Pharm Exam 3

-lasix
-action: blocks reabsorption of sodium and chloride in ascending loop of henle
-effects: hyponatremia, hypochloremia, dehydration, hypotension, hyperglycemia, hyperuricemia

-action: promotes urine production by blocking reabsorption of sodium and chloride in early segment of distal convoluted tubule
-effects: hyponatremia, hypochloremia, dehydration, hypokalemia, hyperglycemia, hyperuricemia

what are the 2 groups potassium-sparing diuretics divide into?

where does the mechanism of action ofpotassium-sparing diuretics take place?

an example of nonaldosterone antagonist

an example of aldosterone antagonist

action: blocks actions of aldosterone in distal nephron, causes retention of potassium and increased excretion of sodium
effects: hyperkalemia and endocrine effects
direct inhibitor, by blockage of aldosterone

action: disrupts soidum-potassium exchange in distal nephron like spironolactone; direct inhibitor; quicker response
effect: hyperkalemia, N&V, leg cramps, dizziness

action: promotes diuresis by creating an osmotic force w/in lumen of nephron
effects: edema, HA, N&V, F&E imbalance

prevent reabsorption of water, sodium and chloride
increases urine flow

study of movement of blood throughout the circulatory system

receptor specificity:beta1, causes selective beta1-adrenergic receptors --> only indication of HR
effect: tachycardia (effect)

receptor specificity (dopamone, beta1, @high doses it is alpha1)
-increases myocardial contractility, which in turn increases cardiac output
effect: tachycardia, dysrythmias, anginal pain
-shcok is a major indicator for use
-increases cardiac output, therefore increases tissue perfusion

indicated fr HF and control of dysrythmias, can reduce symptoms, increase exercise tolerance and decrease hospitalizations
*exerts positive INOTROPIC action on the heart

what does postive inotropic action mean?

myocardial contractility by inhibiting enzyme (Na+, K+-ATPase). K+ ions compete w/ digoxin for binding to Na+, K+-ATPase. B/c K+ competes w/ digoxin: decrease in K+, increase in binding digoxin + Na+, K+-ATPase. increase in this can produce excessive inhibition of Na+, K+-ATPase which results in toxicity.

digoxin therapeutic range?
what is the level at when there is a risk for toxicity?

symptoms of toxicity with digoxin?

how do you treat toxicity from digoxin?

digoxin's half-life?

indications for use of digoxin?

normal range for potassium?

hypokalemia + diuretics?

hypokalemia + digoxin?

foods high in potassium?

types of angina?

type of angina triggered most often by physical activity. other causes are emotional excitement, large meals, and cold exposure. underlying cause is coronary artery disease (CAD) -- fatty plaque in arterial wall, blood flow reduce, angina result

type of angina that is caused by coronary artery spasm, therefore restricts blood fow to myocardium

type of angina that is caused by severe CAD complicated by vasospasm, platelet aggregation and transient coronary thrmobi or emboli

what are the different ways nitrates can be administered?

what are the side effects of nitrates?

what can happen if nitrates interact with hypotensive drugs?

-vasodilator
-a "cardioselective" agent, produces selective blockade of beta receptors in heart

actions: blocks calcium access to cells therefore causing a decrease in heart contractility and conductivity and leading to a decrease in demand of oxygen
varapamil, nifedipine, dilitazem

assessment made by nurse for CCBs?

-an antidysryhthmias
-class IB (sodium channel blocker), IV
-therapeutic range: 1.5-5 mcg/mL
-accelerates repolarization
-used only for ventricular dysryhthmias (limited to ST therapy of ventricular dysryhthmias)

-an antidysryhthmia
-active against a variety of ventricular and superventricular dysrythmias
-class IC agent (sodium channel blocker)
-prodysrhythmic actions: can intensify exisiting dysryhthmias or provoke new ones
-decreases cardiac conduction and increases effective refractory period

-an antidysryhthmia
-class IB agent (sodium channel blocker)
-delays repolarization
-produces dose-dependent decrease in sodium an potassium conduction, thereby a decrease in the excitability of myocardial cells

-an antidysryhthmia
- class III (potassium channel blocker)
-delays repolarization
-used only fr STtherapy for severe ventricular dysryhthmias

-1st generation beta blocker (nonselective, blocks beta1&beta2)
- 1st beta blocker to receive widespread clinical use and remains one of the most important beta-blocking agents
- highly lipid soluble so it readily cross cell membrane

action of propanalol?

propanalol uses (reasons to use it)?

what are the effects of propanlol?

-a vasodilator
-indications: hypertension
-effects: excessive hyptension (HA, nausea, palpitations), cyanide poisoning, thiocyanate toxicity (disorientation, psychotic behavior and delirium)

-close relative to thiazide diuretic but w/o the diuretic effects
-indications: hypertension
-effects: reflex tachycardia, hyperglycemia, hyperuricemia, GI effects, salt and water retention

-ends in 'pril'
-uses: indication is hypertension, HF, acute MI, L ventricular dysfunction, diabetic and nondiabetic nephropathy

side effects of ACE inhibitors?

-action: cause dilation of aterioles and veins; decrease in release of aldosterone, increase in renal excretion of sodium and water
-uses: hypertension, HF, diabetic nephropathy, MI, stroke prevention, migraine HA
-effects: angioedema, fetal harm, renal failure

anticoagulant, injection, inactivates both thrombin and factor Xa, effects begin and fade rapidly, aPTT, antidote: protamine

anticoagulant, orally, inhibits synthesis ofclotting factors factor Xa, effects begin slowly and then persist several days, PT, antidote: vitamin K

INR

PT

aPTT

-ends in 'ase'
-removes thrombi that have already formed
-action: promote conversion of plaminogen to plasmin

major complication for thrombolytics?

side effects of thrombolytics?

-a cholesterol reducing agent
-lowers LDL and total cholestrol
-action: inhibits HMG-CoA reductase hepatocytes synthesize more HMG-CoA reductase, then cholesterol synthesis is largely restored to premature levels
-labs: LDL, VLDL, triglycerides, liver and renal tests
-effects: uncommon; typically rash, HA

-a cholesterol reducing agent
-increases HDL levels
-action: decreases production of VLDLs
-effects: flushing, itching, gastric upset, N&V, diarrhea, liver injury, hyperglycemia
-labs: liver function tests

-a cholesterol reducing agent
-decreases LDL cholesterol levels
-action: absorbs and combines w/ bile acid to frm insoluble complex that is excreted through feces
-labs: fasting LDL, HDL, total cholesterol, triglycerides, electrolytes
-effects: constipation (main), bloating, indigestion, nausea, decrease in fat absorption

-a cholesterol reducing agent
- decreases triglyceride levels
-actions: interacts w/ specific receptor subtype, increases syntehesis of LPL and decreases production of apolipoprotein C-III
-labs: PTT
-effects: gallstones, myopathy, liver injury

risk factors fr elevated cholesterol?

drugs for hypothyroidism?

drugs for hyperthyroidism?

regular insulin (humulin R)
onset?
peak?
duration?

Lispro (humalog, rapid acting)
onset?
peak?
duration?

NPH (intermediate, humulin N)
onset?
peak?
duration?

Glargine (lantus, long acting)
onset?
peak?
duration?

-an oral hypoglycemic
-action: promotes insulin secretion by the pancreas; may alson increase tissue response to insulin
-pt teaching: only for type 2

-oral hypoglycemic
-action: inhibits CHO digestion and absorption, thereby decreasing the postpradinal rise in blood glucose
-pt teaching: type 2 w/ hyperglycemia that is not controlled

-oral hypoglycemic
-action: decreases insulin resistance, and thereby increases glucose reuptake by muscle and decrease glucose production by the liver
-pt teaching: only for type 2, can expand blood volume, causes edema, poses a risk for pts with HF