Pharmacology test 4 Flashcards
Beta Blockers
Mechanism of action: selectively block beta1-adrenergic receptors in the heart.
Therapeutic effects: slows heart rate and reduces contractility.
Adverse effects: hypotension, bradycardia, hypo/hyperglycemia, and fatigue. Hold if HR <60 and systolic <100. Diabetics need to check CBGs
Nitroglycerin (organic nitrate)
Mechanism of action: relax both arterial and venous smooth muscle, thus decreasing the workload on the heart and lowering myocardial oxygen demand.
Therapeutic effects: Used while in acute angina episode is in progress or just prior to physical activity. If it’s not rapid acting, it is used for maintenance of angina.
Adverse effects: severe headache and hypotension with reflex tachycardia, dizziness. Most side effects diminish after a few doses.
Susceptible to breakdown with UV or sunlight. Must stay in it’s original packaging.
Retaplase/alteplase (Thrombolytics)
Mechanism of action: convert plasminogen to plasmin, which digests the fibrin and dissolves the clot
Therapeutic effects: treatment of stroke due to thrombus, acute MI, DVT, arterial thrombosis, and to clear IV catheters.
Adverse effects: abnormal bleeding, which may occur superficially or internally, and occasionally intracranially.
Things to know: used for ischemic strokes but NOT hemorrhagic stroke because their brain could bleed out.
ACE (Angiotensin-converting enzyme) inhibitors (end in PRIL) Prototype drug: enalapril (Vasotec)
Mechanism of action: decrease blood pressure by reducing angiotensin II and aldosterone levels to produce a significant reduction in blood pressure. Stops angiotensin I from turning into angiotensin II
Therapeutic effects: may be used as mono therapy or in combination with other antihypertensives. Primary use is to treat hypertension.
Adverse effects: angioedema, neutropenia, agranulocytosis. Number 1 side effect: A cough ensues (ACE)
Things to know: Cardio-protective, works on the enzyme in the kidneys, drug of choice for patients with heart failure and HTN
Diltiazem (Calcium channel blocker)
used when beta blockers are not tolerated well by a patient.
Mechanism of action: inhibits the transport of calcium into myocardial cells, reducing cardiac workload and bringing more oxygen to the myocardium.
Adverse effects: headache, dizziness, and edema of the ankles and feet. Abrupt withdrawal my precipitate an acute anginal episode.
Digoxin (Lanoxin) (cardiac glycoside)
Mechanism of action: causes the heart to death more forcefully and more slowly, which improves cardiac output.
Primary use: Increase the contractility or strength of myocardial contraction
Adverse effects: N&V, dysrhythmias (most serious), fatigue, anorexia, and visual disturbances such as seeing halos, a yellow-green tinge, or blurring
Narrow therapeutic index: 0.5-2 is therapeutic >2 is toxic. Take HR for one minute. Rescue med: Digibind. Hypokalemia can cause toxicity. Positive inotropic, negative chronotropic and dromotropic.
Milrinone (Phosphodiesterase inhibitors)
Mechanism of action: Increases myocardial contraction force and increases cardiac output.
Administration: Only given IV for acute, severe HF. Treatment should be limited to 2-3 days. Give fluids
Adverse effects: dysrhythmias (most serious), hypotension, headache, N&V
Hydrochlorothiazide (HydroDiuril) (Thiazide)
Mechanism of action: decreases sodium reabsorption in the kidney tubule, sending more sodium to the urine to be excreted.
Therapeutic effects: mild to moderate hypertension, ascites, edema, heart failure, and nephrotic syndrome.
Adverse effects: dehydration, electrolyte imbalances, and hypokalemia
Heparin (Heplock) (Parenteral anticoagulant)
Mechanism of action: bind to antithrombin III, inactivating several clotting factors and inhibiting thrombin activity, thereby interfering with coagulation cascade and preventing formation or enlargement of clots.
Therapeutic effects: Prevent formation of clots in veins and treat DVT, pulmonary embolism, unstable angina, evolving MI, and thrombosis in high-risk patients. *It has no ability to dissolve existing clots.
Adverse effects: abnormal bleeding and heparin-induced thrombocytopenia (HIT), which results in the opposite effects of excessive bleeding
Administration: IV or subcut, short half life, monitor aPTTs.
Hydralazine (Apresoline) (Direct vasodilators)
Mechanism of action: decrease b/p through direct relaxation of arterial smooth muscle, causing vasodilation
Therapeutic effects: treat severe hypertension and hypertensive emergency.
Adverse effects: sodium and fluid retention, headache, reflex tachycardia, palpitations, flushing, nausea, and diarrhea.
No effects of veins. Works directly on the vessels. *Only used in hypertensive emergencies! Used for hypertensive crisis (MAOIs)
Doxazosin (Cardura) (Alpha1-adrenergic agonist)
Mechanism of action: decrease b/p by dilating arteries and veins (by blocking Alpha 1 receptors), and thus it is capable of causing a rapid, profound fall in b/p.
Therapeutic effects: hypertension
Adverse effects: *orthostatic hypotension, dizziness, nausea, asthenia, headache, hypotension, postural hypotension, and somnolence.
Things to keep in mind: First dose phenomenon, take first dose at night and while resting, after first dose body is better adapted.
Furosemide (Lasix) (Loop diuretic)
Mechanism of action: increase urine output even when blood flow to the kidney is diminished. Blocks reabsorption of sodium and chloride in loop of Henle region of the nephron.
Therapeutic effects: treats acute heart failure and renal failure.
Adverse effects: dehydration, electrolyte imbalances, and hypokalemia
Things to keep in mind: first sign of dehydration in the elderly is confusion. Dehydration S/S: sleepy, dry mucous membranes, tenting, headache.
atorvastatin (Lipitor) (HMG-CoA Reductase Inhibitors)
Mechanism of action: inhibits HMG-CoA reductase, so that the liver makes less cholesterol and increases LDL receptors int he liver cells, removing LDL from he blood.
Therapeutic effect: hypercholesterolemia and reduces the risk of MI and stroke
Adverse effects: headache and GI complaints. A small percentile of patients experience liver damage and rhabdomyolysis.
Things to keep in mind: Pregnancy category X , Most potent med to lower LDL levels, first line therapy
Drug-food interaction: grapefruit juice (lowers the metabolism of the med, increasing the amount of the med in the body, higher chance for toxicity)
Niacin (nicotinic acid)
Mechanism of action: decreases VLDL levels, and, because LDL is synthesized from VLDL, the patient experiences a reduction in LDL levels.
Therapeutic effect: reduces triglycerieds and increases HDL levels.
Adverse effects: Flushing and hot flashes occur in almost every patine. Various uncomfortable intestinal effects, such as nausea, excess gas, and diarrhea, are commonly reported. Hepatotoxicity and gout are also possible.
Things to keep in mind: Small doses of aspirin or NSAIDS taken 30 minutes before Niacin could decrease itching and flushing.
Warfarin (Coumadin)
mechanism of action: inhibits the action of vitamin K, diminishing the synthesis of clotting factors II, VII, IX, and X.
Administration considerations: Often, patients begin anticoagulation therapy with heparin nd are switched to warfarin when their condition stabilizes. When transitioning, the two drugs are administered concurrently for 2 to 3 days because warfarin takes several days to achieve optimum effect. Check INR and PT labs.
INR: between 2 and 3.5 on therapy, 1 if not on therapy
PT: between 10-14 seconds
Therapeutic effects: primarily used to prevent stroke, MI, DVT, and pulmonary embolism.
Adverse effects: Bleeding
Rescue med: Vitamin K
