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Pharmacology 1 > Cardiovascular System 1 > Flashcards

Cardiovascular System 1 Flashcards

1
Q

Inhibitors of RAAS

A
  1. Sympathetic blockers (B blockers)
  2. Direct renin inhibitor (aliskiren)
  3. ACE
  4. ARB
  5. Aldosterone antagonist (spironolactone)
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2
Q

Examples of ACE

A

Captopril
Enalapril
Ramipril

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3
Q

MOA of ACE

A

Inhibit angiotensin converting enzyme and hence bp falls due to vasodilation due to decrease in PVR and increase in compliance of large vessels.
Fall in BP dependent on Na+ levels
Angiotensin 1 converted to 1-7 which are vasodilators
Also inhibit substance P/bradykinin which is also converted by ACE

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4
Q

Pharmacokinetics of ACE

A

Food in stomach decreases bioavailability
70% absorbed

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5
Q

ADR of ACE inhibitors

A

Hypotension
Hyperkalemia
Cough
Dysgeusia
Angioedema
Rashes, urticaria
Foetopathic
Headache dizziness vomiting
Acute renal failure

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6
Q

Interactions of ACE inhibitors

A

Diuretics
NSAID like indomethacin
K+ sparing diuretics
Antacids

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7
Q

Uses of ACE inhibitors

A

Hypertension
CHF
MI
Prophylaxis is high risk CAD
Diabetic nephropathy
Non diabetic nephropathy
Scleroderma crisis

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8
Q

Advantages of using ACE inhibitors in hypertension

A

Free of postural hypotension
No CNS effects
Can be used in asthmatics, PVD, diabetics
Long term reduce incidence of Diabetes Type 2
No K+ loss
Renal blood flow maintained
LVH reversed

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9
Q

ACE inhibitors first choice in

A

Diabetics with hypertension
Renovascular and resistant hypertension

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10
Q

ARB examples

A

Losartan
Telmisartan
Valsartan

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11
Q

MOA of ARB

A

Competitive antagonist and inverse agonist of AT receptors
All actions of angiotensin: vasoconstriction, sympathetic stimulation, release of aldosterone and adr, renal actions promotinh salt and water Reabsorbtion, vasopressin release all inhibited

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12
Q

Advantages of ARB over ACE inhibitors

A

Do not interfere with degradation of bradykinin or substance P hence no cough
No angioedema commonly
No dysgeusia
Complete blockade of AT1 receptor
Oral absorption not affected by food

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13
Q

ADR of ARB

A

Hypotension
Hyperkalemia
Fetopathic
Headache dizziness weakness GI side effects

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14
Q

Uses of ARB

A

Hypertension
CHF
Diabetic nephropathy
MI

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15
Q

Example of direct renin inhibitor and MOA

A

Aliskiren
Acts by blocking attachment of angiotensinogen by binding to renin

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16
Q

Examples of cardiac glycosides

A

Digoxin
Digitoxin
Oubain

17
Q

Actions of digoxin

A
  1. Heart: ionotropic effect, increases contractility, vagomimetic action, CNS actions altering sympathetic activity
    Increases force of contraction
    Decreases heart rate
    ECG changes include Inversion of T wave, Prolonged P-R interval and depressed ST segment
  2. Blood vessels: vasoconstriction
    No increase in BP
  3. CNS: activates CTZ so vomiting, hyperapnoea, mental confusion, visual distrubances
    4.kidney: diuresis in CHF patients
18
Q

MOA of digoxin

A

Inhibits Na-k channels
Increase in NA concentration in cell
Opening of L type transient Ca channels
Increase in Ca
CA activated CA channels: ryanodine receptor channels activated
Further increase in ca from sarcoplasmic reticulum
Increase in contraction

19
Q

Manifestations of digitalis toxicity

A

Extracardiac: anorexia, vomiting, nausea, abdominal pain. Fatigue, mental confusion, hyperapnoea, psychosis

Cardiac: all types of arrhythmia, severe bradycardia, ventricular tachycardia

20
Q

Treatment of digoxin toxicity

A

Tachyarrhythmia: KCL
Ventricular arrhythmia: Lidocaine IV
Supraventricular arrhythmia: propanolol
For AV block: Pacemaker

Digitoxin antibody: DIGIBEND, DIGIFAB

21
Q

Uses of digoxin

A

Atrial fibrillation, Atrial flutter
Cardiac failure

22
Q

Two goals of treatment of heart failure

A
  1. Relief of congestive/low output symptoms, restoration of cardiac performance
  2. Arrest/reversal of disease progression
23
Q

Drugs for relief of congestive symptoms

A

Inotropic drugs: digoxin digitalis dobumatine dopamine
Diuretics: furesemide, thiazide
RAS inhibitor: ACE, ARB
Vasodilator: nitrates, hydralazine, nitroprusside
B blocker: Metoprolol, bisprolol

24
Q

Drugs for arrest/reversal of heart failure progression

A

ACE and ARB
B blocker
Aldosterone antagonist: spironolactone, eplerenone

25
Q

Why diuretics given in HF

A

Decrease preload and improve ventricular efficiency by reducing circulating volume
Remove peripheral edema and pulmonary congestion

26
Q

Why RAS inhibitors given

A

To prevent remodeling

27
Q

Vasodilators examples

A

Veins: nitrates
Artery: hydralazine
Both: nitroprusside

28
Q

Why vasodilators are given for HF

A

Decrease pre load : nitrates
Decrease after load : hydralazine
Pre and after load reduction: nitroprusside

29
Q

Why B blockers are given in HF

A

To reduce sympathetic counter mechanism that cause remodeling

30
Q

Why aldosterone antagonist are given in HF

A

To prevent:
1. Expansion of ecf volume: increase preload
2. Remodeling of heart due to proliferation of fibroblast and fibrotic change in myocardium
3. Hypokalemia and hypomagnesemia: leads to ventricular arrhythmia

31
Q

Inamrinone/Amrinone and Milrinone MOA

A

Phosphodiesterase 3 inhibitors
No degradation of cAMP
Hence increase contraction

32
Q

What is inamrinone? Most imp adr

A

It is a ionodilator
Thrombocytopenia

33
Q

Use of drugs in asymptomatic LVD

A

ACE/ARB

34
Q

Use of drugs in mild HF( class1)

A

ARB/ACE
B blocker
Diuretic

35
Q

Use of drugs in moderate HF(class2)

A

ACE/ARB
B blocker
Diuretic
Digoxin

36
Q

Use of drugs in severe HF( class3)

A

ACE/ARB
B blocker
Diuretic
Digoxin
Spironolactone

37
Q

Use of drugs in refractory and emergent HF (class 4)

A

ACE/ARB
DIURETIC
Digoxin
spironolactone
Iv vasodilator
Iv inotropes

Pharmacology 1 (14 decks)

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