Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CVS Pharmacology > Drug Therapy Of Heart Failure > Flashcards

Drug Therapy Of Heart Failure Flashcards

1
Q

Treatment of diastolic heart failure

A

BB, verapamil, diuretics (in volume overload), ACEI (to prevent remodeling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Compare compensated & decompensated heart failure

A
  • Inability of heart to pump blood results in dec blood pressure whicha ativates renin-angiotensin system & adrenergic, leading to VC & inc Aldisterone w salt & water retention, inc HR & ventricular hypertrophy, thus compensated heart failure.
  • Persistent activation of adrenergic & renin-angiotensin systems causing inc after & preload on diseased heart , leading ventricular dilation & inc O2 consumption with constant supply, damage of cardiac myocytes. Inc EDV & EDP with dec COP, thus it is decompensated HF.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Mention drugs used to dec preload in AHF & CHF

A

CHF, ACEI, ARBs, nitrates, loop diuretics

AHF, nitroprusside, nitrates, loop diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Mention drugs used to dec afterload in AHF & CHF

A

CHF, hydralazine, ACEI, ARBs

AHF, nitroprusside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mention drugs which inc contractility in AHF

A

Dopamine
Dobutamine
Inamrinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Mention drugs which protect heart & dec mortality in CHF

A 
Beta bloccker (MBC)
Spironolactone/eplerenone
(ACEI/ARBs/ARNI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Compare hydralazine & nitrates

A

H: causes arteriodilatation, dec afterload, inc COP, improved symptoms of low COP.
N: cause venodilation, dec preload & venous return, dec psystemuc, pulmonary conhpgestion, improve congestive symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe mechanism of action of ACEI

A

Inhibit ACE which converst ang I to ang II and breaks down bradykinin
Leading to dec ang II & inc bradykinin w inc in vasodilator PG & NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mention advantages if ACEI

A
  1. Vasodilatation in both arteries (inc COP) and veins (dec venous congestion)
  2. Inhibition of aldosterone secretion ( Na & water loss, K retention)
  3. Prevent ventricular hypertrophy & cardiac remodelling after myocardial infarction
  4. Dec central & peripheral NE thus it blunts sympathetic reflexes, dec BP with no reflex tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mention drug acting on tissue ACE & having dual elimination

A

Fosinopril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Advantages of ACEI

A
  1. Improve exercise tolerance & congestive symptoms
  2. Renoprotective esp in diabetics
  3. Dec CVS mortality
  4. Does no induce tachycardia/salt & water retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mention indications of ACEI

A
  1. Hypertension
  2. Heart failure (all cases of LV dysfunction)
  3. Myocardial infarction
  4. Nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

GR: ACEI is used in AMI

A
  1. Dec aldosterone-induced remodelling & prevent heart failure
  2. Dec sudden death (dec arrhythmia 2ry to hypokalemia & symp overactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Mention members of ACEI which are NOT prodrugs

A

Captopril

Lisinopril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Lisinopril can be used in ….

A

Liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Only ACE used in emergeny

A

Enalaprilat (given IV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ACEI need dose adjustment in ……

A

Renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Most common side effect of ACEI & most serious one.

Why?

A

Chronic dry cough (common)
Angioedema (rare but fatal)
Both due to accumulation of bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Mention less common adverse effects of ACEI

A
  1. 1st dose hypotension
  2. Hyperkalemia
  3. Hypersensitivty
  4. GIT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mention serious side effects of ACEI

A

Renal impairment in high renin states (parients on diuretics, bilateral renal stenosis)
Fetotoxic & teratogenic
Bone marrow depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe mechansim of action of ARBs

A

Block AT1 receptor which mediates most of the pathological CVS effects of Ang II
Spare AT2 receptor, VD & anti-proliferative effects

22
Q

Advantages if ARBs over ACE

A
  1. No dry cough, no BK production (angioedema still occurs)
  2. Antagonize Ang II produced by ACE & non ACE pathways
  3. Avoid hormonal escape (inc renin) with prolonged ACEI use
  4. Inc AgII activity on AT2, VD & antiproliferative effects
23
Q

Mention mechanism of action & disadvantages of hydralazine

A

K channel opener, hyperpolarization, prevent Ca influx causing arteriodilatation
Dis: rapid tolerance due to sympathetic & renin-angiotensin systems activation leading to salt & wtaer retention & inc HR

24
Q

Mention inidcations of hydralazine

A
  1. Heart failure with nitrates (alternative to ACEI)

2. HYPERTENSION (IV in eclampsia)

25
Describe mechanism of action of nitroprusside & its indication
NO donor, in cGMP, VD by inhibiting Ca influx in wall of bv Ind: most hypertensive emergencies (hypertensive encephalopathy), acute severe HF esp if associated with severe rise in BP
26
Describe toxicity of nitroprusside
1. Severe hypotension & myocardial infarction (due to reflex tachycardia) 2. Cyanide & thocyanate toxicity 3. Thiocyanate toxicity: CNS side effects & delayed hypo-thyroidism
27
GR: Diuretics are used in HF
Dec plasma volume and venous return (preload), dec pulmonary congestion (improve orthopnea & nocturnal dyspnea), dec peripheral (ankle) edema.
28
Mention advantages of spironolactone in HF
Dec mortality by 30%, dec Na retention and worsening of edema Minimize diuretic induced hypokalemia, dec arrhythmia & sudden death Dec myocardial hypertrophy & fibrosis induced by local aldosterone
29
Mention orecautions of using spironolactone in HF
Use cautiously to avoid hyoerkalemia esp if combined w ACEI or in patients with renal impairment
30
Mention drawbacks of chronic sympathetic stimulation
1. Induce tachycardia & inc O2 demand 2. Inc infarct size and propensity of cardiac remodelling MI 3. Increase effect of RAAS on heart 4. Persistent stimulation: myocyte hypertrophy, apoptosis, cardiac dilatation & ven thinning 5. Inc cytokines as TNF & Interleukins, hypertrophy & apoptosis & fibrosis with ven wall stiffness
31
Mention effects of carvedilol on HF
Inc EF Improve symptoms Slow disease progression Dec hospitalization & mortality
32
Mention the beneficial effects of BB in HF
Dec HR, improve coronary filling Dec afterload, inc COP Cardioprotection against adrenergic & Ag II-induced arrhythmia, myocardial damage & apoptosis Improve LV remodeling Resensitize downregulated B1 receptors in long standing cases, thus improve cardiac contractility
33
Mention mechanism of action of bipyrimidine
Inodioator Inhibit PDE-3, inc cAMP: Inc cardiac contractility & COP VD, dec afterload (PR) & preload (pulmonary congestion)
34
Mention adverse effects of inodilators
Thrombocytopenia | Arrhythmia
35
Describe mechansim of action of digoxin
1. Inhibit Na/K/ATPase pump, thus Na conc increases IC, dec Ca outflux, so Ca IC conc increases Ca release from SR, +ve inotropic effect. 2. Indirect vagal stimulation, -ve chrono & dromotrpoic effects. Also reduce sympathetic tone 2ry to inc COP.
36
Describe mechanical effects of digoxin
1. Inc COP 2. Dec EDV & ESV 3. Reduce cardiac size 4. Reduce sympathetic tone, dec pre & afterload 5. Diuretic effect due to inc COP & aldosterone antagonism 6. Mobilize edema fluid
37
Describe direct electrical effects of digoxin
Inc Ca IC, spontaneous delayed afterdepolarization, risk of extrasystole & vent tachycardia (dec ERP in cardiomyocytes)
38
Mention effect of vagal stimulation of digoxin
1. Dec HR in AF 2. Overdose may lead to bradycardia & AV block 3. Trun Af to AF by dec APR & ERP
39
Mention indications of digoxin
1. Systolic HF 2. HF + AF 3. Chronic AF 4. PSVT
40
Mention drugs combines w digoxin in chronic AF
1. BB & verapamil to control ventricular rate | 2. Before procainamide to control to countract atropine like action
41
Describe pharmacokinetics of dugoxin
2/3 absorbed rest is broken down by intestinal flora 2/3 is bound to plasma protein 2/3 is excreted in urine rest in stool T1/2 is 36 hrs
42
Describe pharmacokinetic interactions of digoxin
Erythromycin , inc absorption | Antiarrhythmics, dec renal excretion & displace it from tissue & plasma proteins
43
Describe pharmacodynamic interactions of digoxin
Diuretics, hypercalcemia, sympathomimetics (tachyarrhythmias) BB & CCB, comlete heart block
44
Mention CIs of digoxin
1. Acute MI & rheumatic carditis 2. AF+WPW 3. Ventricular tachycardia (precipitates AF) 4. Sick sinus syndrome 5. HOCM 6. Incomplete hert block
45
Describe manifestations of digitalis toxicity
1. GIT upset 2. Cardaic arrhythmias (tachyarrhythmias or sinus bradycardia/heart block) 3. CNS manifestations 4. Gynecomastia
46
Steps of treatment of treatment of digitalis toxicity
1. Stop digitalis & K losing diuretics 2. KCl ,CI in heart block 3. Lidocaine/phenytoin 4. Stropine in bradycardia/heart block 5. Digibind in fatal toxicity
47
Mention effect of digoxin of ECG
1. Prolonged PR interval 2. Shortened QRS & QT interval, dec APD & ERP 3. Depressed ST, flat or inverted T wave
48
Mention mechansim & side effect of nestiritide
Increase cGMP with VD of arteries & veins | Side effects: hypotension
49
Mention class of drugs of sacubitril
Neprilysin inhibitor
50
…… is an alternative if BB are CI
Ivabradine
51
Mention benefits of natruitic peptide
VD, inc GFR, reduced renin from kidneys
52
Mention role of tolvaptan in HF
ADH antagonist, excretion of electrolyte-free water, correct dilutional hyponatremia secondary to ADH inc in HF.

CVS Pharmacology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions