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100 Cards in this Set

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cardiovascular therapy: Changes in CO affect two major pathways?
1. Carotid sinus firing, sympa discharge

2. Renal blood flow, renin-ang pathway
cardiovascular therapy: What is the effect of the following drugs:

1. Positive inotropic drugs
2. Beta blockers
3. Ace inhibitors
4. AII antagonists
5. Vasodilators and
6. Diuretics
1. Increases cardiac output
2. Inhibit renin release.
3. Inhibit ACE
4. Inhibits effects of AngII including increasing the preload, increasing the afterload and remodelling.
5. Decrease the preload and afterload.
6. Decrease the preload and afterload
antihypertensive drugs: What are the adverse effects of these two diueretics: hydrochlorothiazide, loop diuretics
1. Hypokalemia, hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia (HyperGLUC)

2. Hypokalemia, met alk, hypotension, ototoxicity
antihypertensive drugs: These drugs belong to what class?
clonidine, methyldopa, ganglionic blockers, reserpine, guanethidine, prazosin, beta blockers?
sympathoplegics
antihypertensive drugs: Adverse effects of clonidine?
(alpha2 agonist)

dry mouth, sedation, severe rebound HTN
antihypertensive drugs: Adverse effects of methyldopa?
sedation, positive coombs test

is safe to use for HT during pregnacy
antihypertensive drugs: Adverse effects of ganglionic blockers?
orthostatic HTN, blurred vision, constitpation, sexual dysfuncction
antihypertensive drugs: Adverse effects of reserpine?
sedation, depression, nasal stuffiness, diarrhea
antihypertensive drugs: adverse effects of beta blockers?
impotence, asthma, cardiovascular, cns
antihypertensive drugs: Adverse effects of guanethidine?
orthostatic and exercise Hypotension, sex dysfxn, diarrhea
antihypertensive drugs: Adverse effects of prazosin?
1st dose orthostatic hypotension, Syncope, GOOD effect on LDL

(dizziness, headache)
antihypertensive drugs: The following belong to what class...?

hydralazine, minoxidil, nifedipine, verapamil, nitroprusside
vasodilators
antihypertensive drugs: which one causes lupus like syndrome? What are its other toxicities?
hydralazine (arterial selective)

nausea, headache, reflex tachycardia, angina, salt retention
antihypertensive drugs: adverse effets of minoxidil?
What are its MOA and other uses?
hypertrichosis (hair growth - think Rogaine with minoxidil!) AND pericardial effusion

(reflex tachycardia, angina, salt retention)

MOA: opens K channels--> hyperpolarization of smoothe muscle; used for severe HT and male pattern baldness
antihypertensive drugs: Side effects of nifedipine, verapamil?
dizziness, flushing, constipation, nausea
which antihypertensive drug causes Cyanide toxicity?
nitroprusside, releases CN

also causes orthostatic HT
antihypertensive drugs: Adverse effects of ACE-I Captorpil?
C: cough, A: angioedema, P: proteinuria, T: taste changes, O: hypOtension, P: pregnancy problems like fetal renal damage, R: rash, I: increased renin, L: lower angiotensin.

Also hyperkalemia
cuases an accumulation of Bradykinin which leads to cough
antihypertensive drugs: Losartan is a ----------- R-Inhibitor? With ____-toxicity and ____kalemia
angiotensin II, fetal renal, hyper
Hydralizine: Which two anti-HTN drugs do you use with B blockers to prevent reflex tachycardia, and with diuretics to block salt retention?
hydralizine, minoxidil
Hydralizine (Nesiritide, Isosbridenitrate): mechanims and clinical use?
increase cGMP --> smooth muscle relaxation.
Vasodilates arteries > veins; Reduces afterload.

Used for severe HTN or CHF
What are the 3 Calcium channel blockers used for CV therapy and what is their MOA?
Nifedipine, Verapamil, Diltiazem

block of voltage dependednt L type Ca Channels of Cardiac and smooth muscle --> reduced muscle contractility
Calcium channel blockers, name three: Rank their effects on vascular smooth muscle ad on the heart.
smooth muscle nifed> diltia > verapamil

heart: vera> diltia> nifedepine
Nifedipine, Verapimil, and Diltiazem: What is their use and toxicity?
HTN, angina, arrythmias (not nifedipine)

Cardiac depression and Constipation
Name the 3 ACE inhibitors used in CV therapy

What is Losartan?
captopril, enalapril, lisinopril

Losartan is a Ang II receptor antagonist. It does NOT cause cough.
WHat is the mechanim of the ACE inhibitors considering bradykinin and renin release?
inhibit ACE reducing the levels of ang II, preventing the inactivation of bradykinin. Renin release is increased to to loss of feedback inhibition
What are the clinical uses of the ACE inhibitors?
HTN, CHF, diabetic renal disease
Diuretics- site of action: What is the site of action of
1. Acetazolamide
2. Osmotic agents
3. Loop agents
4. Thiazides
5. Potassium sparing
6. ADH antagonists
1. PCT
2. PCT, thin desc limb, CD
3. Thick ascending limb
4. Distal conv tubule
5. DCT a bit later
6. CD in inner medulla
Diuretics: How does mannitol work?
increase tubular fluid osmolarity, producing increased urine flow
Mannitol: what is the use and toxicity?
Use: Decrease intracranial/intraocular pressure.

Toxicity - pulmonary edema, DEHYDRATION. Contraindicated in anuria, CHF
Acetazolamide: Is a ______inhibitor. Causes ______diuresis and _____ in total body HC03 stores.
Carbonic anhydrase, self-limited NaHCO3, reduction.
Acetazolamide: What electrolye disturbace does it treat? Does it cause?
treats met alk, causes in toxicity hyperchloremic met acidosis. ACIDazolamide caues ACIDosis.
Acetazolamide: Other toxicity?
neuropathy, NH3 toxicity, sulfa allergy
Acetazolamide: uses?
glaucoma, urinary alk, met alk, altitude sickeness
Furosemide: This sulfonamide loop diuretic inhibits _______cotransport
NA, K, 2CL
Furosemide: Furosemide also works by?
abolishes hypertonicit y of medulla, prevent concentration of urine. Increase Caexcertion. Loops Lose calcium
Furosemide: The three uses for this loop diuretic?
edematous states, htn, hypercalcemia
Furosemide: Toxicities?
ototoxicity, hypokalemia, dehydration, allergy, nephritis interstitial, gout

OH DANG!!
Ethacrynic Acid: How is this drug different from furosemide? And how does that affect its use?
Although both have the same action, ethacrynic is a phenoxyacetic acid derivative not a sulfonamide. Therefore use this drug when you are allergic to sulfa.
What loop diuretic can be used for hyperuricemia, acute gout?
ethacrynic acid, but never used to treat gout
What are the clinical uses of Hydrochlorathiazide? What are its toxicities and CIs?
HTN, CHF, NEPHROGENIC DI

HyperGLUC, Sulfa Allergy, INC digoxin toxicity, CI in Diabetics
Hydrochlorothiazide: Hydrochlorothiazide is a thiazide diuretic that inhibits the reabsorption of ----- in the ---- tubule
NaCl; early distal tubule
Hydrochlorothiazide: Does hydrochlorothiazide increase or decrease the excretion of calcium ion?
decrease
Hydrochlorothiazide: A toxic dose of hydrochlorathiazide will do what to the blood levels of these electrolites: potassium, sodium, glucose, lipid, uric acid, calcium
hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC)
K+-sparing diuretics: Spironolactone is a competitive antagonist to the --- receptor in the ---- tubule
aldosterone; cortical collecting tubule

**Spironolactone is K sparing diuretic shown to decrease the morbidity and mortality in CHF patients; its usually used with ACE inhibitors, must watch for HYPERkalemia**
K+-sparing diuretics: Name two K+-sparing diuretics that block Na+ channels in the cortical collecting duct
Triamterine and amiloride
K+-sparing diuretics: Besides causing hyperkalemia, a toxic dose of spironolactone will cause this endocrine effect
Gynecomastia (antiandrogen effect)
K+-sparing diuretics: Name three K+-sparing diuretics. What are their Clinical Uses?
Spironolactone, Triamterene, Amiloride (The K+ STAys.)

Hyperaldosteronism, K+ depletion, CHF
Amilioride/ Triamteride--> Lithium induced DI
Diuretics: electrolye exchange: Diuretics are classified as carbonic anhydrase inhibitors, loop diuretics, thiazides, and K+-sparing diuretics. Which of these causes in increase in urine NaCl?
All of them!
Diuretics: electrolye exchange: Which types of diuretucs increase urine K+?
All except K+-sparing diuretics. Carbonic anhydrase inhibitors, loop diuretics, thiazides.
Diuretics: electrolye exchange: Do carbonic anhydrase inhibitors increase or decrease blood pH?
Decrease, cause acidosis
Diuretics: electrolye exchange: Do K+-sparing diuretics cause acidosis or alkalosis?
Acidosis, decreases pH
Diuretics: electrolye exchange: Do loop diuretics cause acidosis or alkalosis?
Alkalosis, increases pH
Diuretics: electrolye exchange: Do thiazide diuretics cause an increase or decrease in blood pH?
Increase, cause alkalosis
Diuretics: electrolye exchange: Do loop diuretics increase or decrease levels of urine calcium ion?
Increase
Diuretics: electrolye exchange: Do thiazide diuretics increase or decrease levels of urine calcium ion?
Decrease
Antianginal therapy: Name the determinants of the level of myocardial oxygen consumption
There are five: end diastolic volume, blood pressure, heart rate, contractility, ejection time
Antianginal therapy: Do nitrates affect preload or afterload?
preload
Antianginal therapy: Do Beta-blockers affect preload or afterload?
afterload
Antianginal therapy: What is the effect of nitrates on: diastolic volume, blood pressure, contractility, heart rate, ejection time?
decrease EDV, decrease BP, increase contractility (reflex response), increase HR (reflex response), decrease ejection time
Antianginal therapy: What is the effect of Beta-blockers on: diastolic volume, blood pressure, contractility, heart rate, ejection time?
increase EDV, decrease BP, decrease contractility, decreased HR, increase ejection time
Antianginal therapy: The effects of using nitrates and Beta-blockers together will: a) decrease myocardial oxygen demands by the same amount as using either alone, b) decrease myocardial oxygen demands by an amount greater than if each were used alone, or c) have no effect on myocardial oxygen demand
b) Decrease myocardial oxygen demands by an amount greater that if each were used alone
Antianginal therapy: Nifedipine blocks -- channels
calcium
Antianginal therapy: In its effects on myocardial oxygen consumption, is Nifedipine similar to Nitrates or B-blockers?
Nitrates (Nifedipine is similar to Nitrates)
Antianginal therapy: In its effects on myocardial oxygen consumption, is Verapamil similar to Nitrates or B-blockers?
B-blockers
Nitroglycerine, isosorbide dinitrate: Dose nitroglycerin dilate arteries or veins more?
Veins>>arteries
Nitroglycerine, isosorbide dinitrate: Does nitroglycerin increase or decrease cGMP in smooth muscle?
Increase
Nitroglycerine, isosorbide dinitrate: In industrial exposure to nitroglycerine, weekend withdrawal is characterized by which three symptoms?
Tachycardia, dizziness , and headache ("Monday disease")
Nitroglycerine, isosorbide dinitrate: Toxic dosage of nitroglycerine causes which three symptoms?
Tachycardia, hypotension, headache
Cardiac drugs: sites of action: Digitalis has its action on which cell membrane transporter?
Na/K ATPase
Cardiac drugs: sites of action: Ryanodine has its action on which channel?
Calcium release channel in the sarcoplasmic receptor
Cardiac drugs: sites of action: Calcium enters cardiac cells through which channel?
Voltage-gated calcium channel
Cardiac drugs: sites of action: Cytoplasmic calcium concentrations in cardiac cells can be decreased by sequestering calcium in the sarcoplasmic reticulum. Calcium enters the SR through which transporter?
Calcium pump in the wall of the SR
Cardiac drugs: sites of action: Calcium channel blockers have their effect on which calcium transporters?
Voltage-gated calcium channel
Cardiac Glycosides: What is Digoxins MOA?
Inhibits the Na/K ATPase of the cardiac cell membrane, causing and INC in intracellular Na. The Na/Ca antiport does not fxn causing an INC in intracellular Ca ---> Increase Ionotropy
Cardiac Glycosides: What other conditions have an effect on digoxin toxicity? What is the antidote to Dig toxicity?
Dig tox is INC by renal failure, hypokalemia, and quinidine

To tx, slowly normalize k+; Lidocaine, cardiac pacer, anti-dig Fab fragments
Cardiac Glycosides: Name two ECG changes ellicited by digoxin administration
There are 4: increase PR, decrease QT, scooping of ST segment, T-wave inversion
Cardiac Glycosides: Name three symptoms of digoxin toxicity
Nausea, vomiting, diarrhea, blurry vision, arrhythmia
Cardiac Glycosides: Which K+ imbalance potentiates the effects of digoxin?
hypokalemia
Antiarrhythmics- Na+ channel blockers (classI): Which phase of the cardiac action potential do antiarrhythmics decrease the slope of?
Phase 4 depolarization
Antiarrhythmics- Na+ channel blockers (classI): Name the Class 1A antirarrythmics.
Quinidine, Amiodarone, Procainamide, Disopyramide

"Queen Amy Proclaims Diso's pyramid."
Antiarrhythmics- Na+ channel blockers (classI): Do class 1A antiarrhythmics increase or decrease the effective refractory period, AP duration, and QT interval?
Increase ERP, increase AP duration, increase QT interval
Antiarrhythmics- Na+ channel blockers (classI): What do class 1B antiarrhythmics do to the AP duration?
Decrease AP duration
Antiarrhythmics- Na+ channel blockers (classI): Name the drugs in Class 1B?
LIDOCAINE, mexiletine, tocainide

they are given IV and have aprefernece for abnormal/ischemic cardiac tissue; they are especially useful POST MI and in digitalis induce arrythmias
Antiarrhythmics- Na+ channel blockers (classI): Name the drugs in Class 1C.
FLECAINAMIDE, encainide, propafenone

they are usually used as a last resort in refractory tachyrarrythmias; they are proarrythmic (esp. post MI)
Antiarrhythmics- Na+ channel blockers (classI): What effect do class 1C antiarrhythmics have on the AP duration?
No effect!
Antiarrhythmics- Beta-blockers (classII): What are there MOA?
decreases cAMP --> DEC Ca++ currents. Suppress abnormal pacemakers by DEC the slope of the phase 4; DEC SA and AV nodal activity (AV node esp sensitive)
Antiarrhythmics- Beta-blockers (classII): What is esmolol used for specifically?
acute SVTS, its very short acting
Antiarrhythmics- Beta-blockers (classII): How do they affect the slope os the phase 4 and the PR interval?
DEC the slope of phase 4
INC the PR interval
Antiarrhythmics- Beta-blockers (classII): What are their toxicities?
Impotence, exacerbation of asthma, CV efx, CNS efx; may mask the signs of HYPOglycemia
Antiarrhythmics- Beta-blockers (classII): Is esmolol a short- or long-acting beta blocker?
short-acting
Antiarrhythmics- K+ channel blockers (class III): Does amiodarone increase or decrease AP duration?
Increase (K+ channel blocker)
Antiarrhythmics- K+ channel blockers (class III): Does sotalol increase or decrease the effective refractory period?
Increase (K+ channel blocker)
Antiarrhythmics- K+ channel blockers (class III): Does bretylium increase or decrease the QT interval?
Increase (K+ channel blocker)
Antiarrhythmics- K+ channel blockers (class III): Name a symptom of sotalol toxicity.
Torsades de pointes (K+ channel blocker)
Antiarrhythmics- K+ channel blockers (class III): Name three of the symptoms of amiodarone toxicity.
Pulmonary fibrosis, corneal deposits, hepatoxicity, skin deposits resulting in photodermatitis, neurologic effects, constipation, bradychardia, heart block, CHF, hypothyroidism/hyperthyroidism. (Therefore, should check PFTs, LFTs, and TFTs)
Antiarrhythmics- Ca2+ channel blockers (class IV): Does verapamil increase or decrease the conduction velocity of the AV nodal cells?
Decrease (calcium channel blocker)
Antiarrhythmics- Ca2+ channel blockers (class IV): How does diltiazem affect the effective refractory period and the PR interval?
Increases ERP, increases PR (calcium channel blocker)
Other antiarrhythmics: Name a potential use of Mg+ to treat arrhythmias.
To treat torsades de pointes and digoxin toxicity
Other antiarrhythmics: Name a potential use of K+ to treat arrhythmias.
Depress ectopic pacemakers, especially in digoxin toxicity
Other antiarrhythmics: Name a use of adenosine in treating arrhythmias.
To diagnose and abolish AV nodal arrhythmias.