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

anti-hypertensives + lipid lowering drugs Flashcards

(47 cards)

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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

Study These Flashcards
A

hydralazine
alpha adrenergic antagonists
mineralocorticoid receptor antagonists

20
Q

examples of alpha adrenergic antagonists

Study These Flashcards
A

prazosin, alfuzosin, terazosin
“ZOSIN”

21
Q

MOA of alpha adrenergic antagonsts

Study These Flashcards
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

Study These Flashcards
A

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

23
Q

examples of mineralocorticoid receptor antagonsits

Study These Flashcards
A

eplerenone, finerenone
“erenone”

24
Q

6 types of lipid lowering drugs

Study These Flashcards
A
  • HMG CoA reductase inhibitor
  • PCSK9 inhibitor
  • Fibrates
  • bile acid binding resin (cholestyramine)
  • ezetimibe
  • omega 3 acid ethyl ester
25
examples of HMG CoA reductase inhibitor
atorvastatin, pravastatin, sinovastatin "STATIN"
26
MOA of HMG CoA reductase inhibitor
1. inhibit HMG CoA reductase -> decreases cholesterol synthesis 2. increase LDL receptor on cell surface -> increase peripheral clearance
27
when to administer HMG CoA reductase inhibitor
give orally in the evening - less dietary cholesterol in the evening so need to synthesis cholesterol which makes HMG CoA reductase more activ
28
AE of HMG CoA reductase inhibitor
Hepatotxicity Myopathy GI effects rhabdomyolysis Contraindicated: pregnancy, breastfeeding, child -> affect neurodevelopment of foetus
29
examples of PCSK9 inhibitor
monoclonal antibody: evolocumab, alirocumab "CUMAB"
30
MOA of PCSK9 inhibitor
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
can PCSK9 inhibitor be taken orally
Cannot be taken orally because it will be digested since the body considers protein
32
AE of PCSK9 inhibitor
hypersensitivity, inflammation at injection site, nasopharyngitis, sinusitis
33
examples of fibrates
gemfibrozil, fenofibrate
34
MOA of fibrates
interact with PPAR-alpha protein to increase activity of lipoprotein lipase lipoprotein lipase splits triglyceride -> decrease in VLDL, TG, increase HDL
35
AE of fibrates
GI effects rash gall stones myositis
36
MOA of cholestyramine (bile acid binding resin)
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
AE of cholestyramine
GI effects (nausea, constipation) impaired absorption of fat soluble vitamins (ADEK)
38
MOA of ezetimibe
inhibit sterol transporter -> block absorption of cholesterol at small intestine USe: decrease LDL (used tgt with simvastatin)
39
AE of ezetimibe
diarrhoea rhabdomyolysis reversible hepatotoxicty
40
MOA of omega 3 acid ethyl esters (EPA+DHA ethyl ester)
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
AE of omega acid ethyl esters
- 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
drug specifically indicated for hypertriglyceridemia
fibrates like gemfibrozil
43
MOA of hydralazine
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
AE of hydralazine
- 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
AE of sacubitril + valsartan
hypotension, hyperkalemia, renal failure, cough (neprilysin breaks down bradykininO)
46
can diabetic patients be given beta blockers
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
why can't ACE inhibitors be used for preganancy
potential teratogenic effects - for statin, it decreases cholesterol but cholesterol impt for neuro development in child

cvs drugs (3 decks)

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