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Pharmacology > CVS drugs > Flashcards

CVS drugs Flashcards

1
Q

what are the 5 classes of CVS drugs to know

A
  • lipid lowering drugs
  • anti-hypertensives
  • ischaemic heart disease drugs
  • heart failure drugs
  • anti-arrhythymic drugs
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2
Q

what are the 5 types of lipid lowering drugs?

A

SENd the FBi

S: statins
E: ezetimibe
N: niacin
F: fibrates
B: bile acid sequestrants
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3
Q

what are examples of statins?

A

simvastatin/lovastatin

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4
Q

what is the MOA of statins?

A

it is a HMG-CoA reductase inhibitor = prevents production of cholesterol and increases LDL receptor

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5
Q

after statins, what drug is next?

A

ezetimibe

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6
Q

what is the MOA of ezetimibe?

A

inhibits intestinal absorption of cholesterol (both from dietary and biliary sources)

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7
Q

after statins and ezetimibe, what drug comes next?

A

niacins (which are essentially vitamins b3)

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8
Q

what is the MOA of niacins?

A

inhibits lipolysis in adipose tissue and hence the triacylglyceride is used to make HDL instead of LDL/VLDL

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9
Q

after statins, ezetimibe and niacins, what drug class is next?

A

fibrates e.g. gemfibrozil

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10
Q

what is the MOA of gemfibrozil?

A

ligand activator of PPAR-alpha, which is involved in many general pathways; one of which involves activation of lipoprotein lipase

thus more LPL is activated to breakdown TG into free fatty acids which are stored by adipocytes = plasma TG decreases

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11
Q

after statins, ezetimibe, niacins and fibrates, what drug class is next?

A

bile acid sequestrants e.g. cholestyramine

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12
Q

what is the MOA of cholestyramine?

A

binds to bile salts in GI and decrease its reabsorption back into the system = hence depletes hepatic cholesterol to make more bile salts

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13
Q

when and how are statins administered?

A

orally in the evening, as cholesterol synthesis happens are night when the body is in a fasting state and there’s no dietary cholesterol to supplement

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14
Q

how are all these drugs administered?

A

all orally as you want into to enter GIT

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15
Q

what are the DDI’s of fibrates e.g. gemfibrozil?

A

recap: gemfibrozil is PPAR-a activator

it also displaces warfarin and potentiates anti-coagulants so risk of bleeding

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16
Q

what are the contraindications/side effects of bile acid sequestrants e.g. cholestyramine?

A

inhibits absorption of vitamin ADEK too, as well as many other drugs

so need to adjust dose and consider giving vitamin supplements

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17
Q

what is the general contraindication of lipid lowering drugs?

A

safe bet is to say that almost all are hepatotoxic (note that fibrates have additional renal toxicity)

except for statins (which cannot give at all), the rest are pregnancy cat c which means give with precautions

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18
Q

what is the standard therapy for lipid lowering?

A

first line is always to change diet and lifestyle

if that doesn’t work, consider giving drugs; in which statins will be first line

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19
Q

moving on from lipid lowering drugs, what are the anti-hypertensive drugs?

A 
A: ace-1 inhibitor or angiotensin-2 type 1 inhibitor
B: b blockers 
C: calcium channel blocker
D: diuretics
V: vasodilators
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20
Q

what are the drug examples of ace-1 inhibitor and angiotensin-2 type 1 inhibitor?

A
  1. -prils = ACE1 inhibitor

2. -sartans = Angiotensin 2 type 1 inhibitor

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21
Q

what is the MOA of ACE 1 inhibitor?

A
  • blocks angiotensin-converting enzyme
  • decreases vasoconstriction
  • blocks inactivation of bradykinin so it can continue to vasodilate
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22
Q

what is the MOA of angiotensin-2 type 1 inhibitor?

A

blocks angiotensin 2 type 1 receptor directly

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23
Q

what is important about the effects of ACE-1 inhibitor?

A

it simultaneously resets pressure sensor sensitivity and hence blocks the baroreceptor reflux to increase BP when the BP drops

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24
Q

what are the drug examples of b blockers?

A

should be b1 blockers such as atenolol and betaxolol

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25
Q

what is the MOA of b1 blockers?

A

decrease HR and contractility

26
Q

what are the drug examples of calcium channel blockers?

A
  • verapamil/diltiazem

- nifedipine

27
Q

what is the MOA of verapamil/diltiazem?

A

blocks Ca channel to decrease intracellular Ca = decreased conductivity

28
Q

what is the MOA of nifedipine?

A

blocks Ca channel + decrease smooth muscle tone

29
Q

recap: what is the pathway of depolarisation and repolarisation of cardiac myocytes?

A
  1. sodium-potassium pump maintains negative membrane potential
  2. depolarisation happens when Na+ channels open and enters cell
  3. repolarisation begins when K channels open again to let K+ out
  4. repolarisation slows down as Ca2+ channels open and works against the repolarisation
  5. Ca2+ channels close and K+ continues to go out until repolarisation is complete
30
Q

what are examples of diuretics?

A

loop diuretics like furosemide

and thiazides

31
Q

what is the MOA of loop diuretics like furosemide?

A

affects ascending limb of Loop of Henle

blocks the Na/K/2Cl so there’s less K in the tubular cells, which means there’s less K available to be exchanged out for Mg and Ca that is taken back in during reabsorption = more Mg and Ca excretion along with water

32
Q

what are the side effects/contraindications of loop diuretics?

A
  1. hypokalaemic metabolic alkalosis

ultimately K is taken from blood in exchange with Na (which is then in the blood), so that this K can be used to exchange with Mg and Ca

  1. dehydration
  2. acute renal failure
33
Q

what is the MOA of thiazides?

A

affects distal convoluted tubule

blocks NaCl transporter so there’s less NaCl in the tubular cells, thus cell compensates by increasing Ca channel uptake

34
Q

what are the side effects/contraindications of thiazides?

A

tbh same as loop diuretics

  1. hypoK metabolic alkalosis
  2. dehydration
  3. acute renal failure
35
Q

what are the drug examples of vasodilators?

A

minoxidil

36
Q

what is the MOA of minoxidil?

A

it is dilates arterioles only and not veins

it is a K+ channel opener = makes cell hyper polarised and prevents Ca channel from opening = decreased contractility

fun fact: can be used to help male pattern baldness

37
Q

what are the side effects/contraindications of minoxidil?

A

it can cause reflex sympathetic stimulation (which ACE-1 inhibitor does not)

hence must be used together with diuretics and is used only for severe to malignant hypertension

38
Q

drug combinations for angina

A

you can’t really work with the vessels so you just aim to increase contractility

  1. b1 blockers
  2. Ca channel blockers
39
Q

drug combinations for congestive heart failure

A

you want to work on reducing volume load so use ACE inhibitors

40
Q

drug combinations for MI

A

you want to increase contractility and also hope to decrease preload

  1. b1 blockers
  2. ACE inhibitors
41
Q

what anti-hypertensive is contraindicated in renal patients?

A

ACE inhibitors

42
Q

what anti-hypertensives are contraindicated in pregnant?

A

ACE inhibitors

43
Q

what anti-hypertensives are contraindicated in asthmatics?

A

B blockers

44
Q

moving on from lipid lowering drugs and anti-hypertensives, what is a drug used in ischemic heart disease?

A

drug class: nitrates

drug example: nitroglycerin

45
Q

what is the MOA of nitroglycerin?

A

releases NO in smooth muscles, leading to smooth muscle relaxation of both veins and arteries

(compared to minoxidil which is only arteries)

46
Q

how does venodilation and arteriole dilation help IHD?

A

venodilation = decreased preload

arteriole dilation = decreased afterload

together = decreased O2 consumption

47
Q

therapy for heart failure can be split based on early HF and late HF; name the aims of therapy for each type

A

early HF: aim to increase contractility

late HF: aim to decrease volume load

48
Q

what drugs are used in early HF (with the aim to increase contractility)?

A

positive inotropic drugs:

  1. cardiac glycosides e.g. digoxin
  2. beta 1 agonist e.g. dobutamine
  3. PDE inhibitor (also used for late HF)
49
Q

what drugs are used in late HF (with the aim to decrease volume load)?

A
  1. vasodilators like nitrates e.g. nitroglycerin
  2. anti-hypertensive drugs (ACE inhibitors and diuretics)
  3. PDE inhibitor (also used for early HF)
50
Q

what is the MOA of cardiac glycosides like digoxin?

A

inhibits NA/K ATPase = increased Na = less Ca efflux = more Ca in the cells = increased contractility

opposite of calcium channel blockers

51
Q

what is digitoxin?

A

more toxic version of digoxin that has a longer half-life and a stronger affinity

52
Q

when do we use digitoxin preferentially over digoxin?

A

when the patient has renal impairment, use digitoxin instead

53
Q

what are drug examples of PDE inhibitors?

A

sildenafil (viagra) and other -afils

54
Q

what is the MOA of PDE inhibitors?

A

increase cAMP = increases Ca = increased contractility

55
Q

finally we move on to the last drug type, which is anti-arrythmics - what are the 4 diff drug classes?

A 
class 1A, 1B, 1C
class 2
class 3
class 4
56
Q

what is the MOA of class 1?

A

targets Na channel and blocks it = prolongs phase 0 so the cardiac myocytes cannot be depolarised

57
Q

what are examples of class 1 drugs?

A

1A: procainamide
1B: lidocaine
1C: flecainide

58
Q

what is the MOA of class 2?

A

B blocker = suppresses phase 4

59
Q

what are the examples of class 2 drugs?

A

any b blocker e.g. propranolol

60
Q

what is the MOA of class 3?

A

targets K channel and blocks it = prolongs phase 3 repolarisation

61
Q

what are the examples of class 3 drugs?

A

amiodarone

62
Q

what is the MOA of class 4?

A

targets Ca channel and blocks it = delays phase 2 repolarisation = prolongs action potential

Pharmacology (11 decks)

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