You are on page 1of 34

SAINT GABRIEL COLLEGE KALIBO, AKLAN MR. HARLEY L.

DELA CRUZ RN MAN Instructor PHARMACOLOGY

1. Fundamentals of Pharmacology o Pharmacology -The study or science of drugs -Study of the biological effects of chemicals. -The study of drugs and their interactions with living systems
o

Drugs -Chemicals that are introduced in the body to cause some sort of change. - Any chemical that affects the physiologic processes of a living organism Pharmacokinetics - The study of what the body does to the drug -Absorption, distribution, metabolism, and excretion of drug(s) in the body. Pharmacotherapeutics - The use of drugs and the clinical indications for drugs to prevent and treat diseases  Empirical therapeutics effective, but mechanism of action is unknown  Rational therapeutics specific evidence has been obtained for the mechanisms of drug action Pharmacodynamics -The biochemical and physical effect of drug(s) and the mechanism of drug action. -The study of what the drug does to the body, i.e. the mechanism of drug actions in living tissues

o Pharmaceutics -The study how various drugs form influence pharmacokinetic and pharmacodynamic activities -Dosage form design affects dissolution o Pharmacognosy -The study of natural (plant and animal) drug sources

2. Sources: o Plants  Earliest drug source (leaves, roots, bulbs, fruits, blossoms, extracts)  Ex. Alkaloids most active component in plants, reacts with acids to form a salt that easily dissolves in body fluids (caffeine, Nicotine, Atropine)  Glycosides naturally occurring plant active components that has both toxic and good effect (lanoxin, digoxin)  Resins local irritants and caustic agents (laxatives)  Oils thick greasy liquids volatile:( peppermint, spearmint, juniper)/ fixed:( castor oil, olive oil) o Animals  Body fluids, glands of animals are also natural drug source  Ex. Hormones (insulin)  Oils & Fats (liver oils)  Enzymes catalyst produced by living cells (pepsin)  Vaccines suspension of killed, modified, or attenuated microorganism o Minerals  Metallic and non metallic minerals that provides inorganic materials not available in plants or animals.  Usually combined with other ingredients Ex. ( Fe S04, Mg SO4, ) 3. Nursing Responsibilities o Administer drug by using 10 RIGHTSs o Assessing drug effects

o o o

Intervening to make the drug treatment more tolerable Health teaching abt. The drug Monitoring overall px care plan to prevent medication error Legal/Ethical Considerations Control of Drug Development, Evaluation {Pre clinical trials} {Phases of Drug studies I - IV} {Approval} {Continual Evaluation} Pregnancy Category {A X} Production {Controlled Substance, Generic Drugs, Orphan Drugs,} Dispensing {OTC Drugs, Generic Drugs, DAW Drugs}

4.
o o o o o

5. RIGHTSs of Drug Administration o Right drug and patient o Right storage of drug o Right route o Right dosage o Right preparation o Right timing o Right recording/ documentation o Take complete px drug hx o Know if px has any drug allergies o Be aware of potential drug drug or drug food interactions o Teach your px about the drug he is receiving 6. Routes / Sites of Administration o Enteral:  Oral  Solid  Liquid  Meds by NGT  Enteral feedings o Rectal o Disposable Enemas o Parenteral  Intradermal  Subcutaneous  Intramuscular  Intravenous o Percutaneous  Topical  Creams, lotion, ointments  Patch testing for allergies  NTG (Transdermal)  Medication to Mucus membranes  Topical powder 7. PHARMACODYNAMICS - how the drug affects the body DRUG ACTIONS: o To replace or acts as a substitute for missing chemicals. o Increase or stimulate certain cellular activities. o To decrease or slow cellular activities. o To interfere with the functioning of foreign cells such as invading microorganism or neoplasm Receptor Sites specified areas in the cell that allows certain chemicals to cause an effect in the cell o AGONIST direct interaction of drug that causes same activity (Ex. Insulin-Insulin Receptor) o ANTAGONIST has an affinity for a receptor but displays no intrinsic activity  Prevents a response from occurring o COMPETITIVE ANTAGONIST - competes c agonist for receptor sites Ex. (Curare vs. acethylcholine receptor sites)

NON COMPETITIVE binds to receptor sites & blocks the effect of the agonist (protects / prevent another antagonist from entering) o DRUG ENZYME INTERACTIONS drug effects by interfering c enzyme system that acts as a CATALYST for various chemical reactions  blocks the cascade effect of enzyme o SELECTIVE TOXICITY choosy? Ex. (penicillin attacks enzyme system unique to bacterial cell death) o NON SELECTIVE TOXICITY not so choosy? Ex. (chemotherapeutic drugs destroying normal & neoplastic cells)
o

8.

PHARMACOKINETICS how the body acts on the drug  CRITICAL CONCENTRATION sufficient / high concentration of the administered drug working at the (molecular level ) reactive tissues  DOSAGE based on the amount that must be given to eventually reach the critical concentration  LOADING DOSE usually drugs that are needed to take effect quickly Ex. (Aminophylline, Lanoxin)  DYNAMIC EQUILIBRIUM actual concentration that a drug reaches the body  FACTORS:  ABSORPTION FROM THE SITE OF ENTRY  DISTRIBUTION ON THE ACTIVE SITE  BIOTRANSFORMATION IN THE LIVER  EXCRETION FROM THE BODY 1. ABSORPTION- what happens to a drug from the time it is introduced to the body until it reaches the circulating fluids and tissues. -The rate at which a drug leaves its site of administration, & the extent to which absorption occurs
 

Bioavailability a measure of the extent of drug absorption in the body (0% to 100%) Bioequivalent two drugs have the same bioavailability and same concentration of active ingredients

o Areas of Absorption: GI, Orally, Rectally, Skin, Mucus Membranes, Lungs, Muscles, Subcutaneous How Drugs are absorbed? A. Passive Diffusion- major process of absorption  - when there is concentration in one side, drug molecules moves towards the area of concentration  - movement towards the other side is faster if the molecules are smaller, soluble in water and lipid  - no electrical charge that could repel it from the cell membrane  Effortless process, passive process. Most common in oral form of medication. B. Active Transport uses energy to actively move a molecule across a cell membrane  - Molecule moves from an area of concentration to area of concentration (usu. electrolytes)

ADMINISTRATION & ABSORPTION ORAL most common, non invasive, practical & viable  easily broken down by the gastric juices  affected by presence or absence of food in the stomach  Ideal timing for administration o INTRAVENOUS drugs that cannot survive in enough quantity w hen given orally  - Reaches their full strength @ the time of injection  More likely to cause toxic effect ( margin for error )
o

o o o o o o o o o o o

INTRAMUSCULAR absorbed directly in the capillaries in the muscles & sent into circulation (1-5cc) (site of giving?)  - Takes effect faster in men than in women SUBCUTANEOUS small amt(0.5 1cc)usually in the upper arm, abdomen, thigh  - drugs move rapidly in vessels than in oral RECTAL / VAGINAL absorbed by the perfusion of local blood flow in the rectum/ vagina  - treatment of local irritation or infection RESPIRATORY available in all forms that targets the lungs  - mostly in gas or inhalation form or mist BUCCAL/SUB LINGUAL & TRANSLINGUAL common route for certain cases of emergency  - drugs prevent destruction/transformation in the GI TOPICAL superficial or external use only  - used for dermatologic, ophthalmic, otic and nasal preparation SPECIAL AREAS / INFUSIONS given to a specific area of the body Epidural injected in epidural space Intrapleural injected in the pleural cavity Intraperitoneal injected in the peritoneal cavity Intraosseus injected in the rich vascular bone network(long bone) Intra-articular injected into a joint

FIRST PASS EFFECT liver synthesizes and breakdown much of the component thereby needing a dose to have a desired effect  -drug -> stomach -> small intestine -> portal venous system (liver)-> heart( side) > heart (left side)-> systemic circulation-> area (affected) in need of drug THINGS to consider in first pass effect:  Px diet / food preference  Drug preparation / formulations  Liver affectation 2. DISTRIBUTION movement of the drugs that survived the first pass effect thru the body tissues Factors That Affect Absorption:
o o o o o o

Food or fluids administered with the drug Dosage formulation Status of the absorptive surface Rate of blood flow to the small intestine Acidity of the stomach Status of GI motility BLOOD FLOW - blood flow distribution & absorption SOLLUBILITY fat soluble (easily crosses cell membrane, can cross BBB CNS) or HO soluble BINDING drugs bind c plasma protein (albumin)  FREE / UNBOUNDED exerts effectiveness, excreted quickly  BOUNDED slow release, long duration of action, hard to dispose 3. METABOLISM / BIOTRANSFORMATION Conversion of drugs by the LIVER thru the use of bodily system, enzymes  Ability of the body to change a drug from its dosage form to a more water soluble form

4. EXCRETION Elimination of drugs from the body (kidneys, lungs, skin, salivary, mammary glands, GI tract) o HALF-LIFE - The time it takes for the amt. of drug in the body to to of the peak level it previously achieved  - time it takes for of the drug to be excreted by the body o Factors to be considered:  Rate of absorption

  

Metabolism Appropriate dose Excretion

The elimination of drugs from the body


o o o

Kidneys (main organ) Liver Bowel  Biliary excretion  Enterohepatic recirculation

9. Variables Influencing Drug Action  Age  Gender  Weight  Physiological  Pathological  CV  Liver / Kidney dse.  Genetic  Psychological  Environmental
o o o

TOLERANCE -

Resistance to a drug effect 2 to

biotransformation of drug components.

DEPENDENCE may come about if px manifest withdrawal S/Sx when drug is stopped. CONTRAINDICATION - any characteristic of the patient, especially a disease state, that makes the use of a given medication dangerous for the patient Intended therapeutic action (beneficial) Unintended but potential adverse effects (predictable, adverse reactions) THERAPEUTIC INDEX - the ratio between a drugs therapeutic benefits and its toxic effects

o o o

10. DRUG DRUG INTERACTION SITUATIONS:  At the site of absorption (tetracycline vs. Ca & Ca products*)  During distribution (ASA* vs. methotrexate)  During metabolism (coumadin* vs. anti tb)  During excretion (Lanoxin vs. Quinidine*)  At the site of action (Anti HPN vs. AHs*) DRUG TO FOOD INTERACTIONS : SOME FOODS AFFECTS DRUG FUNCTION AND EFFICIENCY  TETRACYCLINES vs. Fe / Ca o DRUG TO LAB TEST : GIVING DRUGS PRIOR TO A LAB TEST CAN ALTER THE RESULT  ATB prior to sputum/ wound GS/ CS  Anti DVT (Fragmin) alters ( ) liver fxn test exams
o

11. PHARMACOTHERAPEUTICS USE OF DRUG TO TREAT/ CURE A DISEASE  ACUTE THERAPY CRITICALLY ILL Px THAT REQUIRES INTENSIVE THERAPY Ex.(Thrombolytics for AMI )  EMPERICAL BASE ON PRACTICAL EXPERINCE RATHER THAN SCIENTIFIC DATA Ex.( EMPERIC ATB prior to GS / CS)  SUPPLEMENTAL/ REPLACEMENT REPLENISH / SUBSTITUTE FOR MISSING SUBSTANCE IN THE BODY Ex. (Ca for Osteoporotic px. Vit. B complex for DM px)  SUPPORTIVE DOES NOT TREAT THE CAUSE OF THE DISEASE BUT MAINTAINS OTHER BODY SYSTEMS INTEGRITY UNTIL Px CONDITION IMPROVES Ex. ( O in a PTB px)  PALLIATIVE FOR END STAGE / TERMINAL Dse. PROMOTION OF COMFORT IS TOP PRIORITY Ex. (Bone CA px having continous M SO4 drip)  Maintenance therapy  Prophylactic therapy
o

Drug actions: The cellular processes involved in the drug and cell interaction

Drug effect: The physiologic reaction of the body to the drug Onset-The time it takes for the drug to elicit a therapeutic response Peak-The time it takes for a drug to reach its maximum therapeutic response Duration-The time a drug concentration is sufficient to elicit a therapeutic response

ADVERSE EFFECTS HARMFUL / UNDESIRABLE EFFECTS THAN HAT HAS BEEN EXPECTED OF A DRUG  KINDS:  DOSE RELATED ?  Px RELATED ? DRUG INTERACTIONS:  Primary can be caused by simple overdose Ex. (overdose of blood thinners can lead to profuse bleeding)  Secondary good or bad effect Ex. (AHs can promote sleeping but what if the px will drive a vehicle)  Hypersensitivity - response to 1 / 2 drug actions that can lead to a pathological condition DRUG ALLERGY Occurs when the body forms an antibodies to a particular drug causing an immune response upon re- exposure  TYPES  ANAPHYLACTIC  CYTOTOXIC  SERUM SICKNESS  DELAYED RESPONSE IDIOSYNCRATIC EFFECT Non pharma related but can be genetic in origin IATROGENIC EFFECT Adverse drug reaction that tends to mimic a pathology Ex. (ASA cause GI irritation that mimics PUD) ADDICTIVE EFFECT SYNERGISTIC EFFECT ANTAGONISTIC EFFECT INCOMPATIBILITY Teratogenic results in structural defects in the fetus Mutagenic permanent changes in the genetic composition and chromosome structure of living organism Carcinogenic cancer-causing effects of drugs

o o

o o o o o o

12. Nursing process Asssessment Nursing Dx Planning Intervention Evaluation




 

DERMATOLOGICAL RASH / HIVES - Assessment: color, turgor, pattern & other pertinent data Intervention: frequent skin care, avoid friction, rubbing, and tight clothing, hydration STOMATITIS Assessment: observe for gingivitis, glositis, odinophagia, halitosis Intervention: frequent, proper oral care a non irritating solution, evaluate diet tolerance SUPER INFECTION Assessment: S/Sx on infection(fever, diarrhea, itching, redness, pain, warmth, discharge Intervention: proper body hygiene (bathing, hand washing etc.,) DC causative meds.

BLOOD DYSCRASIA Assessment: fever, chills, Hct /Hgb (Anemia), Platelet count (thrombocytopenia), WBC (leukopenia), CBC (pancytopenia) Intervention: supportive tx, prevent injury, monitor all lab exam / result

13. TOXICITY  LIVER TOXICITY Assessment: fever, malaise, N & V, jaundice, stool change, altered LOC, liver enzyme lab results Intervention: hygiene, frequent rest periods, DC causative drugs, monitor for bleeding and altered LOC.  RENAL TOXICITY Assessment: URINE (color, character, amount) monitor BUN, CREA level, edema Intervention: Strict / accurate I & O ( q 1 q shift q 24), DC causative meds 0 (gentamycin, ampothericin B) o POISONING Occurs when an overdose of drugs affects multiple body systems c possible or potential fatal reactions.

EXAMPLES: ALTERATIONS IN GLUCOSE METABOLISM o Hypoglycemia- OHA, Insulin o Assessment: S/Sx: fatigue, drowsiness, hunger, , anxiety, headache, cold clammy skin, shaking and lack of coordination, HR, BP, numbness and tingling of mouth, tongue and lips, confusion, rapid shallow respiration, seizure and coma o Interventions: Give hyperglycemic agents IV or Oral to prevent injury and falls Hyperglycemia: Ex. (Ephedrine- bronchodilator/ Anti asthma that relieves nasal congestion causes glucogenolysis o Assessment: fatigue, polyuria, thirst (polydipsia), deep respirations (kausmauls), restlessness, polyphagia, nausea, dry flushed skin, fruity odor breath o Intervention: Insulin, OHA
o

ELECTROLYTE IMBALANCE o Hypokalemia- drug affects kidneys can cause K level in serum by altering renal exchange system (proximal tubules) o Assessment: weakness, numbness, muscles cramps, nausea and vomiting, bowel sounds, Hypokalemic paralysis o Interventions: K rich diet (unless CIx, K supplements prevent injury or falls)
o o o

HYPERKALEMIA - K supplements, K sparing diuretics, K rich diets in renal problems Assessment: weakness, DOB, bradycardia, Ms cramps, Numbness Intervention: Monitor px status (CV,LOC, Homeostasis) diet modification, K wasting drug regimens / protocols, monitor lab exams.

SENSORY EFFECTS  OCCULAR TOXICITY Tiny blood vessels in the retina END ARTERIES are affected, occluded by some drugs Ex. ( Chloroquine) Aralen causes inflamation, retinal damage, blindness o ASSESSMENT: observe for visual acquity, color or vision changes, corneal, retinal affectation o INTERVENTION: supportive tx, prevent injury, optic care hygiene, proper drug administration


 

AUDITORY TOXICITY : Tiny vessels & nerves can be affected by some drug hearing affectation / disturbance Ex. (ASA can cause tinnitus or aural fullness hen given in excessive doses) ASSESSMENT: hearing acquity, Rinnes test, Rombergs test, INTERVENTION: Prevent injury, monitor for perceptual losses, symptomatic drug treatment, (speak in medium tone firm voice)

14. Drug Labels and Packaging y y y y y y y y y y y y y y y y Chemical name the drugs chemical composition and molecular structure Trade name- brandname or proprietary name; first letter always capitalized; The drug has a registered trademark; use of the name restricted by the drugs owner (usually the manufacturer) Generic name- listed in US pharmacopeia; name given by the United States Adopted Name Council ; official accepted name of the drug; not capitalized NDC number- national drug code; a number used by the pharmacist to identify the drug and the method of packaging; NSN- national supply number- a code for ordering the drug Total amount of drug in the container- top left or right or at the bottom Strength of the drug- in metric weight or liquids Form of the drug- preparation of the drug Usual dosage- how much drug is given in a single dose or within 24 hours and who should use the drug Route of administration- how the drug will be administered Storage- describes the condition necessary to protect the drug from losing its potency Directions for preparation- steps how to prepare and use the drug Precaution- specific instructions related to safety, effectiveness and administration that must be noted or followed Manufacturer- the laboratory made the drug LOT number- the batch of drug from which the stock came Expiration date- the drug cannot be used after the last day of the month indicated Date manufactured- the date the drug was made

15. Drug Preparations y Tablets- are powdered drugs that are compressed or molded into solid shapes a. scored tablets- have line down the center can be broken into halves b. unscored tablets- should not be broken not evenly distributed c. coated or film-coated tablets- are smooth and easy to swallow d. enteric-coated tablets- dissolve in more alkaline secretions in the intestine; protects the drug from being inactivated in the stomach and reduces the possible gastric irritation; should not be crushed e. prolonged or extended-released tablets- disintegrates more slowly and have a longer duration of action; should not be crushed f. sublingual tablets- dissolve quickly under the tongue g. coded tablets- have numbers or letters or both for easy identification y Capsules- are gelatin containers to hold powder or liquid drugs; some are enteric-coated called spansule, timespan, time release or sustained- release; dissolve at different times and these are long acting and should not be opened y Syrups- are solutions of sugar in water y Elixirs- clear, hydroalcoholic liquids that are sweetened y Fluid extracts- most concentrated and tinctures- are alcoholic liquid concentrations of drug; potent usually ordered in small amount- 2 teaspoon or less

y y y y y y

Solutions clear liquids that contain a drug in water, IVTT, nebule Suspensions- solid particles of a drug dispersed in a liquid or water Magmas- contains large bulky particles ex- milk of magnesia Gels- have small particles ex. Magnesium hydroxide gel Emulsions- creamy, suspensions of fats or oils in an agent to reduces surface tensions and makes the oil easier to swallow ex. Emulsified castor oil Creams- semi-solid applied externally to skin or mucous membrane

y y y y y y

Ointments- semi-solid drug in petroleum or lanolin base for topical use Pastes- thick ointments to protect the skin; absorb secretions and soften the skin Powder- dry, finely ground drugs, can be applied to the skin in dry form Aerosols- liquid or powders; combined with propellant, used to spray on the skin or in nebulizers and inhalers to reach mucous membrane Suppositories- film base such as cocoa butter, that melts at body temperature Transdermal patches- in a unique polymer patch effective in hour or days that sticks in the skin; drugs are slowly released and absorbed thru the skin

16. DOSAGE AND SOLUTIONS


o o o o

Common household measurements: 1quart= 4 cups 1pint = 2 cups 1cup= 8 ounces 1tbsp= 3tsp: 15 16 ml 1tsp = 60ugtts: 4-5ml Apothecary Measurements: 60minims = 1fluidram 8fluidram=1fl oz; 480minims 16 fl oz =1 pint 2pints=1quart 4quarts = 1gallon

o o

17. Metric measurements: o Units of length (meter) o 1mm = .001m 1cm = .01m o 1hectometer = 100 meters o Units of volume (liter) o 1ml = .001L 1decaliter = 10 Liters o Units of wt (gram) o 1ug/mcg = .00001gm 1mg = .001gm o 1cg = .01gm 1dg = .1gm o 1dg = .1gm 1kg = 1,000grams 18. Other unit equivalents o 1gm = 15 gr. 1gr. = 60mg o 1mg = 1oooug o 1ml =1cc;15gtts;60ugtts;1gram o 1L = 1qt;1000ml o 1gal = 4L; 4qt; 4000cc o 1oz = 30gm;30cc o 1kg = 2.2lbs o 1lb = 16 oz 19. Drug computations o Formulas:  VOL. OF DRUG TO BE GIVEN:  d= desired dose (mg) / s=stock preparation(cc) X h = what you have in vol Stock dose o Ex: give 1000mg sulperazone iv q8 stock dose is 1500mg dillute it in 10cc o Solution:1000mg/ 1.5mg x 10cc = 6.67cc iv q 8 o Ex: dormicum 7.5 mg was ordered for a px having difficulty to sleep stock dose of dormicum is 15mg/tab. How many tablet will you give? What time will you give the drug? o Ex: glucophage tab 750mg od was started for a diabetic px. Stock dose is 500mg /tab. Ho many will you give? Nursing considerations? 20. IV FLUID RATE: o Macrodrops per minute(gtts/min) o = total IVF vol(cc) x 15gtts/cc #hrs(infusion time) x 60min/hr o Ex hook D5Lr 1L x 8 hrs, 16 hrs, 4 hrs. o Solution: 1000cc x 15 gtts /cc o 8 hrs x 60 min/ hr  =15000 gtts / cc  480 min/hr  =31.25cc/min

21. cc / hour o Volume of iv fluid = cc/ hr o # hours to be infuse o Ex: start Pnss 1Liter x 8 hours for a DM patient o 1000cc = 125cc/ hr o 8 hour 22. Conversion (annex) o Conversion of T o C to F = ( C x 1.8) + 32 = F o F to C = (F - 32) (.55) =C o Or FORMULA: F= (C x 9/5) +32 C= (F 32) x 5/9 o Ex. px has 39.5c during admission.using the formula, convert it to F o (39.5C x 1.8) + 32 = 103.F o Ex.3y/o child has dengue,100.3 F convert it to C using the formula o (100.3F - 32) (.55) = 37.5C 23. Computation (annex) pediatric doses o Friedss rule: for a child less than 1y/old o childs dose(age 1y/o)= infants age(in mos.) o 150 mos. o x ave. adult dose o Youngs rule: children 1-12 y/o o childs dose (age1-12 y/o) = childs age (in yrs.) o childs age (in yrs.) +12 o x ave. adult dose o Clarks rule : o wt. in lbs x usual adult dose = safe childs dose o 150 lbs

Ex. Computation: 1. The physician orders digoxin (Lanoxin) 0.125 mg I.M. The ampule reads 1ml= 0.25 mg. How many milliliters of this cardiac glycoside should be prepared? a. 0.25 ml b. 0.5 ml c. 0.75 ml d. 1 ml 2. The physician ordered 1500 ml of D5W in 12 hours. What is the correct flow rate of this isotonic solution when the drop factor is 15 gtt = 1 ml? a. 31 gtt/min b. 21 gtt/min c. 83 gtt/min d. 30 gtt/min 3. 104 F TO C= ?

24. Six Elements of a Drug Order (RA 5921) 1. Patient's name 2. Date order is written

3. Name of medication 4. Dosage (includes size, frequency, and number of doses) 5. Route of delivery 6. Signature of the prescriber

RA 6675- generic act of 1988, prescribed drugs should be written in generic name; prescription should be written clearly with signature

25. NERVOUS SYSTEM - operates through the use of electrical impulse and chemical messengers to transmit information throughout the body and to respond into internal & external stimuli.  CENTRAL NERVOUS SYSTEM  AUTONOMIC NERVOUS SYTEM  PERIPHERAL NERVOUS SYSYTEM o NEURONS basic functional unit of the nervous system, about 14 billion are located in the brain the rest in the SC, PNS .  PARTS:  DENDRITE Short, branchlike projections that conveys information from one neuron towards another neuron .  CELL BODY ( SOMA ) largest part of the neuron  AXON - Elongated, carries information away from the neuron .  EFFECTOR CELLS Receives the signal sent by the axon(cells, muscles, glands, or another nerve)  AFFERENT FIBERS - Nerve axons that run from PNS to CNS  EFFERENT FIBERS - Nerve axons that carry impulse from the CNS to Periphery 26. o Action potential Electrical impulse sent by the nerves
o

cell membranes & nerve membranes have pores or channels that controls the movement of a substance in & out of the cell  some of these channels allows entry & exit of Na, K, Ca  when cells are at rest, membranes are impermeable to Na but permeable to K o Depolarization Na channels open in response to the stimulus Na ions rush inside the cell (positive rush of Ion ) a nerve cannot be stimulated again during depolarized stage o Repolarization - return of the cellular environment to the resting membrane potential stage of responding / balance bet. Na & K occurs o Resting membrane potential- negative environment inside the cell 27. o NERVE SYNAPSE Where the communication bet.2 nerve occurs thru the release of a Neurotransmitter  NEUROTRANSMITTER - chemical that stimulates the receptor sites by exciting or inhibiting them  may either be reabsorbed (reuptake) or broken down by the enzymes in the area Ex. (MAO breaks down the neurotransmitter Epinephrine) (Acetylcholinesterase breaks don the neurotransmitter acethylcholine) o SELECTED NEUROTRANSMITTER o Acetylcholine communicates in the Ms & N, neurotransmitter in the ANS & Parasympathetic o Norepi / Epi classified as catecholamines eurotransmitter released by the sympathetic branch of the ANS, released as a hormone by the adrenal medulla o Dopamine found in amts. In the brain for coordination of impulse & responses both motor & intellectual. heart ? 28. o Gamma amino butyric acid (GABA) found in the brain, inhibits or stimulation nerve activity & important in preventing overexcitability or stimulation such as seizure activity o Serotonin found in the limbic system, important for the in arousal and sleep, prevention of depression and motivation promotion o limbic system area of the brain that contains amounts of neurotransmitters ( epi / norepi / serotonin) if responsible for the expressions of emotions ( anger, pleasure, motivation, how a person learns & react to stimuli) 29. o ANXIOLYTICS & HYPNOTIC AGENTS o ANXIOLYTICS D rugs that alter s the individuals response to the environment, prevents feelings of tension or fear  ANXIETY - a feeling of tension, nervousness, apprehension, or fear that usually involves unpleasant reactions to stimulus o HYPNOTICS Drugs causes sleep or minor tranquilizers (provides hypnosis & sense of tranquility in anxious pxs)  HYPNOSIS Result of extreme sedation & CNS depression / sleep. o SEDATIVES Drugs that cause calmness, unaware of environment  SEDATION - Loss of awareness and reaction to environmental stimulus. Desirable in (restless, nervous, irritable, or overreacting to a stimulus pxs) 30. o BENZODIAZEPINES: Most frequently used anxiolytics: prevents anxiety w/out causing much sedation  ALPRAZOLAM / XANOR  LORAZEPAM / ATIVAN  DIAZEPAM / VALIUM o Action: Acts in the limbic system & RAS to make GABA more effective causing interference in neuron firing. o Indication : anxiety d/o, AWS, hyperexcitability,agitation. o Pharmacokinetics: well absorbed in the GI,peaks30min- 2hrs, lipid soluble, crosses the placenta, enters breastmilk, o CIx : +allergy, psychosis, shock, coma, narrow > glaucoma, acute alcohol intoxication, pregnancy, o Cautions: elderly or debilitated px o Adverse effects : Mild drowsiness, depression, lethargy,fatigue, restlessness, bradycardia, changes in libido, drug dependence. o Antidote: Flumazenil / Romazicon : 31. o BARBITURATES: former drug of choice prior to benzodiazepines, risk of addiction , and dependence  PHENOBARBITAL / LUMINAL  BUTABARBITAL/ BUTISOL o Action : CNS depressants neuronal impulse conduction in the RAS, cerebral cortex, alters cerebellar fxn, motor output .


Ix : Anxiety, sedation, insomnia, seizures, acute manic reactions. Pharmacokinetics: absorbed well, peaks20-60mins.,induces liver enzymes systems. lipid soluble, crosses placenta, enters breast milk o CIx: +allergy, hepatic / kidney / respiratory d/o dse., pregnancy. o Cautions : acute or paradoxical pain (masking?), lactating women o Adverse effects : somnolence, agitation, confusion, hyperkinesia, BP, syncope, apnea, StevensJohnsons 32. o OTHER ANXIOLYTICS & HYPNOTICS : does not fall to benzodiazepines or barbiturates.  AHs: Benadryl / Dipenhydramine, Phenergan / Promethazine: can be sedating for some peoples, Tx for mild insomnia  Paraldehyde / Paral : sedates px c delirium tremens or psych conditions characterized by extreme excitement. Excreted by the lungs and urine  Buspirone / Buspar : anti anxiety agent, (-) sedative, anticonvulsant,Ms relaxant properties, 33. o AUTONOMIC NERVOUS SYSYTEM: involuntary, visceral nervous system (hypothalamus, medulla & SC) o DIVISIONS:  PARASYMPATHETIC / CRANIO SACRAL DIVISION  SYMPATHETIC / THORACOLUMBAR DIVISION o SYMPATETHIC - fight or flight CV fxn, BP, PR, RR, dilated pupils, bronchis dilate, blood flow to the skeletal Ms., sweating , piloerection , RAAS, GLYCOGENOLYSIS, o Adrenergic Transmission: sympathetic nerves that synthesize,stores, release Norepinephrine  RECEPTORS:  ADRENERGIC :  ALPHA ADRENERGIC : (ALPHA 1,) FOUND IN THE BLOOD VESSELS(VASOCONSTRICTORS), IRIS(DILATION), URINARY BLADDER(CONSTRICTION)  ALPHA ADRENERGIC :(ALPHA 2) LOCATED IN THE NERVE MEMBRANES, MODULATORS FOR THE RELEASE OF NOR EPI  BETA RECEPTORS :  BETA 1: FOUND IN CARDIAC TISSUE HAVING (+) INOTROPIC, CHRONOTROPIC EFFECT, LIPOLYSIS  BETA 2 : FOUND IN THE SMOOTH Ms.,PERIPHERY( Ms & LIVER GLYCOGEN BREAKDON) BLOOD VESSELS(VASODILATION), PERIPHERY, UTERINE Ms.(RELAXED UTERINE MS. 34. o PARASYMPATHETIC - Rest & digest GI motility & secretions, HR, BP,RR, pupillary dilation o Cholinergic Transmission:Neurons that uses ACh  Cholinergic drugs: promotes the action of Acetylcholine  Aka parasympathomimetic drug o Major classes o Cholinergic agonist mimics the action of acetylcholine, stimulates cholinergic receptors o Anticholinesterase inhibits acetylcholinesterase, as a result, acetycholine is not broken down and begins to accumulate thus the effect of acetylcholine is prolonged 35. o DIRECT CHOLINERGIC AGONIST:  URECHOLINE  PILOCARPINE o Action: Parasympathetic action that HR,(-)inotropic effect, vasodialtion, bronchoconstriction, mucus, GI activity, bladder tone, relaxed GI, Bladder sphincters, pupil constriction(miosis). o Indications: Acute post op, non obstructive urinary retention, bladder atony c retention o Pharmacokinetics: short half life (1-6hrs), well absorbed o CIx: (+) allergy,pregnant & lactating pxs, Bradycardia, Hypotension, CAD,asthma, o Adverse effects: N & V, cramps, diarrhea, salivation, Bradycardia, heart block,hypotension, Cardiac arrest , Urinary urgency. 36. o INDIRECT CHOLINERGIC AGONIST: does not react c ACh receptor sites directly. reacts c Acetylcholinesterase(enzyme responsible for breakdown of Ach)  NEOSTIGMINE  PYRIDOSTIGMINE o Action: cholinesterase inhibitor, ACh level faciltation of nerve transmission o Indication: Myasthenia gravis , myasthenic crisis o Pharmacokinetics: duration of 2-4 hrs,must be given every few hours  (Pyridostigmine=3-6hrs), does not need to be taken frequently, Oral & Parenteral form, can be given in px that inhaled nerve gases o CIx: cholinergic crisis
o o

(Endophonium iv=used to distinguish if the px is having w/c type of crisis is happening to the px.) Adverse effects:Bradycardia, Cardiac arrest, tearing,dysphagia, N & V, bronchial secretions, incontinence, urinary frequency. Myasthenic Crisis px condition improved p endophonium iv injection Cholinergic Crisis px condition gets worst p giving endophonium iv injection Tensilon Test Dx test for Myasthenia Gravis ALL MYASTHENIA GRAVIS DRUGS DOES NOT CROSS THE BLOOD BRAIN BARRIER

37.
o o o o o

38. Alzheimers dse progressive neural degeneration in the cortex leading to a marked memory loss & inability to do ADLs.- loss of Ach producing hormones  TACRINE (COGNEX)- mild mod. dementia .  GALANTAMINE (REMINYL)- mild mod dementia  RIVASTIGMINE (EXCELON)- liquid, capsule prep  DONEZEPIL (ARICEPT)- o.d. dose only o Action:indirect cholinergic blocks Achase at the cells of the cortex & crosses the BBB o Pharmacokinetics- metabolized by the liver, excreted by the kidney o CIx Cautions:(+) allergy, Liver dse. Pregnant & lactating,bradycardic, intestinal & urinary obstruction o Adverse effect:Insomnia, fatigue, rash,N&V,Ms cramps 39. o Anticholinergic Drugs- used to block the effects of Ach & the PNS (Parasympatholytic agents) o BELLADONA:  ATROPINE ( oral, parenteral, topical ) o Action : blocks the effect of PNS there by promoting SNS effects(dilate pupils, HR,RR,PR, GI, URINARY, BLADDER FXN,salivation,bronchial secretions,) o Ix: preop px, severe bradycardia,hyperactive bowel,pylorospasm o Pharmacokinetics: well absorbed,cross the BBB,excreted in the urine o CIx / Cautions: (+) allergy, glaucoma,GI obstruction,Prostate enlargement,bladder obstruction,tachycardia,myocardial ischemia,liver & kidney problem,breastfeeding & lactating px. o Adverse effects: blurred vision, IOP , cyclopegia,Gi disturbance,dry mouth, insomnia,heartburn, constipation etc  SCOPALAMINE, DICYCLOMINE,PROPANTHELINE 40. o PARKINSONS DSE - progressive neurologic d/o due to marked degeneration in the brain(basal ganglia & substantia nigra) thereby affecting Corpus striatum (helps maintain Ms tone not related to any movement)  tremors leading to rigidity, weakness, bradykinesia, simian posture, difficulty in performing intentional movements, shuffling gait, slurred speech, mask face o * corpus striatum is connected to substantia nigra by series of neuron that uses inhibitory GABA o * substantia nigra sends back impulse to corpus striatum using the inhibitory neurotransmitter Dopamine 41. o higher neurons from the cerebral cortex secrete Ach in the corpus striatum as an excitatory neurotransmitter to coordinate intentional movements of the body= o dopamine in the area causes imbalance that allows the cholinergic / excitatory cells to dominate = o affecting the fxn of basal ganglia & extrapyramidal motor system (provides coordination for unconscious Ms movements Ex. Position, posture, movement) 42. o type 1(inhibition) antiparkinsonian drug:  Dopaminergic : effects of dopa @ receptor sites,does not cross BBB proven to be much more effectve than Anticholinergics o * effective only if theres enough intact neuron in the substantia nigra (unextensive degeneration)  Levodopa (Dopar): precursor of dopamine, crosses the BBB then converted to dopamine usually given c  Carbidopa (Sinemet)= the effect of dopa decarboxylase enzyme in the GI tract & periphery leading to dopamine converted in the brain  Amantadine(Symmetrel)- antiviral, release of dopa  Bromocryptine (Parlodel)- dopa agononist acting on dopa receptor directly-does not need further metabolism(more effective than dopar & Sinnemet 43.  Pergolide (Permax )- adjunct to carbi-levodopa.  Pramipexole (Mirapex)- effective if levodopa effect has decreased  Ropinirole (Requip) new drug. Used in early & late stage of PD when levodopa has lost its adequate effect.
o

 o o o o

Apomorphine iv (Apokyn)- new drug.dopa agonist that manages hypomobility in PD.given SQ route Actions: level of dopa in the substantia nigra Pharmacokinetics: absorbed well in GI & body CIx/ ^Cautions : (+)allergy, closed angle glaucoma,^CVD, asthma,liver, renal dse. Adverse effects:anxiety,nervousness,arrythmias

44. type 2 (stimulation) antiparkinsonian drug:  Anticholinergics: opposes the effects of Ach @ receptor sites in the  Benztropine (Cogentin)- oral,im,iv for parkinsons due to phenothiazines  Biperiden (Akineton)- oral, im, adjunctive tx for PD due to phenothiazines  Dipenhydramine (Benadryl) used in px ho cannot tolerate more potent type of anti PD drugs(Old pxs)  Procyclidine (Kemadrin)- oral,for any type of parkinsonism, controls excessive salivation due to use of neuroleptics  Trihexyphenidyl ( Artane)- used c levodopa, used alone for control of drug induced Extrapyramidal d/o. 45. o Action: tremors & rigidity, drooling assoc. c PD o Ix: Parkinsons dse., Parkinsonism(idiopathic, atherosclerotic,postencephalitic)releif of Extrapyramidal d/o due to phenothiazines o Pharmacokinetics :variable absorption in GI, 1-4 hrs, metabolized in the liver o CIx /^ Cautions: (+) allergy, closed angle glaucoma,GI, GU obstructions, prostate enlargement ^tachycardia, hypo/hypertension, pregnant & lactating px o Adverse effects : disorientation,confusion, memory loss, agitation,delirium,weakness,dry mouth, N & V, GI, GU activity 46. o Psychotherapeutic Agents: drugs aiding in the Tx Mx of mental d/o. o Psychosis: perceptual & behavioral d/o  Schizophrenia- most common type. (hallucinations, paranoia, delusion, speech abnormality, affective problems) strong genetic predisposition  Mania- assoc. c bipolar illness (manic-depressive) periods of extreme depression followed by hyperactivity & excitement.  Narcolepsy- char. by daytime sleepiness &sudden loss of wakefulness. Problem c RAS  Attention-deficit d/o- inability to concentrate on an activity for longer than a few minutes & hyperkinesis 47. o Antipsychotic /Neuroleptics, Major tranquilizers  Antipsychotic - eliminate S/Sx of psychosis  Neuroleptic- adverse neurobiologic effect causing abnormal body movements  Major Tranquilizers- can calm agitated patient o Major types: Typical & Atypical  TYPICAL dopamine receptor blocker{Phenothiazines} Ex: Chlorpromazine/Thorazine, Fluphenazine/Prolixin,Haldol/haloperidol o Action: blocks dopa receptor,prevents stimulation of neuron by dopa,depress RAS 48. o Ix : hallucination, schizophrenia, anxious/agitated px, dellusions, ADHD o Pharmacokinetics: absorbed in GI, still present 6mos, p last dose, children metabolizes drugs faster than old px o CIx/^ Cautions: (+) allergy, PD, CAD, blood dyscrasia, ^glaucoma, PUD, GI/Urinary obstruction o Adverse Reaction: weakness, EPS (dystonia, akathisia, tardive dyskinesia), hypotension, urine color turns pink to reddish brown (minor harmless effect) 49. o Atypical- blocks dopa & serotonin receptors o Ex. Clozapine, Olanzapine, Risperidone,Quetiapine, o Action: blocks dopa & serotonin receptors, depress RAS o Ix: Schizophrenia unresponsive to typical type, o Pharmacotherapeutics: 4-12hrs, metabolized in the liver excreted in urine & feces. o Adverse effects: drowsiness, sedation, seizures, diziness 50. o MANIC- opposite of depression, overstimulation of certain neurons in the brain o ANTI MANIC DRUGS- drugs used to treat manic d/o Ex: Lithium salt, Lamictal, Seroquel,Zyprexa o Ix: Manic d/o, Manic-depressive (bipolar) o Action: alters Na transport in Ms & Nerves;( dopa & norepi but not serotonin) Neurons; ( storage of neuronal dopa & nor epi, content of 2 nd messengers )
o

Pharmacokinetics- absorbed in GI,30min-3hrs peak level when px is dehydrated: lithium more absorbed than Na=toxic level,enters breastmilk. o CIx / ^Caution:(+) allergy, Renal, Liver, Cardiac Dse. Dehydration( Na ),pregnant & lactating px 51. o Adverse effects: therapeutic level: 0.6- 1.2mEq/L o Serum level 1.5=CNS problem: lethargy, slurred speech, Ms. weakness, fine tremor,renal gastric toxicity o Serum level 1.5-2= Intensified above S/Sx +ECG changes o Serum level 2~2.5= progression of effects renal pulmonary fatalities o Serum level >2.5= Complex multi organ toxicity c significant risk of death 52. o CNS Stimulants: Tx for attention deficit d/o & narcolepsy,  Methylpenidate/Ritalin,Concerta-both  Dexmethylpenidate/Focalin- Ix:6y/o px only  Dextroamphetamine/Dexedrine  Modafinil/Provigil-narcolepsy  Pemoline/Cylert-adhd o Action: releases catecholamines from presynaptic neuron= increase stimulation of post synaptic neurons o Pharmacokinetics: rapidly absorbed in GI,peaks 2-4hrs. Half life =2-15hrs 53. o CIx /^Cautions : (+) allergy, anxiety, agitation,fatigue, galucoma,^hx of seizures, drug dependence,alcoholics o Adverse effects : nervousness,insomnia,dizziness, headache,blurred vision & difficulty c accomodation, anorexia, nausea, wt. loss, HPN, arrythmias, angina, 54. o Epilepsy - sudden dc of excessive electrical energy from the cells of the brain. o Classifications:  Generalized- begins in one area of the brain & rapidly spread throughout both hemispheres.px often loses consciousness as a result of massive abnormal electrical brain activity  Tonic-clonic -aka Grand mal, loss of consciousness, confusion & exhaustion upon recovery  Absence- aka petit mal, abrupt, brief(3-5secs)loss of consciousness 55.  Myoclonic- short, sporadic periods of Ms contraction for several minutes  Febrile-most common in children,  Status epilipticus- most dangerous type seizures recur over & over o Partial aka focal seizures , involves one area of the brain, S/Sx depend on exactly where the abnormality occurs.  Simple partial single area of the brain affects a single Ms.  Complex partial- hallucinations,mental distortion,involuntary urination 56. o Drugs for tonic-clonic seizures o HYDANTOINS- stabilizes N membranes & limit the spread of excitability.  Phenytoin (Dilantin) therapeutic level10-20ug/ml  Ethotoin (Peganone) therapeutic level 15-50ug/ml  Fosphenytoin (Cerebyx) short acting  Mephynytoin (Mesantoin) sev. multi system toxicity o Ix: tonic-clonic seizures o Pharmacokinetics: 6-4hr:met. In liver,excreted by kidney o CIx ^Cautions: (+)allergy, hepatic & renal dse. o Adverse effects: nystagmus, ataxia, slurred speech, confusion, Ss Js syndrome fatigue. 57. o BARBITURATES & B -LIKE DRUGS  Phenobarbital( Luminal)therapeutic level 15-40ug/ml  Primidone (Mysoline)-therapeutic level 5-12ug/ml  Mephobarbital (Mebaral)-causes BP, HR, circulatory collapse. o Action: CNS depressants, inhibits impulse & conduction in the ascending RAS, cerebellar fxn, motor output o Pharmacokinetics: 79 hr: metabolism o Adverse effects: Somnolence, insomnia, vertigo, nightmares, lethargy, nervousness, bradycardia, depression, withdrawal syndrome 58. o BENZODIAZEPINES- the effects of GABA(causes stimulation of Limbic & RAS)  DIAZEPAM (Valium)-releives tension, anxiety & Ms spasm, not used for long time Tx of seizures half life= 20-50 hrs  CLONAZEPAM (Klonopin)-usu for petit mal & myoclonic half life =18-50hrs
o

o o o

Ix: Anxiety d/o, AWS, Ms relaxant, Status Epilipticus CIx ^ Cautions: allergy, pregnant, liver kidney dse. Adverse effects: drowsiness, sedation, depression, disorientation,diarrhea, incontinence, withdrawal

59. PETIT MAL DRUGS SUCCINIMIDES supresses the abnormal elctrical activity in the brain  ETHOSUXIMIDE (Zarontin)- drug of choice for petit mals/ absence seizures,often used first. thera level=40-100ug/ml  METHSUXIMIDE (Celontin)- can cause bone marrow depression. o Pharmacokinetics: peaks 1-7 hrs, halflife: 30-60hrs, metabolized in liver, excreted in the urine & bile o CIx ^ Cautions: allergy, renal, hepatic dse, pregnancy o Adverse effects: drosiness, ataxia, headache,diarrhea 60. o PETIT MALS DRUGS (annex)  Depakene (Valproic acid)- drug of choice in tx myoclonic seizures peaks 1-4 hrs. half life 616 hrs  Acetazolamide (Diamox)- for absence seizure in children, for open angle glaucoma, edema in CHF px s, half life 2.5 6 hrs.  Zonisamide (Zonegram) new drug. Inhibits voltage sensitive Na & Ca channels, px should be hydrated due to possibilities of renal calculi 61. o FOCAL SEIZURE DRUGS  CARBAMAZEPINE (Tegretol) drug of choice, ability to block Na channels to prevent repetitive action potentials in the abnormal focus  CLORAZEPATE (Tranxene) also used for anxiety, alcohol wihtdrawal  FELBAMATE (Felbatol) usually given if other medications fail.causes liver toxicity & aplastic anemia  GABAPENTIN (Neurontin) adjunctive therapy for other seizure drugs  LAMOTRIGINE (Lamictal) adjunctive therapy 62.  LEVETIRACETAM (Keppra)- newer drug,renal toxicity  OXCARBAZEPINE (Trileptal) for px 4-16 y/o  TOPIRAMATE (Topamax)- interferes Na channels causing stability of nerve membranes o CIx^ Cautions:(+) allergy, bone marrow supression,^pregnancy, liver & kidney dse. o Adverse effects: drowsiness, ataxia, dizziness, nausea, vomiting, hepatitis, CV complications, Ss Js syndrome 63. o PAIN sensory & emotional experience assoc.w /actual or potential tse damage. o PAIN PERCEPTION: o Painful stimulus free nerve endings (nociceptors) release of prostaglandin pain receptors (A-delta-small, fast,myelinated fiber / Cfiber-slow,unmyelinated) ascending tracts (spinothalamic tracts-beginning of the gate control theory) hypothalamus thalamus cerebral cortex 64. o NARCOTICS - aka opiods. o OPIOD RECEPTORS- receptors (CNS, GI, Periphery)that respond to endogenous opiates (Endorphin, Enkephalin)  BRAINSTEM-opioid receptors helps control BP, pupil diameter.  GI- opioid receptors regulates N & V cough  SC & THALAMUS- opioid receptors help integrate & relate incoming info abt. Pain  HYPOTHALAMUS- opioid rceptors interrelate the endocrine & neural response to pain  LIMBIC SYSYTEM- opioid receptors incorporate emotional aspects of pain & response to pain. 65. o Peripheral Nerve sites- opioid receptors may block release of neurotransmitters that are related to pain & inflammation o 4 types of opiod receptors  Mu(u) - 1pain blocking receptors (analgesia) RR, GI activity, euphoria, pupil constriction  Kappa (k)- assoc. c some analgesia, pupil constriction, sedation, dysphoria  Beta()- reacts c enkephalins in the periphery to modulate pain transmission  Sigma( E )- pupillary dilation, maybe responsible for hallucinations, dysphoria, psychose assoc. c narcotic use 66. o NARCOTIC AGONIST- drugs that react c opioid receptors throughout the body to cause analgesia sedation, euphoria (controlled substance)
o o

FENTANYL (Duragesic) MEPERIDINE (Demerol) OXYCODONE (OxyContin) MORPHINE (Astramorph) o Action: analgesia, antitussive, adjuncts to general anesthesia o Ix : severe acute or chronic pain, pre op meds, analgesia during anesthesia o Pharmakokinetics: fastest route is iv, greater absorption in male, most are in preg. category C (except oxyxodone B- do not cut, crash meds!! -Fast effect) 67. o CIx ^ Cautions: (+) allergy, pregnancy, labor, lactation,^ respiratory dysfxn, recent GI & GU surgery, head injuries, alcoholism, liver & kidney dse. o Adverse effects: respiratory depression, hypotension, shock, biliary spasm, constipation, hallucinations, anxiety, fear, ureteral spasms, dependence 68. o NARCOTIC AGONIST AGONIST stimulates certain opioid receptors & blocks some. Has less abuse potential than pure narcotics  BUPRENORPHINE (Buprinex)- mild-mod. Pain  BUTORPHANOL (Stadol) preop med mod.-sev. Pain, effective in tx of migraine headache.  NALBUPHINE (Nubain) mod. sev. Pain, adjunct for gen anesthesia  PENTAZOCINE (Talwin)- prefered in shifting iv- oral pain killer, highly hallucinogenic & euphoric (+ tripelannamine) o Pharmacokinetics: well absorbed iv-im, crosses placenta 69. o CIx /^Cautions: allergy,pregnancy, lactation, ^COPD & CV dse px. o Adverse effects: respiratory depression, apnea, suppression of cough reflex, N & V, constipation, biliary spasm,psychose, lightheadedness, GU & GI affectations 70. o NARCOTIC ANTAGONIST  NALMEFENE (Revex)  NALOXONE (Narcan)- tx & dx of narcotic use  NALTREXONE (ReVia) o Actions: blocks opioid receptors & reverse the effects of opioids. o Ix: narcotic overdose (resp. depression, sedation) o Pharmacokinetics- well absorbed p injection, passes in the placenta & breast milk. o CIx^Cautions: allergy,^ pregnant / lactating px. o Adrese effects: acute narcotic abstinence syndrome (n & v, svveating, tachycardia, hypotension, pulmonary edema. 71. o Nsg implementation:  Maintain patent airway /provide artificial ventilation  Continous px monitoring  Administer narcotic antagonist  Comfort, safety measures  Thorough health teaching abt. drug ( brand name , dosage, time of taking, cautions etc. ) 72. o MIGRAINE HEADACHES- sev. Throbbing headaches on one side of the head. 2 to arterial dilation  COMMON- occurs s aura, sev. Unilat. Pulsating pain usu. accompanied by N&V light & sound sensitivity (aggravated by physical activity)  CLASSIC- preceded by aura, sensation (sensory & motor disturbances .5 hrs prior to headache o CLUSTER HEADACHES- starts during sleep (Sharp, steady eye pain 15-90mins) c sweating, flushing, tearing & nasal congestion o TENSION HEADACHE-during stress (dull band of pain around entire head 30mins-1wk.) anorexia, fatigue, mild intoleranec to light / sound. 73. o ERGOT DERIVATIVES-cause cranial vasocontrictions, pulsations of cranial arteries  DIHYDROERGOTAMINE (Migranal)-po, iv,nasal spray  ERGOTAMINE- previous drug of choice, SL o Actions: blocks alpha adrenergic & serotonin sites in the brain causing constriction of vessels & arterial pulsation o Ix: prevent & abort vascular & migraine headaches o Pharmacokinetics: rapidly absorbed c in 30 mins. o CIx ^Cautions : allergy, pregant & lactating px, ^ pruritus, GI reactions. o Adverse effects: numbness, tingling fingers & toes, Ms pain, thready pulse, chest pain 74. o Nsg implementation:
   

    

Know px drug Hx/allergy, Hx taking for CV dse. r/o pregnancy & lactation Continous monitoring for any adverse reaction post drug administration. Health teaching abt drug being administered.

75. TRIPTANS- new class. Causes cranial vasoconstriction & migraine relief (-) CV, GI effects vs ergot derivatives  SUMATRIPTAN (Imitrex)- very effective in cluster headache  NARATRIPTAN ( Amerge) causes birth defects  RIZATRIPTAN (Maxalt) for migraine (c / s )aura o Actons: binds to selective serotonin sites causing vasoconstriction o Ix: Tx but not prevention of migraines o Pharmacokinetics: liver metabolizes, excreted by kidney, crosses placenta 76. o CIx ^ Cautions: allergy, pregnant / lactating px. ^ elderly px , CAD px o Adverse effects: dizziness, vertigo, weakness, myalgia, chest pain, tingling, numbness o Nsg. Implementation:  know drug allergy / Hx  Use 10 Rs of drug administration  Px comfort & safety  Monitor CV functioning & other VS  Observe for any adverse effects  Health teaching 77. o ANESTHETICS: drugs that cause complete/partial loss of sensation  GENERAL- CNS depressants produces loss of pain & consciousness. blocks body reflex  Goals: (analgesia, unconsciousness, amnesia)  Risk Factors: o CNS= neurological d/o dse (SE, CVA, MG) o CV= cv dse/abnormality (CAD, hypotension) o RESPI= abnormal V/Q perfussion ratio (COPD, Asthma, etc) o Renal & Hepatic: altered met & excretion of drug (ARF, ESRD, Hepa A-E, cirrhosis, etc.)  LOCAL- cause loss of pain sensation & feeling in a designated area or body part 78. o Balance Anesthesia- use of combination of drug(s) each c a specific effect (analgesia,Ms relaxation, unconsciousness, amnesia)  Pre op meds- anticholinergics, atropine SO4  Sedative-hypnotics - dormicum  Antiemetics - plasil  Antihistamines - benadryl  Narcotics - nubain (nalbuphine) o Stages of Anesthesia o Stage 1: Analgesia stage(loss of pain sensation) px is still consciouss & able to communicate o Stage 2: Excitement stage(excited & may be combative behavior) usu. c SNS response ( PR, BP, RR) 79. o Stage 3 Surgical Anesthesia (relaxed skeletal Ms, Normal RR, loss of eye reflexes, dilated pupil) surgery can be safely performed o Stage 4 Medullary Paralysis CNS depression, respiratoty & vasomotor stimuli loss. (death can occur) o INDUCTION- from beginning of anesthesia stage 3. *stage 2 = danger pd. o MAINTENANCE from stage 3- until surgery is complete (usu. Gas anesthetics given) o RECOVERY- from dc anesthesia-cosnciousness regained (movement, ability to communicate) *px must be continously monitored* 80. o TYPES OF GEN. ANESTHESIA  BARBITURATES  THIOPENTAL (Pentothal)-most common, rapid onset, short recovery pd (- analgesic prop.)  METHOHEXITAL (Brevital)- rapid onset, must not be in contact c silicon, (- analgesic prop.) causes resp. depression, apnea.  NON BARBITURATES  MIDAZOLAM (Dormicum)peaks 30-60mins, N&V are often  KETAMINE (Ketalar)- causes hallucinations,dreams, psychotic episodes  DROPERIDOL (Inapsine)- CIx in renal & liver dse. 81.
o

ANESTHETIC GASES- enters the bronchi & alveoli capillary system heart systemic circulation tissues/fats (nerves) brain= CNS depression  NITROUS OXIDE ( BLUE CYLINDER )- potent analgesic, least toxic usu in dental practice  Cyclopropane ( orange cylinder ) not good analgesic,causes headache, N & V,  Ethylene ( red cylinder )- less toxic, unpleasant taste in mouth 82. o VOLATILE LIQUIDS- unstable gas @ rm T & release gases  HALOTHANE (Fluothane)- rapid onset & recovery,( HR, BP, ) liver toxic  DESFLURANE (Suprane)- causes cough & laryngospasm  ENFLURANE (Enthrane)- causes renal toxicity, arrythmia  METHOXYFLURANE (Penthrane)- slow onset, used in labor & delivery  SEVOFLURANE ( Uthane)- newest form, 83. o LOCAL ANESTHETICS-loss of sensation in local area of the body ( T, touch, proprioception, skeletal Ms tone) o TYPES OF ADMINISTRATION:  TOPICAL-cream, spray, lotion (skin, nose, throat, mouth, urethra, rectal)  INFILTRATION-injecting directly in area (wound dehis) that needs resuturing  FIELD BLOCK-injected all around the area that ill be affected by the operation (tooth extraction) 84. o NERVE BLOCK-injected some point along the nerve thats responsible for the sensation of area involve o peripheral nerve block- blocks sensory & motor aspectsof a particular nerve for a relief of pain. o central nerve block-injected into the roots of the nerves o epidural block-injected in the space where the nerves emerge from the SC o caudal block-injection in sacral canal below the epidural area 85. o INTRAVENOUS & REGIONAL ANESTHESIA- carefully draining all blood from the extremities, securing it c tourniquet (prevent anesthesia from entering the general circulation) & injecting it in the vein. o GEN. KINDS:  ESTERS : BENZOCAINE, PROCAINE, TETRACAINE  AMIDES: LIDOCAINE, BUPIVACAINE, DIBUCAINE, ROPIVACAINE  OTHERS: DYCLONE, PRAMOXINE 86. o Action: temporary interruption in production & conduction of nerve impulse.  Affects permeability of nerves membranes to Na ions thereby preventing the nerve from depolarization o Ix: infiltration, nerve blocks, spinal anesthesia, local pain relief o Pharmacokinetics: ester types are easily broken down by plasma esterases. amides types are broken down much longer (toxicity prone) o CIx: ^Cautions: allergy, heart block, shock, ^liver & kidney dse. hypotension 87. o Adverse effects: skin injury, headache, restlessness, anxiety, tremors, blurred vision, N & V, arrythmia, cardiac depression o Nsg Intervention:  assess CV & Respiratory function  Maintain patent airway  check for gag & swallowing reflex  Spinal anesth px must remain flat on bed x 12hrs  Proper hydration 88. o NMJ- area of communication bet. the nerve & Ms. o Neuromuscular Junction Blocking Agents- blocks the area of communication bet. Nerve & Ms. o Non Depolarizing NMJ agent: ( CURARE) TUBOCURARINE-adjunct to Gen. anesthesia  Action: occupies the muscular cholinergic receptor site preventing Ach from reacting c the receptor  Ix: induce skeletal relaxation, ECT, Ventilated px.  Pharmacokinetics: metabolized by liver & excreted unchange by the liver  Adverse effects: respiratory depression, apnea, bronchospasm, cardiac arrythmia. 89. o Depolarizing NMJ blocker: attaches to the Ach receptor site on the Ms cell, depolarizing it.hydrophillic & does not cross BBB o Succinylcholine - adjunct to gen. anesthesia o Action: combines c ACh receptors causing flaccid paralysis. Prolongs depolarization (Ms contracts first & then leading to paralysis)
o

o o o

Ix: facilitate ET intubation, induce skeletal Ms relaxation, ECT, Pharmacokinetics: metabolize in the plasma & liver by the use of cholinesterase CIx ^ Caution: allergy, MG, renal & hepatic Dse. pregnant^ CV dse. Malignant hyperthermia, Adverse effects: respiratory depression, Ms paralysis, bronchospasm, hypotension, arrythmias,, GI, dysfxn, paralysis, decubitus ulcer Nsg. Implementation: Must be given by specialist Not be mixed c alkaline soln. Monitor pxs overall status & recovery Maintain cholinesterase inhibitor Maintain cmfort & safety Close monitoring of VS & neuro VS

90.
o o o o o o o o

Pharma(Cardio Resp) Midterm - Presentation Transcript 1. Nsg. Pharmacology midterm 2. o CARDIOVASCULAR SYSTEM- responsible for delivering oxygen & nutrient rich blood to all of the body & removes w aste products for excretion o HEART- hollow muscular organ loc inside the thoracic cavity bet T 2-T4, inverted triangle, main organ for pumping blood. o Chambers:  ATRIUM- 2 upper parts of the heart  VENTRICLE- 2 lower parts of the heart o Frank starlings law-the further heart Ms is stretched, the stronger in returns to its original form o Cardiac cycle:  Systole  diastole 3. 4. o Electrophysiological properties:  EXCITABILITY  AUTOMATICITY  CONTRACTILITY  REFRACTORINESS  CONDUCTIVITY o Receptors: o ALPHA adrenergic  ALPHA 1  ALPHA 2 o BETA adrenergic  BETA 1  BETA 2 5. 6. o Cardiac Valves:  Atrioventricular Valves  Semilunar Valves o CONDUCTION SYSYTEM: o SA node AV node Bundle Of His Purkinje fibers 7. o ACTION POTENIAL OF CARDIAC MUSCLE o 5 PHASES:  PHASE 0 : CELL IS STIMULATED, Na gates open Na enters the cells ( + flow of electrons) DEPOLARIZATION  PHASE 1 : SHORT PERIOD- Na IN THE CELL equals those outside  PHASE 2 : PLATEU STAGE cell membrane are less permeable to Na., Ca slowly enters the cell., K begins to leave the cell (REPOLARIZATION)  PHASE 3 : Gates are closed & K rapidly moves out of the cells (RAPID REPLARIZATION)  PHASE 4 : CELLS COME TO REST. Electrolytes go to their respective places 8. o MECHANICAL ACTIVITY SARCOMERE - basic functional unit of the heart muscle  ACTIN 2 contractile proteins of sarcomere (thin filaments)  MYOSIN protein of sarcomere that is thick & has small projections  TROPONIN protein that seperates actin & myosin when the sarcomere is at rest

* when heart Ms is stimulated, Ca enters the cells ( starts to repolarize) & Ca reacts c troponin & inactivates it. Allowing actin & myosin to react c each other thus, SLIDING FILAMENT THEORY occurs NORMAL BLOOD FLOw (TO & FROM THE HEART): Inf. Vena Cava & Sup. Vena Cava ( UN O2 BLOOD) R. Atrium ( TRICUSPID VALVE ) R. Ventricle ( PULMONIC VALVE ) PULMONARY ARTERY LUNGS ( OXYGENATED BLOOD ) PULMONARY VEIN L. Atrium ( MITRAL VALVE ) L. Ventricle ( AORTIC VALVE ) ASCENDING AOTA SYTEMIC CIRCULATION metabolic demands & expenditures

9.
o o o o o o o o

10. 11. Anti lipidemic drugs- drugs that lipid amount in the blood. Cholesterol-base unit for formation of steroids(sex & cortical hormones),basic unit for the formation & maintenance of cell membrane o (HMG-Co A): hydroxymethylglutaryl-coenzyme A reductase= regulates the early step in the cellular synthesis of cholesterol 2 to cholesterol amt.  HDL : high density cholesterol (good cholesterol), transports cholesterol to the liver for excretion  LDL : low density cholesterol (bad cholesterol), transport to peripheral tissues (CAD associated ) 12. o CAD (coronary artery dse.)- progressive growth of atheromas in the coronary arteries thereby causing thickrning of the blood vessel ( oxygenated blood in the heart vs. oxygen demand & expenditure) o Risk factors:  Modifiable:  Cigarette smoking  Sedentary lifestyle  High stress level  Hypertension  Obesity  Diabetes  Gout  Chlamydia infection  Non modifiable:  Genetic predisposition  Age  gender 13. 14. o Hyperlipidemia- level of lipids in the blood o Flow of cholesterol: dietary fats stomach Small intestine gall bladder (releases bile in S. Intestine) Bile sythesizes fat (micelles) micelles absorb in the S.intestine (chylomicrons)/ bile recycled to liver chylomicrons absorbed in lymphatics heart syytemic circulations & metabolic purposes o ANTIHYPERLIPIDEMIC AGENTS: drugs that cholesterol amount  BILE ACID SEQUESTRANTS  HMG-Co A REDUCTASE INHIBITOR  CHOLESTEROL ABSORPTION INHIBITOR  OTHER ANTILIPIDEMIC AGENTS 15. o BILE ACID SEQUESTRANTS- binds c bile acids , levels of bile acid (contains cholesterol) reentering hepatic circulation.  CHOLESTYRAMINE (QUESTRAN)- powder that must be dilluted  COLESTIPOL (COLESTID)- powder & tablet  COLESEVELAM ( WELCHOL)- tablet o Actions: the liver use of cholesterol to make more bile acid(thus, LDL in the periphery) o Ix: hyperlipiemia, pruritus, biliary obstruction o Pharmacokinetics: not absorbed systemically, binds c bile acids in the intestine & excreted in fecal form o CIx^Cautions: allergy, biliary obstruction, abnormal intestinal function^pregnancy & lactation 16. o Adverse effects: headache, anxiety, fatigue, N & V, bleeding time ( absorption of Vit. K), clottin factor, Vit A & D
o o

o o o o o o o

Nsg Intervention: Do not administer powder agents in dry form Ensure the consistency, viability of tablets(affects absorption) Avoid any drug combinations Asses GI functioning (frequency of BM) Health teaching about drug Support & encouragement

17. HMG CoA REDUCTASE INHIBITORS- blocks the enzyme LDL levels , HDL . Usually referred as statins  ATORVASTATIN (LIPITOR)-can be used in children10-17y/o  FLUVASTATIN (LESCOL)- fungal product  LOVASTATIN (MEVACOR)- old version, limited s/effects but can lead to RHABDOMYOLYSIS  PRAVASTATIN (PRAVACHOL)- effective in CAD & MI px  ROSUVASTATIN (CRESTOR) newest, HDL , LDL but causes RHABDOMYOLYSIS in asians  SIMVASTATIN (ZOCOR)- also prevents MI, CAD but no severe toxicity 18. o Actions:blocks the formation of cellular cholesterol (LDL) & may or my not HDL. o Pharmacokinetics: all absorbed in the GI, & undergo first pass in the liver, excreted by urine or feces. Peak effects in 2-4 wks. o CIx^Cautions: allergy, liver & renal dse. (Pregnancy cat X), endocrine abnormality o Adverse effects: flatulence, abdominal pain, N & V, headache, dizziness, insomnia, liver & renal affetation. o Nsg. Implementationo Administer drug in pm / hs ( bld cholesterol occurs during night 5am) o Monitor cholesterol levels 19. o Monitor liver enzyme levels o Must be in conjunction c exercise & diet o Suggest lifestyle changes o Periodic opthalmic exam o Stop lovastatin, atorvastatin, fluvastatin in any acute serious medical condition (infection, BP, major surgery, trauma, endocrine d/o) o Pregnancy & lactating caution / alternatives o Health teaching abt. Medication 20. o CHOLESTEROL ABSORPTION INHIBITORS- absorption of cholesterol in the small intestine, dietary cholesterol delivered in the liver & liver cholesterol clearance  EZETIMIBE (ZETIA) o Ix: hyperlipidemia, adjunct to diet & exercise o Pharmacokinetics: absorbed properly. Peaks 4-6hrs. o CIx^Cautions: allergy, pregnant & lactating, liver & kidney dse. o Adverse effects: diarrhea, abdominal pain, back pain, URTI, muscle aches & pain 21. o Nsg Implementation:  Monitor cholesterol, triglyceride LDL levls  Monitor liver function test  Advise diet & exercise regiment  Discuss possibilty of lifestyle changes  Patient teaching o Other Antilipidemic drugs  FIBRATES (fibric acid derivatives)  NIACIN 22. o FIBRATES- stimulate breakdown of lipoproteins from tissue & remove it in plasma, lipoprotein & triglyceride synthesis & secretion  FENOFIBRATE (TRICOR)- inhibits triglyceride synthesis in the liver, decreases LDL, increases uric acid secretion, may stimulate triglyceride breakdown  GEMFIBROZIL (LOPID)- inhibits lipid breakdon in periphery, reduces production of triglycerides & LDL, increases HDL . Should not be combined c statins (RHABDOMYOLYSIS) o NIACIN-VIT. B3, inhibits the release of free fatty acids from adipose tse. rate of triglyceride removal from plasma & generally LDL, HDL  NIACIN (NIASPAN / NICOTINIC ACID)23.
o

BLOOD P - P exerted by the heart to the arterial walls DETERMINANTS:  HEART RATE  STROKE VOLUME-amt. of bld pumped out of the left ventricle c each heartbeat  PERIPHERAL RESISTANCE- resistance of muscular arteries to the bld being pumped through o VASOGENIC CENTER- loc in the medulla oblongata o BARORECEPTORS / P RECEPTORS- can be found in the atria,arteries 24. o RENIN-ANGIOTENSIN SYSTEM- compensatory mechanism by the kidney (hypotension / lack of oxygen in the kidneys occurs) o Renin liver (produces angiotensin) angiotensin I bloodstream LUNGS (converts I-II by the use of A.C.E. Angiotensin II angiotensin II receptor in the blood vessels VASOCONSTRICTION o Angiotension II angiotensin III stimulates adrenal cortex (produces aldosterone)m = Water & Na retention. o HYPERTENSION / HPN / HTN- bld p is above normal 140/90 mmhg  Pre hypertension, Stage 1 & 2 o HYPOTENSION- bld pressure is below normal 25. o HYPERTENSION CONTROL  STEP 1: lifestyle modifications ( diet, exercise, etc.)  STEP 2: drugs are added (failed step 1) DIURETICS (dec. serum Na levels), BETA BLOCKERS (dec. HR & strength of contrcation, & vasodilaion), ACE inhibitor (blocks conversion of angiotensinI II), Ca CHANNEL BLOCKER ( relaxes Ms contraction), or AUTONOMIC BLOCKER  STEP 3: inadequate response to former step, drug may be changed, combined or increased.  STEP 4: combination of the 3 former steps. 26. o DIURETICS- drugs that promote urination (excretes Na & K) o Classifications:  THIAZIDES & THIAZIDE LIKE DIURETIC / K sparing diuretics = prevents K loss, K is reabsorbed in the proximal renal tubule  Ex: INDAPAMIDE, METALAZONE, HYDROCHLOROTHIAZIDE,CHLOROTHIAZIDE  LOOP DIURETICS / K w asting diuretics = does not promote K reabsorption  Ex: FUROSEMIDE, ETHACRYNIC ACID, BUMETANIDE 27. o SYMPATHETIC BLOCKERS  BETA BLOCKERS: blocks vasoconstriction, HR cardiac Ms contraction, bld flow to kidneys ( release of renin), these drugs have many side effects, not recommended for all people, often used in monotherapy in step 2  Ex: ACEBUTOLOL, ATENOLOL, METOPROLOL,PROPANOLOL  2. ALPHA & BETA BLOCKERS: useful in combination c other agents. More potent in blocking the SNS response. Px often complain of fatigue , inability to sleep, GI & Gu disturbance  Ex: CARVEDILOL, LABETALOL, GUABENZ, GUANADREL, GUANETHIDINE 28.  ALPHA ADRENERGIC BLOCKERS: inhibit the postsynaptic receptor sites. alpha1 receptor blocker (dec. SNS tone,= vasodilation), alpha2 receptor blocker (prevents norepinephrine release)  Ex: PHENOXYBENZAMINE, PHENTOLAMINE  ALPHA2 AGONIST- stimulate the alpha2 receptors in CNS (inhibits the CV center to lower Sympathetic outflow)  Ex: CLONIDINE, GUANFACINE, METHYLDOPA  ALPHA1 BLOCKER: decreases vascular tone, vasodilation.  Ex: DOXAZOSIN, PRAZOSIN, TERAZOSIN 29. o ANGIOTENSIN CONVERTING ENZYME- blocks the conversion of (RAAS), can be combined c diuretics  BENAZEPRIL (LOTENSIN)- for HPN only, can cause cough  CAPTOPRIL ( CAPOTEN)- HPN & CHF, DIBETIC NEPHROPATHY, LVF p MI. can cause cough, GI distress  ENALAPRIL (VASOTEC)- HPN, CHF, LVF  LISINOPRIL (ZESTRIL)- HPN, CHF, a day POST MI px. o Pharmacokinetics: crosses placenta & breastmilk. o CIx^Cautions: allergy, renal & liver dse. Pregnant & lactating^ CHF, hyponatremic px o Adverse effects: tachycardia, MI, rash, pruritus, GI irritation, pancyopenia, proteinuria
o o

30.
o o o o o o

Nsg. Implementation: Encourage px to implement lifestyle changes (diet, exercise, smoking cessation etc.,) Complete medical Hx (pregnant / Lactating) Getting baseline data (VS) proior to giving the drug Provide thorough px teaching about the drug Know appropriate actions / interventions to do due to occurrence of side effects

31. CALCIUM CHANNEL BLOCKER- prevents the movement of calcium into the cardiac & smooth Ms hen the cells are stimulated (inability to contract & loss of smooth Ms tone, vasodilation, dec. peripheral resistance) can be also effective in treatment of angina (dec. cardiac workload)  AMLODIPINE (NORVASC)- hpn & angina  DILTIAZEM (DILZEM)- hpn (sustained release)  FELODIPINE (PLENDIL)- hpn  VERAPAMIL (CALAN)- hpn , arrythmia (sustained release) o Pharmacokinetics: gen absorbed in the body. Crosses the placenta o CIx^Cautions : allergy, pregnant & lactating, renal & hepatic dse. 32. o Adverse effects : dizziness, headache, fatigue, hypotension, bradycardia, edema, heart block, skin flushing o Nsg. Implementation : o Complete medical & drug Hx o Take VS & baseline data full minute o Thorough assessment prior, during & after drug administration o Do appropriate protocol during adverse effects & refer accordingly 33. o VASODILATORS - used when other therapies fail. Produces relaxation of vascular smooth Ms. dec. peripheral resistance & BP. Do not block reflex tachycardia. Used in severe hypertension  HYDRALAZINE (APRESOLINE )-maintains increase blood flow while relaxing smooth Ms.  NITROPUSIDE (NIPRIDE)- used in the tx of hypertensive crisis o Pharmacokinetics: rapidly absorbed & widely distributed o CIx^Cautions: allergy, renal & hepatic dse., pregnant & lactating px., ^ CHF, CAD, cerebral insuficiency, hypotension o Nsg. Implementation : o Monitor VS & other baseline data o Health teaching about the drugs & related factors o Observe px for adverse reaction to drug o Manage px (reacted adversely) properly 34. o OTHER ANTI HPN DRUGS- tx of severe HPN  MECAMYLAMINE ( INVERSINE)- occupies cholinergic receptor sites of autonomic neuron (blocks Ach at Sympathetic & Parasymoathetic ganglion) o ANTI HYPOTENSIVE DRUGS- usually indicated if px BP is decreased. Use of (SYMPATHOMIMETIC DRUGS) o SYMPATHOMIMETIC DRUGS- react c sympathetic adrenergic receptors( BP, blood vol., Cardiac Ms contraction)  MIDODRINE (Pro-Amatine)- tx for orthostatic hypotension  Action: activates alpha receptors in arteries & veins to BP (can also be used in px having liver dse)  Pharmacokinetics: absorbed in GI,  CIx^Cautions: supine hpn, CAD, ARF, pregnant & lactating px  Adverse effects: piloerection, rash, vision changes, vertigo, headache, problem in urination. 35. o Nsg. Implementation o Monitor VS (BP prior to giving meds) o Comfort measures o CIx in bedridden px o OTHER SYMPATHOMIMETIC DRUGS  DOBUTAMINE  DOPAMINE  EPHEDRINE  EPINEPHRINE  ISOPROTERENOL  METARAMINOL 36. o CONGETIVE HEART FAILURE- dropsy heart fails to pump blood around the body. o CAUSES:
o

   

CAD- 95% cause of CHF, insufficiency of blood to meet O 2 demand of the myocardium (Ms becomes hypoxic & capacity to contract ) CARDIOMYOPATHY- viral infection, alcoholism, steroid abuse, collagen d/o HPN- leads to enlarged cardiac Ms ( puts cardiac Ms in constant oxygen demand) VALVULAR HEART DSE.- overload of the ventricles due to inadequate closing of the valves (leakages of blood / backflo w) RIGHT SIDE HEART FAILURE vs. LEFT SIDE HEART FAILURE COMPENSATION: CO stimulation of barroreceptors (aortic arch &carotid sinus) SNS response ( HR, BP, rate & depth of RR, +inotropic effect , blood volume ) RAAS (kidneys) compensated CHF overtime prolonged stress to the heart (cardiomegaly) heart Ms increases due to over work & chambers of the heart dilate ( blood volume they have to handle ) will further lead to aggravated CHF.

37.
o o o

38. TREATMENT: VASODILATORS (ACE inhibitors & NITRATES)- work load of the heart DIURETICS- blood volume, venous return & BP BETA ADRENERGIC AGONIST- stimulate beta receptors in SNS ( Ca flo w in heart cells, myocardial contraction)  CARDIOTONIC (INOTROPIC / PRESSORS)- heart contraction  4. 1 CARDIAC GLYCOSIDES (lanoxin)- most often used in CHF rapid action onset & can be safely be excreted unchanged in the urine ( antidote=digoxin immune fab) o Action: intracellular Ca, allows Ca to enter myocardial cells during depolarization.  myocardial contraction (inotropic effect)  CO & renal perfusion( urine output, blood vol. renin release & renin angiotensin system)  HR (- chronotropic effect) conduction velocity in AV node 39. o CIx^Cautions: allergy, Vtach & Vfib, heart block,SSS, AMI,^ pregnant & lactating px. o Adverse effects: headache, yello w halo around objects=digitalis toxicity o Nsg. Implementation : o Monitor apical pulse 1 full min o Check dosage & preparation o Standby emergency equipments & meds (lidocaine, K salts, dilantin, atropine, Ca monitor) o Avoid combining it c food & antacids o Monitor px for therapeutic level (0.5-2ng/ml) o Monitor electrolyte level (K) 40.  4. 2 PHOSPODIESTERASE INHIBITORS- used for px unresponsive to glycoside tx. Short term CHF tx only  INAMRINONE (INOCOR)- iv prep only  MILRINONE (PRIMACOR)o Action: blocks the enzyme phospodiesterase & myocardial cell adenosine monophospate ( Ca levels in the cells=stronger contraction & prolongs the effect of sympathetic stimulation) o Pharmacokinetics: widely distributed post injection o CIx^Cautions: allergy, aortic & pulmonic valvular dse. Acute MI, hypovolemia, elderly px, pregnant & lactating px. o Adverse effects : ventricular arrythmias (Vfib), hypotension, chest pain, N & V, etc., o Nsg. Implementation: o Monitor BP & PR (hook px to cardiac monitor) o Monitor px for adverse effects (arrythmias) o Accurate I & O 41. o ARRYTHMIA / DYSRYTHMIA- abnormality / disturbance in normal & rate & rhythm of the heart  Bradycardia  Tachycardia  (PAC / PVC, Atrial flutter / Atrial fibrilation, Vtach / Vfib, AV heart blocks 1-3, bundle blocks) o CAUSES: changes in automaticity & conductivity) o Electrolyte disturbance alters action potential o Oxygen deprivation (hypoxia / anoxia) o Structural damage in the conduction pathways through the heart o Alteration in bld. Acidity / alkalinity (waste products accumulation) 42. o ANTIARRYTHMIC AGENTS- corrects dysrythmia  CLASS 1(a,b,c),2 ,3 ,4 & others
o   

CLASS 1: blocks the Na channels in the cell during action potential ( local anesthetics / membrane stabilizers)  1a: & prolongs phase 0 of the action potential  DISOPYRAMIDE (NORPACE)- tx for ventricular arrythmia (adult & young px)  MORICIZINE (ETHMOZINE)- cardiac deaths (proarrytmia)  PROCAINAMIDE (PROCAINE)-for tx of ventricular arrythmia (po, im, iv prep)  1b: & shorten duration of action potential  LIDOCAINE (XYLOCAINE)- vtach / vfib in MI or cardiac surgery px.  1c: markedly phase 0 (extreme slo wing of conduction)  FLECAINIDE (TAMBOCOR)-tx Vtach & PAT,( mortality) 43. o CLASS 2: beta adrenergic blockers causing depressed phase4 of the action potential( slows cell recovery, conduction & automaticity)  ACEBUTOLOL (SECTRAL)- anti hpn drug, tx of PVCs  ESMOLOL (BREVIBLOC)- short term tx for SVT  PROPANOLOL (INDERAL)- anti hpn, anti angina, anti migraine headache & anti SVT due to digoxine or cathecolamine overdose o CLASS 3: blocks K channels & prolongs phase 3 of action potential (delays repolarization & conduction rate)  AMIODARONE (CORDARONE)- not usually 1 st choice  SOTALOL (BETAPACE)-tx for maintenance of NSR & can cause any arrythmia (proarrythmia)  BRETYLIUM-for unresponsive arrythmia to other drugs  IBUTILIDE (CORVERT)- converts atrial fibrillation to flutter of recent onset (less 90 days) 44. o CLASS 4: blocks Ca channel in the cell membranes( depolarization, prolongation of phase 1&2 replarization)  DILTIAZEM (CARDIZEM)- treats PSVT  VERAPAMIL ( CALAN)- treats SVT, atrial flutter & fibrillation 45. 46. o ANTIANGINAL DRUGS- helps restore 0xygen supply Vs. demand by 1. dilating tha coronary vessels, 2. decreasing load of the heart.  NITRATES / NITROGLYCERIN: cause smooth Ms relaxation & Ms tone (fast acting, dilates veins, arteries & capillaries. o NITRO-BID / NITROSTAT- given SL / TL (spray), IV, patch, transmucosal, PO. Fast acting.  ISOSORBIDE DI NITRATE (ISORDIL) slow effect but last upto  ISOSORBIDE MONO NITRATE (IMDUR)4 hrs. taken prior to angina attacks  AMYL NITRATE (GENERIC)- inhaled & takes effect in 30 secs. o CIx^Caution: allergy, hypotension, cerebral bleeding, pregnant & lactating px o Adverse effects: BP, headache, dizziness, tachycardia, N & V 47. o CORONARY ARTERY DSE- narro wed lumen of the bld vessel ( blood & oxygen are decreased) due to atheromas therby causing atherosclerosis. o ANGINA PECTORIS- chest pain suffocation of the chest o STABLE ANGINA- relieved by rest & NTG no damage to heart cells are noted o UNSTABLE ANGINA- more pronounced. Heart is having ischemia. Unrelieved by rest & NTG. No complete damge to heart is noted o PRINZMETAL ANGINA- spasm of blood vessels not narrowing occurs. Pain occurs at rest at the same time of the day (each day) o MYOCARDIAL INFARCTION- completely occluded coronary vessels leading to injury, ischemia, necrosis 48. 49. o Nsg. Iplementation: o Give drug in SL route not oral o Asks the px if the tablet given fizzles or burns o Check for the expiry date o Assess VS one full minute & baseline data o Instruct the px to maintain sitting / lying position during & after administration to prevent fall o Health teaching about the drug 50. o BETA BLOCKERS- blocks SNS ( BP, HR, myocardial contractility)  METOPROLOL (NEOBLOC)- dilates cardiac & renal vessels, decrease cardiac load & potentiates every cardiac beat  PROPANOLOL (INDERAL) NADOLOL (CORGARD)o

o o o

Pharmacokinetics- metabolized in liver excreted by urine CIx^Caution: allergy, bradycardia, heart block, cardiogenic shock^ DM, PVD Adverse effects: dizziness, vertigo, CHF, arrythmias, flatulence, impotence, decreased exercise tolerance. Nsg. Implementation Do not abruptly DC these drugs Must be given c food for better absorption Assess VS prior & after giving the medication Health teaching for px Prevent falls

51.
o o o o o o

52. CALCIUM CHANNEL BLOCKER- prevents Ca movement into cardiac & smooth Ms cells upon stimulation.  AMLODIPINE (NORVASC)-prinzmetal angina, coronary  DILTIAZEM (DILZEM) vasospasm, chronic angina,  NICARDIPINE (CARDENE)effort associated angina pectoris  NIFEDIPINE (CALCIBLOC) hypertension  VERAPAMIL (ISOPTIN)- arrythmia o Pharmacokinetics: gen. absorbed, metabolized in liver. Crosses placenta & breast milk o CIx^Cautions: allergy, pregnant & lactating, liver & kidney dse. o Adverse effects: hypotension, bradycardia, dizziness, heart block, flush & rush 53. o BLOOD COAGULATION- complex process involving vasoconstriction, platelet clamping, & clotting factor o CLOTTING FACTOR- produced in the liver & breaks do w n fibrinogen into insoluble fibrin threads. o INTRINSIC PATH W AY: o HAGEMAN FACTOR- clotting factor XII (chemical found in the bld.) activated due to exposure of damage bld vessels to collagen o EFFECTS: o Clot formation activated o Clot dissolving process iniated o Inflammatory response started o Activation of clotting factor XI (plasma thromboplasmin antecedent / PTA) & activates cascade sereies of coagulant substances intrinsic pathway: o ends in the conversion of prothrombin to thrombin (converts fibrinogen to insoluble fibrin threads) (thrombus) plugs the injury & seal the sysytem 54. o EXTRINSIC PATH WAY: clotting outside the vessel. Tissue Thromboplastin released by injured cells. o PLATELET AGGREGATION- adhesion of platelets in the endothelial lining / site of injury.  Once they stick, releases ADP & other chemicals to attract other platelets to stick as well. o CLOT RESOLUTION & ANTICLOTTING- blood plasma contains anti clotting substances:  ANTITHROMBIN III- prevents thrombin formation  PLASMIN / FIBRINOLYSIN- blood protein that breaks do w n blood clot o THROMBOEMBOLIC D/O- common  CORONARY ARTERY DSE.  CVA, PVD , AMI, DVT  HYPOXEMIA, HYPOXIA, NECROSIS DUE TO LO W OXYGEN & BLOOD SUPPLY 55. o HEMORRHAGIC D/O- rare.  HEMOPHILIAS, BLOOD DYSCRASIAS, DENGUE, OVERDOSE OF ANTICOAGULANT THERAPY o ANTICOAGULANTS- drugs that interfere c normal coagulation process. o ANTIPLATELET DRUGS: formation of platelet plug by responsiveness of the platelets to stimuli that cause them to stick in the vessel  ASPIRIN (ASA)- TIA, CVA, & MI  PLAVIX (CLOPIDOGREL)- MI, CVA, ISCHEMIA  PLETAAL (CILOSTAZOL)- INTERMITTENT CLAUDICATION o Pharmacokinetics: higly bound to proteins o CIx^Cautions: allergy, bleeding d/o, pregnant & lactating px o Adverse effects: bleeding, bruising, headache, dizziness, weakness, N & V, GI distress, rash 56. o Nsg. Implementation: o Small frequent feeding (GI disturbance) o Symptomatic treatment for (aches & pain)
o

Precautions against bleeding Health teaching about the drug ANTICOAGULANT - alters coagulation process clotting cascade, thrombin formation  WARFARIN (COUMADIN)- DVT, PULMO EMBOLUS A-FIB, MI *3days to effect & lasts 4-5 days (not ideal for acute cases)*  HEPARIN (GENERIC)- DVT, A-FIB,PULMO EMBOLUS, DIC, ABG, CLOTTING IN IV LINE *does not cross breast milk (ideal-lactating) o Pharmacokinetics: varies in each drug 57. o CIx^Cautions: allergy, bleeding d/o, liver & kidney dse. ^CHF, o Adverse effects: bleeding (gums to sever internal hge.), hair loss, N & V, GI upset, diarrhea, bruising, o Nsg. Implementation: o Monitor for therapeutic level (Heparin: clotting time & APTT) o (Coumadin: PT & INR) o Observe for S / Sx of excessive bleeding o Keep antidotes available (Heparin: Protamine SO4) (Coumadin: Vit. K / Konakion) o Safety & comfort measures 58. o LO W MOLECULAR Wt. HEPARIN- blocks factor Xa , IIa & angiogenesis ( process that allows CANCER cells to develop new bld vessels. used pre or post surgery & prolonged bed rest ( risk of thrombus formation ) & is continued for 7days - 2wks.  TINZAPARIN (INNOHEP)- DVT, used c coumadin  DALTEPARIN (FRAGMIN)- DVT, Pulmo Embolus, Unstable Angina  ENOXAPARIN (CLEXANE)- DVT, Angina, Pulmo Embolus,MI o CIx^Cautions: bleeding d/o, pregnant & lactating, should be used c standard heparin 59. o THROMBLOLYTICS- destroys formed thrombus by activating natural anticlotting system (conversion of plasminogen to plasmin)  STREPTOKINASE (STREPTASE)- Coronary Artery Thrombosis , Pulmo embolus, MI, DVT  UROKINASE ( ABBOKINASE)- Coronary Artery Thrombosis, MI, o Pharmacokinetics: fast acting , iv preparations only. o CIx^Cautions: allergy, liver & kidney dse, pregnant & lactating, bleeding d/o o Adverse effects: bleeding (gums & internal organs), bruising, rash, flushing (allergic reaction), bronchospasm, o Nsg. Implementation: o Administer AH prior to giving thrombolytics o Prepare for blood typing & cross matching (F WB) o Monitor for bleeding 60. o Nsg. Implementation o DC heparin if px is having thrombolytics (unless ordered) o Monitor & assess px for S/Sx of bleeding o Monitor blood coagulation results o Bleeding precautions o Thorough px teaching & evaluate teaching plan 61. o BLEEDING D/O  HEMOPHILIA genetic d/o px lacks clotting factor  LIVER Dse. affects production of clotting factors & proteins needed to prevent bleeding  BONE MARRO W d/o platelet are not formed in sufficient quantity to be effective o Anti Hemophilic agents:  ANTIHEMOPHILIC FACTOR (Bioclate, ReFacto) factor VIII (clotting factor missing in Hemophilia A)  COAGULATION FACTOR VIIa (NovoSeven) for Hemophilia A & B  FACTOR IX COMPLEX (Benefix, Profilnine SD) contains plasma fractions of many of the clotting factors & blood levels of factors II, VII, X, used for tx of (hemophilia B (christmas dse. - factor IX), control bleeding episodes in Hemophilia A & factor VII deficiency. 62. o Cautions^CIx: allergy, pregnant & lactating liver dse c DIC o Adverse effects: headcahe, flushing , chills, fever, lethargy , N & V, o Nsg. Implementation: o Should be administered IV route only o Monitor px response & clotting factor levels o Monitor px for S/Sx of thrombosis ( compressive stockings, positiioning, ambulation, exercise ) o Decrease rate of infusion if allergic reaction occurs o Arrange bld typing & cross matching in case of serious blood loss.
o o o

o o

Provide px teaching. Offer support & encouragement Systemic Bleeding: result of excessive plasminogen activity & risk of bleeding from clot dissolution HEMOSTATIC DRUGS drugs used to control / treat bleeding  APROTININ (Trasylol) IV drug that forms complexes c kinins, plasmins, & other clot dissolving factor to block the activation of plasminogen system. Usu for CABG pxs.  AMINOCAPRIC ACID (AMICAR) inhibits plasminogen activating substance & some antiplasmin activity. Oral & IV form usually prevents recurrence of SAH Cautions^CIx: allergy, DIC, ^ cardiac conditions, renal & hepatic dysfxn., Adverse effects : clotting, hallucinations, dizziness, N & V, diarrhea, fatigue, malaise, etc., Nsg. Implementation: Monitor px for S/Sx of thrombosis Orient px & safety measures if hallucination occurs

63.
o o

o o o o o

64. 65. RESPIRATORY SYTEM: brings O 2 in the body, allows exchange of gases & expels CO 2 & other end products. o MAJOR PARTS  UPPER RESP. TRACT  - nose c (conchae) entry & filters inhaled air  nasal cavity c (epithelial lining) - warms & humidifies air  contains goblet cells that produce mucus, traps dust & microorganisms, pollen & other foreign substances  Contains cilia , microscopic hair-like projections of the cell membrane, constanly moving to profell mucus down towards the throat  Sinuses (pairs) air filled passages through the skull  Phaynx funnel shaped tube extends from nose to larynx  Has 3 parts (na sopharynx , oropharynx, larygopharynx )  Larynx aka voice box lies anterior to esophagus. 66. 67.  LO WER RESP. TRACT  Trachea aka windpipe from larynx to T7 then divides into  R & L bronchus R is shorter, wider more vertically downward than L  Segmental bronchi & subsegmental bronchi  - Bronchioles final path wat to the alveoli  Terminal bronchioles last airways of the conduction system (nose terminal bronchioles = antomic dead space ) o LUNGS paired organs in the thoracic cavity capable of oxygenting blood & expelling CO2 apex= T1, base= diaphragm o ALVEOLI ( RESPIRATORY BRONCHIOLES, ALVEOLAR DUCTS, ALVEOLAR SACS) = RESPIRATORY ZONE = GAS EXCHANGE / VENTILATION o PERFUSION alveoli receives UnO 2 blood from the R ventricle 68. o RESPIRATION act of breathing, controlled by CNS (medulla Oblongata controls inspiratory Ms., diaphragm, Ext. intercostals & abdominal Ms) o MEDULLA OBLONGATA DORSAL PART controls inspiration  VENTRAL PART usu. dormant unless needs to ventilation or active exhalation. o PONS apneustic center rate & depth of respiration  pneumotaxic center allo ws talking & breathing o VAGUS NERVE parasympathetic nerve. Stimulation of diaphragm contraction & inspiration, may also lead to bronchoconstriction. o CEREBRAL CORTEX allo ws voluntary control of breathing (holding out breath or altering rate & depth of breathing) 69. o Upper resp. tract conditions Common cold viral invasion leading to activation of inflammatory response (histamine & prostaglandin)  Mucus membranes engorged c blood, tissue s w ells, goblet cells produce more mucus  Sinus pain, nasal congestion, sneeze, runny nose, teary eyes, scratchy throat, headache, can block the eustachian tube & affects hearing or evn otitis media.  Sinusitis inflammation reaction that leads to pain ? Or even lead to brain infection  Pharyngitis & Laryngitis common bacteria or virus. Cardiac affectation ? o Lo wer Resp. tract conditionso

 

Atelectasis lung collapse as a result of outside P against the alveoli thus, lung expansion does not occur Pneumonia viral / bacterial invasion by aspiration leading to gas exchange = poor oxygentation ( DOB, fatigue, fever, abnormal breath sounds)

70. Bronchitis bacteria, virus or foreign materials infect the inner layer of the brochi that leads to narro wing of the airway due to inflammation (Acute / Chronic)  Bronchiectasis chronic dse. Involving bronchi & bronchioles char. by dilation of the bronchial tree, chronic infection & inflammation, normal cells are replaced by fibrous scar tse. o Obstructive pulmonary dses.  Asthma char. by reversible bronchospasm, inflammation, hyperactive airways triggered by allergens, irritants, stress, exercise, emotions. Releasing histamine = bronchospasm / bronchoconstriction in minutes then cytokines in 3-5 hrs = mucus production & edema = obstruction  COPD permanent obstruction of airways often related to cigarette smoking. 71.  Emphysema loss of elastic tissue of the lungs, destroyed alveolar walls, hyperinflated lungs that can lead to collapse c experition.  Cystic Fibrosis hereditary dse. Accumulation of copious amts. of very thick secretions in the lungs. Secretions obstruct airway & destroys lung tse. 72. o RESPIRATORY DRUGS works to keep the airways open & gases moving efficiently. o ANTITUSSIVES drugs that supresses the cough reflex  BENZONATATE local anesthetic on resp. passages blocks the stretch receptors that stimulate the cough reflex  CODEINE *  DEXTROMETORPHAN *  HYDROCODONE * o Ix: common (non productive cough) o Actions: *acts directly on medullary cough cough center of the brain to depress the cough reflex o CIx^Cautions: post op px (thoracic & abdominal), ^ asthma & emphysema, hypertension, Hx of addiction, driving px. 73. o Adverse effects: drying effect on the mucous membranes, increase viscosity of resp. secretions. dro wsiness & sedation, nausea, constipation, dry mouth. o Nsg. Implementation: o Evaluate & assess cough if c (fever, rash, or excessive secretions) o Ensure that drug is not taken morethan prescribed o Provide other measures to relieve cough (humidity, cool temperatures, fluids, o Health teaching about drug & foods to be taken (vit c & natural fruit juices) 74. o Decongestants usu. Adrenergics / sympathomimetics causing local vasoconstriction, bld. flo w to irritated & dilated capillaries in nasal & sinus cavities  EPHEDRINE  OXYMETAZOLINE  PHENYLEPHRINE  TETRAHYDROZOLINE o Action: cause vasocontriction = edema, inflammation of nasal membranes mostly applied topically (sprays),fast acting o Ix: common cold, sinusitis, allergic rhinitis o CIx^Cautions: lesion / erosion in the mucous that could lead to systemic absorption, glaucoma, hypertension. 75. o Adverse effects: local stinging, burning sensation. If used for >5days can lead to rebound congestion o Nsg. Implementation: o Proper administration of meds & positioning (parkinsons position, proetts position) o Safety measures (dizziness, sedation) o Drug drug interaction (OTC drug) o Oral Decongestants po drugs for Mx/Tx of nasal congestion rel. to common cold, pain reliever & decongestant in otitis media  DECOLGEN  DECOFED  DORCOL 76. o Action: shrinks the nasal mucous membranes by stimulating the alpha adrenergic receptors in nasal cavity = dec. in size & drainage of sinuses = improve airflo w.


o o o o o o o o

CIx^Cautions: glaucoma, hypertension. Adverse effects: rebound congestion, anxiety, restless, tremors, hypertension, arrythmias, sweating, pallor. Nsg. Implementation: Drug drug interaction Safety measures if (CNS effects occurs) Monitor PR, BP etc. Shld not be used longer than 7days Patient education Topical Nasal Steroids decongestants used for thx of allergic rhinitis. Action: topical anti inflammatory = blocks inflammatory reaction. Ix: allergic rhinitis CIx^Cautions: acute Infections, avoid exposure to airborne infection (chickenpox, measles) Adverse effects: local burning, stinging, irritation, dryness of mucosa, headache. Nsg. Implementation Clear nasal passages prior to drug administration Position px properly (parkinsons & proetts) Monitor px for devt of acute infection Thorough teaching for px ANTIHISTAMINES relieves respiratory symptoms & treat allergies BENADRYL- PHENERGAN CLARITINE MECLIZINE CELESTAMINE Action: blocks histamine 1 & its effect = relief for itchy eyes s welling, congestion 7 drippy nose. Also has some anticholinergic effects. Ix: seasonal perrinnial allergic rhinitis allergic conjunctivitis, uncomplicated urticaria, angioedema, amelioration of allergic reactions during BT, anaphylactic reactions. CIx^Cautions: pregnancy, lactation ^ renal, hepatic, CV px c arrythmia (prolonged QT interval) Adverse effects: dro wsiness, sedation. Anticholinergic effect: dryness of the mouth, GI upset, Nausea, dysuria, itching, dry skin. Nsg. Implementation: Administer drug on empty stomach ( 1hr ac, 2hr pc) Encourage having( sugarless) candies / lozenges to dec. dry mouth effect. Increase fluid intake unless CIx Provide skin care regiment (prevent dry skin S/Sx) Avoid intake of alcohol (sedation prec.)

77.
o o o o o o o o o o

78.
o    o o o o

79.
o o o o o o

80. EXPECTORANTS liquefy secretions in the resp. tract, reduces viscosity, easy to cough it out.  GUAIFENESINE  GLYCERYL GUACUOLATE o Action: enhances the output of resp. tract fluids = dec. adhesiveness = easier movements of less viscous secretions. o Ix : dry non productive cough, excessive mucus in the resp. tract, common cold, acute bronchoitis, influenza o Adverse effects: N & V, headache, rash, o Nsg. Implementation: o Caution px ( drug shld. Not be used > 7days o Advise small frequent feeding if px is taking this drug o Avoid driving or other tasks that needs coordination o Do not overdose 81. o MUCOLYTICS - breaks do wn mucus in order cough out thick tenacious secretions. (inhalation / nebulization, p.o., i.v.)  ACETYLCYSTEINE can also be antidote (acetaminophen poisoning)  MUCOMYST o Ix: COPD, cystic fibrosis, PTB, atelectasis due to thick mucus production. o Adverse effects: N & V, stomatitis, urticaria, bronchospasm, rhinorrhea. o Nsg. Implementation: o Avoid combining c other drug & dilute c sterile water in neb kit o If acetylcysteine is used, wipe off residue in px face (risk for skin breakdown) o Most mucolytics drugs used in nebs are photo sensitive & must be kept in refrigerator. 82. o BRONCHODILATORS /ANTI ASTHMATICS facilitates respiration & oxygenation by dilating air ways.
o

ZEMAIRA Tx for alpha protease deficiency (hereditary) = sev. emphysema o Ix: bronchial asthma, bronchospasm c COPD o XANTHINES inhibits release of slow reacting substance of anaphylaxis (SRSA) & Histamine  CAFFEINE / CAFFEDRINE  AMINOPHYLLINE / THEOPYLLINE o Ix: relief & prevention of Bronchial Asthma, bronchospasm c COPD. o Adverse effect: Therapeutic level = 10-20ug/ml > normal level = GI upset, Nausea, irritability, tachycardia, seizures, brain damage, death. 83. o Nsg. Implementation: o Administer oral drug c food or milk o Monitor px response to drug o Provide rest & quiet environment o Monitor px & lab exam for toxic level o SYMPATHOMIMETICS dilates bronchi c rate & depth of respiration (BETA 2 SELECTIVE ADRENERGIC AGONIST)  ALBUTEROL / PROVENTIL long acting neb & po > 2 y/o px  BITOLTEROL / TORNALATE long acting neb. >12 y/o  EPHEDRINE for old & young px  EPINEPHRINE / EPIPEN drug of choice in adult & children for acute bronchospasm due to anaphylaxis, CIx in CVD px. o CIx^Cautions: CVD, vascular dse., DM, hyperthyroidism, pregnant & Lactating px. 84. o Adverse effects: Sympathetic effects: HPN, arrythmia o Nsg. Implementation: o Reassure that the chosen drug may have varied effect in px o Advise minimal use only o Teach px to use these drugs 30-60 mins prior to exercise (prevent exercise induced asthma) o Safety measures if CNS effects arises o Anticholinergic bronchodilators for px that cant tolerate (symphatomimetics) might respond to these:  IPRATROPIUM / ATROVENT not as effective compared to  TIOTROPIUM / SPIRIVA - symphatomimietics. maintenance for COPD o Pharmacokinetics: effects 15-30 mins.peaks1-2hrs o CIx^Cautions: allergy,for atropine like S/Sx 85. o Adverse effects: anxiety, nervousness, dizziness, headache, nausea, GI distress, palpitations. o Nsg. Implementation: o Ensure adequate hydration o Encourage the px to void prior to each dose o Provide small frequent meals, sugarless lozenges o Advice px not to drive post drug intake o INHALED STEROIDS very effective Tx for bronchospasm.  BUDESONIDE / SIMBICORT  FLUNISOLIDE / AEROBID  TRIAMCINOLONE / AZMACORT o Action: inflammatory resp. in the air way = a. dec. swelling, b. promote beta drenergic receptor activity_promote smooth Ms relaxation & inhibit bronchoconstriction 86. o Pharmacokinetics: well absorbed in Resp. Tract. Crosses placenta & enters breastmilk. o CIx^Cautions: not for emrgency use (acute asthma attack & status asthmaticus), pregnant & lactating px, ^ active infection of resp. system. o Adverse effects: Irritability, headache, rebound congestion, epistaxis, local infection o Nsg. Implementation: o Do not give drug to acute asthma & status asthma attacks o Taper systemic steroids carefully during transfer to inhaled steroids (adrenal insufficiency c sudden withdrawal) o Have px use decongestants prior using inhaled steroids o Have px rinse mouth post drug inhalation (prevent Gi effects) o Monitor px for S/Sx respiratoty infection o Thorough health teaching 87. o LEUKOTRIENE RECEPTOR ANTAGONIST newer class of drugs. Dev. to specifically act at the site of the problem assoc. c asthma but not for acute asthmatic attacks  ZAFIRLUKAST / ACCOLATE - prophylaxis & chronic Tx of  MONTELUKAST / SINGULAIR bronchial asthma  ZILUETON / ZYFLO - > 12 y/o px


o o o o

Action: blocks production of Leukotrienes D4, E4 (components of SRSA) Pharmacokinetics: rapidly absorbed from GI tract, crosses the placenta & breastmilk CIx^Cautions: allergy, renal & hepatic dse. Pregnant & lactating px Adverse effect: headcahe, dizziness, nausea, generalized pain, fever & infection.

88. Nsg. Implementation: Administer drug on EMPTY stomach Not to be used in Tx of acute asthma attacks Should be take continuously & do not miss dose Urge px to avoid OTC that contains ASPIRIN LUNG SURFACTANTS Surfactant ( naturally occurring compounds or lipoproteins contains lipid & apoproteins that surface tension c/in the alveoli = expansion of alveoli for gas exchange  BERACANT / SURVANTA rescue Tx for infants c RDS;  CALFACTANT / INFASURF - prophylactic Tx for px c high risk  COLFOSCERIL / EXOSURF - in dev. RDS px .  PORACTANT / CUROSURF - rescue Tx for infants c RDS; 89. o Pharmacokinetics: acts immediately into trachea. Metabolized in the lungs o CIx^Cautions: pregnancy & lactating. Usually used as emergency drugs. o Adverse effcets: PDA, interventricular Hge., pneumothorax, hyprbilirubinemia, sepsis due to reaction to lipoprotein or the invasive procedures the px under went. o Nsg. Implementation: o Provide life support during administration o Ensure proper placement of ET tube (bilat. Chest movement, lungs sounds) o Suction infant immediately prior to giving drug but do not suction 2 hrs post administration o Continue other supportive measures o Support & encourage parents of the child. 90. o MAST CELL STABILIZERS Anti asthma & Anti allergy  CROMOLYN / INTAL Tx of Chronic Bronchial Asthma, exercise induced asthma & allergic rhinitis. CIx: acute attack, younger than 2 y/o px  NEDOCROMIL / TILADE / ALOCRIL Mx of mild-mod bronchial asthma. CIx: px less than 12 y/o o Action: Cromolyn: limits release of Histamine by the mast cell in response to inflammation & irritation. Usu. Inhaled from a capsule & takes effect 7days.  Nedocromil: inhibits activity of inflammatory mediators (eosinophils, neutrophils, macrophages, mast cells) = blocking the effect of histamine. o Pharmacokinetics: cromolyn=active in lungs & excreted during exhalation. Nedocromil=excreted unchanged in the urine o CIx^Caution: allergy, Pregnant & lactating px. 91. o Adverse effects: headache, dizziness, nausea, sore throat, dysuria, nasal congestion.
o o o o o o

You might also like