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Pharmacology > Antihyperlipidemic > Flashcards

Antihyperlipidemic Flashcards

1
Q

Hyperlipidemia (Hyperlipoproteinemia) means
———– plasma lipoproteins which is one of the
risk factors for————– ( coronary heart
disease).

A

increased-atherosclerosis

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2
Q

Other risk factors include ———- as a
major risk factor for coronary disease. Also, reduced
levels of ———–, increased ———— of lipoproteins,
and stimulation of————- . , ————-also a
major risk factor, is another source of oxidative
stress. Also, and,—————-and————– .

A

Cigarette smoking-HDL-oxidation-thrombogenesis-Diabetes-obesity-hypertension

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3
Q

Plasma lipids include: ———and—————and—————

A

cholesterol, triglycerides

(TG) and phospholipids

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4
Q

Metabolic disorders that involve elevations in any

lipoprotein are termed———————–or ——————–

A

hyperlipoproteinemias or hyperlipidemias

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5
Q

———–denotes increased levels of

triglycerides

A

Hyperlipemia

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6
Q

Types of lipoproteins
——————— → formed in GIT from
dietary TG.

A

Chylomicrons (TGs):

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7
Q

Types of lipoproteins
———— (TGs and cholesterol) → endogenously
synthesized in liver. Degraded by ——- into free fatty
acids (FFA) for storage in——— and for
————– in tissues such as cardiac and skeletal
muscle.

A

VLDL-LPL -adipose tissue-oxidation

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8
Q

Types of lipoproteins
———— (TGs, cholesterol); and —— (cholesterol) →
derived from ——— hydrolysis by lipoprotein
lipase. Normally, about——– of LDL is removed from
plasma by —————-

A

IDL-LDL-VLDL-70%- Hepatocyte

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9
Q

Types of lipoproteins
- ———— (protective) →exert several —————-
effects. They participate in ————- of cholesterol
from the artery wall and inhibit the —————- of
atherogenic lipoproteins& removes cholesterol from
tissues to be degraded in ———-.

A

HDL - Anti atherogenic - retrieval - oxidation - liver

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10
Q

Etiology of hyperlipidemias
• 1- ———–(genetic origin): hereditary.
• 2- Secondary to:
• Diseases e.g. ———————
• Drugs: ———————, alcohol, ——————-

A

Primary - hypothyroidism - beta blocker - thiazides

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11
Q

Types of Hyperlipidemia
• Primary Chylomicronemia (I):
Chylomicrons are not present in the serum of normal
individuals who have fasted——–hours. The recessive traits
of deficiency of——————– are usually
associated with severe lipemia.

A

10-lipoprotein lipase or its cofactor

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12
Q

Types of Hyperlipidemia
• Familial Hypercholesterolemia (IIA):
Familial hypercholesterolemia is an——————–
trait. Although levels of ———– tend to increase with normal
.

A

autosomal dominant -LDL-VLDL

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13
Q

Types of Hyperlipidemia
Familial Combined (mixed) Hyperlipoproteinemia (IIB):
elevated levels of———– ,————– .

A

VLDL-LDL

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14
Q

Types of Hyperlipidemia
• Familial Dysbetalipoproteinemia (III):
Increased ——— resulting increased ———– and cholesterol
levels.

A

IDL-TG

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15
Q

Types of Hyperlipidemia
• Familial Hypertriglyceridemia (VI):
increase———- production with normal or decreased LDL.

A

VLDL

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16
Q

Types of Hyperlipidemia
Familial mixed hypertriglyceridemia (V):
• Serum ——— and ————- are increased

A

VLDL and chylomicrons

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17
Q

Management of Hyperlipidemias
• I- Diet:
• Avoid —————- (animal fats) and give
—————-(plant fats).
Regular consumption of fish oil which contains
omega——- fatty acids and vitamins — and —-
(antioxidants).

A

saturated fatty acids-unsaturated fatty acids-3-E-C

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18
Q

Management of Hyperlipidemias
II. Exercise:
• ————- HDL and insulin —————

A

increase sensitivity

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19
Q

Management of Hyperlipidemias
III- Drug therapy: the primary goal of therapy is
to —————- levels of ——— . Also, 2nd goal, ———- in ——–
is recommended

A

decrease-LDL-increase-HDL

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20
Q 
HMG –COA reductase inhibitors
(statins)
Production of this enzyme and of LDL
receptors is transcriptionally regulated by
the------------------- in the cell.
• -Inhibit the  step ----------------in
cholesterol synthesis.
A

content of cholesterol-first enzymatic

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21
Q

Mechanism of action of statin: - Structural analogues of HMG –COA reductase (the rate limiting enzyme in
cholesterol synthesis)
→ reduction of
cholesterol synthesis in liver →
compensatory ↑ in synthesis of —————- on hepatic and extra hepatic tissues →Increase in hepatic uptake of circulating———— which decreases plasma LDL cholesterol .
- low intracellular cholesterol decreases the secretion of —————
- Decrease TGs to some extent and ↑ HDL.
- ————–protective: vaso——— and
decrease ————- formation and
stabilize plaque.————–action.

A

LDL receptors-LDL-VLDL-Cardio-dilators-platelet thrombus- Anti-inflammatory

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22
Q

Simvastatin - Rosuvastatin -lovastatin- Pitavastatin are include in which group ?

A

HMG –COA reductase inhibitors ( Statin)

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23
Q

Pharmacokinetics of statin :
————, ——— (prodrugs). The others
are active as given.
- ————— & —————– are the most
potent.
- Well absorbed when taken ————-. Excreted
mainly in ———–
- T1/2= 2 hrs Except:
Atrovastatin (———), Rosuvastatin (———)
* Should be given at night except:
—————————and—————-

A

Simvastatin-lovastatin-Atorvastatin-Rosuvastatin-orally-bile-14 hr-19 hr
Atrovastatin and Rosuvastatin

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24
Q

Effective in all types of hyperlipidemia except those who
are ———————————– (lack of
LDL receptors)
Usually combined with other drugs.

A

homozygous for familial hypercholesterolemia

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25
Q

Adverse effects of statin:

5

A

1- Increase in liver enzymes (serum transaminases should be monitored continuously ,CI in hepatic
dysfunction).
• 2-Myopathy and muscle damage leading to renal failure (myoglobinuria) in patients with renal dysfunction especially when combined with fibrates or nicotinic acid,
erythromycin, itraconazole and cyclosporine (plasma
creatine kinase level should be monitored continuously).
• 3- Cataract and GIT upset.
• 4- Increase in warfarin levels.
• 5-CI in pregnancy and nursing mothers , lactation, children
and teenagers.

26
Q

The most common affect of all 5 groups ?

A

GIT upsets

27
Q

Enumerate the high intensity statin and they lower LDL an averge of more than and equal ——?
2

A

Rosuvastatin
Atorvastatin
50%

28
Q

Enumerate the moderate intensity statin and they lower LDL an averge of more than and equal ——?
8

A 
Atorvastatin
Rosuvastatin
Simvastatin
Pravastatin
Lovastatin
Fluvastatin
Pitavastatin 
30% to less than 50%
29
Q

Enumerate the low intensity statin and they lower LDL an averge of more than and equal ——?
5

A 
Lovastatin
Pravastatin
Fluvastatin
Simvastatin
Pitavastatin 
less than 30%
30
Q

FDA is revising drug label for ———–to clarify the risk of myopathy

A

Lovastatin

31
Q

The first and cheapest anti hyperlipidemic———————————-.Decrease both TGs (—————) and cholesterol
(————-) levels

A

Niacin; Nicotinic acid (Inhibitors of lipolysis)-VLDL-LDL

32
Q

• Mechanism of action of Niacin ( Nicotinic Acid)(inhibitors of lipolysis):
• It is a ————inhibitor of lipolysis in adipose
tissues → ↓ mobilization of FFAs (major
precursor of ——- and needed for VLDL
production) to the liver → ↓ VLDL (after few
hours).
• Since ——- is derived from VLDL so ↓ VLDL
→ ↓ LDL (after few hours).
• - ↑ HDL levels ( the most potent
antihyperlipidemic).
• - ↓ endothelial dysfunction →↓ thrombosis

A

potent-TGs-LDL

33
Q

The most potent antihyperlipidemic drug in raising HDL ?

A
  • Niacin; Nicotinic acid (Inhibitors of

lipolysis)

34
Q

—————–will dec endothelial dysfunction →↓ thrombosis

A
  • Niacin; Nicotinic acid (Inhibitors of

lipolysis)

35
Q

someone use statin and has a low level of HDL which drug could he use to improve his HDL level ?

A
  • Niacin; Nicotinic acid (Inhibitors of

lipolysis)

36
Q

Pharmacokinetics of Niacin:
• ———– given, converted to——— which
does not decrease plasma lipids alone(must be
incorporated with NAD).

A

Orally-nicotinamide

37
Q

Therapeutic uses of Niacin :
• Familial ————- (type IIB) (↑VLDL and↑
LDL).
• Sever hypercholesterolemia, combined with
————– or ————-.

A

hyperlipidemias-fibrates -cholestyramine

38
Q

Fibrates (activators of lipoprotein
lipase)
————-fibrate (prodrug 20 hours) and ————-(2h)

A

Fenofibrate-Gemfibrozil

39
Q

Mechanism of action of Fibrates
: Agonists at PPAR(—————) →
expression of genes responsible for increased
activity of plasma lipoprotein lipase enzyme →
hydrolysis of———– (by 30%) and
chylomicrons→ ↓ serum TGs
• - Increase clearance of———(by 10%) by liver &
↑ HDL

A

Peroxisome proliferator activated receptor- VLDL- LDL

40
Q

The most effective in reduction TGs —————

A

Fibrate

41
Q

Therapeutic uses of Fibrate:

1 thing

A

• Hypertriglyceridemia (the most effective in
reduction TGs) - combined hyperlipidemia (type
III) if statins are contraindicated.

42
Q

patient who take fibrate should also becareful about Ingestion of high amount of simple
sugars especially ————-enhances
FFA, and formation of TGs and VLDL,
thus reduction of fructose and other free
sugars is an effective mechanism to
lower FFA synthesis.

A

fructose

43
Q

Fibrates-Efficacy
lower TG by ———-to———
Lower LDL-C by ———–to———– with normal ———–
Raise HDL-C by ——- to ——-
reduce progression of ——————lesions

A

30 - 55 %
5-20%
18-22
coronary

44
Q

Pharmacokinetics of fibrate:
• - Completely absorbed after ——-administration.
• - ————- bound to plasma proteins(pp),
extensively metabolized, excreted in ———–

A

oral-Highly-urine

45
Q

Adverse effects: of fibrate
• ——— disturbances.
• ———– (increased biliary cholesterol
excretion).
• - Muscle pain and myopathy (patients with ——–
impairment are at risk).
• - Increase ———- (something like warfarin) levels (compete for pp).
• -CI in pregnancy (safety in pregnancy is not
established), , lactating women, renal and hepatic
dysfunction, gall stones.

A

GIT
Gall stones
renal
coumarin

46
Q
  • Bile acids Sequestrants(resins):

3 example

A

Cholestyramine, colestipol and colesevalem

47
Q

• Mechanism of action of resins : are——- exchange resins; bind bile acids in the intestine forming complex →loss of bile acids in the stools →↑ conversion of
cholesterol into———— in the liver.
Decreased concentration of intrahepatic cholesterol →
compensatory increase in ——– →↑ hepatic
uptake of circulating LDL → ↓ serum LDL
cholesterol levels.
• -Modest increase in ————-

A

anion- bile acids-LDL receptors-HDL

48
Q

Pharmacokinetics of resins :
Orally given but——— neither ———-nor
altered by intestine, totally excreted
in feces

A

absorbed-metabolically

49
Q

Bile Acid-Binding Resins efficacy

  • Reduce LDL-C by ——-to———–
  • Raise HDL-C by —–to———
  • May increase ————-concentration
  • Reduce major ———– events
  • Reduce ——– mortality
A 
15-26%
3-6%
TG concentration
major coronary events
coronary-CHD
50
Q

Therapeutic uses of resins:
• Of choice in treatment of type ——and ———-
hyperlipidemias (along with statins when response to
statins is inadequate or they are contraindicated).
• - useful for Pruritus in biliary obstruction (↑ bile acids).

A

IIA and IIB

51
Q

————————useful for Pruritus in biliary obstruction (↑ bile acids).

A

resins(Bile acid sequestrants)

52
Q

AVERSE EFFECTS of resins:
• ——–, ————– but not ———- ↓
absorption of fat soluble vitamins (—-, —–, —-, —–) , ↓ Vit K → ———————–
• —————is the most common adverse effect.
• ↓ absorption of many drugs as digitoxin, warfarin,
aspirin, phenobarbitone. Thus, these drugs should be
taken —–to—– hours before , or —-to— hours after bile acids
binding resins
Cholestyramine can sometimes cause ————

A 
Cholestyramine, colestipol , colesevalem
k,a,d,e
hypoprothrombinemia.
Constipation
1-2
4-6
Hypertriglyceridemia
53
Q
  • Ezetimibe (cholesterol absorption inhibitors)
    Inhibits intestinal ———- absorption
    → ↓ delivery of intestinal cholesterol to
    liver→ ↓ concentration of intrahepatic stores
    of cholesterol→ compensatory ↑ in LDL
    receptors →↑ uptake of circulating LDL
    →↓ serum LDL cholesterol levels(
    comparable or even more than statins)
A

cholesterol

54
Q

Ezetimibe (cholesterol absorption inhibitors)

Adverse effects: 3 things

A

diarrhea and abdominal
pain.
• - CI in patients with liver dysfunction

55
Q

-Therapeutic uses
• —————May be synergistic with statins : so good for
combination therapy (adjunct therapy).
• Recent data suggest that ——— with
Simvastatin is supperior than Simvastatin
alone in reducing cardiovascular events.

A

Ezetimibe

56
Q

Omega - 3 fatty acids
Mechanism of action:
• Essential fatty acids inhibit ———-and———-
• Decrease TG by ————- with small
increases in LDL and HDL.
• Does ———— CV morbidity and motality.

A

VLDL and TG.
25- 30 %
not affect

57
Q

• Adverse effects:

2 things

A

• GIT disturbances.
• Increase bleeding tendency with
anticoagulants and antiplatelets.

58
Q

Combination drug therapy:
If no improvement within ————weeks with a
single drug therapy, the dose should be
————-.

A

6

increased

59
Q

Combination drug therapy:
If no improvement after——— months
change the drug or consider combination
therapy

A

3

60
Q

Combination drug therapy:
Bile acid resins can be safely combined
with ———- or ————- (↓ LDL, VLDL
cholesterol levels respectively).
- Ezetimibe + statins → synergistic effects.
• - Fibrates and statins are——- → ————.
• - Nicotinic acid and statins (must be
cautiously used) → —————.

A 
statins
nicotinic acid
CI 
myopathy
myopathy
61
Q

Efficacy of Ezetimibe
Lowers LDL-C by — to —–
May raise HDL-C by —- to ——-
Lower TG by ——– to ———

A

18-20%
1-5%
5-10%

62
Q

Adverse effects of Niacin :
5 things
3G 1C 1M

A 
1-Cutaneous flush (PG-mediated , dec by Aspirin 30 min before niacin ) and pruritus
2-GIT disturbances
3-Glucose intolerance 
4- Gouty arthritis(hyperuricemia)
5-Myopathy (rare)

Pharmacology (6 decks)

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