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CVS pharm Flashcards

1
Q

What are the different drug classes used for arrhythmia treatment

A

1A, 1B, 1C =Na+ channel blockers
II = B-blocker
III = K+ channel blocker
IV = Non-DHP Ca2+ channel blocker

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2
Q

Describe the MOAs of 1A, 1B, 1C anti-arrhythmics

A

1A = Procainamide = Na+ channel blocker => slows phase 0 depolarisation and prolongs ERP

1B = Lidocaine = Na+ channel blocker = > slows phase 0 depolarisation & shortens phase 3 repolarisation and APD

1C = Flecainide = Na+ channel blocker => slows phase
0 depolarisation

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3
Q

What is the MOA of class III anti-arrhythmics

A

Amiodorone = K+ channel blocker => blocks Ikr/Iks => prolong phase 3 repolarisation and ERP

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3
Q

How do B-blockers treat arrhythmias

A

Meta/Bisoprolol = suppress phase 4 depolarisation

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3
Q

What is the MOA of class IV anti-arrhytmics

A

Verampil = Non-DHP Ca2+ channel blocker => Prolongs APD and ERP

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3
Q

What is the drug used for emergency supra ventricular tachycardia

A

Adenosine

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3
Q

What are the adverse effects of amiodorone

A

Bradycardia
Prolonged heart block
Thyroid dysfunction

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4
Q

What is the MOA of adenosine

A

Stimulate K+ channel and inhibits Ca2+ current Decrease AVN conduction
Increase ERP

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4
Q

What are the contraindications of verampil

A

Depressed cardiac function
Hypotension

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5
Q

What are the first line anti-hypertensives

A

ACE-I/ AT1 blockers
B-blockers
Ca2+ channel blockers (DHP)
Diuretics (Thiazides)

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6
Q

What are some ACE-Is used for hypertension

A

Lisinopril
Captopril
Enalapril

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6
Q

What is the MOA of ACE-I

A

-Prevents AngI -> AngII
=>Decrease aldosterone release => decreased Na/H2O retention
=>Decrease vasoconstriction => Decrease PR
- Prevent bradykinin inactivation => Increase NO and PG

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6
Q

What are some AT1 blockers used

A

Valsartan
Losartan

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6
Q

What are the adverse effects of ACE-Is

A
  • Decrease BP and renal blood flow => decreased eGFR => acute renal failure
  • Increase NO and PG => inflammatory like response => angioedema and dry cough
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7
Q

What is the MOA of AT1 blockers

A

Prevents AngII - AT1R binding => Decreased vasoconstriction and PR

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7
Q

Why are B-blockers contraindicated in asthma patients

A

B2R blockade => Decreased PKA activity => Unhibited MCLK activation and MLC phosphorylation => Increase risk of bronchoconstriction

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7
Q

What are the adverse effects of AT1 blockers

A

Less dry cough and angioedema than ACE-Is

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7
Q

What are some B-blockers used for hypertension

A

Non-selective = Carvedilol
Cardioselective = Biso/Metaprolol
3rd Gen = Nebivolol

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8
Q

What are the contraindications of ACE-Is and AT1 blockers

A

Pregnancy

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8
Q

What is the MOA of B-blockers

A

B1R antagonist => inactivated Gs protein => Decrease Adenyl cyclase activity => Decrease ATP -> cAMP => Decrease PKA activity => Decrease L type Ca2+ channel phosphorylation = > Decrease Ca2+ influx and Ca2+ -calmodulin complex => Decrease MCLK activation and MLC phosphorylation = > Impairs vascular smooth muscle contraction => Relaxation

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8
Q

What are some DHP Ca2+ channel blockers

A

Nifedipine
Amlopidine

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8
Q

How do DHP Ca2+ channel blockers help as anti-hypertensives

A

Decrease Ca2+ influx
- Decrease myocardial contractility => Decrease CO
- Decrease vascular SM tone => Decrease PR
=> Decrease BP

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9
Q

What are some thiazide diuretics

A

Hydrochlorothiazide
Indapamide

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9
Q

What is the MOA of thiazide diuretics

A
  • Blocks Na/Cl transporter => Decrease NaCl reabsorption
  • Increase Ca2+ reabsorption
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9
What are the second line anti-hypertensives
Hydralazine A-antagonists Mineralocorticoid antagonists
9
What are the adverse effects of thiazide diuretics
- Hypokalaemia metabolic acidosis = Increase Aldosterone mediated K+, H+ excretion at collecting duct - Hyponatraemia = Decrease Na/H2O reabsorption - Hyperglycaemia = Hypokalaemia => Prolonged K+ channel opening => Hyperpolarisation => Decrease exocytosis of insulin granules activated by Ca2+ influx - Hyperuricaemia = Increase urate reabsorption at prox tubule
9
What are the adverse effects of hydralazine
Baroreflex associated sympathetic activation Hydralazine induced lupus syndrome
9
What is the MOA of hydralazine
Arteriole vasodilator => inhibits IP3 induced Ca2+ release => Decrease PR and BP
10
What is the MOA of A-antagonists
Oppose A1 mediated vasoconstriction => Increase vasodilation => Decrease PR and BP
10
What are some A-antagonists used for hypertension
Prazosin
11
What are some side effects of A-antagonists
Increased urinary freq
11
What is the MOA of mineralocorticoid antagonists
Blocks aldosterone receptor => Decrease Na+ channel activation and reabsorption
11
What are some mineralocorticoid receptor antagonists
Spironolactone Triamterene
12
What are the adverse effects of mineralocorticoid antagonists
Hyperkalaemia Metabolic acidosis Spironolactone => Gynecomastia Triamterene => Kidney stones
12
Which lipoproteins contribute to increase atherosclerosis risk
LDL and VLDL
12
What is the MOA of statins
Inhibit HMG-CoA reductase => Decrease cholesterol synthesis in cells => Increase LDL receptors => increase LDL uptake and decrease circulatory LDL
13
What drug classes are used for hyperlipidemia
HMG-CoA reductase inhibitors (statins) PCSK9 inhibitors (Evolo/Alirocumab) Fibrates (Gemfibrozil/Fenofibrate) Omega-3-acid ethyl esters (DHA +EPA) Resins Ezetimide
14
What are the adverse effects of statins
Decreasse liver function Myopathy
14
What are the contraindications of statins
Pregnancy and young
15
Explain the best time to take statins
Evening =>Eat less => decrease cholesterol intake => Body has to synthesise more cholesterol => Increase HMG-CoA reductase activation
15
What is the MOA of PCSK9 inhibitors
Inhibit hepatic PCSK9 => decreased LDL receptor degradation
16
What drug is used for statin intolerant patients
PCSK9 inhibitors
17
What are the adverse effects of PCSK9 inhibitors
Hypersensitivity reactions Nasopharyngitis/ sinusitis
17
What is the MOA of fibrates
PPAR-A ligand => Increase lipoprotein lipase activity => Decrease circulatory VLDL
17
What are the adverse effects of fibrates
Nausea Rash Gall stones
18
What are the adverse effects of Omega-3-acid ethyl esters
Fish allergy DHA => Increase LDL-C DHA + EPA => TXA2 decrease => Bleeding GI problems
18
What is the MOA of Omega-3-acid ethyl esters
- Increase free fatty acid breakdown - EPA + DHA = weak substrates of Diglyceride Acyltransferase => Decrease hepatic triglyceride production
18
What is the MOA of resins
Bind bile acid with salts => prevents bile reabsorption => hepatocytes increase cholesterol breakdown to synthesise more bile acid
18
What is the MOA of ezetimibe
Inhibits sterol transporter NPC1L1 in intestine => decrease sterol uptake
18
What are the adverse effects of resins
Constipation and flatulence Decrease vit absorption
18
What drug classes are used for IHD
Cardiac pacemaker retardant = Ivabridine Vasodilators = Nitrates (NItroglycerin) and Ca2+ channel blockers Cardiac depressants = Ca2+ channel blockers and B-blockers
19
What are the adverse effects of ezetimibe
Steatorrhoea
19
What is the MOA of ivabradine
Inhibits pacemaker I(f) current => Decreases spontaneous diastolic depolarisation & HR => Decrease cardiac workload and O2 consumption
19
What are the adverse effects of ivabradine
Visual problems Bradycardia
20
What is the MOA of nitrates
Release NO => increase guanylyl cyclase activity => increase GTP => cGMP => MLC deactivation => decrease vascular SM tone - Venodilation => Decrease preload - Arteriolar dilation => Decrease after load => Decrease O2 consumption
21
What are the adverse effects of nitrates
- Decrease venous return and PR => hypotension => baroreflex sympathetic activation in aortic arch => reflex tachycardia - Dilation of cerebral blood vessels => Increase intracranial pressure => Headache
22
How do Ca2+ channel blockers act as vasodilators
Decrease Ca2+ influx => vascular smooth muscle tone
22
What are the drug classes used for HF
B-blockers Sacubitril-Valsartan Diuretics (Loop and K+ sparing) Cardiac glycosides Hydralazine Nitrates Ivabradine
23
What are the approved B-blockers for HF
Carvedilol Biso/Metaprolol Nebivolol
24
What are the adverse effects of Sacubitril-valsartan
Hypotension Hyperkalaemia Renal failure Angioedema and cough
24
What is the MOA of sacubitril-valsartan
Sacubitril = Inhibits Neprilysin => prolongs BNP vasodilation and diuresis effects Valsartan = Blocks AngII vasoconstriction and aldosterone release (AngII breakdown inhibited by sacubitril)
24
Name one loop diuretic
Furosemide
24
What is the MOA of loop diuretics
- Inhibits Na+/K+/2Cl- transporter => decrease reabsorption of electrolytes & Mg2+ & Ca2+ - Increase renal blood flow
25
What are the adverse effects of loop diuretics
Hypokalaemia Ototoxicity Hyperuricaemia Hypomagnesemia Decresse PG synthesis
26
Compare the onset between K+ sparing and loop diuretics
K+ sparing = slower onset Loop diuretics = faster onset
26
Explain which drugs should not be prescribed with loop diuretics
Aminoglycosides => exacerbate ototoxicity NSAIDs => exacerbate Inhibition of PG synthesis
27
Compare the different indications of loop and K= sparing diuretics
Loop = Acute oedema, Acute hyperkalaemia, Acute renal failure K+ sparing = Hyperaldosteronism
27
Name 2 cardiac glycosides
Digoxin and digitoxin
28
What is the MOA of cardiac glycosides
Increase contractility and CO - Increase carotid sinus firing => Decrease symp - Increase renal blood flow and decreaserenin release => Decrease AngII => Decrease preload/afterload Increase parasympathetic activity => Decrease AV conduction => invcrease AV nodal delay and decrease Ventricular rate
29
Describe the toxicity effects of cardiac glycosides and its uses
Increase Ca2+ influx => Treat fib, systolic dysfunction, tachycardia
30
How do you treat digitalis toxicity
Discontinue dosare Correct K+/Mg2+ deficiency Anti-arrhythmic treatment Digoxin antibodies

Linganguliguliguli (7 decks)

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