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cvs drugs > anti-hypertensives + lipid lowering drugs > Flashcards

anti-hypertensives + lipid lowering drugs Flashcards

1
Q

example of ace inhibitor

A

captopril
enalapril
lisinopril
“PRIL”

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2
Q

MOA of ACE inhibitor

A

prevents conversion of angiotensin I to angiotension II

effect:
decreased vasoconstriction
decrease aldosterone
prevent breakdown of bradykinin which forms NO and prostaglandin (vasodilation)

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3
Q

use of ACE inhibitor

A

hypertenion
HF
renal insufficiency
protective effect after MI

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4
Q

AE of ACE inhibitor

A

hypotension, renal failure, hyperkalemia
drug cough (bradykinin)

contraindicated: pregnancy

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5
Q

example of ang II type I blocker

A

candesartan
losartan

“SARTAN”

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6
Q

MOA of ang II type I blocker

A

block binding of Ang II to receptor

contraindicated: pregnancy

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7
Q

advantage of ang II type I clocker over ACE inhibitor

A

less/no dry cough
- does not prevent breakdown of bradykinin

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8
Q

MOA of beta blockers

A

block phosphorylation of ATP to cAMP so Ca2+ channel not activated, blocking calcium induced calcium release to trigger bronchoconstriction

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9
Q

examples of beta blockers

A

non-selective -> propanolol, carvedilol
cardio-selective -> bisoprolol, metoprolol XL
mixed (3rd gen) -> nebivolol
- at low dose, cardio selective
- at high dose, non-selective

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10
Q

AE of beta blockers

A

CVS: hypotension, bradycardia, heart block
CNS: depression

Contraindicated: asthmatics (bronchoconstriction esp from non-selective)

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11
Q

examples of calcium channel blockers

A

dihydropyridines
nifedipine
amlodipine
“DIPINE”

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12
Q

MOA of calcium channel blockers

A

decrease vascular smooth muscle tone -> decrease BP

decrease contractility ->decrease CO -> decrease BP

Uses: stable angina, HTP, protective effect for MI

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13
Q

AE of calcium channel blockers

A

hypotension, HF, MI

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14
Q

example of diuretics

A

thiazides
- hydrochlorothiazide
-indapamide

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15
Q

MOA of thiazides

A
  • block NaCl reabsorption at DCT
  • less blood volume
  • decrease CO
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16
Q

uses of thiazide

A

CVS: HTP, congestive HF
Renal: kidney stones due to hypercalciuria
- enhance Ca2- reabsorption to since less cations in reabsorbed

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17
Q

AE of thiazides

A
  • hyponatraemia
  • hyperuricemia
    • hypokalameia
      => NA+ excretion may trigger aldosterone release which causes excretion of K+
  • hyperglycaemia
    => decrease K+ in pancreatic B cells keeps K+ channels open which causes hyperpolarisation of cell
    => voltage gated Ca channels remain closed so exoctyosis of insulin granules decreased becasue it is activated by calcium influx
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18
Q

what are 1st line hypertensives

A

beta blockers
ACE inhibitors
calcium channel blockers
diuretics (thiazides)

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19
Q

what are the 2nd line hypertensives

A

hydralazine
alpha adrenergic antagonists
mineralocorticoid receptor antagonists

20
Q

examples of alpha adrenergic antagonists

A

prazosin, alfuzosin, terazosin
“ZOSIN”

21
Q

MOA of alpha adrenergic antagonsts

A

oppose alpha 1 mediated vasoconstriction-> decrease peripheral resistance -> decrease BP

PK:
half-life: 7h
reach peak plasma conc in 2.5h (fast acting)
metabolised in liver

22
Q

AE of alpha adrenergic antagonist

A

CVS: reflex tachycardia (moment to moment response is to increase HR)
CNS: depression
Renal: urinary frequency

23
Q

examples of mineralocorticoid receptor antagonsits

A

eplerenone, finerenone
“erenone”

24
Q

6 types of lipid lowering drugs

A
  • HMG CoA reductase inhibitor
  • PCSK9 inhibitor
  • Fibrates
  • bile acid binding resin (cholestyramine)
  • ezetimibe
  • omega 3 acid ethyl ester
25
Q

examples of HMG CoA reductase inhibitor

A

atorvastatin, pravastatin, sinovastatin
“STATIN”

26
Q

MOA of HMG CoA reductase inhibitor

A
  1. inhibit HMG CoA reductase -> decreases cholesterol synthesis
  2. increase LDL receptor on cell surface -> increase peripheral clearance
27
Q

when to administer HMG CoA reductase inhibitor

A

give orally in the evening
- less dietary cholesterol in the evening so need to synthesis cholesterol which makes HMG CoA reductase more activ

28
Q

AE of HMG CoA reductase inhibitor

A

Hepatotxicity
Myopathy
GI effects

rhabdomyolysis

Contraindicated: pregnancy, breastfeeding, child -> affect neurodevelopment of foetus

29
Q

examples of PCSK9 inhibitor

A

monoclonal antibody: evolocumab, alirocumab
“CUMAB”

30
Q

MOA of PCSK9 inhibitor

A

by inhibiting PCSK9, prevent LDL receptor degradation (LDL receptor cannot be endocytosed and degraded in lysosome). More LDL receptors on surface so absorb more LDL into cell
* reduce LDL level in blood to doesnt get stuck in blood vessel

31
Q

can PCSK9 inhibitor be taken orally

A

Cannot be taken orally because it will be digested since the body considers protein

32
Q

AE of PCSK9 inhibitor

A

hypersensitivity, inflammation at injection site, nasopharyngitis, sinusitis

33
Q

examples of fibrates

A

gemfibrozil, fenofibrate

34
Q

MOA of fibrates

A

interact with PPAR-alpha protein to increase activity of lipoprotein lipase

lipoprotein lipase splits triglyceride -> decrease in VLDL, TG, increase HDL

35
Q

AE of fibrates

A

GI effects
rash
gall stones
myositis

36
Q

MOA of cholestyramine (bile acid binding resin)

A

bind to bile salts in small intestine
- bile salts emulsify huge fat globules in small intestine and once done, bile salts will be recycled
- when cholestyramine bind to bile salts, bile salts cannot be recycled so hepatocytes use cholesterol to produce bile salts

RESULT: reduce intracellular cholesterol con and increase uptake of LDL cholesterol

Use: LDL elevation in combined hyperlipidemia

37
Q

AE of cholestyramine

A

GI effects (nausea, constipation)
impaired absorption of fat soluble vitamins (ADEK)

38
Q

MOA of ezetimibe

A

inhibit sterol transporter -> block absorption of cholesterol at small intestine

USe: decrease LDL (used tgt with simvastatin)

39
Q

AE of ezetimibe

A

diarrhoea
rhabdomyolysis
reversible hepatotoxicty

40
Q

MOA of omega 3 acid ethyl esters (EPA+DHA ethyl ester)

A

decrease TG synthesis by inhibiting diglyceride acyltransferase -> increases free fatty acid breakdown

EPA and DHA ethyl ester are poor substrates because their fatty acids have lots of kinks so cannot fit properly into enzyme binding site

PK: oral, mtabolised by liver

41
Q

AE of omega acid ethyl esters

A
  • GI effects (constipation, flatulence, pain, diarrhoea)
  • increase LDL cholesterol
  • increased bleeding time due to decreased production of thromboxane A2

Contradicated: allergic to fish, ppl on anticoagulants

42
Q

drug specifically indicated for hypertriglyceridemia

A

fibrates like gemfibrozil

43
Q

MOA of hydralazine

A

vasodilation of arterioles -> decrease afterload -> decrease BP

so compensatory release of NE to increase HR so increase venous return and CO

use: HFrEF (systolic dysfunction)

PK:
oral-> HFrEF, essential hypertension (when 1st line anti-hypertensives dont work) => slow onset but long DOA
IV-> severe post partum hypertension (acute onset and short DOA)

44
Q

AE of hydralazine

A
  • baroreflex associated sympathetic activation -> flushing, hypotension tachycardia
  • hydralazine induced lupus syndrome (HILS)
    => arthalgia, myalgia, serositis, fever
    => dose dependent, > 6 mths use
    solution: discontinue hydralazine

Contradiction:
coronary artery disease (due to hydralazine activation of SNS -> increase CO and oxygen demand -> worsen myocardial ischaemia)

45
Q

AE of sacubitril + valsartan

A

hypotension, hyperkalemia, renal failure, cough (neprilysin breaks down bradykininO)

46
Q

can diabetic patients be given beta blockers

A

sympathetic NS alert person when hypoglycemic (increase HR, feel faint)

beta blockers prevent patients from feeling palpitations because beta blockers block contractility of heart, masking symptoms of hypoglycemia

47
Q

why can’t ACE inhibitors be used for preganancy

A

potential teratogenic effects
- for statin, it decreases cholesterol but cholesterol impt for neuro development in child

cvs drugs (3 decks)

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