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Pharmacology MBBS > Hypolipidemics and vasodilators > Flashcards

Hypolipidemics and vasodilators Flashcards

1
Q

Receptor which absorbs cholesterol into the intestinal cell

Drug which inhibits it

A

NPC1L1 receptor
Niemann Pick C1 like1 receptor
Exetimibe inhibits this receptor

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2
Q

MTP of lipid metabolism

Inhibited by

A

Microsomal Transport Protein
Transports lipids into the RER of liver to be combined with proteins (to form VLDL)
Inhibited by Lomitapide (used along with Icosapent)

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3
Q

Avasimibe

A

Inhibitor of ACAT (Acyl CoA transferase) which esterifies cholesterol
Under trial

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4
Q

Icosapent

A

Blocks secretion of VLDL from liver

Used along with Lomitapide against genetic condition called familial hypertriglyceridemia.

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5
Q

Fibrates

A

Derivatives of fibric acid
Increases activity of LPL (lipoprotein lipase) ➡️
increased removal of TAG from lipoproteins ➡️
decrease in TAG, VLDL and chylomicron
Side effect: increases LDL

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6
Q

Mipomersen sodium

A

Blocks synthesis of apo B-100 ➡️ decreases LDL

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7
Q

LDL receptor are increased by

A
  1. Statins
  2. Ezetimibe: decreased extrinsic cholesterol
  3. Bile acid binding resins
  4. PESK-9 inhibitors:
    Evolocumab, Alivocumab
    PESK-9 facilitates degradation of LDL receptor
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8
Q

Statins

Decreases LDL receptor by which mechanism

A

Competitive inhibitor of HMG CoA reductase inhibitors ➡️ intrinsic cholesterol decreases ➡️ increased demand for extrinsic cholesterol

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9
Q

Statins examples

A 
Rosavastatin
Atorvastatin
Pravastatin
Fluvastatin
Simvastatin
Pitavastatin
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10
Q

Mechanism of action of statins

A

Competitive inhibition of HMG CoA reductase activity (activity increases at night)

  1. ➡️ Decreased cholesterol synthesis ➡️ LDL receptor increases ➡️ decreased plasma LDL
  2. Inhibits VLDL synthesis ➡️ decreased TAG
  3. Increases HDL
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11
Q

Pleiotrophic effects of statins

A

Non lipidemic beneficial effects:

  1. Anti aggregant effect
  2. Anti coagulant effect
  3. Anti inflammatory effect (decreased CRP)
  4. Vasodilation (increased NO)
  5. Plaque stabilising effect
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12
Q

Uses of statins

A
  1. DoC for treatment of dyslipidemia (eg., type II hyperlipoproteinemia)
  2. 1°and 2° prophylaxis of atherosclerotic cardiovascular disease (stable angina, MI, stroke)
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13
Q

Absorption of statins

A

Good oral absorption

Maximum with prodrugs like lovastatin and simvastatin (which are highly lipid soluble) which can cross BBB

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14
Q

First pass metabolism of statins

A

High first pass metabolism of statins
(But they have high plasma protein binding)
Reflux pump called OAT P1B1 (organic anionic transporter)
This is inhibited by gemfibrozil ➡️ increased bioavailability of statins

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15
Q

Metabolism of statins

A

Phase-1:
By CYP3A4, except fluvastatin, pravastatin, rosuvastatin
Phase-2:
By glucuronidation
t1/2 maximum: rosuvastatin > atorvostatin

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16
Q

Most potent statins

A

Pitavastatin > Rosuvastatin

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17
Q

Bile acid binding resins

Mechanism and examples

A 
Block enterohepatic circulation of bile acids
➡️ Decreases bile acid in liver 
➡️ decreases cholesterol 
➡️ increases LDL receptors 
➡️ decreases plasma LDL
Examples:
1. Cholestyramine 
2. Cholesevelam
3. Colestipol
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18
Q

Side effects of statins

A
  1. Myopathy:
    don’t monitor CPK since myopathy can be delayed by years
  2. Hepatotoxicity:
    Monitor ALT/AST every 3-6 months
  3. Insulin resistance
  4. Pravastatin decreases fibrinogen levels
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19
Q

CI of statins

A
  1. Pregnant women
  2. Children <10 years
    Except pravastatin, which is CI for children <8 years
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20
Q

Uses of bile acid binding resins

A
  1. Add on to statins
  2. Dyslipidemia with increased LDL
  3. DoC in pregnant women and children instead of statins
  4. Treatment of biliary gastritis and diarrhoea
  5. Colesevelam is used for treatment of type II DM
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21
Q

Side effects of bile acid binding resins

A
  1. Increased VLDL➡️ hypertriglyceridemia (used only if TAG <300 mg/dl)
  2. Bloating
  3. Constipation
  4. Dyspepsia
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22
Q

Niacin mechanism of action

A
  1. Stimulates Gi receptors of adipocytes
    ➡️ decreases cAMP
    ➡️ inhibits HSL
    ➡️ decreases FFA, TAG, VLDL, IDL and LDL
  2. Increases HDL (maximum among hypolipidemics)
  3. Only drug that decreases Lp(a)
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23
Q

Uses of niacin

A
  1. Add on to statins
  2. Dyslipidemia to increase HDL
    Not preferred nowadays
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24
Q

Side effects of niacin

A
  1. Increases PG ➡️ niacin induced flushing (DoC: aspirin)
  2. Hepatotoxic: ALT/AST monitoring required
  3. Insulin resistance: blood glucose monitoring
  4. Increased uric acid level
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25
Q

Examples of fibrates

Uses

A

Clofibrate
Bezafibrate
Fenofibrate
Gemfibrozil
Uses:
1. DoC for type III hyperlipoproteinemia
2. DoC for hypertriglyceridemia and chylomicronemia syndrome
3. Fenofibrate: decrease uric acid, so used in gout with hypertriglyceridemia

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26
Q

Dosage, side effects and CI of fibrates

A

Dose: 30 minutes before food (food increases absorption)
Side effects:
1. Myopathy except bezafibrate
2. Choledocholithiasis: maximum with clofibrate
CI: renal failure

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27
Q

Mechanism of action of fibrates

A

Stimulates PPAR (paraoxysmal proliferation of activated receptor-α) ➡️ stimulates lipoprotein lipase:

  1. Decreases TAG, VLDL and chylomicron
  2. Increases LDL, IDL and HDL (maximum with gemfibrozil)
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28
Q

Classification of vasodilators

A 
1. Arterial dilators:
 decrease after load
2. Venodilators and mixed dilator:
 decreases preload 
 S/E: postural hypotension
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29
Q

Examples of arterial vasodilators

A
  1. Calcium channel blockers like amlodipine
  2. Hydralazine
  3. Minoxidil
  4. Diazoxide
  5. Fenoldopam
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30
Q

Classification of CCB

A 
1. Non-DHP:
 •Verapamil (most potent)
 •Diltiazem
2. DHP (dihydropyridines):
 •Amlodipine
 •Clevidipine
 •Nifedipine
 •Nicardipine
 •Nimodipine
All are racemic mixture of enantiomers except diltiazem and nifedipine
31
Q

Special features of amlodipine

A

A DHP CCB like clevidipine
Longest acting CCB
Has maximum oral bioavailability

32
Q

Special features of clevidipine

A

A DHP CCB like nicardipine

Shortest acting CCB since it is metabolised by plasma esterase

33
Q

Uses of CCBs

A
  1. HTN (mild/moderate): 1st line drugs
  2. HTN urgency: oral nifedipine
  3. HTN emergency: IV nicardipine (DoC) > IV clevidipine
  4. DoC in Raynaud’s disease
  5. Cerebral vasospasm (2° to SAH)
34
Q

Special features of nimodipine

Special use

A

A DHP CCB like amlodipine
Has high lipid solubility and high affinity for cerebral blood vessel
DoC for cerebral vasospasm (2° to subarachnoid haemorrhage SAH)

35
Q

Side effects of calcium channel blockers CCBs

A
  1. Head ache: M/C
  2. Ankle edema:
    Cause by pre-capillary dilation
    Prevented by ACEi/ARB (via post-capillary dilation)
    For verapamil:
  3. Constipation
  4. AV node block
    Hence verapamil is CI with β-blocker (both causes AV node inhibition)
36
Q

Hydralazine

A 
Arterial vasodilator Mechanisms:
1. IP3 induced Ca release 
2. Opens K+ channel
3. Release of NO
Uses (IV route):
 HTN emergency in pregnancy (DoC labetolol IV)
37
Q

Side effects of hydralazine

A 
Arterial dilator
1. Head ache
2. Hypotension
3. SLE: M/C in females
 Within 6 months of drug use 
4. Sweet’s syndrome:
 Neutrophilic dermatosis
38
Q

Minoxidil

A 
Potent vasodilator (arterial)
Mechanism:
 Opens K+ channel
Uses:
1. Severe/resistant HTN
2. Androgenic alopecia (topically):
 DoC finasteride 
 (S/E: decreased libido)
39
Q

Side effect of minoxidil

A

Arterial dilator
S/E:
1. Hirsutism (via systemic route)
2. Na+/H2O retention- some very potent vasodilator

40
Q

Classes of vasodilator drugs which act via increasing NO release

A
  1. Hydralazine
  2. Nitrates
  3. Nitroprusside
41
Q

Diazoxide

A 
Arterial dilator
Mechanism:
 Opens K+ channel ➡️ potent vasodilator
Uses:
1. DoC for insulinoma
2. Was used for HTN emergency via IV (S/E- severe hypotension)
42
Q

Examples of venodilators

A
  1. Nitroglycerin

2. Isosorbide dinitrate and mononitrate

43
Q

Nitroglycerin mechanism of venous dilation (immediate)

A

It is metabolised by aldehyde dehydrogenase to NO
NO stimulates Guanylate cyclase ➡️ increases CGMP ➡️
Inhibits MLCK myosin light chain kinase ➡️:
1. In blood vessel:
Vasodilation
Uses in angina/MI
2. In GIT:
Relaxation
Oesophageal/biliary spasm

44
Q

Effects of continuous nitroglycerin exposure

A 
Continuous nitroglycerin exposure ➡️
 ADH down-regulation ➡️
 nitrate tolerance
Prevention:
 8 hours of nitrate free period every day, especially at night time ➡️ decreased risk of acute angina
45
Q

Nitroglycerin drug interactions with PDE-5 inhibitors

A

PDE-5 which metabolises cGMP is inhibited by Sildenafil and Tadalafil
These cause vasodilation and are used against pulmonary HTN and erectile dysfunction
Combination of these is CI as it causes severe hypotension

46
Q

Drug interaction of guanyl cyclase simulator with nitroglycerin

A

Both produce vasodilation using similar effect
Examples of guanyl cyclase simulator:
1. Cinaciguat
2. Riociguat (used for pulmonary HTN)

47
Q

Uses of nitroglycerin

A

High first pass metabolism do not preferred orally
1. Sublingual- DoC for:
•acute attack of angina
•acute prophylaxis is angina
2. IV: HTN emergency, pulmonary oedema
3. Transdermal, buccal: long term prophylaxis of angina (slow absorption)

48
Q

Isosorbide dinitrate IDN

A 
Venodilators 
In liver it is denitrated to IMN (active form)
Uses:
 Orally
1. Long term prophylaxis of angina
2. Chronic CHF (IDN + hydralazine)
 Via sublingual route
3. Acute attack of angina
49
Q

Isosorbide mononitrate IMN

A

Venodilator
Active form of IDN
No first pass metabolism
Use: orally for long term prophylaxis of angina

50
Q

Side effects of nitrates (venodilators)

A
  1. Hypotension
  2. Head ache
  3. Dizziness
  4. Monday disease (workers of nitrate industry)
51
Q

Mixed dilators

A
  1. α blockers

2. Nitroprusside

52
Q

Nitroprusside

A

Mixed dilator
Metabolised in endothelium
Mechanism similar to nitroglycerin
Gets metabolised to 2° product cyanide which is metabolised by rhodonase to thiocyanate
Thiocyanate effects:
1. Hypothyroidism (anti thyroid substance)
2. Neuropsychiatric effects

53
Q

Uses of nitroprusside

A
  1. HTN emergency (2nd line)
  2. Pulmonary oedema
  3. Aortic dissection always with β blocker (to inhibit reflex tachycardia due to vasodilation)
54
Q

Functions of Angiotensin II and AT III

A
  1. Blood vessels:
    Acts on AT-I receptor causing vasoconstriction
  2. Increases aldosterone:
    Na+ / H2O retention and K+ loss
  3. Glomerulus:
    AT-II receptors of efferent arteriole constriction and
    PGs cause afferent arteriole dilation
55
Q

Angiotensin IV

A

In CNS
Increases cognition
AT IV analogue under trial for treatment against Alzheimer’s disease

56
Q

RAAS inhibitors types

A
  1. DRI: direct renin inhibitor
  2. ACEi:
    angiotensin converting enzyme inhibitor
    Increases renin and AT-I
  3. ARB:
    angiotensin receptor blockers
    Blocks AT-I
57
Q

Effects of RAAS inhibitor

A
  1. Blocks kininase
  2. Blood vessel
  3. Decreases aldosterone
  4. Efferent arteriole dilation
58
Q

Effects of RAAS inhibitor wrt kininase

A

ACEi blocks kininase
➡️ increases bradykinin, substance P, PGs
Side effects:
1. Angioedema
2. Dry cough (due to medullary cough centre irritation)

59
Q

Effect of RAAS inhibitors on blood vessels and aldosterone levels

A 
1. Causes vasodilation and loss of Na+/H2O ➡️ decreases bp:
 S/E postural hypotension
 1st line drug in HTN
2. K+ retention:
 S/E hyperkalemia
 Should not conbine ACEi with ARB
60
Q

Effect of RAAS inhibitor in glomerulus

A 
1. Efferent arteriole dilation ➡️ decreased GFR
CI:
 • Renal failure
 • B/L renal artery stenosis
2. Decreases proteinuria
Used in:
 • DM
 • CKD
 • Nephrotic syndrome
DoC of HTN with proteinuria
61
Q

Examples of ACEi

A 
C. Captopril
L. Lisinopril
E. Enalapril
R. Ramipril
Q. Quinapril
f. Fosinopril
b. Benzapril
The above Clerq fb are given orally
Enalaprilat is given IV due to poor absorption
62
Q

ACEi which are not prodrugs

A

Captopril and Lisinopril

63
Q

Elimination of ACEi

A 
1. Uniphasic: shortest acting and least potent
 Clearance from plasma
 Captopril
2. Biphasic:
 \+ high affinity for ACE
 most ACEi
3. Triphasic: longest acting
 biphasic + high AVd 
 Ramipril
64
Q

Uses of ACEi

A
  1. Hyperreninemic HTN: first line drug
  2. HTN+ proteinuria: DoC
  3. HTN urgency: oral captopril
  4. HTN emergency: IV enalapril
  5. History of MI or chronic CHF: to reduce mortality
  6. Captopril test
65
Q

Captopril test

A

Differential diagnosis b/w renovascular or essential HTN
In RV HTN the increase in renin is much more than in essential HTN
Confirmatory test is renal angiography
Captopril preferred as shortest acting

66
Q

Specific side effects of ACEi

A
  1. Angioedema
  2. Dry cough M/C
  3. Dysgeusia
  4. Rash with itch
    The last 2 are maximum with captopril
67
Q

Examples of ARB angiotensin receptor blockers

A 
T. Telmisartan
E. Eprosartan 
C. Candesartan 
I. Irbesartan 
L. Losartan 
O. Olmesartan
In tequila, the prodrugs are Ca and Ol
Telmisartan has maximum PPAR γ agonist
68
Q

Losartan

A 
Angiotensin receptor blocker ARB
Non specific
1. Blocks thromboxane A2:
 Anti aggregant
2. Uricosuric effect:
 2° use for chronic gout
3. PPAR γ agonist
 Decreases insulin resistance
69
Q

Pharmacokinetics of Angiotensin Receptor Blockers

A 
Poor oral bioavailability
Increased plasma protein binding
t1/2: 
 max in Telmisartan
 min in Eprosartan
70
Q

Uses of ARBs angiotensin receptor blockers

A

Uses are similar to ACEi

  1. Preferred in case of ACEi intolerance and ineffectiveness
  2. Losartan- portal HTN
  3. Irbesartan - rhythm control on atrial fibrillation
71
Q

Side effects of ARBs

A
  1. Alopecia
  2. Agranulocytosis
  3. Vasculitis
  4. Olmesartan can cause sprue like syndrome (with characteristics of weight loss and abdominal pain)
72
Q

Direct renin inhibitor DRI

A 
Aliskiren - only FDA approved drug
Use: 2nd line for HTN
S/E: 
 hyperuricemia
 diarrhoea, GERD
73
Q

Common side effects of all RAAS inhibitors

A

Postural hypotension

Hyperkalemia

74
Q

Common contraindications of all RAAS inhibitors

A
  1. Renal failure
  2. B/L renal artery stenosis
  3. Pregnancy:
    In 1st trimester- CNS defects
    In 2nd/3rd trimester- renal defects

Pharmacology MBBS (19 decks)

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