Fa Pharm: Cardiovasc Therapy

Front 1

cardiovascular therapy: Changes in CO affect two major pathways?

Back 1

1. Carotid sinus firing, sympa discharge

2. Renal blood flow, renin-ang pathway

Front 2

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

Back 2

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

Front 3

antihypertensive drugs: What are the adverse effects of these two diueretics: hydrochlorothiazide, loop diuretics

Back 3

1. Hypokalemia, hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia (HyperGLUC)

2. Hypokalemia, met alk, hypotension, ototoxicity

Front 4

antihypertensive drugs: These drugs belong to what class?
clonidine, methyldopa, ganglionic blockers, reserpine, guanethidine, prazosin, beta blockers?

Back 4

sympathoplegics

Front 5

antihypertensive drugs: Adverse effects of clonidine?

Back 5

(alpha2 agonist)

dry mouth, sedation, severe rebound HTN

Front 6

antihypertensive drugs: Adverse effects of methyldopa?

Back 6

sedation, positive coombs test

is safe to use for HT during pregnacy

Front 7

antihypertensive drugs: Adverse effects of ganglionic blockers?

Back 7

orthostatic HTN, blurred vision, constitpation, sexual dysfuncction

Front 8

antihypertensive drugs: Adverse effects of reserpine?

Back 8

sedation, depression, nasal stuffiness, diarrhea

Front 9

antihypertensive drugs: adverse effects of beta blockers?

Back 9

impotence, asthma, cardiovascular, cns

Front 10

antihypertensive drugs: Adverse effects of guanethidine?

Back 10

orthostatic and exercise Hypotension, sex dysfxn, diarrhea

Front 11

antihypertensive drugs: Adverse effects of prazosin?

Back 11

1st dose orthostatic hypotension, Syncope, GOOD effect on LDL

(dizziness, headache)

Front 12

antihypertensive drugs: The following belong to what class...?

hydralazine, minoxidil, nifedipine, verapamil, nitroprusside

Back 12

vasodilators

Front 13

antihypertensive drugs: which one causes lupus like syndrome? What are its other toxicities?

Back 13

hydralazine (arterial selective)

nausea, headache, reflex tachycardia, angina, salt retention

Front 14

antihypertensive drugs: adverse effets of minoxidil?
What are its MOA and other uses?

Back 14

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

Front 15

antihypertensive drugs: Side effects of nifedipine, verapamil?

Back 15

dizziness, flushing, constipation, nausea

Front 16

which antihypertensive drug causes Cyanide toxicity?

Back 16

nitroprusside, releases CN

also causes orthostatic HT

Front 17

antihypertensive drugs: Adverse effects of ACE-I Captorpil?

Back 17

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

Front 18

antihypertensive drugs: Losartan is a ----------- R-Inhibitor? With ____-toxicity and ____kalemia

Back 18

angiotensin II, fetal renal, hyper

Front 19

Hydralizine: Which two anti-HTN drugs do you use with B blockers to prevent reflex tachycardia, and with diuretics to block salt retention?

Back 19

hydralizine, minoxidil

Front 20

Hydralizine (Nesiritide, Isosbridenitrate): mechanims and clinical use?

Back 20

increase cGMP --> smooth muscle relaxation.
Vasodilates arteries > veins; Reduces afterload.

Used for severe HTN or CHF

Front 21

What are the 3 Calcium channel blockers used for CV therapy and what is their MOA?

Back 21

Nifedipine, Verapamil, Diltiazem

block of voltage dependednt L type Ca Channels of Cardiac and smooth muscle --> reduced muscle contractility

Front 22

Calcium channel blockers, name three: Rank their effects on vascular smooth muscle ad on the heart.

Back 22

smooth muscle nifed> diltia > verapamil

heart: vera> diltia> nifedepine

Front 23

Nifedipine, Verapimil, and Diltiazem: What is their use and toxicity?

Back 23

HTN, angina, arrythmias (not nifedipine)

Cardiac depression and Constipation

Front 24

Name the 3 ACE inhibitors used in CV therapy

What is Losartan?

Back 24

captopril, enalapril, lisinopril

Losartan is a Ang II receptor antagonist. It does NOT cause cough.

Front 25

WHat is the mechanim of the ACE inhibitors considering bradykinin and renin release?

Back 25

inhibit ACE reducing the levels of ang II, preventing the inactivation of bradykinin. Renin release is increased to to loss of feedback inhibition

Front 26

What are the clinical uses of the ACE inhibitors?

Back 26

HTN, CHF, diabetic renal disease

Front 27

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

Back 27

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

Front 28

Diuretics: How does mannitol work?

Back 28

increase tubular fluid osmolarity, producing increased urine flow

Front 29

Mannitol: what is the use and toxicity?

Back 29

Use: Decrease intracranial/intraocular pressure.

Toxicity - pulmonary edema, DEHYDRATION. Contraindicated in anuria, CHF

Front 30

Acetazolamide: Is a ______inhibitor. Causes ______diuresis and _____ in total body HC03 stores.

Back 30

Carbonic anhydrase, self-limited NaHCO3, reduction.

Front 31

Acetazolamide: What electrolye disturbace does it treat? Does it cause?

Back 31

treats met alk, causes in toxicity hyperchloremic met acidosis. ACIDazolamide caues ACIDosis.

Front 32

Acetazolamide: Other toxicity?

Back 32

neuropathy, NH3 toxicity, sulfa allergy

Front 33

Acetazolamide: uses?

Back 33

glaucoma, urinary alk, met alk, altitude sickeness

Front 34

Furosemide: This sulfonamide loop diuretic inhibits _______cotransport

Back 34

NA, K, 2CL

Front 35

Furosemide: Furosemide also works by?

Back 35

abolishes hypertonicit y of medulla, prevent concentration of urine. Increase Caexcertion. Loops Lose calcium

Front 36

Furosemide: The three uses for this loop diuretic?

Back 36

edematous states, htn, hypercalcemia

Front 37

Furosemide: Toxicities?

Back 37

ototoxicity, hypokalemia, dehydration, allergy, nephritis interstitial, gout

OH DANG!!

Front 38

Ethacrynic Acid: How is this drug different from furosemide? And how does that affect its use?

Back 38

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.

Front 39

What loop diuretic can be used for hyperuricemia, acute gout?

Back 39

ethacrynic acid, but never used to treat gout

Front 40

What are the clinical uses of Hydrochlorathiazide? What are its toxicities and CIs?

Back 40

HTN, CHF, NEPHROGENIC DI

HyperGLUC, Sulfa Allergy, INC digoxin toxicity, CI in Diabetics

Front 41

Hydrochlorothiazide: Hydrochlorothiazide is a thiazide diuretic that inhibits the reabsorption of ----- in the ---- tubule

Back 41

NaCl; early distal tubule

Front 42

Hydrochlorothiazide: Does hydrochlorothiazide increase or decrease the excretion of calcium ion?

Back 42

decrease

Front 43

Hydrochlorothiazide: A toxic dose of hydrochlorathiazide will do what to the blood levels of these electrolites: potassium, sodium, glucose, lipid, uric acid, calcium

Back 43

hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC)

Front 44

K+-sparing diuretics: Spironolactone is a competitive antagonist to the --- receptor in the ---- tubule

Back 44

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**

Front 45

K+-sparing diuretics: Name two K+-sparing diuretics that block Na+ channels in the cortical collecting duct

Back 45

Triamterine and amiloride

Front 46

K+-sparing diuretics: Besides causing hyperkalemia, a toxic dose of spironolactone will cause this endocrine effect

Back 46

Gynecomastia (antiandrogen effect)

Front 47

K+-sparing diuretics: Name three K+-sparing diuretics. What are their Clinical Uses?

Back 47

Spironolactone, Triamterene, Amiloride (The K+ STAys.)

Hyperaldosteronism, K+ depletion, CHF
Amilioride/ Triamteride--> Lithium induced DI

Front 48

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?

Back 48

All of them!

Front 49

Diuretics: electrolye exchange: Which types of diuretucs increase urine K+?

Back 49

All except K+-sparing diuretics. Carbonic anhydrase inhibitors, loop diuretics, thiazides.

Front 50

Diuretics: electrolye exchange: Do carbonic anhydrase inhibitors increase or decrease blood pH?

Back 50

Decrease, cause acidosis

Front 51

Diuretics: electrolye exchange: Do K+-sparing diuretics cause acidosis or alkalosis?

Back 51

Acidosis, decreases pH

Front 52

Diuretics: electrolye exchange: Do loop diuretics cause acidosis or alkalosis?

Back 52

Alkalosis, increases pH

Front 53

Diuretics: electrolye exchange: Do thiazide diuretics cause an increase or decrease in blood pH?

Back 53

Increase, cause alkalosis

Front 54

Diuretics: electrolye exchange: Do loop diuretics increase or decrease levels of urine calcium ion?

Back 54

Increase

Front 55

Diuretics: electrolye exchange: Do thiazide diuretics increase or decrease levels of urine calcium ion?

Back 55

Decrease

Front 56

Antianginal therapy: Name the determinants of the level of myocardial oxygen consumption

Back 56

There are five: end diastolic volume, blood pressure, heart rate, contractility, ejection time

Front 57

Antianginal therapy: Do nitrates affect preload or afterload?

Back 57

preload

Front 58

Antianginal therapy: Do Beta-blockers affect preload or afterload?

Back 58

afterload

Front 59

Antianginal therapy: What is the effect of nitrates on: diastolic volume, blood pressure, contractility, heart rate, ejection time?

Back 59

decrease EDV, decrease BP, increase contractility (reflex response), increase HR (reflex response), decrease ejection time

Front 60

Antianginal therapy: What is the effect of Beta-blockers on: diastolic volume, blood pressure, contractility, heart rate, ejection time?

Back 60

increase EDV, decrease BP, decrease contractility, decreased HR, increase ejection time

Front 61

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

Back 61

b) Decrease myocardial oxygen demands by an amount greater that if each were used alone

Front 62

Antianginal therapy: Nifedipine blocks -- channels

Back 62

calcium

Front 63

Antianginal therapy: In its effects on myocardial oxygen consumption, is Nifedipine similar to Nitrates or B-blockers?

Back 63

Nitrates (Nifedipine is similar to Nitrates)

Front 64

Antianginal therapy: In its effects on myocardial oxygen consumption, is Verapamil similar to Nitrates or B-blockers?

Back 64

B-blockers

Front 65

Nitroglycerine, isosorbide dinitrate: Dose nitroglycerin dilate arteries or veins more?

Back 65

Veins>>arteries

Front 66

Nitroglycerine, isosorbide dinitrate: Does nitroglycerin increase or decrease cGMP in smooth muscle?

Back 66

Increase

Front 67

Nitroglycerine, isosorbide dinitrate: In industrial exposure to nitroglycerine, weekend withdrawal is characterized by which three symptoms?

Back 67

Tachycardia, dizziness , and headache ("Monday disease")

Front 68

Nitroglycerine, isosorbide dinitrate: Toxic dosage of nitroglycerine causes which three symptoms?

Back 68

Tachycardia, hypotension, headache

Front 69

Cardiac drugs: sites of action: Digitalis has its action on which cell membrane transporter?

Back 69

Na/K ATPase

Front 70

Cardiac drugs: sites of action: Ryanodine has its action on which channel?

Back 70

Calcium release channel in the sarcoplasmic receptor

Front 71

Cardiac drugs: sites of action: Calcium enters cardiac cells through which channel?

Back 71

Voltage-gated calcium channel

Front 72

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?

Back 72

Calcium pump in the wall of the SR

Front 73

Cardiac drugs: sites of action: Calcium channel blockers have their effect on which calcium transporters?

Back 73

Voltage-gated calcium channel

Front 74

Cardiac Glycosides: What is Digoxins MOA?

Back 74

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

Front 75

Cardiac Glycosides: What other conditions have an effect on digoxin toxicity? What is the antidote to Dig toxicity?

Back 75

Dig tox is INC by renal failure, hypokalemia, and quinidine

To tx, slowly normalize k+; Lidocaine, cardiac pacer, anti-dig Fab fragments

Front 76

Cardiac Glycosides: Name two ECG changes ellicited by digoxin administration

Back 76

There are 4: increase PR, decrease QT, scooping of ST segment, T-wave inversion

Front 77

Cardiac Glycosides: Name three symptoms of digoxin toxicity

Back 77

Nausea, vomiting, diarrhea, blurry vision, arrhythmia

Front 78

Cardiac Glycosides: Which K+ imbalance potentiates the effects of digoxin?

Back 78

hypokalemia

Front 79

Antiarrhythmics- Na+ channel blockers (classI): Which phase of the cardiac action potential do antiarrhythmics decrease the slope of?

Back 79

Phase 4 depolarization

Front 80

Antiarrhythmics- Na+ channel blockers (classI): Name the Class 1A antirarrythmics.

Back 80

Quinidine, Amiodarone, Procainamide, Disopyramide

"Queen Amy Proclaims Diso's pyramid."

Front 81

Antiarrhythmics- Na+ channel blockers (classI): Do class 1A antiarrhythmics increase or decrease the effective refractory period, AP duration, and QT interval?

Back 81

Increase ERP, increase AP duration, increase QT interval

Front 82

Antiarrhythmics- Na+ channel blockers (classI): What do class 1B antiarrhythmics do to the AP duration?

Back 82

Decrease AP duration

Front 83

Antiarrhythmics- Na+ channel blockers (classI): Name the drugs in Class 1B?

Back 83

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

Front 84

Antiarrhythmics- Na+ channel blockers (classI): Name the drugs in Class 1C.

Back 84

FLECAINAMIDE, encainide, propafenone

they are usually used as a last resort in refractory tachyrarrythmias; they are proarrythmic (esp. post MI)

Front 85

Antiarrhythmics- Na+ channel blockers (classI): What effect do class 1C antiarrhythmics have on the AP duration?

Back 85

No effect!

Front 86

Antiarrhythmics- Beta-blockers (classII): What are there MOA?

Back 86

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)

Front 87

Antiarrhythmics- Beta-blockers (classII): What is esmolol used for specifically?

Back 87

acute SVTS, its very short acting

Front 88

Antiarrhythmics- Beta-blockers (classII): How do they affect the slope os the phase 4 and the PR interval?

Back 88

DEC the slope of phase 4
INC the PR interval

Front 89

Antiarrhythmics- Beta-blockers (classII): What are their toxicities?

Back 89

Impotence, exacerbation of asthma, CV efx, CNS efx; may mask the signs of HYPOglycemia

Front 90

Antiarrhythmics- Beta-blockers (classII): Is esmolol a short- or long-acting beta blocker?

Back 90

short-acting

Front 91

Antiarrhythmics- K+ channel blockers (class III): Does amiodarone increase or decrease AP duration?

Back 91

Increase (K+ channel blocker)

Front 92

Antiarrhythmics- K+ channel blockers (class III): Does sotalol increase or decrease the effective refractory period?

Back 92

Increase (K+ channel blocker)

Front 93

Antiarrhythmics- K+ channel blockers (class III): Does bretylium increase or decrease the QT interval?

Back 93

Increase (K+ channel blocker)

Front 94

Antiarrhythmics- K+ channel blockers (class III): Name a symptom of sotalol toxicity.

Back 94

Torsades de pointes (K+ channel blocker)

Front 95

Antiarrhythmics- K+ channel blockers (class III): Name three of the symptoms of amiodarone toxicity.

Back 95

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)

Front 96

Antiarrhythmics- Ca2+ channel blockers (class IV): Does verapamil increase or decrease the conduction velocity of the AV nodal cells?

Back 96

Decrease (calcium channel blocker)

Front 97

Antiarrhythmics- Ca2+ channel blockers (class IV): How does diltiazem affect the effective refractory period and the PR interval?

Back 97

Increases ERP, increases PR (calcium channel blocker)

Front 98

Other antiarrhythmics: Name a potential use of Mg+ to treat arrhythmias.

Back 98

To treat torsades de pointes and digoxin toxicity

Front 99

Other antiarrhythmics: Name a potential use of K+ to treat arrhythmias.

Back 99

Depress ectopic pacemakers, especially in digoxin toxicity

Front 100

Other antiarrhythmics: Name a use of adenosine in treating arrhythmias.

Back 100

To diagnose and abolish AV nodal arrhythmias.