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Cardiovascular System > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the main function for antiarrythmic drugs?

A

They are used to restore normal cardiac activity by targeting proarrhythmic areas of heart.

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2
Q

Which drugs are apart of Class Ia Antiarrhythmics?

A

Double - Disopyramide
Quarter- Quinidine
Pounder - Procainamide

” Double Quarter pounder”

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3
Q

Which drugs are apart of the Class Ib Antiarrhythmics?

A

Lettuce - Lidocaine
Mayo - Mexiletine
Pickles - Phenytoin
Tomato - Tocainide
on my Burger

” Lettuce, Mayo, Pickles on my B(Ib)urger”

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4
Q

Which drugs are apart of Class Ic Antiarrhythmics?

A

Can - Ic
get
Fries - Flecainide
Please- Propafenone

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5
Q

What is the Mechanism of action for Class 1 Antiarrhythmics?

A

The are Sodium ( Na+ ) channels blockers. They leave fewer channels available to open in response to membrane depolarization thereby raising threshold for Action potential firing and slowing rate of depolarisation.

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6
Q

Which phase is affected by Class 1 antiarrhythmics drugs?

A

Phase 0 ( depolarization )

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7
Q

Class 1 antyarrythmic drugs decreases re-entry and prevent arrhythmia by ?

A
  1. Decreasing conduction velocity
  2. Increasing refractory periods of ventricular myocytes.
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8
Q

Which Class 1 antiarrhtyhmic drug provides a marked Na+ block?

A

Class Ic

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9
Q

Which class 1 antiarrhtyhmic drug prolongs action potential?

A

Class Ia

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10
Q

Which class 1 antiarrhtyhmic drug shortens action potential?

A

Class Ib

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11
Q

Which Which class 1 antiarrhtyhmic drug does not change action potential?

A

Class Ic

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12
Q

What is a diuretic?

A
  • Drug that ↑ volume of urine flow
  • Primarily inhibit Na + reabsorption
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13
Q

What are the classification of diuretics?

A
  • Thiazide/ Thiazide like diuretics
  • Loop diuretics
  • K+ sparing Na channel inhibitors
  • Aldosterone receptor antagonists
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14
Q

What are examples of Thiazide/ thiazide-like diuretics?

A

Metolazone
Indapamide
Chlorthalidone
Chlorothiazide
Hydrochlorothiazide (prototype)

“MICCH is thiazide”

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15
Q

What are examples of K+ sparing Na channel inhibitors?

A

Eplerenone
Amiloride
Triamterene
Spironolactone

” K+ sparing Na channel inhibitors EATS everytime !”

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16
Q

What are examples of Loop diuretics?

A

Tammy- Torsemide
Eat- Ethacrynic acid
Bunny’s - Bumetanide
Fruit - Furosemide
Loops

” Tammy Eat Bunny’s Fruit LOOPS’

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17
Q

What are the aldosterone receptor antagonists?

A

SpironolactONE
EplerenONE

AldosterONE inhibitors

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18
Q

Fill in the blanks. “An example of an osmotic diuretic is ____________ and a carbonic anhydrase inhibitor is __________.”

A

Osmotic diuretics - Mannitol
Carbonic anhydrase inhibitors - Acetazolamide

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19
Q

What is the principal site of action for Loop diuretics?

A

Loop of Henle duuhhh

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20
Q

What is the principal site of action for Thiazides?

A

The distal convoluted tubules

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21
Q

The cortical collecting tubules is the principal site of action for which drug?

A

– K sparing – amiloride, triamterene & spironolactone , eplerenone

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22
Q

What is the mechanism of action for Thiazides?

A

It inhibits Na+/Cl- transporter on the luminal side of Distal Convolutes Tubule.

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23
Q

What are the adverse effects of Thiazides?

A

HYPERcalcemia
HYPERuricemia
HYPERglycemia
Hypokalemia
Hypomagnesemia
Hyponatremia
Hypocholemia

Increase in LDL cholesterol & triglycerides

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24
Q

What is the Mechanism of Action for Loop Dieuretics?

A

Inhibition of Na+/K+/2Cl- co-transport system in the thick ascending limb of the Loop of Henle.

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25
Q

What are the clinical uses of Loop Diuretics?

A
  • Oedematous states ( pulmonary oedema due to CHF, ascites due to cirrhosis)

*↑ urine output in acute renal failure

  • Hypercalcemia, hyperkalemia, hypermagnesemia
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26
Q

What are the adverse effects of Loop Diuretics?

A
  • HYPERuricemia
  • Metabolic alkalosis
  • Hypokalemia
  • Volume depletion
  • Ototoxicity ( reversible)
  • Hypokalemia
  • Volume depletion
  • Hypocalcemia
  • Hypomagnesemia
  • Hyperuricemia
  • Interstitial nephritis
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27
Q

True or False? Loop diuretics DECREASES calcium content of urine.

A

FALSE!! It INCREASES calcium content in urine.

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28
Q

What is the mechanism of action for Spironolactone?

A

Competitive antagonist of aldosterone at aldosterone receptor in DCT.

*Binds to receptor preventing formation of mediator proteins that stimulate Na+/K+ pump

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29
Q

What is the mechanism of Amiloride & Triamterene?

A

Directly inhibits Na+ reabsorption in collecting tubule – works INDEPENDENT of presence of aldosterone.

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30
Q

What is the clinical use of Amiloride & Triamterene?

A

Can be used in the treatment of Hypoaldosteronism

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31
Q

What is the Clinical uses of Spironolactone?

A
  • Hypertension – often added to other diuretics (thiazides) to limit K + loss
  • Oedema 2 0 CHF, cirrhosis, nephrotic syndrome
  • Primary hyperaldosteronism
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32
Q

What are the adverse effects of Spironolactone?

A
  • Hyperkalemia (esp. in patients w renal impairment)
  • Hyponatremia
    *Metabolic acidosis [intracellular shift of H+]
  • Irregular menstrual cycle
  • Gynaecomastia & impotence
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33
Q

True or False? Amiloride causes HYPERcalcemia while Spironolactone causes HYPOcalcemia.

A

TRUE!!

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34
Q

What are the examples of α-1 blockers ?

A

Prazosin
Doxazosin
Terazosin

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35
Q

What are the clinical uses for Prazosin?

A
  • Hypertension
  • BPH – relaxes smooth m in bladder neck
  • Raynaud’s phenomenon (vasospam → digital ischemia)
36
Q

What are the adverse effects of Prazosin?

A
  • Orthostatic hypotension
  • Syncope
  • Nasal congestion
  • Dry mouth
  • Nightmares
  • Sexual dysfunction
  • Lethargy
37
Q

Fill in the blanks. “ Propanol on the pulmonary (β 2): cells causes ________.

A

Bronchoconstriction - by blocking β 2 adrenoceptor mediated relaxation of bronchial smooth muscle

38
Q

Fill in the blanks. “ Propanol on the β 2 receptors on the Juxtaglomerular cells causes ________.

A

A decrease in Renin secretion - ( blocks β 1 – adrenoceptors on the juxtaglomerular apparatus)

39
Q

What are the clinical uses of Propranolol ?

A
  • Ischemic heart disease, hypertension, arrhythmias, aortic dissection.
  • Portal hypertension: splanchnic vasodilation →↓ portal pressures &↓ GI bleeding.
  • Thyrotoxicosis, anxiety disorders
  • Migraine prophylaxis
40
Q

What are the adverse effects of Propranolol?

A
  • Sinus bradycardia, AV block, hypotension, CHF
  • Fatigue, depression, ↓libido
  • May precipitate bronchospasm
  • ↑ VLDL, ↓ HDL
41
Q

Metoprolol is a what type of drug ?

A

β 1 adrenoceptor competitive antagonist

42
Q

Which drug can be used in the treatment of chronic Congestive Heart failure?

A

Carvedilol

43
Q

What are the contraindications of Carvedilol?

A

Acute CHF
Heart block
Asthma
COPD

44
Q

What are the adverse effects of Carvedilol?

A
  • Dizziness
  • Fatigue
  • Hypotension
  • Weight gain
  • Hyperglycaemia
  • Diarrhoea
45
Q

What are the clinical uses of Statins?

A

*Drug therapy of choice to reduce hypercholesterolemia & achieve LDL cholesterol goals in pts at risk for /or with CAD.

  • Reduces cardiovascular mortality and risk of myocardial infarction , coronary revascularization and stroke
46
Q

What are the lipid modulating properties of statins?

A
  • Reduces lipid content of atherosclerotic lesions & promotes plaque stability.
  • Decrease vulnerability of plaque to rupture.
  • Decrease likelihood of thrombus formation & vascular occlusion
47
Q

What are the Cardioprotective effects of statins?

A
  • Improve endothelial function by enhanced synthesis of NO.
  • Diminish vulnerability of lipoproteins to oxidation —-> inhibiting unregulated uptake of modified LDL by macrophages.

*Suppress inflammation - key component of atherogenesis

  • Promote plaque stability by inhibiting monocyte penetration into arterial wall & reducing macrophage secretion of metalloproteinases - degrade & weaken fibrous caps of plaques
48
Q

Which statin drug should not be taken at night?

A

Atorvastatin & Rosuvastatin

49
Q

Which statin drugs are inhibited in the liver by Cytochrome P450 CYP3A4 ?

A

Lovastatin, Simvastatin, Atorvastatin

50
Q

Which substance is a Potent inhibitor of Cytochrome P450 CYP3A4 ?

A

Grapefruit Juice

51
Q

Fill in the blanks. “ ___________ &______________ are metabolised by CYP2C9

A

Rosuvastatin & Fluvastatin

52
Q

What are the adverse effects of HMG CoA Reductase inhibitors?

A
  • Elevation of serum transaminase
  • ↑ risk of diabetes ( largely in prediabetics)
  • Constipation
  • GI upset
  • Myalgia
  • Myopathy
  • Rhabdomyolysis
  • Headache
  • Rash
  • Cataracts
  • ↓ Coenzyme Q 10
  • Cognitive impairment (rare) (amnesia, memory impairment, confusion)
53
Q

What is the effect of Ezetimibe?

A

WResults in ↓total cholesterol and LDL-C with minimal effects on HDL & trigylcerides

54
Q

What drugs should Ezetimibe be combined with to increase its efficacy?

A

Statins

55
Q

What is the MOA of Ezetimibe?

A

Inhibits cholesterol absorption at small intestine brush border.

56
Q

What are examples of Bile acid binding resins / sequestrants ?

A

Cholestyramine
Colestipol
Colesevelam

57
Q

What is the MOA of Bile acid resins/sequestrants?

A

Prevent intestinal
reabsorption of bile acids; liver must use cholesterol to make more.

  • Resins bind negatively charged bile acids in small intestines, forming insoluble complexes that are then excreted in faeces.
  • Loss of bile acids stimulates liver to increase conversion of stored cholesterol into new bile acids.
58
Q

What are examples are Fibric acid derivatives (Fibrates)?

A

GemFIBRozil
FenoFIBRate
BezaFIBRate
CiproFIBRate

59
Q

What are the mechanisms of action of Fibric acid derivatives (Fibrates)>

A

Reduces plasma triglycerides

  • ↑ activity of lipoprotein lipase → promote catabolism of VLDL (rich in TGs).
  • ↓hepatic synthesis & secretion of VLDL.
  • ↑ HDL ( ↓ TG → ↓exchange of cholesteryl esters from HDL to TG – rich lipoproteins)
60
Q

What are the adverse effects of Fabric acid derivatives?

A
  • GI upset
  • Skin rash
  • Alopecia
  • Myalgias
  • Lithiasis (formation of gall stones due to  biliary excretion of cholesterol)
  • Abnormal LFTs
61
Q

What is the mechanism of Niacin (Vitamin B3)?

A
  • Inhibits lipolysis (hormone- sensitive lipase) in adipose tissue;↓ transport of FFA to the liver and ↓ hepatic synthesis of triglycerides. It reduces hepatic VLDL synthesis
62
Q

What are the adverse effects of Niacin?

A
  • Severe flushing (prostaglandin mediated, may be reduced if aspirin taken beforehand/ taking sustained-release preparations)
  • Pruritus
  • Headache
  • Nausea
  • Constipation

↑ transaminases

  • Hyperglycaemia

*Hyperuricemia (inhibits tubular secretion of uric acid)

63
Q

What are examples of PCSK9 (proprotein convertase subtilisin/ kexin type 9) inhibitors ?

A

Alirocumab, evolocumab

64
Q

What is the MOA of PCSK9 inhibitors?

A

They inactivate the LDL-receptor degradation, increasing amount of LDL removed from bloodstream.

PCSK9 inhibitors decrease LDLR degradation by PCSK9 → improve LDL clearance & ↓ LDL

65
Q

What are the examples of ACE inhibitors?

A

Captopril
Enalapril
Lisinopril
Ramipri
Trandolapril

all the prils lol

66
Q

What is the mechanism of action for ACE inhibitors?

A

Reversibly inhibit ACE which catalyzes Angiotensin I → Angiotensin II → blocking RAAS axis

Inhibition ofACE also prevents inactivation ofbradykinin, a potent vasodilator.

67
Q

What are the adverse effects of ACE inhibitors ?

A
  • Cough (persistent dry cough)
  • Angioedema (both due to
    increase bradykinin; contra indicated in C l esterase inhibitor deficiency},
  • Teratogen (fetal renal malformations),
    *Creatinine increase (because of decrease GFR),
  • Hyperkalemia,
  • Hypotension.

CATCHH

Used with
caution in bilateral renal artery stenosis because ACE inhibitors will further l CFR - renal failure.

68
Q

What are the examples of Angiotensin II receptor blockers (ARB’s)?

A

Losartan
Candesartan
Eprosartan
Irbesartan
Olmesartan
Telmisartan
Valsartan

” the sartans”

69
Q

What is the mechanism of action of Angiotensin II blockers (ARB’s)?

A

Competitive AT11 receptor blocker but they DO NOT increase bradykinin

70
Q

What are the adverse effects of ARB’s?

A
  • dizziness
  • nausea
  • angioedema
  • hyperkalemia esp. in patients taking K sparing diuretics
  • fatigue
  • hypoglycemia
  • chest pain
  • diarrhoea
  • hypotension
71
Q

Which drug is a direct inhibitor of renin?

A

Aliskiren

72
Q

What are examples of Calcium channel clockers?

A

Dihydropyridine (DHP)
- Nifedipine
- Amlodipine
- Felodipine
- Nicardipine
- Isradipine
- Nisoldipine
- Clevidipine
- Nimodipine

Non- dihydropyridine
- Verapamil
- Diltiazem

73
Q

What is the mechanism of action for Dihydropyridine (DHP) CCB?

A

CCB binds to L type Ca 2+ channels inhibiting inward movement of Ca 2+, decreasing the rate of recovery of these channels

74
Q

What are the clinical uses of Nifedipine?

A
  • Hypertension
  • Ischaemic heart disease
  • Relief of coronary vasospasm in Prinzmetal’s angina
  • Pulmonary hypertension
  • Raynaud’s phenomenon
75
Q

What are the adverse effects of Nifedipine?

A
  • Ripheral oedema
  • Dizziness
  • Flushing
  • Headache
  • Heartburn
  • Hypotension
  • CHF
  • Nausea
76
Q

What is the Main clinical uses of Methyldopa?

A

It is used to treat Hypertension in Pregnancy .

77
Q

What are rapidly - acting Nitrates?

A

Nitroglycerin

78
Q

What are examples of long-acting nitrates?

A
  • Sustained- release nitroglycerin
  • Isosorbide dinitrate
  • Isosorbide mononitrate
79
Q

What is the MOA of Nitrolycerine?

A

Nitrates via nitric oxide (NO), stimulate guanylate
cyclase→↑ cGMP → activation of
cGMP-dependent protein kinases.

This causes ↓intracellular Ca 2+ & activation of
myosin light chain (MLC) phosphatase, both of
which result in MLC dephosphorylation

80
Q

What are the clinical uses of Nitroglycerine?

A

Treatment of angina (often w β- blocker * to
minimize reflex tachycardia that occurs w
nitrates)

Congestive heart failure

Hypertension esp. in patients w coronary disease

81
Q

Which drug is a PDE V inhibitor?

A

Sildenafil

82
Q

What is the MOA of PDE V inhibitor (Sildenafil)?

A

PDE V inactivates cGMP - ↑cGMP→ MLC dephosphorylation → smooth m
relaxation

83
Q

What is the MOA Ranolazine ( Anti-anginal drug )?

A
  • Inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption. Does not affect heart rate or blood pressure.
84
Q

What is the MOA of Trimetazidine ( abtianginal drug)?

A

Trimetazidine inhibits the utilisation of FFA for energy production by inhibiting the enzyme mitochondrial 3-ketoacyl CoA thiolase ( 3-KAT) activity in Beta oxidation

85
Q

What are the clinical uses of Trimetazidine (anti-anginal drug)?

A

Angina
Vertigo, Tinnitus

86
Q
A

Cardiovascular System (10 decks)

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