Vascular Disease

blocker-Labetolol

1, 2, 1 blocker

DM, Asthma, CHF

Vasodilators (Hydralazine, Minoxidil, Diazoxide; Nirtoprusside))

TPR Hydralazine Minoxidil Diazoxide: TPR and VR Nitroprusside

Angina

Nitroprusside (IV only); Others oral

Ca++ Channel Blockers


SDFX = TPR (all), HR (V,D>>N), CF (V>>D,N)

Name

MOA

Pharmacology

Toxicities/SDFX

Reflex

Drug Drug Interactions

Contraindications

Administration

Misc

Phenylalkylamine (Verapamil)

Benzothiazipine (Diltiazem) Dihydropyridines (Nefedipine et al)

constipation, Hypotension, some HA, Peripheral Edema (no RE to diuretics), AV block, some CHF a little hypotension, peripheral edema, AV block (nyeh) Hypotension, HA, Peripheral Edema Tachycardia (does not RE to diuretics)

blockers; Cardiac Failure considered the safest Ca channel blocker highest affintiy x heart of other Ca chnl blkrs; good in ER situation

OK to use w blockers

w blockers HR THIS IS BAD!

blockers

sublingual, short duration

All antihypertensive mx cause in RAAS (via: BP and CO blood flow to kidney RAAS), chance of Orthostatic Hypotension (via contractilty, volume or CF).

Dyslipidemia Drug Therapy


Name MOA Pharmacology
Reduces esterificationof TG in liver, May reduce hepatic cholesterol formation, Reduces VLDL, TH and LDL, HDL, Effective vs Hyperlipidemia Types IIV, Cho-ol levels reduced 25% @ 3gm/day. clotting via tissue plasminogen factor and plasma fibrinogen

Toxicities/SDFX

Reflex

Drug Drug Interactions

Contraindications

Administration

Misc

Nicotinic Acid/Niacin

Inhibits adipose Lipase

Flushing, Pruitis (itching), Abdominal pains, Dyspepsia Peptic ulcers (at first), Hepatic dysfx (jaundice, transaminase levels)

Give w Aspirin; Use Poor pt compliance; in pts w TGs Use in pt w TGs

Fibrates (Gemfibrozil)

serum TG, extrahepatic LPL, aplipoprotein synths, HDL?

extrahepatic lipoptotein lipase (LPL), aplopotrotin syths, serumTG, VLDL, kinda HDL; plasma fibrinogen levels :: Gallstones, chance of arrythmias, Nausea, Cramps, Bleeding due to platelet adhesiveness bleeding

w Statins = chance of Rhabdomyolysis

Type I hyperlipidemia

Indicated x pts w TG>750 mg/dL; esp Use x pts w TH good x Type III >750mg/dL, esp hyperlipidemia; Not good if pt is Type III good x pts w Type I; (elevated IDL) phtyp Ppl use x in surviival w/o evidence.

Binds bile acid which are Bile Acid Sequestrants precursors to cholesterol LDL, Not absorbed in (Cholestyramine, which shifts bile acid GI tract, Colestipol, Colesevelan) prodx instead of cholesterol

Major Constipation, impaction, abd cramps, Hemrrhoid aggrevation

Absorbs other drugs as well as bile acids so Cholestyramine will also bind vitamins, digoxin etc

Stagger administration of other drugs

Chlestipol & Colesevelan are newer and more potent w less SDFX and help CHD mortality and major coronary events

Cholesterol Absorption Inhibitor (Ezetimibe)

Diarrhea, Hepatic cholesterol absorption insuffx; These SDFX are from guy mild/more tolerable vs cholesterol, TG BASeqeuestrants

HMG CoA Reductase Inhibitors ("Statins")

inhibit HMG CoA Reductase cholesterol synths

Works in liver, cholesterol, LDL, HDL

Myalgias, rhabdomyolysis (rare)

NEVER USE IN PREGNANT WOMEN

Good Compliance but Expensive; Must Perform LFT bf and after tx

ANTICOAGULANTS
Antithrombotics
Name MOA Pharmacology Toxicities/SDFX Reflex Drug Drug Interactions Contraindications Administration Misc
Aspirin is used to help prevent thrombus formation; used to help prevent 2nd stroke. NOT useful to prevent 1st seizure

Aspirin

Stroke, Hemorrhage, Bleeding, GI Distress, ulcers

ADP Inhibitors (Clopidogril)

irreversibly inhibits ADP DOC x preventing prehibiting platelet 2ndary stroke or MI aggregation

Bleeding of hemorrhage, easy burising, GI, Intracranial Used during invasive cardiac procedures CABG, PTA

GP Iib/IIIa Inhibitors Inhibit fibrinopen receptor on platelets to inhibit fibrin binding and scaffold forming Inhibit fibrinogen receptor on platelets to inhibit fibrin binding and scaffold forming Inhibit fibrinogen receptor on platelets to inhibit fibrin binding and scaffold forming

IV ONLY

ABCIXIMAB

GP Iib/IIIa Inhibitors

Bleeding, immune reaction

IV ONLY

EPTIFIBATIDE

GP Iib/IIIa Inhibitors

Bleeding immune reaction

IV ONLY

Tirofiban

GP Iib/IIIa Inhibitors

Bleeding,

IV ONLY

Anticoagulants (prevent fibrin scaffold formation after platelet aggregation)


Name MOA Pharmacology Toxicities/SDFX Reflex Drug Drug Interactions Contraindications Administration Misc

Heparin

Spontaneous hemorrhage, alopecia, HMW Heparin binds to HSS, fever, skin ncrosis Binds to Antithrombin III AT III bound to factor Iia osteoporosis/sponatneo thus preventing or Xa. LMW heparin us bone brkg @ chronic inactivation of thrombin. binds to ATIII bound to doses, dangerous lvls XA only of AT III, thrombocytopenia, antiplatelet AB's

pts w religious wishes against pork (it comes from pig glycosaminoglycans)

Do NOT Give Orally. Do NOT Give IM.

Does not cross BBB or placenta. Treat spontaneous hemorrhage w protamine sulfate

Direct Thrombin Inhibitors (Hirudin Argatroban)

by inhibiting Factor Iia it stops fibrin from being made, and prevents scaffold formation; Lepirudin/Hirudin is used Inhibit Thrombin (Factor prolongs PTT (so does to replace Heparin in Iia) Heparin) Heparin-Induced Thrombocytopenia; Argatroban is used to tx Heparin induced Throbocytopenia DOC x DVT prevention after hip surgery Reduced vit K is crucial x turning Preprothrombin into Prothrombin thus the Ca++ on gamma Carboxyglutamic acid can't bind FIIa or FIXa to Stops the reduction of vit the platelets. -wiki; K. Warfarin is used to tx A fib, Prevent Thromboemboli stroke, acute MI, Venous Thromnosis and Pulmonary embolism. Warfarin activity if in conjunction w Cimetidine (OTC H2 blocker) via warfarin metabolism, w Phenylbutazone via binding to prots, w Aspirin = Platelet fx:: Warfarin activity if in conjunction w Cholestyramine due to absorption, Phenobarbital by inducing cyt450, w Phenytoin by inducing cyt450

Lepirudin is derived from leech saliva

Enoxaparin

Warfarin/Coumadin

pregnant women (crosses BBB and causes fetal death birth defects)

Oral (good good thing) w 100% bioavailability. Dose is calculated by finding INR PT so that PT 2.

cyto 450 metabolization; binds to prots.

How to treat SDFX: Mild bleeding w dose Reduction; Severe Bleeding w stopping regimen and give Vit k; BAD bleeding via all of the above w concentration or plasma

Thrombolytic Agents
Dissolve clots by activating the conversion of plasminogen to plasmin that hydrolyzes fibrin. Therapeutic window 2-6 hrs after ssx usu IV

Name

MOA

Pharmacology

Toxicities/SDFX

Reflex

Drug Drug Interactions

Contraindications
Thrombo-Embolic Stroke

Administration

Misc
t1/2=23 mins; NOT an enzx

Streptokinase

Activates Plasminogen

Tissue Plasminogen Activator (Alteplase, Reteplase, Tenecteplase)

Alteplase repidly activates plasminogen bound to fibrin inthrombus (low affinity for free plasminogen); Urokinase

Desmoteplase Aminocaproic Acid Protamine Sulfate Vitamin K inhibits plasminogen activation antagonizes heparin

Bleeding Thereapeutic window 2(antidote=AminoCaproic 6hrs after ssx. Used x Acid), Immune Rxn, DVT, Acute MI Fever, Anaphylaxis Thereapeutic window 26hrs after ssx. Used to tx MI (not better vs streptokinase), Thromboembolic Strokes(not that great); GI and intracranial Alteplase is good @ bleeding treating MI (90 min window), Massive pulmonary embolism, Ischemic stroke (3 hr window) Thereapeutic window 26hrs after ssx. maybe intravascular Used to tx bleeding thrombus HSS, Dyspnea, Used to tx bleeding Flushing, Bradycardia Used to tx bleeding

IV ONLY

IV

IV

Antianginal Drugs

Name

MOA
Mimics endogenous NO the cGMP pathway which relaxes myosin. Effort angina - preload, SV MVO2; Variant angina- coronary flow by relieving coronary spasm; Mixed angina - coronary blood flow MVO2

Pharmacology
Dilates the viens>>coronary aa>>peripheral aa. Used to tx Effort Angina. Venous Flow Preload LVEDV/P Ventricular stretch Systole time Stroke Volume MVO2/Cardiac work Venous Return

Toxicities/SDFX

Reflex

Drug Drug Interactions

Contraindications

Administration
Sublingual to bypass liver, Oral, Topical (ointment ?looks like toothpaste?) Dispensed in Lactose to prevent combustion. Should have burning sensation when placed in tongue

Misc

Nitrates (Nitroglycerin, ISDN, ISMN)

Flushing of face neck, Pulsating HA due dilation of meninges (esp if topical) , Postural Hypotension due to antagonism of SAS, Halitosis, Methemoglobinemia

Keep away from air, light. Tolerance develops to low doses @ 4 wks. Stagger w drug free periods to avoid tolerance

Blockers (Nadolol, Propranolol, Timolol, Atenolol, Bisoprolol, Metoprolol)

HR & CF CO & MVO2

Use to tx Effort angina and Acute MI. Not that great x Variant angina

Bronchospasm (esp nonselectives), Heat failure, Bradycardia, AV Block, Peripheral Vascular Disese, Raynaud's, Depression, "Vivid" dreams, Sexual Dysfx.

maybe: LVEDV Heart size duration of systole coronary perfusion O2 delivery O2 demand reflex CF or HR. damn

Calcium Channel Blockers (Verapamil, Ditiazem, Nifedpiine)

block voltage gated Ca channels esp in aa>>vv; Verapamil - HR, CF TPR and coronary flow; Ditiazem - HR TPR & coronary flow; Nifedipine - TPR & coronary flow

Used to tx Prinzmetal angina; Effort angina refractory to NO's/ blockers, or pts w bad SDFX to blokrs and NO's. Only Verapamil and Ditiazem are indicated x pure effort angina.

Ditiazem - AV block, Hypotension; Verapamil Hypotension, HA, Periph Nifedipine has Edema, Constipation, only Ditiazem is safe to contractility and HR as AV block, CHF; use w blockers reflexes Nifedipine Hypotension, HA, Perip Edema

Oral, prot bound, No Orthostatic Hypotension

Coronary Vasodialtion - D, V, N); Peripheral Vasodilation - N, V; Contractility - N (reflex), V ; HR - D , N (reflex) , V

Aspirin Thromblytics Ranolazine Fatty Acid Oxidation Inhibitor (pFOXI) Effort angina + HTN? Treat w Ca Channel Blockers or blockers. Effort Angina + Asthma/COPD? Treat w Ca Channel Blocker. Variant angina + HTN + Sinus Bradycardia? Treat w Nifedipine

Antiarrhythmic Agents
Class I Na Channel Blockers (Impede Diastolic Depolarization at some point?)
Name MOA Pharmacology Toxicities/SDFX Reflex Drug Drug Interactions Contraindications Administration Misc

Ia Procainamide

bind to open/active Na channel

Ia Disopyramide

bind to open/active Na channel

Fever, Rash, AntiNuclrAntibodies, K channel blocking, widen upstroke of AP QRS cmplx, widen QT duration (APD); K flow; intervals; 20% phase 2, and AP converted to NAPA in depolarization liver so watch x NAPA toxicity, Lupus in slow acetylaters upstroke of AP; K flow; phase 2, and AP depolarization

toxicity w Amiodarone Cimetidine Ranitidine Procaine

IV

No evidence shows it works. Ia and Ic kill ppl.

No evidence shows it works. Ia and Ic kill ppl.

Ib Lidocaine

bind to inactive/closed Na channel

K flow, APDl and phase 2

Ib Tocainide

bind to inactive/closed Na channel bind to inactive/closed Na channel

K flow, APD and phase 2 K flow, APD and phase 2

Ib Mexiletine

Ib Phenytoin

bind to inactive/closed Na channel

K flow, APD and phase 2;

Mouth numbness, Tinnitus, slurred speech, confusion, somnolescence, sxrs, CNS depression; activates K channels AP duration from hyperpolarization activates K channels AP duration from hyperpolarization activates K channels AP duration from hyperpolarization Death via Hypotension, Cardiac Failure, Asystole esp in old ppl, Teratogenesis, Gingival Hyperplasia, Hirsutism; activates K channels AP duration from hyperpolarization

toxicity w Propranolol, Verapamil Cimetidine

IV

Not as deadly as Ia

oral

Not as deadly as Ia

oral

Not as deadly as Ia

oral

Not as deadly as Ia

Ic Flecanide Ic Moricizine Ic Propafenone

upstroke of AP BIG TIME

Just as deadly as Ia Just as deadly as Ia Just as deadly as Ia

All Class I antiaryhthmics Excitability, Responsiveness, and ischemia; also, by phase 2 they stop the cells from becoming prematurely "ready"/primed? for another contration. (except for lidocaine). Quinidine (Ia) just tells all the cells to STFU so it can reset the rhythm

Class II - Blockers
Name MOA Pharmacology Toxicities/SDFX
Bronchospasm, Hrt Failure, Bradycardia AV Block, Raynauds, Depression, Sex Dysfx: see above*: Sotalol may cause Torsades de Pointes Esmolol is new It looks like Ach, blocks the AV node and then is destroyed.

Reflex

Drug Drug Interactions

Contraindications

Administration

Misc

Non-selective (Propanolol, Sotalol, Timolol)

Propanolol - use x Atrial Tachyarrhythmias

Cardio-Selective (Atenolol, Metoprolol, Esmolol)

Atenolol DOC x something; automaticity by SAS; SAS related responsiveness of ischemic tissue; AV nodal conduction

ISA (Acebutolol) & blockers (Labetolol) Class II - Blockers are GREAT x Tachyarrhthmias

Class III K+ Blockers


Name MOA Pharmacology Toxicities/SDFX Reflex Drug Drug Interactions Contraindications Administration Misc

Pulmonary Fibrosis (fatal), Irreversible Liver damage, Constipation, Good x ischemic tissue bluish discoloration, Delays repolarization; Amiodarone (also Ia Na and during V Tachy to thyroid dysfx (from I's) marked in APDuration channel blocker and Ca slow down excitability Hz yellow discoloraton of and ERP (effective channel blocker) by prolonging AP eyes, Torsade de refractory period) duration Pointes Fatal arrhthmias but these are rare. Life saving prop's far outweigh. Torsades de Pointes; Prolongs QT interval Ibutilide use x A Fib/Flutter; when acting as K channel blocker use x Atrial Torsades de Pointes, Dofetilide Tachyarrhythmias, A Prolongs QT interval Fib; use x Atrial Sotalol (oooh also a Torsades de Pointes blocker) Tachyarrhythmias

w blocker inhibition of both; w blocker conduction velocity in all cardiac tissue; Toxicity w Procaine

Has a 30 day half life (bad)

orally BID

Class IV Ca Antagonists (Nifedipine Is NOT an Antiarrhthmic agent)


Name
Verapamil

MOA
SA automaticity; AV nodal conduction velocity SA automaticity; AV nodal conduction velocity Not Nifedipine

Pharmacology
use x Atrial Tachyarrhythmias

Toxicities/SDFX

Reflex

Drug Drug Interactions

Contraindications

Administration

Misc

Don't use w Propranolol AV SA Dysfx, Asystole or Disopyramide

Diltiazem Not Nifedipine

Not Nifedipine

Not Nifedipine

Not Nifedipine

Not Nifedipine

Not Nifedipine

Not Nifedipine

Not Nifedipine

Class V Cardiac Glycosides


Name MOA Pharmacology Toxicities/SDFX Reflex Drug Drug Interactions Contraindications Administration Misc
Tx toxicity w K (to lvl @ 5 mEq/dL), Lidocaine to hyperpolarize, Dig Fab Fragments, DO NOTUSE PADDLES, VERAPAMIL or BRETYLIUM

Digoxin/Digitoxin?

SA automaticity; ventricular Delayed After Depolarization (DAD); Excitability bc depolarize use x Atrial membr pot; Toxic doses Tachyarrhythmias have adverse effect.; Conduction velocity in atria, in AV node, in ventricles at toxic doses cAMP, gK, automaticity of SA node; Conduction velocity in DOC x PVST atria (vagomimetic), in AV node

SA Bradycardia, SVT, AV Block, Jxal Tachycardia, V Tach, V Fib (20% of pts have SDFX)

Adenosine

Flushing, SOB, Bronchospasm, HA, Hypotension, Nausea, Paraesthesia

Heart Transplant

Atrial Tachyarrhythmias - Tx w Propanolol, Dofetilide, Sotalol, Digoxin or Verapamil SVT - DOC=Adenosine (but may cause asthma attack) Vagal Maneuvers, Digoxin, Phenylephrine ( TPR vagal RE), blockers, Verapamil (IV): Prophylaxis via Verapamil, blocker (NOT Esmolol) AVOID CAFFIENE CIGARETTES Wolf Parkinson White (WPW) Syndrome (a ventricular pre excitation thing) - AV Node via Vagal Maneuvers, Verapamil Digoxin, Propranolol; Accessory (kent bundle) w Amiodarone QPD Flecanide Propanlolol V Tach - tx w Lidocaine ( V automaticity, Rapid depolarization in nml, Bidirectional block in Ischemic), Procainamide ( phase 0, ADP, ERP, V automaticity), Propranolol, Bretylium ( ADP, ERP) DC Cardioeversion (the paddles)::: None of these incr survival. HA! Torsades de Pointes - Stabilize w MgSO4 (DOC) remove causative agents (eg quinidine, amiodarone), give K to serum K lvls to 5+/- .5mEq/L Paroxysmal Ventricular Tacnycardia (PVST) - DOC is Adenosine

Beta Lactam Antibiotics


Penicillins
Name Class Spectrum MOA DOC Toxicities/SDFX Drug Drug Interactions or Combos
Oral contraceptives lose activity if + PNC b/c gut bact activate BCPs; lose activity if + TTCCL

Metabolism

Contraindications

Resistance

GENERALLY

cell wall synthesis inhibitor @ transpeptidase enzx; Staph Strep?? activation of autolytic enzx

Anaphylaxis (immediate, accelerated, delayed), epilepsy, nephritis, hematuria, hemolytic anemia (rare), GI, incr Na+

excreted in the urine; picks up protein at lactam ring creating a hapten leading to allergic rxn

no metabolism, drug destroying, drug can't penetrate, mutation, bioch indux, conjgx, transdx, transposition

Penicillin A Penicillin F combine w Probenicid (weak acid) to compete for excretion; Add procain (charged) to decrease short T1/2 (<60 mins), renal absorption and incr T1/2; add excretion phenoxyacetic acid to make acid stable and thus available orally penicillinase penicillinase

Penicillin G

Narrow Spectrum G+

Penicillin V

Narrow Spectrum G+ Narrow Spectrum

Methicillin

not used all too much

staph aureus

Nephrotoxic Ampcl+Sulbactam (B lactamx inhibtr) x incr efficacy; BCP lose contraceptive activity w Ampcln loses activity if + gentamycin b/c chem rxn so give staggered Given w Na so watch Na levels

B lactamase resistant :); staph aureusdamn penicillinase; NOT active vs Klebsiella or Pseudomonas penicillinase; NOT active vs Klebsiella or Pseudomonas B lactamase resistant :) B lactamase resistant :) B lactamase resistant :) B lactamase resistant :) Amox+Clavulinic acid (B lactamx inhibtr) x incr efficacy

Ampicillin

created to overcome the Broad Narrow Spectr of PNC G Spectrum

shigella

Carbenicillin

created to overcome the Broad Narrow Spectr of PNC G. Spectrum Not much used anymore Staph aureus starting to become resistant Staph aureus starting to become resistant Staph aureus starting to become resistant Staph aureus starting to become resistant Narrow Spectrum Narrow Spectrum Narrow Spectrum Narrow Spectrum

(pseuodmonas, proteus)

poor absorption

Oxacillin

Nafcillin Cloxacillin Dicloxacillin Amoxicillin Bacampicillin

Metabolized to Ampicillin

prodrug (ampicilin is active compound klebsiella Pseudomonas Pseudomonas (best vs Psuedomonas of PNCs), GPseudomonas AND klebsiella Gklebsiella klebsiella

Geocillin (Carbenicillin Derivative of carbenicillin Inodyl) Ticarcillin Azlocillin Mezlocillin/Pipercillin D Penicillamine Not an Antibacterial Chelates Copper Narrow Spectrum, G-

Wilsons Disease

D-Cycloserine

disrupts erasamase at stage 2 of cell wall synths; erasamase converts L(2ry tx of TB (1 of 4)) alanine to D-alanine so it disrupts the bact cell wall synths

Cephalosporins
Name Class Spectrum MOA DOC Toxicities/SDFX
More toxic vs PNC esp 1st gx; irritation at IM inj site; thrombophlebitis @ IV; hypersensitivity; superinfx; Nephrotoxic synergistic w AG

Drug Drug Interactions or Combos


Synergistic w other nephrotoxc drugs

Metabolism

Contraindications

Resistance

GENERALLY

Broad Spectrum 1st Genertion 1st Genertion 1st Genertion 1st Genertion 2nd Generation G+ G+ G+ G+ Broad Spectrum G+ some GBroad Spectrum G+ some GBroad Spectrum G+ some GBroad Spectrum G+ some GBroad Spectrum more GBroad Spectrum more GBroad Spectrum more GBroad Spectrum more GBroad Spectrum more GBroad Spectrum Good GBroad Spectrum Good G-

same as PNC, cell wall (proteus, E. coli, synths inhibition, auto lysis klebsiella) induction, and (staph endocarditis) (E. coli, Klebsiella) (klebsiella) (UTI) (ear infx, sinusitis)

excreted in the urine

cross rxn w PNC allergy

less susceptible to B lactamase vs PNC

Cephalothin Cefazolin Cephalexin Cefadroxil Cefamandole

MTT causes bleeding. GIVE W VITAMIN K; disulfram reaction MTT causes bleeding. GIVE W VITAMIN K; disulfram reaction MTT causes bleeding. GIVE W VITAMIN K; disulfram reaction

alternative if allergic to ampicillin or amoxicillin

Cefoxitin

2nd Generation

(anaerobes)

Cefaclor

2nd Generation

Cefuroxime

2nd Generation

(meningitis)

MTT causes bleeding. GIVE W VITAMIN K; disulfram reaction Cross BBB (good if you have CNS infections) Cross BBB (good if you have CNS infections) Cross BBB (good if you have CNS infections) Cross BBB (good if you have CNS infections) Cross BBB (good if you have CNS infections)

Cefotaxime

3rd Generation

Ceftizoxime

3rd Generation

Ceftriaxone

3rd Generation

Cefixime

3rd Generation

Cefpodoxime Proxetil

3rd Generation

Cefepime

4th Generation

(pseudomonas)

Cross BBB (good if you have CNS infections) Cross BBB (good if you have CNS infections)

Cefpirome

4th Generation

(pseudomonas)

Other Beta Lactam Drugs


Name
Carbapenem Imipenem Carbapanem Meropenem Monobactam

Class

Spectrum
Broad Spectrum anaerobes Broad Spectrum anaerobes G- rods ONLY

MOA

DOC
(anaerobes, UTI, LRI, GI, Gyn infxs) (anaerobes, UTI, GI, Gyn infxs)

Toxicities/SDFX

Drug Drug Interactions or Combos


must give w cilastatin to inhibit kidny metabolism does not need inhibitor

Metabolism
kidney enzx inactivates so must give w inhibitor

Contraindications

Resistance

superinfx may occur

NO PNC cross hypersensitivity :-)

lactamase resistant :-)

Beta Lactamase Inhibitors (Clavulanic acid, Sulbactam, Tazobactam)

inhibit beta lactamase (no antibacterial activity by themselves)

Clavulanic Acid + Ticarcillin or Amoxicillin; Sulbactam + Ampacillin; Tazovactam + Pipercillin/Mezclocillin (combos needed x activity) Red Man SSx, (hives, HoTN, flushing, rush, chest pain); ototoxic, injx site irritation,, rash, AG + vanc = Synergistic chest pain, hypotension, Nephrotoxicity synergistic w Nephrotoxic drugs (AG)

Vancomycin

G+

(staph aureus, C. diff, cell wall sythesis inhibtr commonly used x PNC via binding D-ala D-ala resistant drugs)

Bact chg the D-ala D-ala so drug has nowhere to bind

Bacitracin

(staph infx that don't RE Nephrotoxic if given IV (less so cell wall synthesis inhibitor to PNC meth, oxa naf or if given orally) cloxacillins) G- infx G- infx detergent, cell membr disruption detergent, cell membr disruption Nephrotoxic if given IV Circumoral paresthesias if IV, nephrotoxic

Synergistic w other nephrotoxc drugs

Polymixin B Colistin Sulfate

AntiFolates
Sulfonamides
Name Class Spectrum MOA DOC Toxicities/SDFX Drug Drug Interactions or Combos
incr warfarin activty (wfn is bumped off plasma prot by sulfmds causing unwanted bleeding); hydantoin (same as wfn but is an anticonvulsant), incr T1/2 Phenytoin (competes x micrsomal enzx),

Metabolism

Contraindications

Resistance

GENERALLY

compeltes with paba for coupling enzyme so bact Broad Spec can't make vit. B9. free (G+ cocci, G- drug is active drug; pH cocci/rods dependant (will crystalize out at low pH so drink lots of water

none but alt x (UTI, nocardiosis, shigella, trachoma, chlamydia, pneumocystis jirovechi)

StvJonSSx (from long lasting sulf Rx), decr vit K synth(by wiping out gut bact), hypoglycemia/GI, hepatitis, crytalluria, CNS-rare-,

good distribution, bound to plasma prot making it difficult to metabolize, renal excretion (unchanged), acetylation in liver loses activity but retains toxicity, T1/2 depends on kidny fx

gluc6phos DH defx (NADPH is depleted and can't reduce G6PDH-causes hemolytic anemia), AIDS, kernicterus (new borns; bumps off bilirubin and causes mental retardation), allergic to SO2 (e.g. Celexa)

decreased permeability, coupling enzyme changes, paba prodx incr.

sulfasalazine

Methotrexate

large molec antifolate

cancer

5aminocyclocyclic acid is cleaved off (active part) Inhibit folate synths (Folate to FH2; or FH2 to THF4) | Cancer-MTX forms complx w polyglutamate and is trapped inside cell to incr activity

Reum. Arth, colitis Acute Lymph Leuk, choriocarcinoma, Burkitts lymphoma, Psoriasis, immunosuppres (x organ transplants). TOO TOXIC x antibact GI ulcers, bone marrow depression, hepatic toxicity, HA, pulmonary, renal, pseudolymphoma. (Tx x toxicity = Folinic acid or folic acid) sulfa w trimethoprim (UTI, prostatitis, otitis med, chronic bronchitis, pneumocystis prodrug jirovechi (not AIDS pts) shigellosis, toxoplasmosis prodrug UTI, prostatitis,otitis media, shigella, toxoplasmosis incr [creatine], StvJonSSX, displaces drugs bound to plasma prot causing incr lvls e.g. warfarin

pregnant fem, fem trying to get preg.

Small Molec Antifolates thymine derivatives

Depends on R1, R2

Inhibit folate synths (Folate to FH2; or FH2 to (malaria) THF4) Thymine Derivative, some are prodrugs metablized to sulfanilamide (active cmpd)

StvJonSSx, hypersensitivity, GI, megaloblastic anemia, N/V, anemia, incr serum creatinine

incr folate reductase

Prontosil

Sulfonamide

Bactrim (Septra)

Slufamethoxazole/Trimet hoprim combo

AIDS

Pyrimethamine

small molecule antifolate

plasmodia, sporozites

inhibit dihydrofolate reductase inhibiting folate synths inhibit dihydrofolate reductase inhibiting folate synths

suppression of chlorq resist falciparum sp usu in combo w other TB mx

b9 defx, macrocytic normochromic anemia, megaloblastic bone marrow; leukopenia, granulocytopenia rare StvJonSSX NVD

synergism w sulfa drugs

Trimethoprim

small molecule antifolate

synergism w sulfa drugs

prodrug

DNA Synthesis Inhibitors


Quinilones
Name Class Spectrum MOA DOC Toxicities/SDFX Drug Drug Interactions or Combos Metabolism Contraindications Resistance

GENERALLY

(STD, UTI, GI infx, URI, DNA gyrase SSTI, bone/joint infx topoisomerase II (G-) or IV {better vs sulfa}, TB, (G+) mycobacterium avium cmplx) (STD, UTI, GI infx, URI, DNA gyrase SSTI, bone/joint infx topoisomerase II (G-) or IV {better vs sulfa}, TB, (G+) mycobacterium avium cmplx) DNA gyrase topoisomerase II (G-) or IV (G+)

Nalidixic Acid

Cinozacin

Fluoroquinilones
Name Class Spectrum MOA DOC Toxicities/SDFX Drug Drug Interactions or Combos Metabolism Contraindications Resistance

GENERALLY

STD, TB (2ry), SSTI, GI, cartilege growth inhibition mycobacterium infx; (in children), cardiac arrythmias, better than sulfa drugs crystalluria (drink lots of water)

Liver metabzd, Excreted in urine/bile (depends on children, preg Fem which) acid pH decr activity, rapidly absorbed, Liver metabzd, Excreted in urine/bile (depends on children, preg Fem which) acid pH decr activity, rapidly absorbed,

Ciprofloxacin

Levaquin/Levafloxacin

Norfloxacin

Ofloxacin

DNA gyrase topoisomerase II (G-) or IV (G+) DNA gyrase topoisomerase II (G-) or IV (G+) DNA gyrase topoisomerase II (G-) or IV (G+) DNA gyrase topoisomerase II (G-) or IV (G+) NOT a quinolone, but damages DNA.

ANTHRAX

NVD, HA, abnml LFTs,

NVD, HA, abnml LFTs,

children, preg Fem

Nitrofurantoin

unk

UTI

RARE-liver, lung, GI, skin

pts w severe renal insfx

Protein Synthesis Inhibitors

Name
GENERALLY

Class

Spectrum

MOA

DOC
depends on geography

Toxicities/SDFX

Drug Drug Interactions or Combos

Metabolism

Contraindications

Resistance
conjugation

stop ribosomal complex G+, G-, Broad from moving, disrupt aa Spectrum binding

Erythromycin

Macrolides

G+, Bacteriostatic (cidal @ high doses but w toxicities

Binds to 50S ribosomal subunit, inhibits translocation step and inhibsc cmplx formation

Mycoplasma pneumonia, Legionella, Diphtheria, also used to tx bacterial bronchitis, otitis media, acne(topical). Prophylax endocarditis colon/oral surgx [2ry Staph Strep, tetanus, chlamydia, lyme; some G- N. Meningitidis, H. flu, B. pertussis]

estolate form - cholestatic hepatitis (GI pain, hepatomegaly, incr bilirubin, eosinophlia; reversible); free (active) form- N/V/D

ERTHX + Clindamycin is antagonistic; ERTHX + PNC = syng renal damage; decr cytochrome P450 activity concentrated in the liver, so other Rx/herbs have bile excretion more activity Chloramphenicol+Erythromyci n=antagonism by 50S competition

Liver/kidney damage

Induced resistance, 50S ribosome mutation, efflux pumps, hydrolysis/destrx of Rx; cross resistance to other macrolides and clindamycin

Clarithromycin

Macrolides

Broad Specturm

Binds to 50S ribosomal subunit, inhibits translocation step and inhibsc cmplx formation

H. flu, mycobacterium avium (AIDS pts usu), H. pylori

decr cytochrome P450 activity so other Rx/herbs have more activity

Azithromycin

Macrolides

Broad Specturm

Binds to 50S ribosomal subunit, inhibits translocation step and inhibsc cmplx formation

(mycobacterium avium, Toxoplasmosis encephalitis, chlamydia urethritis) Erythromycin 1st too toxic to use, 50S inhibition, blocks translocation step anaerobic infx (bacterioides fragiles), strep pyogenes, diplo pneumoniae, staph aureus; 2ry choice if allergic to PNC

Lincomycin (not used anymore)

Lincosamides

Broad Specturm

50S inhibition, translocation inhibition

antagonize macrolides

Clindamycin

Lincosamides

G+, Bacteriostatic 50S inhibition, (cidal @ high translocation inhibition doses but w toxicities

Pseudomembaranous enterocolitis (can be fatal so change to vancomycin)

antagonize macrolides/erythromycin

metabzd in liver, excreted by kidneys

cross resistance w erithromycin, ribosomal mutations

Tetracycline

Tetracycline

Brucella Bacteroides Broad 30S inhibition previnting t(Lyme, spirochetes, Specturm G+, aminoacyl binding; inhibits mycoplasmas amebae, GfMet tRNA from binding cholera, STDs); SIADH

GI (staph enteritis could cause superinfx), hypersstvy, photosenstvy, liver damage, renal damage, dizzy/vertgo, damage to teeth/bones causes discolored teeth

Chelates heavy metals (Ca, Mg) which reduces absorption; TTCCL decreases activity of BCPs via killing gut bact needed for BCP activation; PNC+TTCL=antagonistic

Lower dose if kidney disfx. Excretion depends on GFR (except for minocycline and doxycycline); kids <10 preg fem

Gradual reisistance via R factor and efflux, overuse. Cross resistance w streptomycin, erythromycin, ampicillin, chloramphenicol, oxacillin, and cephalosporins. G- usu have cross resistance w chloramphenicol (not G+)

Minocycline

Tetracycline

Broad 30S inhibition previnting tLyme Specturm G+, aminoacyl binding G-

teeth discoloration

not good for UTIs

Doxycycline

Tetracycline

Broad 30S inhibition previnting tSpecturm G+, Lyme aminoacyl binding G-

teeth discoloration

not good for UTIs; Carbamazepine + doxy = decr doxy lvls via induction; PHB + doxy = decr levels via induction; PHT + doxy = ditto;

Tigecycline (not important)

Tetracycline

Broad 30S inhibition previnting tssti, intra-abdominal infx Specturm G+, aminoacyl binding G-

GI, N/V/D superinfx, hypersensitivity, irreversible delayed aplastic anemia Gray Baby SSx (renal damage, cardiac collapse), good diffusion to CNS, and inner eye (good thing), pancytopenia (rare/severe), GI, neuro sdfx, superinfx,

Do NOT use to tx Proteus/Pseudomonas

Chlorapmphenicol

Broad Spectrum

prevents 50S from binding to mRNA, inhibits peptidyltransferase (also inhibits euka cells w diff mechanism)

Salmonella typhosa (rickettsia, mycoplasma, lymphogranuloma). NOT USED FOR TRIVIAL INFX

not good w TTCCL, Polymyxin B, vancomycin, hydrocortisone b/c of antagoinism; Chloramph+Erythromycin=ant agonism by 50S competition

liver glucuronidation or hydroxylation inactivates, inactive drug excreted by kidny, incr plasma lvls if liver disfxing

lower dose if liver disease

R factor transmits gene x acetylation

Aminoglycosides
Name Class Spectrum MOA DOC Toxicities/SDFX Drug Drug Interactions or Combos Metabolism Contraindications Resistance

GENERALLY

Aminoglycosides

Narrow Spectrum G-

prot synths inhibition; cell (G- rods causing membr damage via; binds meningitis) to 30S ribosome

CN VIII damage, renal damage allergic dermatitis (topical), neuromuscular jx blocker, vertigo, dysmetria, +Romberg sign

ototoxicy if +Ethacrynic acid

resistance via R factor transfor; mutation of 30S unchgd excreted form by subU; adenylation in kidny via GFR; short T1/2, kanamycin streptomycin, low TI, dosing schedule is renal disfx incr plasma lvls so gentamycin, tobramycin; tricky so instead of lots of lower dose; synergistic renal phosphorylation in small doses Rx is a few tox w other renal toxic drugs kanamycin, streptomycin; heavy doses instead of lots acetylation in kanamycin, of small doses neomycin, tobramycin, amikacin, gentamycin strreptoycin

Streptomycin

Aminoglycosides

inhibits fMet binding; inhibits translocation step (aminoacyl binding to tRNA); require O2 for transport thru cell walll

vestibular system disruption, hearing loss if high doses, peripheral neuritis, facial TB (must combo); plague paresthesia, NMJ blocked in high doses, rash/hives, kidny damage 2ry TB

Must combo w other TB drugs; strpmcn + PNC to tx enterococci; DO NOT GIVE ALONE b/c resistance develops quickly; synergistic activity w Erhthromycin to tx Strep faecalis endocarditis

mutation of 30S subU

Kanamycin Broad Spectrum bacteremia

Neomycin

Aminoglycosides

E. coli, Proteus, Shigellae,, Klebsiella; Nephrotoxic ototoxic, contact prophylactic x bowel dermatits surgx (staph enterocolitis)

NOT effective x Pseudomonas or Bacterioides

Tobramycin Parommycin

Aminoglycosides Aminoglycosides

Gentamicin

Aminoglycosides

G-

Pseudomonas resistant to Polymyxin Nephrotoxic, vestibular B(Klebsiella, Proteus , Gototocicity, CNS toxicities rods causing meningitis; E. coli, ); Plague

Genta + Carbenicillin = decr genta activity via chemical rxn; Genta + Cephalothin = synergistic nephrotoxicity via tubular necrosis; Genta + Polymyxin B = synerg nephrotoxicity and NMJ block; Genta + Kanamycin = synerg ototoxic effects;

Renal excretion via GFR

Viomycin

Aminoglycosides

2ry choice x TB gonorrhea in urethra, prostate or cervix if N. gonorrhea is susceptible pain at injx site, hives, N/V, insomnia, dissiness; rarerenal/liver damage, incr BUN, decr clearance, incr LFTs

arises quickly

Spectinomycin

Aminocyclotol

30S subU inhibitor

pts sensitive to PNC usu tolerate spectomycin

Ineffective in extragenital gonorrhea/syhp

Streptogramins
VR E. faecium, bactremia, URI caused by MRStaph/Strep PNC resistant Strep pneumoniae R factor transmits binding site mutation

Quinupristin

streptogramin

G+

50S inhibitor

joint muscle pain, decr cytoP450 combo drug w Dalopristin

Linezolid Netilmycin

Oxazoladinone Oxazoladinone

G+

multi-drug resistant organisms

GI, HA, MAOI inhibition

poor people

Antifungal Drugs
Name Class Spectrum MOA DOC Toxicities/SDFX Drug Drug Interactions or Combos Metabolism Contraindications Resistance

Polyenes
Candida albicans; Moniliasis (oral or topical) (Cryptococcus, Histoplasma, Blastomyces, Trichophytion, Epidermophyton, Microsporum; sometimes mycoplasma bact),

Nystatin

Polyene

yeasts and fungi

binding to ergsterol causes cell membrane leakage

none unless given systemically (oral - mild N/V, diarrhea; IV hemolytic anemia, kidny damage)

N/A

Amphtericin B

Polyene

.3 mg <MIC< 1 mg. Dose is binding to sterol causes 2x MIC that cell membrane leakage lab gives you.

Use only in hospital w fatally ill pts and make sure pt is VERY TOXIC: NEPHROTOXIC, "healthy" enough to take th hypersensitivity, chills, fever, Rx. Daily dose not to exceed severe deep fungal infx phlebitis, HA, anemia, anorexia, 1.5 mg/kg; AmphoB allows (e.g. meningitis, bone, Rifampicin (usu bact Rx) to decr renal fx HoTN, hepatic pnemonia); topical penetrate fungal cell wall and failur, jaundice, hepatocullular kill fungi, but is toxic to host); disfx, intrathecal administration causes chemical meningits

DO NOT EXCEED 4g else renal damage, do LFT's, renal fx test b/f tx

N/A

Imidazoles/Triazoles
systemic infx (coccidiomycosis, paracoccidiomycosis, histoplasmosis-formally txd w Amph B Keto + antacids decr keto activity b/c keto needs acid environment to be soluable/active; keto + cyclosporine incr cyclosp lvls; keto decr steroid metablzm

Ketoconazole

Broad Spectrum

Inhibition of ergosterol syths causing membr disruption

inhibits cytchrP450 (disrupts steroid hormone metbz and other drug metabz), elevates LFT's

5-Flucytosine

Deaminated to 5fluoracil (active cmpd) which replaces U in mRNA resulting in screwy Candida peptides. Also converted albicans Candida albicans (Cryptococcus to (Cryptococcus) , Torulopsis, 5fluorodeoxyriboseMonoP hos. Which inhibits Aspergillus) thymidylate synthase. Basically commits suicide

Usefulness lmtd b/c cytopls membr not permeable to Fatal Bone Marrow 5Flu, so AmphoB Depression, diarrhea, AIDS pts potentiates 5-flu have trouble tolerating effectiveness (tx x Candida & cryptococcus infx)

prodrug

HIGH lots of things become resistant

Griseofulvin

fungastatic

binds to cell membr, kills(?) growing fungi by disrupting mitotic spindle. Binds to host keratin creating an environment where fungi can't grow and the fungi is shed w natural shedding process

skin and nail infx, athletes foot. (Microsporum, mild; HA (gone in a few days), trichophyton, memory probs, GI Epidermophyton; athletes foot and stuff): (systemic x candida albicans)

Gris + PHB decr Gris lvls by decr absorption; Gris + warfarin decr warfarin activity by induction; Gris induces prophyrin synths causing porphyria attack to those pts w porphyrias

N/A

Miconazole

Broad Spectrum

Inhibition of ergosterol syths causing membr disruption

Tinea pedis, cruris, vesicolor (vulvovaginal candidasis) coccidiomycosis

synergistic with coumadin systemic - arrythmias, phlebitis, (anticoagulate), use if HA AmphoB not an option

low vit K, pts taking anticoagulants

Fluconazole

Inhibition of ergosterol syths causing membr disruption

oral/esophogeal candidiasis in AIDS pts GI, vomiting. In AIDS pts (cryptococcal meningitis; StvJon SSx, liver damage, prevent relapse after thrombocytopenia, rash) Amph B)

give antiemetic to counteract vomiting; phenytoin lvls incr; anticoagulant lvls incr if + flucon

teratogenic (don't give to preg fem)

Resistance

Name

Class

Spectrum

MOA

DOC

Toxicities/SDFX

Drug Drug Interactions or Combos

Metabolism

Contraindications

Resistance

Undecylenic Acid

Fatty acid?

???

Tinea pedis, cruris, vesicolor, ringworm

GI

Tolnaftate

Fatty acid?

Squalene epoxidase inhibitor (ergosterol syths inhibition)

Trichophyton rubrum

GI

Terbinafine

Allylamine

fungicide by squalene buildup

Squalene epoxidase inhibitor (ergosterol syths inhibition)

Trichophyton, Epidermophyton, HA, diarrhea, dyspepsia, abd Microsporum (aspergillus, pain; chg in tast patterns; incr candida, sporothrix LFT (severe hepatotoxicity rare) schenckii, malassezia furfur) Aspergillosis after AmphoB has failed nyeh, GI, incr LFT

T1/2=16 days, liver metabolizes, inactive cmpd excreted in feces kidny

Caspofungin

Echinocandin

Aspergillosis

Inhibits beta 1-3 glucan syths

Anti TB Drugs
Name Class Spectrum MOA DOC Toxicities/SDFX Drug Drug Interactions or Combos Metabolism Contraindications Resistance
INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Ototoxicity, nephrotoxicity (all Start to see improvement of Rifampin + pyrazinamide morbidity in 2 weeks AG do) (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem Seizures (esp if predisposed), must be given w B6 peripheral neuorapothy GI, HoTN, liver toxicities AG AG AG 2ry 2ry prot syths inhibitor prot syths inhibitor 2ry TB 2ry TB ototoxicity ototoxic nephrotoxic ppl w seizures, depression (exacerbated)

Streptomycin

Aminoglycosides

1ry

inhibits fMet binding; inhibits translocation step (aminoacyl binding to tRNA); require O2 for transport thru cell walll

Cycloserine Ethionamide Levofloxacin Viomycin Kanamycin Amikacin

2ry

Rifabutin/Rifampin

1ry

inhibits RNA polymease (initiation step)

TB combo, active systemic TB, TB mingitis,eradication of meningiococcal carrier state; Mycobacterium avium

reare hepatitis, turns host fluids orange, flu like ssx

must combo; maybe can use AmphoB to let rifampin into fungal infx; Rifampin + AminosAcid block the absorption of the other from gut (bad thing); INH + induces P450 Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem

INH+Rifampin have additive liver toxicity <-toxicity; causes from RNA pol mutation loss of BCP activity

Capreomycin

peptide

2ry agent when 1ry no longer useful

ototoxicity, renal toxicity (not as bad as AG)

Aminosalicyclic acid

2ry b/c of GI probs

folic acid synths

Rifampin + AminosAcid block the absorption of the other bad diarrhea b/c of high dose from gut (bad thing); BCPs (8g) lose effectiveness; induction of liver;

Ciprofloxacin

Isoniazid

isonicotinic acid uses up causing OH buildup in cell; 1ry TB tx, NO interferes w mycolic acid TB combo G-/+ activity synths causing cell wall damage

INH + Rifampin + Pyraz + Ehambutol or Streptomycin is INH metabolit causes toxicity B6 standard 4 Rx tx. use INH + defx, peripheral neuropathy; Rifampin + pyrazinamide liver toxicity esp w EtOH (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x (death); szr if prone; preg fem; give w B6; INH inhibits metbz of Phenytoin

prodrug (active cmpd is converted by catalase to isonicotinic acid); LONG T1/2 you can give; acetylation inactivates; P450 metabolism

Treat <20yos. DO NOT TREAT if >35yos

mutation of catalase TB has high mutation rate so selectivity is common :(

Ethambutol

1ry TB tx, NO mycolic acid inhibition ro G-/+ activity RNA syths inhibtion

TB combo, mycobacterium avium cmplx

retrobulbar neuritis @ high doses (decr visual acuity, red green color blindness)

INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide excreted in urine/feces (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem

DO NOT use in kids

Pyrazinamide

1ry

reinfection

Liver Toxicity TOXICITY MANDATES hospitalization

INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem

HIGH if tx w/o other drugs

Dapsone Clofazimine Amithiozone Thalidomide Ethionamide 2ry

Leprosy Leprosy Leprosy Leprosy Leprosy teratogen

use 3-4 leprosy mx to start use 3-4 leprosy mx to start use 3-4 leprosy mx to start use 3-4 leprosy mx to start use 3-4 leprosy mx to start pregnant women (day 20-50 cuases seal limbs in fetus)

AntiViral Drugs
Name
Amantadine and Rimantadine (better mx)

Class

Spectrum

MOA

DOC

Toxicities/SDFX

Drug Drug Interactions or Combos

Metabolism

Contraindications

Resistance
NOT USED CURRENTLY B/C OF RESISTANCE IN ALL STRAINS OF FLU

Blocks binding to cell

nervousness, depression, prophylactic tx of Flu epilepsy esp if prone to A2 in elderly (parkinson) psychosis

do not use w bactrim, antihistamines (causes decr dose in geratric pts neurotoxicity; esp in older ppl, hmmm)

Idoxuridine (historical significance only)

antimetabolite; DNA synths inhibitor by stopping DNA elongation; (herpes keratitis from incorporated into DNA herpes type I, if nothing causing DNA breakage, else left) muation rate incr; selectivity due to rapid rate of virus replication

photosensitivity, edema causing lacrimal duct occlusion; slows down healing process

prodrug

teratogenic, carcinogenic,

Vidarabine

purine

(DNA viruses via decr synthesis)

replaces adening to stop DNA synths

(herpes keratitis from herpes type I, if idoxuridine not available); chicken pox, herpes encephalitis via systemic; ocular herpes infx

at high doses stops host DNA synths (polymerase); carcinogen, teratogen, mutagen

systemic - allopurinol + vida causes decr activity of gout mx

deamination causes inactivity; prodrug

Interferon alpha

inhibit virus binding by binding to virus; inhibit at all steps of virus rep

neurotoxic, flu like ssx usu Chronic Hepatitis (B, C) resolves in days, bone marrow (Karposis sarcoma, suppresion, exacerbate melanoma) depression/suicide

Acyclovir Ganciclovir Ribavirin Cidofovir Trifluridine Foscarnet

purine

inhibits viral DNA polymerase; syths inhibition

Herpes (all kinds and manifestations)

inactivated if taken w allopurinol

prodrug

HIV Drugs- 1PI + Ritonavir + 2NRTI (specific combo) = 4 drug Tx; or NRTI (combo)+ NNRTI = 3 Drug Tx
Zidovudine NRTI incorporation into DNA causing early DNA HIV @ all stages; termination and slow replx prophylaxis x exposure by blocking reverse and newborn transcriptase incorporation into DNA causing early DNA HIV @ all stages; termination and slow replx prophylaxis x exposure by blocking reverse and newborn transcriptase incorporation into DNA causing early DNA HIV @ all stages; termination and slow replx prophylaxis x exposure by blocking reverse and newborn transcriptase damage tissue that are constantly turning over via mt combo toxicity; lactose acidosis, liver Lamivudine+Zidovudine failure low platelets damage tissue that are constantly turning over via mt combo toxicity; lactose acidosis, liver Lamivudine+Zidovudine failure low platelets prodrug concerted to nucleotide @ low lvls or monothpy

Lamivudine

NRTI

prodrug concerted to nucleotide

@ low lvls or monothpy

Emtricitabine

NRTI

damage tissue that are constantly turning over via mt combo Tenofovir + toxicity; lactose acidosis, liver Emricitabine failure low platelets

prodrug concerted to nucleotide

@ low lvls or monothpy

Tenofovir

NRTI

incorporation into DNA causing early DNA HIV @ all stages; termination and slow replx prophylaxis x exposure by blocking reverse and newborn transcriptase nonompetetive inhibitor of HIV @ all stages; reverse transcriptase HIV @ all stages; inhibit final prot metabz of prophylaxis x exposure HIV prot and newborn HIV @ all stages; inhibit final prot metabz of prophylaxis x exposure HIV prot and newborn HIV @ all stages; inhibit final prot metabz of prophylaxis x exposure HIV prot and newborn HIV @ all stages; inhibit final prot metabz of prophylaxis x exposure HIV prot and newborn

damage tissue that are constantly turning over via mt combo Tenofovir + toxicity; lactose acidosis, liver Emricitabine failure low platelets, renal insfx

NOT prodrug

@ low lvls or monothpy

Efavirenz

NNRTI

teratogen

cytP450 indux

preg fem, liver disfx

@ low lvls or monothpy

Atazanavir

Protease inhibitor

long lasting DM, hyperlipidemia, diarrhea long lasting DM, hyperlipidemia, diarrhea long lasting DM, hyperlipidemia, diarrhea long lasting DM, hyperlipidemia, diarrhea inhibits cytP450 painful injx; incr chance of bact pneumonia

combo w low dose Ritonavir, then combo w NRTI combo w low dose Ritonavir, then combo w NRTI combo w low dose Ritonavir, then combo w NRTI combo b/c incr T1/2 of other drugs; but contraindicated if pt taking other mx

@ low lvls or monothpy; cross resistance @ low lvls or monothpy; cross resistance @ low lvls or monothpy; cross resistance

Fosamprenavir

Protease inhibitor

Lopinavir

Protease inhibitor

Ritonavir

Protease inhibitor

inhibits cytP450

@ low lvls or monothpy; cross resistance

Enfuvirtide

Fusion inhibitor; peptide

binds to gp41

HIV @ all stages

don't give if allergic

@ low lvls or monothpy; cross resistance

AntiParasitic Drugs
AntiMalarial
Name
GENERALLY

Class
sulfa drugs, trimethoprim, quinolones

Spectrum

MOA
DNA replication disruption; B9 syths inhibition

DOC

Toxicities/SDFX

Drug Drug Interactions or Combos

Metabolism

Contraindications

Resistance

Chloroquine

Aminoquinolone

Binding to DNA inhibits nucleic acid synths

use during erythrocytic GI, HA, malaise, vertigo, blurry phase of maria cycle; vision. schizonticide;

Coadministration w Primaquine is required to tx /prevent relapse;

Excreted in tears absorbed by corneal epithlm causing edema and opacifications of cornea (retinal aa constrx causes retinal ischemia and visual impairment) not active vs P falciparum; pts w epilepsy or on psychiatric mx; pregn

if Plasmodium sp can't concentrate in cell then mx won't work; falciparum is chloroquine resistant and reqs cinchona and anti-folates

Mefloquine Hydroxychloroquine

blood schizonticide

blood schizonts of P falciparum, vivax, Prophylactic ovale, malariae

interference with w fine coordination and spatial discrimination

Quinine

Cinchona alkaloid

gamete of all Plasmodium sp EXCEPT falciparum

Binding to DNA inhibits nucleic acid synths

Chloroquine resistant falciparum sp

injx site irritation, retinal ischemia, hearing loss, ringing in ears, dizziness, N/V/D; Severe-blindness, deafness, vertigo, HoTN; thrombocytopenia, purpura, hemolytic anemia, agranulocytosis, blackwater fever (hemolysis, clotting, renal failure uremia, death)

usu given w anti-folates, pyrimethamine + sulfadiazine/dapsone (x choroq resist falciparum)

no resistance and we don't know why

Primaquine

8-Aminoquinolone

tissue schizonticide; gametocidal

Exoerythrocytic P vivax well tolerated; acute hemolytic anemia and P ovale

Chloroquine must be given w Prima for complete tx; + 4aminoquinolone x prophylaxis

ppl w Gluc 6 P DH defx

no resistance and we don't want any

Chloroquanide plasmodia, sporozites inhibit dihydrofolate reductase inhibiting folate synths suppression of chlorq resist falciparum sp usu in combo w other mx b9 defx, macrocytic normochromic anemia, megaloblastic bone marrow; leukopenia, granulocytopenia rare b9 defx, macrocytic normochromic anemia, megaloblastic bone marrow; leukopenia, granulocytopenia rare GI, N/V/D, dermatitis, crystalluria, hematuria, hemolytic/aplastic anemia, granulocytopenia Bacrim+Amant=neurotoxicitie s in geriatric pts

Pyrimethamine

Trimethoprim

plasmodia, sporozites

inhibit dihydrofolate reductase inhibiting folate synths

suppression of chlorq resist falciparum sp usu in combo w other mx

Diaminodiphenyl Sulfone (DDS) Sulfa Trimethoprim + Sulfamethoxazole (bactrim)

Folic acid inhibition b/c it is a paba analog

ppl w Gluc 6 P DH defx

pts taking amantadine, old pts

Amebicides, AntiProtozoal Drugs


Name Class Spectrum MOA DOC Toxicities/SDFX Drug Drug Interactions or Combos Metabolism Contraindications Resistance

Metronidazole

teratogenic

Diloxanide furoate

Iodoquinol

Emetine

Dehydroemetine

Chloroquine

Suramin Na

Melarsoprol

Na Stibogluconate

Pentamidine Isethionate

Nifurtimox

Quinacrine

Atovaquone

Name
Piperazine Citrate Thiabendazole Mebendazole Albendazole Pyrantel Pamoate Paromomycin Praziquantel Bithionol Niclosamide Quinacrine

Class

Spectrum

MOA

DOC

Toxicities/SDFX

Drug Drug Interactions or Combos

Metabolism

Contraindications

Resistance

Lactam Antibiotics
Penicillins
Administration

injection b/c not acid stable

oral

oral

oral

injection

oral

injection

oral (better vs Ampicillin) Oral

Cephalosporins
Administration

oral?

IM/IV IM/IV oral oral IM/IV

IM/IV

oral

oral

oral

oral

oral

r Beta Lactam Drugs


Administration

IV (IM) via slow infusion to avoid Red Man SSx, oral x gut bact (e.g C. diff)

topical intrathecal/pleural (IV/IM) topica (ophthalmic/otic)

AntiFolates
Sulfonamides
Administration

pills, orally, cheap :D

treat toxicites w folinic acid (cancer) or folic acid (psoriasis RA); IM, IV, IT

oral

oral

Synthesis Inhibitors
Quinilones
Administration

Fluoroquinilones
Administration

better than sulfa drugs

n Synthesis Inhibitors

Administration
oral

must coat tablet to protect it from stomach pH, so it dissolves in duodenum; good body distr

oral (w/ food?)

oral (w or w/o food :-)

oral not so good absorption, IM/IV

oral not so good absorption, IM/IV

oral good absorption

IV ONLY

oral

Aminoglycosides
Administration

IM, subQ, oral (x gut infx; bad absorption in gut), intrathecal, topical

IM (no CSF distribution)

topical oral x gut infx,

intrathecal (CNS toxicities)

IM

Streptogramins

oral

ntifungal Drugs
Administration

Polyenes

topical, oral (excreted in feces) vaginal tablets,

topical, IV (low doses long time, .5mg/kg)

idazoles/Triazoles
topical, oral (being replaced by itraconazole and vriconazole; voricon does not inhibit P450 as much which is good for polypharmacy)

oral (good absorption)

oral (good absorption if eaten w fats), IV. Up to 12 mos to treat dermatophytes

topical, not given systemically

Administration

topical

topical

oral, topical

Anti TB Drugs
Administration

for all TB tx: oral;

requires 8g per day

oral good absorption; prophylaxis x 9 mos if evidence of expossed (only prophylaxic tx

oral

AntiViral Drugs
Administration

decr dose in elderly b/c of decr renal fx

topical, (systemicHARDLY)

topical, (systemicHARDLY); acyclovir is better

must be taken for 1 yr

c combo) = 4 drug Tx; or NRTI (combo)+ NNRTI = 3 Drug Tx

injx

tiParasitic Drugs
AntiMalarial
Administration

as prophylactic tx must be given x 6 mos straight after leaving endemic area.; as suppressive therapy 2.5 g orally w/in 3 days, IM if necessary; prophylactic vs chloroquine resistant falciparum, ovale, vivax;

IV/IM? as blood schizonticide; oral

des, AntiProtozoal Drugs


Administration

Administration

Actinomycetes General Features Etiology Epidemiology

No Immune RE: b/c it's too far away. Reason for removal is Manifestations Actinomycosis-1)Cervicofacialmost common, usu follows dental caries and happens after trauma 2)Thoracic-pulmonary inf may be initiated by extentision or inspiration. Maybe spread to CNS 3)Abdominalusus due to perforation of intestinal wall e.g. appdx rupture. ss(x) follow infd organ. 4)Genital-common in femms, usu w/ IUDs, ss(x) similar to PID, usu subclinical

Actionmyces israeli, Propionibacterium propionicus, Actinomyces naeslundii

M>F 2:1, 15-35yo, usu after loss of nml flora

Nocardia asteroides

75% of cases in Males unk reasons. 50% of cases to immunocompr, AIDS, EtOHics, cancer, chrnc pulmonary inf. Orgsms are wrdwde, soil and aquatic.

Nocardiosis-Pulmonary inf as transitory or chronic, rarely necrtizing, w/ many large abscesses. 2)May disseminate to organs w/ predilection to brain

M>F b/c of more exposure. Sub/tropical, Sudan, Mxco, usu soil dwellers.

Actinomycetoma-SubQ inf 1)Swollen lesion usu on foot/hand suppurating abscesses w/ grains (same as eumycetoma)

Spirochetes General Features Etiology Epidemiology Manifestations Spiral shaped, Nonsporulating, Motile

Treponema pallidum

Syphillis-1)Primary Stage-Hard chancre nonpainful (genitals-males cervix-fems) 2)Secondary Stage-Flu like ssx, skin lesions, mucous 1)Modes of Inf-Passage through birth membrane lesions 3)Latent Period canal, infection in utero, contact 4)Late Period/Tertiary Stageduring manifestation, blood Neurosyphilis:Asymptomatic or transfusion 2)Adolescent to adults Symptomatic-Meningovascular, Parenchymatous (paresis, Tabes Dorsalis). Late Benign Syph-Gumma Formation

Teponema pertenue Treponema carateum Treponema syphillis

Children, Warm tropics Children, Warm arid tropics Children, Arid subtropical

Yaws-looks like warts on skin. Pinta-Looks like skin is peeling, or becoming unpigmented Bejel/Endemic-Mouth lesions, skin lesions, granulomatous lesions on skin nasophrx, bones Relapsing Fever Tick Born (B. recurrentis )-More relapses but less severe. Louse born (B. hermsii, turicatae, parkerii )-Usu only one severe febrile episode Lyme Disease 1)Primary stgerythema chronicum migrans 2)Secondary stg-rash, arthrits, neuro, cardiac 3)Tertiary stg-arthritis

Borrelia recurrentis, hemsii, turicatae, parkerii

Borrelia burgdoferi, garinii, afzelii

Worldwide Reservoirs-Deer, mice Vector-ticks

Leptospira interrogans, biflexa

Reservoirs-animals (e.g. cows)

Leptospirosis-usu subclinical may cause fevers, conjuctivitis, Icterus jaundice Kidney/Liver dss

More Notes:

General features Etiology

Epidemiology

Oral Microbiology Bact of supragingiva is mostly G(+) sp. Bact of subgingiva is mostly G(-) sp. Disru Manifestations

Streptococcus mutans, Lactobacillus acidophilus

Everybody everywhere is susceptible (babies falling asleep w/ bottle, salivary rate, late weaning). Brushing, Fluoride, Peridex (.12% chlorohexidine)etc etc. helps to prevent. [L. acidophilus ][caries]. S. mutans main cause of oral infs.

Dental Caries-Decalcification of inorganic and organic portions of tooth via acids produced when bact act on CHOs

1)Microbial-brkdwn of epithelial wall provides entry, G(-) rods increase, tissue damage due to endotoxins of G(-) bact 2)Immunologial-allergic rxn of gingiva to mouthwash/toothpast, pemphigus vulgaris, lichen planus, neoplastic dss, carcinoma 3)Traumatic-blunt trauma, plaques, chemical (aspirin is caustic to epithelial tissue)

1)Periodontal Disease-Gingivitis, Periodontitis, Periodontosis, Periodontal Abscess, Drug induced gingival Hyperplasia, ANUG, Primary Herpetic stomatitis, Recurrent Herpetic Stomatitis, Herpetic Whitlow, Aphthous Ulcers, Candidiasis, Hairy Tongue, Dry Socket 2)Endodontic-Pulpitis

General Features Etiology

Epidemiology

Legionella and Bartonella 1)Peru Ecuador, Colombia 2)G(-) rods fastidious (needs humidity w/ CO2) 3) Manifestations

M>F 2:1, 50+yo, Summer, Smokers, 1)Legionairres dss-Flu like ss(x) EtOHics, immcomrsd, pulmo dss Legionella pneumophilia Fatal 2)Pontiac Fever-Flu-like ss(x) Spread via aerosol e.g. swamp Self-limiting coolers

Bartonella bacilliformis

1)Peru Ecuador, Colombia 2)G(-) rods fastidious (needs humidity w/ CO2) 3)Spread via sandfly Phlebotomus

1)Bartonellosis-Acute anemia verruga Anemia caused by removal of infd sensitized RBC's, HA Myalgia. Anemic phase ends when humoral RE induced Chronic Bartonellosis w/ cutaneous lesions1-2cm for years

Bartonella quintana

1)"Trench Fever"-Fevers at 5day 1)Spread via human louse Pediculus intervals 2)Most commonly HA, xtrm humanus wkns tibial pain Varies fr ass(x) to debilitating 3)Angiomatosis

Bartonella henselase

1)Car Scrath Dss-Lymphadenopathy at site of inf 2)SBE 3)Bacillary Angiomatosis

Etiology

Epidemiology

Parasites SubKingdom Protozoa Manifestations

Entamoeba histolytica

Reservoir: Only Humans thus human-human transmission only via fecal contaminated H2O w/ cysts. Flying bugs can transport feces cysts from feces to food Common in Tropics 1)Prot defx, Pregnant, immdfx InfDss, but may assx carriers.

1)Amoebic Dysentery-abd pain, cramps, colitis w/ diarrheaBloody stools w/ 25poops/day. (R lobe of liver may be infrupturelung inf. Length of illness days-yrs

Giardia lablia

WrdWde Childrn<10yo e.g. daycare centers Homosexual Males Reservoir:dogs, muskrats, sheep, lakes, rivers aka "backpackers dss" Transmission fecal-oral cyst is infective form Flying bugs can transport feces cysts from feces to food

1)Giardia-mild drrha to malabsorption syndrm, foul dirrha, abd cramps, farting, steatorrha Malnutrition b/c G. lamblia absorbs fat sol. stuff like beta carotene, B12 exacerbating malabsorption syndrm

Balantidum coli

Plasmodium falciparum

WrdWde, Fem Mosquito is vector. Mosqo ingests diff sex sp., male matures to magetes female into macrogamete, fertilization forming zygote/ookineate/oocyst, oocyst turns 1)Malaria-Early flu-like ss(x), to haploid sporozites, sporozites goto Nausea, vomiting drrha, HA fever mosqo saliva glands, inf humans. In convulsions, joint pain humans sporozites goto hepatocytes to become merozoites, release, inf RBC's, mature into trophozoites, merozoites, rupture, release more merozoites Coccidian parasite, Cat is vector and reservoir. Immcprsd and pregnant are at risk. Cat eats cyst, cyst turns into trophozit, trophozit turns to oocyst, cat poops, humans ingest oocyst, oocyst turns into sporozit, inf and dss Children under 5, Americas Kissing bug is vector, inf but poops on human skin causing irritation, human scratches inf into skin, inf. Trypomastigotes invade phagocytic cells, develp into amastigotes, multiply, ruputure, mature to trypomastigit form, inf new RBC's (get picked up by new Kissing bug). Many reservoirs. Africa Tse Tse fly is vector

Toxoplasma gondii

1)Toxoplasmosis-Acute:chills, fever, HA fatigue, lmphadenitis, myalgia Chronic:rash, encephlitis, myocarditis

Trypanosoma cruzi

1)Chagas Disease-Inflamntn, swelling, facial rash/edema, death bea CNS damage (esp in chldrn) and myocarditis

Trypanosoma grucie g, rhodosaiense More Notes General Features Etiology

1)African Sleeping Sickness SubKingdom Metazoa Phylum Nematodes

Epidemiology 1)Found in 2/3 of world esp (sub)tropics and areas w/ sanitation 2)Most prevalent in Asia SthEast USA 3)4-14yos 4)Access to hlthcr, hygeine, soc.ec cond's also factors

Manifestations 1)Adult worms no acute ss(x) 2)GI obstr, abdom pain oral expulsion 3)Lung phase w/ pulmonary ss(x) (Ascaris coming out of anus?)

Ascaris lumbricoides

Enterobius vermicularis

1)Temperate climates 2)5-10yos 3)Adults inhabit cecum Most common helminthe inf in USA

1)Enterobiasis-usu ass(x) but ss(x) = perianal pruritus at night, anorexia irritability abdom pain Sometimes fem w/ vulvovaginitis or peritoneal granulomas

Stronyloides stercoralis

1)Indigenous to S.E. USA (KY, TN, FL LA etc) esp veterans

1)Skin-Larva currens (fast advancing skin lesion usu on perineum or trunk 2)GI-bloating, anorexia nausea 3)Pulmonarynonspcfc

Wucheria bancrofti

1)inhabit lymph syst and subq tiss Larva is inf agent Tropical

1)ass(x) 2)Acute Lymphadenitis w/ fever Elefantitis(?)

General Features Etiology Schistosoma mansoni

Epidemiology

Phylum Platyhelminthes Class Trematodes Nutrient uptake via absorption Nonsegmente Manifestations hepslpleenomegally

Fasciolopsis buski

Asia Metacercariae is inf agent

General Features Etiology

Epidemiology

Class Cestodes Head w/ scolex suckers, hermaphroditic, no gut, nutrients via abos Manifestations 1)T solium-passing of gravid proglottids >13branches/glottid thus major concern is develping cystercosis 2)cystercosis-depends on where cyst is Neuro is fatal

Taenia solium

wrldwde Humans only definitve host T saginata no hooks Larval cyst in undercooked meat is inf agent High in Latin America/Africa low in USA

Taenia saginata

wrdwde High in Latin america low in USA T solium has hooks, Eggs of undercooked beef are inf agents

1)T sagomata-abd pain, passing proglottids 15-20branches/glottid 2)cystercosis-depends on where cyst is, Neurocyst can be fatal

Echinococcus granulosus

WrdWde Egg causes inf Larva causes dss Protoscolios inf dogs dogs poop eggs other wldlif/humans infected

Cystic echinococcosis Hydatid Cysts Can Be Found In Liver Rickettsia and Ehrlichia I) Rickettiosis Manifestations

Etiology

Epidemiology

Rickettsia prowazekii

Human/Rat Louse (or flea) (respectively) is vector/reservoir, Louse dies b/c of inf, Africa, S. America. No person-person transmission G(-)

A)Typhus Fever 1)Epidemic/Louse bornTyphus-Fever HA myalgia, rash on 4th day (1st on trunk then limbs usu not face), Maculopapular rash w/ petechia, CNS dsf(x)(stupor delerium), uremia Brill's Disease is remanifestation usu mild w/o rash 2)Endemic Flea Born TyphusSame as Epidemic but less severe Rash first on appendages THEN trunk B)Spotted Fever 1)Rocky Mt. Spotted Fever-incubation x 5days, HA fever myalgia, maculopapular rash w/ petechia on 4th day on hands feet then trunk face. Death via circulatory collapse/kidney failure 2)Boutennese Fever milder form of RMSF Rash first on trunk then appendages 3)Rickettsialpox Rash first on trunk then appendages C)Scrub Typhi Rash first on trunk then appendages D)Q Fever Rash first on trunk then appendages E)HumanGranulocyticEhrlichiosis Manifestations

R. typhi

Texas G(-)

Rickettsia rickettsii

E. USA, campers/hikers. Roden/Dog ticks are vectors. Ticks are vecrtor and reservoir. Ticks not killed by inf G(-)

R. conoria

G(-) Transmitted by mite bite of house mouse G(-) SE Asia, Australia. Transmitted by chigger G(-) Farm/Rural area, Slaughterhouse workers Wisconsin, Minnesota Epidemiology

R. akari

Orienta tsutsugamushi

Cocellia burnetti

Ehrlichia ewingii Etiology

omycetes

s too far away. Reason for removal is usu. Cosmetic Key Diagnostics 1)examin sputum, pus tissue, cervical exudates for granules and filaments >1mcmtr side. 2) Culture ID via morph, gram stain (+) and fimaments. 3)Facultative anaerobes Treatment Notes

1)PNC 2)tetracycline, clindamycin, sulfonamides. 3)surgery to drain lesions

Part of normal flora. Propylactics used by dentists and after trauma.Nonsporeforming

1)Distinguish from TB 2)Exam sputum for G+ orgs 3)Culture ID via morph, Aerobic growth, partial acid fast

1)SFM-TMP 2)surgery

20-30% fatal 1)Log phase more virulent vs stationary phase. Virulence due to penetrating growing tip. Effect lysozome fx. Virulent forms grow out of macrophage

1)Examine pus for granule and verify size, color, G+ w/ bact filaments<fungal filmts 2)Culture ID via morph, cell wall composition, use for verification

1)Long term antibx. PNC(Actinomyces ), Chloramphenicol Sulfonamides (Nocardia ) Streptomycin (Actinomadura, Streptomyces ) 2)Amputation-last resort

inf by traumatic implantation

ochetes

al shaped, Nonsporulating, Motile Key Diagnostics Treatment Notes

1)Direct exam 2)Serologic testsNonspecificTrepanoma l Rapid Plasma Reagin for cardiolipin, ELISA, 1)PNC, 2)Ttracycln, Specific Trepanomal Erythromycin, 3)Jarishc (hemaggltzn assay, Herxheimer Rxn fluoroscein antibody tests 3)Demonstration of orgsm via drkfld exam, silver stain, tests under "2)"

NonVenereal ss(x)-Yaws, Pinta, Bejel Dg(x) via demonstration of orgsm T(x)=PNC (or Ttrcycl or Erythrmc) 2)VirulenceOuter membr prots for adherence, hyaluronidase for tissue invasion, fibronectin for mimic, antiphagocytosis (reason for undetectable) 3)May cause still born or late abortion Skin to skin Skin to skin Transmission via mouthmouth contact Usu not fatal

Borrelia in blood, stain w/ Giemsa. Must take sample DURING febrile stage. 1)Clinical exam"Bullseye erythema"(75% of p(t)) 2)Serological tests ELISA, Immunoflrsc Ab

Tick born is Endemic. Louse Born is Epidemic. 1)Ttrcycln, Erythromycin Relapses progressively 2)JH rxn milder. Death via CV probs 1)Early Inf-Doxycycline or Amoxycilin 2)LateCeftriaxone

Can lead to debilitating arthritis Only spirochete resistant to envrnmnt outside body thus is the only spirochete that can be cultivated. Transmission via soil, H2O, food, inf tissue, congenital(rare)

1)Darkfield microsc

1)Long course antibx 2)Vaccinate livestock

crobiology of subgingiva is mostly G(-) sp. Disruption of these proportions disease. Notes Key Diagnostics Treatment

1)Caries excavation. Restore missing s(x)

and Bartonella astidious (needs humidity w/ CO2) 3)Spread via sandfly Phlebotomus Key Diagnostics Treatment

Notes

1)Flurosc antibody 1)Erythromycin 2) staining 2)Culture fr lung Rifampin

G(-) rods Stain better w/ silver stain Antiphagocytic Antibodieskilling Cytotoxin inhibits PMN respiratory bursts Macrophages may kill Orgs produce Blactamase Two other Legionella spp w/ diff DNA but same ss(x)

Gentamycin

1)Can be found w/o dss.

Gentamycin

1)Can be found w/o dss 2)may cause SBE

1)Blood ID esp in immcmpr pts 2)Cultures NOT helpful b/c too few None orgs available due to cell mdtd RE

1)Now reduced in AIDS pts b/c of t(x) for M tb inf

asites om Protozoa Key Diagnostics

Treatment

Notes

20m. 1)Flask shaped ulcers in intestine 2)stool samples mcrscpy (watery-trophozoites w/ ingst RBC solid-cysts)-not helpful after dissemination 3)Ab testing, ELISA, PCR

Phylum Sarcomastigaphora Class Sarcodina NOT 1)Metronidazole (flagyl) commensal, Amoebic cysts follwd by iodoquinol can form in liver maybe 2)t(x) for carriers w/ fatal, Reportable dss in Tx luminal amoebiasis Asexual reprodx. Cyst iodoquinol, furamide and IngestionStomachHCl paromomycin 3)Improve to release trophozoites in sanitation dudnemAttachment to host cell and destruction

1)Exmn stool x trophozits (fresh smple) usu billions of trophzits, Smple at diff time intervals b/c neg sample 1)Metronidazole, inf, Cysts are 11m furazolidine, quinacrine. long commonly found in T(x) of contacts solid samples and survive for 2wks 2)String test, Ab test w/ 98% accuracy

Phylum Sarcomastigaphora Class Mastigaphora Cyst*chlorine resistant* IngestionStomachHCl to release trophozoites in dudnem and jjnmtrophzits attach to intstn villi via ventral suckers and absorb semidigstd food through body, usu encyst in colon, onset of dss b/c of intstn inflmmtn.

Phylum Ciliaphora

1)Exmn RBC's for rings 2)PCR or Ag detction

1)Mefloquin-orally Quinine-IV both to treat blood and liver

Phylum Apicomplexa

1)Ab testing, IgM (not found in AIDS p(x))

1)"Nml" pt-Clindamycin 2)AIDS ptPyrimethamine w/ Trisulfapyrimadine 3)Pregnant-Spiramycin

Prevention via good hygiene and women avoiding cat litter

1)Thk/Thn blood films for trypomastigotes 2)Biopsy-of nodes, spleen, liver for amastigotes 3)xenodiagnosis-inf clean kissing bug w/ p(t) blood

1)Nifurtimox (has little affect on tissue inf) 2)Na Kissing bug eradication as Stibogluconate w/ control method Meglumine antimoniate

SubKingdom Metazoa Phylum Nematodes Key Diagnostics

Treatment 1)Albendazole PO (mebendazole later to treat whipworm), Mebendazole avoid vermifuges 2)VitA to improve growth devl't

Notes 1)Fem > Male 2)15-35cm long Creamy white Cuticle w/ fine circular striations 3)Adult lives in upper sm intest

1)Microsc ID of eggs in stool 2)Poor growth

1)Nocturnal observation 2)Scotch tape test of anal area and view micrscp for eggs (50mcrmetrs)

1)Albendazole PO 1)F>M 2-13cm Yellow, Fem (mebendazole later to w/ pointed tail 2)Gravid fem treat whipworm), migrates to anus to deposit Mebendazole 2)treat eggs 3)Hygeine whole family and school preventative chums

1)Eosinophilia as hallmark of helminthe inf 2)Larva in stool 250m orgnsm=intestinal inf 600m orgnsm=hyperinf 3)Larva in sputum = hyperinf 4)Culture in beef broth 1)Microsc ID of mcrofiliariae of blood sampls at night 2)ICT for Ab-Ag rxn.

1)Ivermectin or Thiabendazole, but usu too late by the time p(t) seeks t(x)

1)Symptoms can occur if p(t) put on corticostrds 2)worms don't need to leave body to finish life cycle Can also be free living 3) prodx of steroids virulence blood/tisse parasite Mosqo vector

1)interruption of dss w Albendazole+Ivermectin( or Diethylcarmazine) for 5 yrs Alleviate/preventlymphedema mngnmt

es Class Trematodes uptake via absorption Nonsegmented Key Diagnostics Treatment Notes Praziquantel (incr cell vaccine dev'lt against Sm membr permeability) p80 would be nice avoids eggs w/ spine in feces Oxamniquine no longer inf via surf membr renewal available in USA elliptoid shaped eggs in Praziquantel (incr cell stool or vomit membr permeability)

Cestodes aphroditic, no gut, nutrients via abosrption aka Tapeworms Key Diagnostics Treatment 1)worm inf dgx via eggs in stool 3mos post inf ID 1)Praziquantel for worm of progolittid for inf. 2)Albendazole or speciation 2)cystercosis- Praziquantel for cysts in involved organ cystercosis 3)Surgy to Eggs in feces Ag-Ab remove calcified cysts tests 1)worm inf dgx via eggs in stool 3mos post inf ID 1)Praziquantel for worm of progolittid for inf. 2)Albendazole or speciation 2)cystercosis- Praziquantel for cysts in involved organ cystercosis 3)Surgy to Eggs in feces Ag-Ab remove calcified cysts tests Imaging Serological tests should be used b/f Surgry w/ postop invasive methds, Albendazole Immunoassys and Ehrlichia kettiosis Key Diagnostics Treatment

Notes cysticercosis ingestion can happen in populations that don't eat pork. b/c a carrier can contaminate the nonpork meal e.g. jews eating food from a dirty pork eater

Notes

Flea born Typhus-Rash on arms/legs THEN trunk Tick born-Rash on trunk first then legs/arms, serology

30%fatal Flea born Typhus Ttcycl, Chloramphenicol is wrdwde Not fatal for w/in 7 days onset fleas. Fatal for louse

Ttcycl, Chloramphenicol w/in 7 days onset

inf in tick is everywhere, <60%fatal w/o t(x). Ttcycl, Chloramphenicol Rickettsia live in nucl of cell w/in 7 days onset 2 and 3 caused by diff sp vs 1) Ttcycl, Chloramphenicol w/in 7 days onset Ttcycl, Chloramphenicol w/in 7 days onset Ttcycl, Chloramphenicol w/in 7 days onset Ttcycl, Chloramphenicol w/in 7 days onset Severity of dss b/c of high Ttcycl, Chloramphenicol [endotoxin] Vector control w/in 7 days onset important esp for human Treatment Notes

Key Diagnostics

General Features Etiology Pedraia hortai Trichosporon beigelii

Epidemiology

Superficial Infections No Immune RE: b/c it's too far away. Reason for removal is usu. C Manifestations Black Piedra-Black gritty nodules in hair shaft

Temperate climates, sporadically in S. White Piedra-soft, mucilaginous, U.S. light colored nodules on hair Tinea nigra-Chronic asymptomatic infection of stratum corneum usu of palm Pityriasis versicolor-Chronic, mildly asymptomatic noninflammatory infection of stratum corneum. Lesions covered w/ sharply delineated furfuraceous scales, w/ variable pigmentation, may be single or coalesed. Cutaneous Infections (Dermatophytosis)

Exophiala werneckii

Teenagers, female, U.S. Gulf Coast, FL, warmth of Caribbean

Malassezia furfur

Normal skin/scalp flora. Ds(x) hightest in tropics. Found equally in wo(men). Recurrent. Excess perspiration, corticosteroids, malnutrition and hydrophobic cmpds on skin.

General Features Etiology M. audouinii T. tonsurans

usu caused by 1) Trichophyton (rubrum , tonsurans , mentagrophytes ) 2) Epidermophyton floccosu audouinii ). colonize keratized tissue. Found on humans, animals, and in soil. Inf fr nml flora are mo acute, more sensitive to t(x) and less likely to reoccur. same sp can cause more than one ss(x), m Epidemiology Manifestations Tinea capitus-1) Epidemic a. Grey childhood disease. Spread frm Mexico patch caused by M. audouinii b. to U.S. Black dot caused by T. tonsurans Tinea favosa-yellow cup shaped common in Mediterranean crusts called scutula occurs in adult males, acquired from Tinea barbae-mild irritation to animals folliculitis Tinea corpus-ringworm on body w/ children, worldwide scaling to inflammatory lesions of glabrous skin Tinea crurus (jock itch)-Lesions usu males. Favors humidity are sharply demarcated raised erythematous border Most common, affects millions worldwide usu occurs w/ tinea pedis Tinea pedis (athletes foot)-often begins on 4th/5th digit Tinea manum-infection of hand Tinea unguium-nail infection

M. audouinii

Trichophyton

More Notes:

Transmission my contact, either fr soil, lesions, or indirect (pool, shower, comb, etc) Microsporum sp :m floccosum :macroconidia, Trichophyton sp :microconidia. Temp sensitive limits inf to surface. Fatty acid patch to pre-puberty.

General features

Subcutaneous Infections Introduced via traumatic implantation. Some occur worldwide w/ endemic areas, Sever

Etiology

Epidemiology

Manifestations

Sporothrix schenckii

Found worldwide, endemic areas in Brazil, Mxco, Zimbabwe. 75% of cases male, in U.S. associated w/ horticulture/gardening as occupational hazard.

Sporotrichosis-4 clinical types: 1) cutaneous lymphatic-75% of cases. Leads to necrotic lymph nodules progressing along lymph vessels 2) cutaneous non-lymphatic-"fixed" form, found in endemic areas

Pseudallescheria boydii

1ly in males b/c of exposure. Wolrdwide w/ endemic areas in Sudan, Mxco. Orgms usu live in soil.

Mycetoma (Eumycetoma)localized, swollen, lesion with pus on foot or hand. Pus contains grains. Looks like random lesions on body with dark, crusty draining blotches.

Fonsecaea pedrosoi, Worldwide, more in Tropics. Phialophora verrucosa, Males>Femes. Usu a soil orgnsm. Inf Cladosporium carrionii via traumatic implantation

Chromo(blasto)mycosis-SubQ, localized chronic inf of skin and subq tissues leading to verrucoid, ulcerated, crusted l(x)s. Starts as small red macule then black stuff on skin, then HUGE swollen warts. Phaeohyphomycosis cerebral1)SubQ Phaeo is subQ cysts (1"x1") red, black 2)Cerebral Phae is cerebral inf w/ abscess, fatal 3)inf of paranasal sinuses

Cladosporium trichoides, Fonsecaea pedrosio, Bipolaris spicifera Aquatic parasite. Occurs in children/young men > femes. Most cases in Sri Lankan divers/fisherman

Rhinosporidium seeberi

Rhinosporidosis-looks like huge wart on/near nose

Loboa loboi

Affects males, usu S. America. Dolphins may be resorvouir

Lobomycosis-chronic inf may spread peripherally w/ verrucous ulcerated lesions. Develops over 20-30 yrs

Conidiobolus coronatus or Basidiolus ranarum General Features

Entomophthoromycosis (C/B?)

Systemic Infections 1)Occur in nml hlthy peeps, asymptomatic/subclinical 2)1ly pulmonary inf that may spread via blood 3) or in endemic areas 6)localized outbrx from exposure to common

Etiology

Epidemiology

Manifestations

white females, immunocompromised (AIDS). Disseminated form occurs in men w/ pigmentation and pregn femms (3rd trimester). Found in Coccidioides immitus, Sonoran Life Zone/Desert (e.g. El Coccidioides posadasii Paso) SW U.S., Mexico. C immitus in San Joaquin Valley. C posadassi elsewhere. Thermly dimorphic moldsoil.

Coccidiomycosis-1)1ry inf is generally inapparent, benign (60%) or mild-severe URI. 2)2ry inf (a)benign chronic pulmonary-thin walled cavities or granulomas (b)progressive pulmonary formmay follow 1ry or from reactivation. May disseminate to skin depending on health status

Histoplasmosis capsulatum

Incidence: Symptomatic pulmonary disease 75% Men. 1:1 sex ration in chldrn. Mildly chronic cases are 7590%male. Immunocompromised p(x) at risk or mortatlity 70% dissemination and mortality in AIDS p(x). Sexual bias in disease but not exposure Geography: Worldwide, endemic areas E of Misspi, incldng Rio Grande areas. Mold-soil microconidia-irrittion on inhalation. Animals as reservoir. Incidence: males>femms AfroAmrcns> All ages but more in 30-50yo's In small epidemics-no sex bias, mostly children inf, usu pulmonary inf. Geography: Thermally dimorphic, Africa, Mxco, Venzla, Israel, India, East U.S. Coast. Lives in soil. Animals (dogs) as reservoir.

Histoplasmosis-1)pulmonary inf 95%subclinical. Leaves cavitary lesions in peeps w/ underlying lung probs 2)Disseminated disease may leave lesions b/c infd retic.edoth cells freely disseminate even in ass(x) p(x). Oropharyngeal cancer due to mildly chronic disase (recurrent over 10-20yrs). 3)African Histoplasmosis disese of skin and bones Blastomycosis-Inhalation of conidia 1)Pulmonary inf w/ variety of ss(x). 2)Chronic cutaneous disease is 80% of presentation w/ 50% having pulmonary ss(x) 3)Disseminated disease generalized w/ bone, UG tract, and CNS as extrapulmonary sites.

Blastomyces dermatitidis

Paracoccidioides brasiliensis

Paracoccidiomycoses 1)Pulmonary inf asymptomatic, self limiting, may become latent, few Incidence:No sexual bias w/ 5-25% of develop ss(x) after exposure. pop skin test +. Symptomatic disease 2)Chronic Progressive Inf occurs are 90%male ag wrkrs. 11:1 following latency in 90% cases w/ male:femm b/c estrogen inhibits mold dissemination to mucosal and to yeast morph. Geography:Central gingival srfcs, may have chronic and S. Amrca. Avoids the Amazon pulmonary disease and some both Thermally Dimorphic Dissemination to other organs also observed 3)Acute progressive form (10%of cases) in children and adults fatal in weeks

Cryptococcus neoformans va grubii

Incidence:most children in NY cty skin test +, 1000cases/yr in nonAIDS pop. Maybe 3:1 male:femms. 50%in healthy peeps, 50% 2ry to DM, AIDS, bone cancer, 4th most common disease in AIDS p(x) Geography:worldwide types B-tropical, type C-S. Calif, type AandDsoil and pigeon guano (pigeon as reservoir) Yeast is inhaled and forms capsule after infection

Cryptococcosis-1)1ry Pulmonary inf usu ass(x) to mild ss(x) thus not often diagnosed 2)Disseminated disease-meningitis in U.S., skin/bone inf-Euro.

General Features Etiology

Opportunistic Infections 1)Inf of immunocompromised 2)becoming more frequent 3)pathogenic ones are ubiquitous 4)a Epidemiology Manifestations

1)Nml flora of mouth, GI, vagina, skin 2)immunocompromised, trauma experience e.g. burn, leukemias, endocrine factors e.g. DM/DI, AIDS are all predisposing factors. Also iatrogenic 3)Plaque made of Candida albicans , and (an)aerobe leading to other sp microenvironment. Deep seated plaque required physical scraping for removal. Biofilm helps colony grow. Abiotic surfaces e.g. dentures, help biofilm adhesion and device deterioration

Candidasis-Thrush, Vaginitis, Intertrigginous, Onychomycosis, Diaper rash 2)Systemic inf 4th most common nosocomial blood stream inf and is life threatening. 3)Endocarditis 4)Recurrent Eye inf 5)Random skin rashes/lesions after sepsis 7)UTI 8)chronic mucocutaneous candidiasis involved cell mediated immunity. epithelial lesions are verrucous and warty

Aspergillus fumigatus and other sp.

Adults, males-unkown sex bias 2)similar predisposing factors as Candida. 3)Worldwide in soil-mold, decaying vegetation, can be aerosolized

Aspergillosis-1)Allergic RE (IgE) as asthma, allergic bronchopulmonary aspergillosis (most common RE), IgG RE for nonatopic inf 2)noninvasive colinization-aspergilloma in preexisting cavity e.g. pulmonary pleura, asymptomatic may lead to fatal hemmorrage, nonpulmonary colonization in head cavities w ss(x) of otitis, sinusitis etc. 3)Invasive disease occurs as 1ry pulmonary inf of compromised host seen as a fatal necrotizing pneumonia, dissemination may spread to GI, liver kidney etc

Rhizopus orysae, Absidia, Rhizomucor, Mucor

Predisposing factors: Acidosisrhinocerbral inf, Leukemia Steroids Immunosupprsant-thoracic form Geography:Worldwide on decaying vegetation-mold, soil, H2O. Produce sporangiospores (conidia)

Muromycosis-1)Cerebral form looks like bells palsy, death w/in 1 week if untreated 2)Thoracic form is usu pulmonary inf.

Pneumocystitis jiroveci Pneumonia-Diffuse pneumonia 1)debilitates infants w/ subtle Immunocompr, AIDS p(x), Ubiquitous, infant, Bcell and Lymphocyte Worldwide, nml flora, animals as Pneumocystitis jiroveci infiltration 2)immnocopmr p(x) reservoir 30-40%mortality in infants, manifest ofver several weeks w/ 10% mortality in AIDS p(x) fever, recurrent/breakthrough tachypnea, massive # of orgnsms invading alveolar spaces.

More Notes

Nosocomial inf x2 fr 1980-1990 at 4/1000 discharge. Candida albicans 60%, Candida sp. 20%, Torulo wound, pneumonia, fungemia, IV catheter most likely cause for inf. Infectious, and expensive. Other o

ections ar away. Reason for removal is usu. Cosmetic Key Diagnostics Treatment Direct exam shows hair shaft w/ nodules. Hair cut (or Terbinifine) Under scope shows fungi 1)Examine skin scrapings for pigmented hyphae. 2)Culture for verification Topicals: miconazole, ointment, sulfur soln's, salicylic acid

Notes These are types of Piedra

Can be confused with malignant melanoma

examine skin scales for shory hyphae and spherical cells

Topicals: 1)SeSulfide micon/ketocon(azole) Oral: ketocon/itracon/flucon(a zole)

lipophilic, hypopigmentation due to interference of fungal melanin synths

Dermatophytosis)

rophytes ) 2) Epidermophyton floccosum or 3) Microsporum (canis , gypseum , mals, and in soil. Inf fr nml flora are more chronic/mild. Inf fr soil/animals more e sp can cause more than one ss(x), more than one sp can cause same ss(x). Key Diagnostics Treatment Notes usu aquired fr animals (dogs)

1)Topical nonRXUndecylenic acid, Tolnatrate, Miconazole, Clotrimazole, USEFUL FOR MOST: Terbinafine, Drying 1)chronicity 2)reoccurence cmps, keratolytic agents. 3)severity 4)spread to nonRx often used b/f others 5)pets/animals 6)distinguish fr C.albicans . seeing a physician. Some sp fluoresce so use 2)Topical Rx-Exonazole "wood's lamp". Examine nitrate, Ketoconazole, hair for spores Oxiconazole, (endo/ecto(thrix). Skin/nail Sulconazole, scraping for hyphae. Ciclopiroxolamine (nail Culture ID via color, txtr, topography etc) lacquer) Naftifine, Butenafine 3)SystemicGriseofulvin, Detoconazole, Itraconazole.

less common nowadays

may require antibacterials for 2ndry inf

, shower, comb, etc) Microsporum sp :macroconidia, Epidermophyton sensitive limits inf to surface. Fatty acids on scalp after puberty help limit grey

nfections ur worldwide w/ endemic areas, Several sp may cause same ss(x)

Key Diagnostics Lesions along lymphatics is pathognomonic. Direct exam for cigar shaped yeast. Culture ID of thermally dimorphic (grows as: mold in soil, yeast at 37. Serology not helpful Direct exam of pus for granule of certain size, color, filaments >1mcromter. Culture for verification based on morphology and asexual conidial formation Direct exam reveals pigmented branching hyphae w/ sclerotic bodies (spore). Culture ID of dark pigmented colonies looking for asexual reproduction Direct exam of tissue shows pigmented fungal elements Culture ID via morphology and conidial formation 6-330 mcrmtr sporangium (filled w/ endospores) No culture available

Treatment

Notes

1) looks like cysts on skin following lymphatics 2) Orally-KI (in milk), looks like you put Itraconazole Topicalyour skin through Amphotericin B (for a meat grinder. lymphatic relapse or 1ry Dissemination is pulmonary inf, Heat rare. Pulmonary inf is becoming common in hospitals

1)Longterm antib(x): Ampho B, topical Nystatin, KI (all w/ little success). 2)Surgery to clean abscess. 3)Amputation.

Actinomycetoma is due to bact. yeast grows faster vs mold

1)Surgery successful if early 2)Itraconazole 3)Antibacterials for 2ry inf 4)AmphoB-partial cure w/ relapse

Drugs w/ variable success. Surgery for certain manifestations

Cerebral Phaeo diagnosed after death.

1) Surgery 2) various drugs tried

Direct exam of tissue for chain of bout 4 lemon shaped cells Surgery bout 9micrmeters. No culture

Similar to chromomycosis

Spontaneous resolution

ections monary inf that may spread via blood 3)immunit to reinf 4)geographically restricted zed outbrx from exposure to common source

Key Diagnostics

Notes HIGHLY INFECTIOUS. Skin test. Differentiate Possible terrorist from other URI's. agent. Virulence Take travel h(x). due to protease, Direct exam of 1)bed rest for 1ry ss(x) estrogen binding sputum for sporangia 2)disseminated w/ prot, Tcell or spherules. Thermly AmphoB or Fluconazole mediated RE in dimorphic grows as (use Fluc in AIDS p(x)) reinf, spherule-tiss. Culture 3)cavities removed alkalinazation of ID for arthrospores in surgcly phagosomeallergi filament (also es to 1ry inf is exoantigen and DNA good b/c it probe) indicates immune RE. 1)Direct exam of sputum, biopsy, blood for intracellular yeast. Culture ID takes 28 days shows spores w/ spikes. Use DNA probe nstead 2)animal inoculation to obtain tissue for ID. Blood test also helpful for d(x) and pr(x) 1)Direct exam of sputum, biopsy, pus, for broad based budding yeast 2)Culture ID yeasttissue mold-nature 3)DNA test, exoantigen

Treatment

1ry Pulmonary-treat ss(x) only. Acute cases use AmphoB or Itraconazole w/ Ketoconazole and fluconazole as alternatives. Surgery to remove pulm lesions

moderate chronic disseminated disease fatal if untreated (6-12 mos) Fulminant disease may occur in infants and adults. Resistant to oxidative burst

1)AmphoB Itrazonazole 2)2hydorxystilbamine 3)Ketoconazole-mixed results 4)Itraconazole for HIV suppression

virulenc factors: morphogenesis, cell wall, anti macrophage adhesion

1)Direct exam of mucosal scrapings for "pilots wheel" yeast 2)Culture ID moldnature yeast-tissue, ID via yeast form 3)serolgy for diagnosis/prognosis

Skin test shows no sex bias for 1)Sulfa drugs x 3-5yrs symptomatic 2)Imidazoles, oral disease Virulence kitoconazole (possiblity factors:morphoge of relapse) Itraconazole nesis, estrgn 3)AmphoB for inpatient binding prot, cell wall, immune suppression

1)Direct exam of sputum or CSF in India ink for capsule 2)Culture ID-cells examined for capsule Phenol oxidase test used for ID 3)Serologic test for capsular antigen.

1)AmphoB 2)Combo AmphoB+5Fluorocytosine 3)Fluconazole (esp in AIDS p(x) to prevent relapse)

1)only fungus w/ capsule 2)Meningitis fatal if untreated 3)Virulence factors:Mating type, growth at 37 degr, capsule is antiphagocytic, immune suppression

nfections t 3)pathogenic ones are ubiquitous 4)any fungus or shroom may cause inf Key Diagnostics Treatment Notes 1)can be 1)Direct exam of acute/chronic, 1)Topicals for sputum, pus, tissue disseminated/supe Cutaneous-Nystatin, for yeasts, rficial/deepseated Miconazole, 2)Concern of pseudohyphae Clotrimazole(OTC x esophigitis in 2)Culture ID looks for vaginitis), Ketoconazlole. AIDS 3)Virulenc germ tubes, 2)Thrush t(x) lozenges Factors:yeast chlamydospores. 3)Esophegitis AmphoB, morph chgs, Yeast ID via physio Fluconazole 4)Systemicprotease rxns 3)Isolation from AmphoB, Fluconazole, phospholipase, skin/vaginal mucosa Ketoconazole adhesins, laminin to confirm. (sometimes combo w/ collagen, Significance in urine Miconazole IV and 5macrophage 'pends on other Flurocytosine 5)t(x) of evasion, immune factors Isolation fr predisposing factors supression, Th1 sterile site significant. helps in t(x) response and Th2 4)Serology ineffective susceptibility 1)Direct exam of sputum, biopsy for septate hyphaew/ acute angle branching 2)Culture ID based on colonial morphology and pattern. Fast growth (white center, green cortex) +blood culture should be considered significant since even invasive cultures can be Serologic test best in noninvasive disease

1)ubiquitous so may be 1)Treat allergy ss(x) contaminate in 2)AmphoB w/ culture so 5Fluorocytosine or repeated cultures surgery for Aspergilloma used. 3)Must treat invasive 2)Virulence:protea disease aggressively b/c se phospholipase, it's fatal. AmphoB or adhesins laminin, Itraconazole gliotoxin (immunosuppresa nt) endotoxin

1)Direct exam of sputum, biopsy for NON-septate hyphae, Disease fatal w/o t(x). usu few to see 50% w/ t(x) 1)AmphoB 2)Culture ID via 2)surgical debridement colony morphgy and sporangial formation Fungus related to ascomycetes. Atypical chrtcs, used to be thought as parasite. Virulence:adhesin s to Type I pneumocytes, disruption of bloodair barrier (lung)

1)Direct exam-Infant looks emaciated, Xrays show diffuse lung cavity 2)sputum, Biobsy (for asci, spores ameboid shaped yeast, 3)No culture available

1)Acute t(x) Trimethoprimsulfamethozoasole 2)Propylaxis for AIDS via TMP-SMX.

lbicans 60%, Candida sp. 20%, Torulopsis, Aspergillus. Inf of UTI, surgical inf. Infectious, and expensive. Other opportunistic sp: Trichosporon (see white

Topicals* Undecyclin Haloprogin Clioquinol Triacetin Ciclopiroxolamine Squalene 2.3, epoxidase inhibitors (tolnaftate, naftifine, terbinafine, butenafine) Allyl Ammines are part of the Squalene 2,3 epixidase inhibitors (Terbinafine, Naftitine, Butenafine) Polyenes* (Nystatin, Amphotericin B*^) Azoles*+^ (Clotrimazole, Econazole, Ketoconazole *+, Miconazole *^, Butoconazole, Oxiconazole, Sulconazole, Terconazole, Tioconazole)

Orals+ Griseofulvin 5-flurocytosine Nikkomycin Z Ketoconazole*+ Fluconazole*^

IV^ Echinocandin Miconazole*^ Fluconazole*^ Voriconazole+^ Amphotericin B*^

Itraconazole

Voriconazole+^

Drugs for Superficial Infections

Drugs for Cutaneous Infections

Drugs for SubCutaneous Infection

cell wall synths

cell wall f(x)

DNA syns

Allylamines of the Squalene 2,3 epoxidase inhibitors Naftifine Terbinafine Butenafine Azoles Clotrimazole* Econazole* Fluconazole*^ Itraconazole Ketoconazole* Polyenes Nystatin Amphotericin B*^

Miconazole*^

Oxiconazole*

Sulconazole*

Terbinifine*+

Terconazole* Tioconazole Voriconazole+^ Drugs for Opportuinistic Infection

Drugs for Systemic Infection

squalene epoxidase inhibitors

DNA syns

competition for subst

DNA Viruses

Enveloped

Naked

Poxviridae

Herpesviridae

Hepadnaviridae

Adenoviridae Papillomaviridae

Polyomaviridae

Parvoviridae *ssDNA

Variola

Vaccinia Monkeypox Molluska contagiosum

HSV

VZV

EBV

CMV

HHV

Hebatitis B

Adenovirus

HPV

JC

BK

Simian

Parvovirus B19

Adenoassociated virus

RNA Viruses
ss RNA

(+) RNA

(-) RNA

NonSegmented

Nonsegmented

Segmented

Naked

Enveloped

Enveloped

Enveloped

Picorividae

Noroviridae

Togaviridae

Flaviviridae

Coronaviridae

Retroviridae

Parmyxoviridae

Filoviridae

Rhabdoviridae

Arenaviridae

Bunyaviridae

Orthomyxoviridae

Rhinovirus

Poliovirus

Echovirus

Coxackie Virus A and B

Hepatitis A

Norwalk

Calcivirida e

Rubella

EEV

WEV

VEV

Yellow Fever virus Dengue Virus

West Nile St. Louis virus virus Corona

SARS

HIV, HTLV 1 and 2

Parinfluenz a

Measles

Mumps

RSV

Ebola

Marburg

Rabies

VSV

LSV

TCV

LCV

CLEV

Hanta virus

Influenza A, B, C

Table 8-4. Transmission and Distribution of Pathogenic Parasites

Organism
Intestinal Protozoa Entamoeba histolytica

Infective Form
Cyst/trophozoite

Mechanism of Spread
Indirect (fecal-oral) Direct (venereal) Fecal-oral route Fecal-oral route Fecal-oral route Fecal-oral route Fecal-oral route Fecal-oral route Direct (venereal) route Direct inoculation, inhalation Anopheles mosquito Ixodes tick Fecal-oral route, carnivorism Phlebotomus sandfly Reduviid bug Tsetse fly Fecal-oral route Fecal-oral route Fecal-oral route Fecal-oral route Direct skin penetration from contaminated soil Direct skin penetration, autoinfection Direct skin penetration, autoinfection Carnivorism Mosquito Mosquito Chrysops fly Biting midges or black flies Simulium black fly Ingestion of infected cyclops Mosquito Ingestion of metacercaria encysted on aquatic plants Metacercaria on water plants Metacercaria encysted in freshwater fish

Giardia lamblia Cyst Dientamoeba fragilis Trophozoite Balantidium coli Cyst Isospora belli Oocyst Cryptosporidium Oocyst species Enterocytozoon bieneusi Spore Urogenital Protozoa Trichomonas vaginalis Trophozoite Blood and Tissue Protozoa Naegleria and Cyst/trophozoite Acanthamoeba species Plasmodium species Sporozoite Babesia species Pyriform body Toxoplasma gondii Oocysts and tissue cysts Leishmania species Promastigote Trypanosoma cruzi Trypomastigote Trypanosom brucei Trypomastigote Nematodes Enterobius vermicularis Egg Ascaris lumbricoides Toxocara species Trichuris trichiura Ancylostoma duodenale Necator americanus Strongyloides Trichinella spiralis Wuchereria bancrofti Brugia malayi Loa loa Mansonella species Onchocerca volvulus Dracunculus medinensis Dirofilaria immitis Trematodes Fasciolopsis buski Fasciola hepatica Opisthorchis (Clonorchis) sinensis Egg Egg Egg Filariform lava Filariform larva Filariform larva Encysted larva in tissue Third-stage larva Third-stage larva Filariform larva Third-stage larva Third-stage larva Third-stage larva Third-stage larva Metacercaria Metacercaria Metacercaria

Paragonimus westermani Schistosoma species Cestodes Taenia solium

Metacercaria Cercaria

Metacercaria encysted in freshwater crustaceans Direct penetration of skin by freeswimming cercaria

Cysticercus, embryonated egg Ingestion of infected pork; or proglottid ingestion of egg (cysticercosis) Cysticercus Sparganum Embryonated egg Ingestion of cysticercus in meat Ingestion of sparganum in fish Ingestion of eggs from infected canines Ingestion of eggs from infected animals, fecal-oral route Ingestion of eggs; fecal-oral route Ingestion of infected beetle larvae in contaminated grain products Ingestion of infected fleas

Taenia saginata Diphyllobothrium latum Echinococcus granulosus Echinococcus multilocularis Hymenolepsis nana Hymenolepsis diminuta Dipylidium caninum

Embryonated egg Embryonated egg Cysticercus Cysticercus

ogenic Parasites

Distribution
Worldwide Worldwide Worldwide Worldwide Worldwide Worldwide North America, Europe Worldwide Worldwide Tropical and subtropical areas North America, Europe Worldwide Tropical and subtropical areas North, Central, and South America Africa Worldwide Areas of poor sanitation Worldwide Worldwide Tropical and subtropical areas Tropical and subtropical areas Tropical and subtropical areas Worldwide Tropical and subtropical areas Tropical and subtropical areas Africa Africa and Central and South America Africa and Central and South America Africa, Asia Japan, Australia, United States China, Southeast Asia, India Worldwide China, Japan, Korea, Vietnam

Asia, Africa, India, Latin America Africa, Asia, India, Latin America

Pork-eating countries: Africa, Southeast Asia, China, Latin America Worldwide Worldwide Sheep-raising countries: Europe, Asia, Africa, Australia, United States Canada, Northern United States, Central Europe Worldwide Worldwide Worldwide

Nephritic = Blood + HTN + Oliguria + Azotemia + Edema


PSGN - Follows group A hemolytic strep infx, usu due to bad hygiene, C3, ASO or antiDNAse B positive, shows "lumpy bumpy" on subepithelium w IF, large hypercellular glom RPGN - Crescents deposition of fibrin in bowman space, monocytes, large pale kidneys Type I - Anti GBM IgG complexes complex deposits on GBM smooth linear appearance on immunofluroscence. e.g Goodpasteurs Type II - Immune complex mediated "lumpy bympy" glomerular BM on immunofluorescence. e.g. Bergers Disease Type III - ANCA associated aka Pauci immune shows nothing on GBM w immunofluorescence but PMNs have either c-ANCA or p-ANCA. Usu a RE to Wegener Granulomatosis or vasculitis'.

Alport Disease - mutation of 5 Type IV collagen nephritis, nerve deafness, and ocular problems and splitting of lamina densa

Nephrotic = Proteinuria +Hypoalbuminemia + Edema + Hyperlipidemia + Lipiduria


MCD/MN/nil disease/Lipoid Nephrosis - Fused/absent podocytes (epithelial foot processes) FSGS - glomerular sclerosis frm persistent glomerular vasodilation Hypercellular Perihilar Collapsing Tip Lesion Membranous Glomurlonephropathy/MN/Membranous Nephropathy/MGN - subepithelial immune complex disease vs GBM but NO Ig's in ciruculation, epimembranous spike and dome appearance, Autoimmune states or heavy metals can predispose Membranoproliferative Glomerulonephritis/MPGN - basement membrane alterations, glomerular cell proliferation, WBC infiltration,Tram Track appearance due to GBM duplication Type I - Subendothelial IgG and complements, Prominent Tram Track appearance, mesangial cells, ganular complement deposits w IF, Ig complexes circulating Type II - Dense Deposit Disease shows some tram trac appearance, C3 next to dense deposists, serum C3, no Ig's in BM complexes, IgG vs C3 convertase, ribbon like deposits w/in capillary, nephrotic and nephritic ssx both present Diabetic Nephropathy - Early stage has large kidneys (later has small granular kidneys), EM shows thick holey GBM, thin lamina rara interna and externa, tubular atrophy Lupus Nephropathy Type I - no ssx Type II - IgGs and C3 in mesangial matrix, Proteinuria, hematuria. Just uncomfortable Type III - Focal Proliferative has extenseive damage, complement, few pts w nephrotic ssx, segmental necrosis, mesangial deposits Type IV - Diffuse Proliferative is most severe form, combo of nephritic and nephrotic ssx, 100% glomeruli involved, scarring, wire loop abnormalities, subendothelial depostis of Ig's and C3 and Fibrin Type V - Looks just like MG HIV Associated Nephropathy - Black Drug users affected, Tamm Horsfall prots IgA Nephropathy/Berger Disease - IgA deposits in medangium, recurrent hematuria Amyloidosis - large kidneys, low BP, congo red stain positive Hypertensive Nephrosclerosis - Black ppl w uncontrolled HTN, proteinuria

Anticonvulsants
Drugs That Work On Na+ Channels Drug MOA SDFX
Nystagmus, Diplopia, Ataxia, Hirsuitism, Coarsening of Facial Features, Mild Peripheral Neuropathy

Source
Website

T(x) For
Anticonvulsant (Partial and General Tonic/Clonic Szr) DOC: Anticonvulsant (Partial Szr), Anticholinergic, antineuralgic, antidiuretic, muscle relaxant and antiarrhythmic Same as CBZ Partial Szr Monotherapy in Partial Seizures (also in adjunct to Valproate acid); Absence & Myoclonic szrs in children

Phenytoin Decrease Influx. Increase Efflux of Na+, Ca2+ (Fosphenytoin is broken and K+ channels in open state down into Phenytoin)

Carbamazepine

Slows recovery rate of inactive Na+ Channels, preventing the PDS. Metabolite also active.
paroxysmal depolarizing shift

Dizzines, diplopia, nausea, ataxia, blurred vision. Aplatstic anemia, Website Agranulocytosis, Thrombocytopenia, StvJohnson Sx

Oxcarbazepine

Metabolized to active cmpd 10, 11Dihydro-10 Hydroxy-5H Dibenz[b,f]azepine5Carboxamide

Same as CBZ but less frequency

notes

Lamotrigine

Inactivates Voltage gated Na+ channels

Dizziness, HA, Diplopia, Nausea, Somnolence, Skin Rash (may progress to StvnJohnson Sx). Increased risk of cleft palate if used during pregn.

notes

Drugs That Work On T-type Ca++ Channels

Drug
Zonisamide

MOA

SDFX

Source

T(x) For
Adjunct thpy for Partial Szrs as induction NOT long term use DOC: Generalized Epilepsy Sx. Absence Szr DOC: Petit Mal; Alternative to Valproic acid

Blocks Na+ channels & decreases Cl- flux via T- StvnJohns Sx, Contraindicated in ppl notes type Ca++ channels w/ allergies to sulfonamid AB At low conc. Blocks voltage Na+ channels. High conc slows influx of Ca++. Increases activity of GABA making enzm (glutamic acid decarbxlylse) and inhibits GABA metabolism. Reduces Ca++ currents in thalamus so that the thalamus is the discharge pacemaker.

Valproic Acid (GABA synth inducer)

Hepatic Toxicity

Ethozuximide

Drugs That Work Via GABA Agonists via increasing GABA prodx, decreasing GABA brkdwn, blocking GABA reuptake, GABA-A
agonists

Drug

MOA

SDFX

Source

T(x) For
Short TermPartial Szr As IV to terminate szr b/f use of long term AED Absent szr As IV to terminate szr b/f use of long term AED Absent szr (Short TermPartial Szr DOC x Myocloninc Szr & Subcortiical Myoclonis 4th DOC x Absent szr Partial Szr, Panic d/o Absent szr Partial Szr

Lorazepam

GABA-A agonist in CNS

Dizzines, atazia, drowsiness

Website

Diazepam

GABA-A agonist in CNS

Dizzines, atazia, drowsiness

Website

Clonazepam

Enhances GABA in Reticular Nucl. Inhibits Ttype Ca+ channel currents

Dizzines, atazia, drowsiness Withdrawl may trigger status epilepticus

Website

Clobazam Binds to GABA receptor increase Cl- current, Blocks AMPA receptor, Blocks L and N type Sedating Ca++ currents and inhibits Na+ channels Sedating, Dizziness, Nausea

Phenobarbital

DOC for infants Absent szr Partial Szr Partial Szr Absent szr

Primidone (metabolized Metabolized to PHB to Phenobarbital)

GABA Reuptake Inhibitors

Drug
Nipecotic Tiagabine

MOA

SDFX
Dizziness, Asthenia, Nrvsness, Tremor, Depression, Emotional Labile

Source

T(x) For
Adjunct thpy x Partial and secondary gen. szr

Inhibits GABA transporter 1

notes

Vigabatrin

Inhibits GABA transaminase

Absence status drowsiness, (rarely: depression agitation, confusion & psychosis)

DOC x Infantile spasm Used as an adjunct x refactory partial szrs

GABA Synthesis Inducers

Drug

MOA

SDFX

Source

T(x) For
Partial Szr Adjunct Generalized Tonic Clonic Szr (Neuropathic pain, Periperal Neuralgia Second line adjunct x Partial Szr Generalized Epilepsy Sx. Absence Szr

Gabapentin (Neurontin)

GABA analog, Decreases GABA metabolism, Inhibits Reuptake

notes

Pregabalin

Incr. GABA in neurons and glial cells At low conc. Blocks voltage Na+ channels. High conc slows influx of Ca++. Increases activity of GABA making enzm (glutamic acid decarbxlylse) and inhibits GABA metabolism.

notes

Valproic Acid (GABA synth inducer)

Hepatic Toxicity

notes

GABA Synthesis Inducers

Drug
Felbamate

MOA
Blocks NMDA receptors

SDFX
Aplastic anemia, SEVERE Hepatitis

Source
notes

T(x) For
Partial Szr 3rd line x refractory cases Adnunct x Partial Szr & Primary Gen TonClon Szr. Szrs frm LemoxGastut Sx

Topiramate

Inhibits Na+channels from inactive state, incr Cl- Acute myopia, secondary closed flux thru GABA receptors (diff from BZD binding angle Glaucoma, Oligohydrosis, site) Hyperthermia

notes

Other AED's

Drug
Progesterone Estradiol

MOA
Increases GABA channel conductivity, Attenuates glutamate excitatory RE: PROconvulsant via decreases Cl- flux, and NMDA agonist in hippocampus

SDFX

Source
notes notes

T(x) For

CarbonicAnhydrase Inhibitors Leveritacetum

Increases intracellular [H+] causing K+ to move out, hyperpolarization increasing the threshold. (Topiramate, Zonisamide and Acetazolamide)

notes notes

Hypnotics/Anxiolytics
BZDs

Drug
Zolpidem Zaleplon Chloral Hydrate Buspirone

MOA
GABA receptor agonist (Hypnotic) GABA receptor agonist (Hypnotic) Metabolized to Trichloroethanol 5HT1a and DA2 AntAg

SDFX
Daytime sedation; Rebound Insomnia (low); Low incidence of rebound insomnia Tolerance/Dependance

Source
notes notes notes

T(x) For
Insomnia Insomnia Anxiety (Atpyical Anxiolytic)

Barbs

Clonazepam (BZD)

Enhances GABA in Reticular Nucl. Inhibits Ttype Ca+ channel currents

Dizzines, atazia, drowsiness Withdrawl may trigger status epilepticus

Website

DOC x Myocloninc Szr & Subcortiical Myoclonis 4th DOC x Absent szr Partial Szr, Panic d/o

Fluvoxamine

SSRI in CNS

Well Tolerated dizziness, HA, insomnia, nervousness, somnolence

ADD/ADHD

Drug
Methylphenidate Dextroamphetamine Atomoxetine Desipramnie Buproprion Venlafaxine (and metabolite) Clonidine Guanfacine

MOA
DA reuptake inhibitor DA and NE reuptake inhibitor NE reuptake inhibitor, Adenyl cyclase desinsitization, Beta adrenergic receptor downregulation, 5HT receptor downregulation 5HT & NE reuptake inhibitor 5HT & NE reuptake inhibitor CNS Alpha2 adrenergic Agonist (activating inhibitory pthwys, reducing symp outflow, ) A2 agonist

SDFX
many Severe, but in few pts

Source
PDR PDR

T(x) For

Antidepressant Smoking cessation

ADD, HTN, Depression HTN

Mood Disorders
Drug MOA SDFX Source
notes

T(x) For
Antidepressant Smoking cessation Antidepressant Antidepressant Antidepressant, usu more effective

Buproprion (similar strx DA, 5HT & NE reuptake inhibitor to amphetamine) TCA alpha2 adrenergic receptor antagonist Mirtazapine causing incr NE, 5HT in synapse Nefazodone SNRI (venlagaxine, duloxetine) Li Divalporex

sedation, INCREASED appetite (wt gain) liver failure (death; not used so much SSRI (little affinity x alpha adrenergic receptors anymore) 5HT & NE reuptake inhibitor alters ion channel leading to decr in NE, 5HT reuptake stabilize temporal lobe effective 50-60% of time

Bipolar Bipolar Bipolar reduces cycling and depression NOTHING for mania Bipolar Bipolar

Lamotrigine

Topiramate Oxacarbamaepine

not effective for most ppl

Carbamazepine

Slows recovery rate of inactive Na+ Channels, preventing the PDS. Metabolite also active.
paroxysmal depolarizing shift

Hepatic induction leading to need for MASSIVE dosages. Dizzines, diplopia, nausea, ataxia, blurred Website vision. Aplatstic anemia, Agranulocytosis, Thrombocytopenia, StvJohnson Sx

Antidepressant DOC: Anticonvulsant (Partial Szr), Anticholinergic, antineuralgic, antidiuretic, muscle relaxant and antiarrhythmic

Gr+ Cocci Anaerobes aerotolerant Strep Enterococcus Staph obligate Peptostreoptococcus Bacilli Anaerobes aerotolerant nonsporforming Lactobacillus Corynebacterium Propionibacterium Actinomycetes Arachnia Bacterionema obligate sporeforming Clostridium Aerobes aerotolerant Rothia GrCocci Aerobes Neisseria-flavens, mucosa, subflava, meningitidis, sicca Anaerobes Viellonella Bacilli Anaerobes aerotolerant nonsporeforming Haemophilus Actinobacillus Eikenella Capnocytophaga obligate Bacteroides Fusobacterium Leptotrichia Wolinella Selenomonas spiral/curved Anaerobes aerotolerant Campylobacter

Spirochetes Anaerobes obligate Treponema Borrelia

Disease Test + TP (++)

Healthy FP (-+)

Test -

FN (--)

TN (+-)

Disease + Risk Factor

Healthy

Diseased Pts Healthy Pts Exposed (++) Exposed (-+)

No Risk Factor -

Disease Pts Health Pts Not Not Exposed Exposed (+-) (--)

Stage Incubation

Duration

Clinical Disease

Syphillis Activity of Treponema pallidum

2 to 6 weeks (most often 3 to 4 weeks)

None

Spirochetes actively proliferate at entry site, spread over body

Primary

8 to 12 weeks

1. Chancre present Chancre teeming with them at inoculation site 2. Regional lymphadenopathy None Inconspicuous

Primary Latent Secondary

4 to 8 weeks

Latent

Tertiary

Variable over period of 5 years (Latent periods with recurrences) Few months to a lifetime (average 6 to 7 years) Variable-rest of patients life

1. Skin and mucosal lesions 2. Generalized lymphadenopathy None

Skin and mucosal lesions rich in spirochetes (highly infectious) Inconspicuous

Related to organ system diseased

Paucity of spirochetes in classic lesion

Diagnosis

Tissue Change

Identification of T. pallidum a) Dark-field microscopy b)Fluorescent antibody 1. Dark-field microscopy of chancre 2. STS positive STS Positive

Chancre appears at inoculation site

Chancre present

1. Dark-field microscopy 2. STS Positive STS Positive

None demonstrable; Chancre has healed with little scarring 1. Infection active 2. Resolution spontaneous

1. STS positive or negative 2. Special silver stains

1. Gumma 2. Healing 3. Scarring 4. Tissue distortion

Actinomycetes General >filaments>1mcmtr. Cell wall w/ peptidoglycan, a.a. Streptomyces-are large family of bact. found in soil, H2O, organic debris-primary source Features Etiology Epidemiology Manifestations Treatment Key Diagnostics Notes Actinomycosis Normal flora of GI tract, oral cavity.

Etiology

Epidemiology

Cutaneous Infections (Dermatophytosis) Manifestations Treatment Key Diagnostics

Notes

Etiology

Epidemiology

Subcutaneous Infections Manifestations Treatment

Key Diagnostics

Notes

Etiology

Epidemiology

Systemic Infections Manifestations Treatment

Key Diagnostics

Notes

Etiology

Epidemiology

Opportunistic Infections Manifestations Treatment

Key Diagnostics

Notes

mal flora of GI tract, oral cavity.

Seizures Generalized General Tonic Atonic Tonic Clonic http://pediatricneurology.com/seizure_intro.htm Clonic Myoclonic Absent

Partial Simple-No ComplexLOC + LOC