Cardio Pharm Flashcards
Diuretics
Overall decrease in blood vessel
increase water excretion
increased sodium
Adverse effects: electrolyte/fluid imbalance, orthostatic hypotension, change in mood, weakness/fatigue
IND: hypertension, CHF
Beta Blockers
decrease HR, force contraction, sympathetic to heart
Adverse effects: bronchodilation, orthostatic hypotension, decrease max exercise capacity, psychotropic effects (depression, libido decrease, lethargy)
other blockers: centrally acting, ganglion, presynaptic adrenergic inhibitors, alpha blockers
IND: angina, arrythmias, heart failure, hypertension, raynauds disease, recovery from MI
Vasodilators
inhibits smooth muscle contracts
Adverse effects: tachycardia, orthostatic hypotension, fluid edema, dizziness/HA, avoid systemic heat
IND: hypertension, heart failure
Renin-angiotensin System drugs adverse effects
adverse effects: dizziness/naseua, allergic reaction/edema, dry cough due to bradykinesia, damage to CV or kidneys, may increase BP
ACE Inhibitor
Angiotensin II converting enzyme inhibitor- prevents ANG II formation= decreased vasocostriction and less vasohypertrophy
Angiontensin II receptor blocker
new drug, milder side effects
blocks receptor=decrease ANG II effect on BV/heart
Renin Blocker
aliskien prevents renin from converting angiotensin into ANG I= no effect of ANG II effect
Calcium channel blocker
stabilizes HR by decreasing Ca entry into smooth muscle
Adverse effects: swollen foot/ankle, orthostatic hypotension, change in HR, increase risk of MI, avoid systemic heat
IND: hypertension, angina, arrythmias
Organic nitrates
administered sublingual or by patch
decrease preload (venous return to heart) decreases postload (blood heart pumps against)
overall decrease in cardiac workload and oxygen demand
Organic nitrates tolerance
patch= decrease effect
discontinuing application may increase effectiveness
prevent tolerance through interval application
Organic nitrates adverse effects
dizziness/HA
orthostatic hypotension
avoid systemic heat
Digitalis Mechanism
autonomic mechanism: decrease HR by stimulating vagus
mechanical: inhibits Na/K pump=increase Na in cell=increase Ca= increase myocardial Ca for contraction
Digitalis Adverse effects
severe effect: fatal
GI problems confusion fatigue depression arrythmias blurred vision
Positive inotropes Mechanism
inhibit phosphodiesterase= prevent cAMP breakdown=increase intracellular Ca for contraction
stimulate dopamine B receptors
Positive inotropes Adverse effects
digitalis just has effective
IV drip
only for acute heart failure
Mechanism of Clot formation
intrinsic: CF XII contacts damaged BV
extrinsic: damaged BV release CF VII
together CF X converts prothrombin into thrombin
thrombin assists fibrinogen form fibrin
Mechanism of clot breakdown
tissue Plasmin activator (tPA) converts plasminogen into plasmin
Anti-coagulants
indicated for DVT
acts rapidly
administered paraenterally
increases effect of anti-thrombin III
Heparin types
unfractionated heparin- unpredictable, IV admin, CF IXa Xa
low molecular weight heparin- predictable, safer, sub Q admin, CF Xa
HIT types
heparin induced thrombocytopenia
type 1=asymptomatic, self resolving
type 2= limb threatening, immunre response to heparin
Oral anticoagulants
inhibit the cycle of vit k conversion to vit k epoxide
Warfin
administered 3-4 times/day to slowly ween into coumadin
warfin use after heparin
Other anticoagulants
direct thrombin inhibitorrs
CF Xa inhibitors
Anti-thrombotics in general
decrease platelet induced clot
Aspirin
prevents formation of PG2 and Thromboxane
men more effective for MI
female more effective for CVA
baby aspirin may be therapeutic: irreversibly inhibit platelets
ADP inhibitors
ADP stimulates platelets, ADP inhibitor inhibits ADP
Glycoprotein inhibitor
GP stims fibrin, GP inhibitor inhibits GP
Thrombolytics
initiates clot break down in coronary arteries
fibrinolytics activation
Use of thrombolytics for MI
no one drug is superior
decreases mortality by 50% in admin within 1hr
effective within 3-12 hours
Use of thrombolytics for CVA
must rule out hemorrhage
effective within 2 hr admin
use of r-TPA
Adverse effects of thrombolytics
hemorrhage
dressing change, manipulation, debridement cautions
Treating clotting deficiency (Hemophilia)
fibrinolytic inhibitors
vit k for new borns
2 types of Hemophilia
type 1= factor VIII replacement
type II= factor IX
2 main drrug to treat Hyperlipidemia
Statin- decreases cholesterol synthesis, increase LDL breakdown, increase HDL, decrease triglyceride
Fibric acid- activates nuclear receptor to affect lipid metabolism
Other drugs to treat hyperlipidemia
niacin- decrease triglyceride
ezetimbe- affect GI lipid absorbtion
bile acid- decreases plasma cholesterol
Antilipd concerns
GI problems
liver/renal toxicity
statin induced myopathy
Statin induced myopathy
decrease cholesterol in muscle
decrease co-enzyme Q10
decrease prenylate protein for gene replication
increase enzyme require to regulate protein
Factors that affect Statin induced myopathy
fixed factors genetic old age female renal/liver disease
modifiable increase in exercise high dose lipophilic drug combining drugs
