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House Pharmacology > Anti Dyslipidemic > Flashcards

Anti Dyslipidemic Flashcards

1
Q

Anti-Dyslipidemic agents are drugs used to treat __________________ in the body

A

dysregulations in the Lipid levels

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2
Q

Lipids are (organic or inorganic ?) compounds that are ________ in water but _____ in organic solvents

A

Organic

poorly soluble

miscible

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3
Q

Lipids are (soluble or insoluble?) in blood

A

Insoluble

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4
Q

TRANSPORT of Lipids

Lipids are bound to _______ in blood an transported as complexes called _______

A

plasma proteins

LIPOPROTEINS

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5
Q

LIPOPROTEIN = _____ + ________

A

LIPIDS + APOLIPOPROTEIN

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6
Q

The main classes of lipoprotein includes

?????

A

CHYLOMICRONS.
VERY LOW-DENSITY LIPOPROTEIN (VLDL) LOW-DENSITY LIPOPROTEIN (LDL) HIGH-DENSITY LIPOPROTEIN (HDL)

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7
Q

Mention the apolipoproteins they have

Chylomicrons- _________

VLDL-_________

LDL-__________

HDL-__________

A

A1, A4, A5, B-48

B100, C, E

B100

A1,A2, E

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8
Q

CHYLOMICRONS

Formed ___GENOUSLY from ______

A

EXO

DIETARY sources

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9
Q

CHYLOMICRONS

Contains mainly _________

Transport them from the ____ to the ___ for ____

A

TRIGLYCERIDES

G.I

TISSUES; STORAGE

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10
Q

VLDL –

Formed ____genously in the ____

A

Endo

liver

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11
Q

VLDL –

Contains ______________

Transports its contents from the _____ to the _____ for _______

A

both TRIGLYCERIDE and
CHOLESTEROL

LIVER; TISSUES; STORAGE

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12
Q

LDL-

Formed _____GENOUSLY through ____________

A

ENDO

the breakdown of VLDL

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13
Q

LDL-

Contains _________

Transports it from the ____ to the _____ for _____

A

only CHOLESTEROL

LIVER

TISSUES

STORAGE

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14
Q

HDL

Formed ___GENOUSLY in ______

A

ENDO

the TISSUES

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15
Q

HDL

Contains _________

Transports them from _______ to ________ for _________

A

only CHOLESTEROL

the TISSUE; the LIVER

EXCRETION

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16
Q

Dyslipidemias means presence of a ___________ in the body

A

deranged Lipoprotein levels

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17
Q

DYSLIPIDEMIA

is characterized by the combination of

( low or high?) LDL-(Cholesterol or triglyceride?)

( low or high?) VLDL - (Cholesterol or triglyceride?)

( low or high?) HDL - (Cholesterol or triglyceride?)

A

High; Cholesterol

High; Triglyceride

Low; Cholesterol

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18
Q

AETIOLOGY of DYSLIPIDEMIAs

PRIMARY DISORDERS
_____________ disease
Includes

????

A

Inherited

TYPE I TYPE IIa TYPE IIb TYPE III TYPE IV TYPE V

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19
Q

AETIOLOGY of DYSLIPIDEMIAs

SECONDARY DISORDERS

Diabetes mellitus
Obesity
Alcoholism
Nephrotic syndrome Chronic renal failure Liver disease Hypothyroidism Drugs

A

You understand 🍻

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20
Q

DYSLIPIDEMIA: CLINICAL FEATURES

______ological
_______ological

____________

A

Dermat

Ophthalm

Gastrointestinal

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21
Q

DYSLIPIDEMIA: CLINICAL FEATURES

Dermatological

————-
__________
___________

A

Xanthomas
Xanthelasmas
Xanthomata

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22
Q

DYSLIPIDEMIA: CLINICAL FEATURES

Ophthalmological

_______

__________/______

A

Lipemia retinalis
Arcus lipoides cornea/ arcus senilis

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23
Q

DYSLIPIDEMIA: CLINICAL FEATURES

Gastrointestinal

________ or _______

A

Fatty Liver or Hepatic Steatosis

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24
Q

COMPLICATIONS of DYSLIPIDEMIA

State which is attributed to cholesterol and which is to triglycerides

Atherosclerosis
Angina pectoris
Myocardial infarction

A

cholesterol

cholesterol

cholesterol

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25
Q

COMPLICATIONS of DYSLIPIDEMIA

State which is attributed to cholesterol and which is to triglycerides

Ischemic cerebrovascular disease/ Stroke Peripheral vascular disease

Pancreatitis

A

cholesterol

triglycerides

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26
Q

DIAGNOSIS of DYSLIPIDEMIA

Lipid Profile:

_______
_________
_________
___________

A

Total Cholesterol
LDL Cholesterol
HDL Cholesterol
Triglyceride

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27
Q

Target cholesterol levels

Total cholesterol - less than ______mg/dL

LDL - less than ______mg/dL

HDL- _____ mg /dL or higher

Triglycerides-less than ______mg/dL

A

200

100

60

150

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28
Q

Non-Pharmacological TREATMENT of DYSLIPIDEMIA

_____ modification
________
________ restriction

A

Dietary

Exercise

Alcohol

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29
Q

Non-Pharmacological TREATMENT of DYSLIPIDEMIA

Dietary modification such as _______ , _____,——— etc

A

Low calories

Low saturated fats

High fiber

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30
Q

Anti-Dyslipidemic agents

Includes
_________
_________
_________
_________
_________
_________

A

STATINS
FIBRATES
NIACIN
BILE ACID RESIN EZETIMIBE
FISH OIL DERIVATIVES.

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31
Q

STATIN

EXAMPLES

???

A

Simvastatin
Lovastatin
Pravastatin
Fluvastatin
Rosuvastatin
Atovastatin

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32
Q

MECHANISM OF ACTION of STATIN

Inhibit the _________ of _______ in the ____

A

endogenous synthesis ; cholesterol; Liver

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33
Q

MECHANISM OF ACTION of STATIN

Bind and block ________________________ in the _____ pathway.

A

3-HYDROXY-3- METHYLGLUTARYL COENZYME A (HMG- COA) REDUCTASE

Cholesterol

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34
Q

Statins lead to reduction in _____

35
Q

The rate-limiting enzyme in cholesterol synthesis is _________, which catalyzes the conversion of ________ to ________

A

HMG-CoA reductase

HMG-CoA to mevalonic acid.

36
Q

Statins

In response to the reduced free cholesterol content within hepatocytes, synthesis of ______ is increased and their degradation is reduced.

A

LDLreceptors

37
Q

Statins also can reduce LDLlevels by _________________ and by _______________

A

enhancing the removal of LDLprecursors (VLDL and IDL)

decreasing hepatic VLDL production.

38
Q

Statins have a triglyceride-lowering effect

T/F

If T, how?
If F, why?

A

T

By decreasing hepatic VLDL production.

39
Q

Statins lead to
___%-___% ↓LDL-C,
__% ↓ TG
__%-____% ↑ HDL-C

A

20; 50

5

5; 15

40
Q

ADVERSE EFFECT of STATINS

______ pain

_____ Distress
Elevated _________

Insomnia

A

Muscle (Myalgia)

GI

liver enzymes

41
Q

ADVERSE EFFECT of STATINS

Insomnia

________.

_________lysis

__________

A

Rash

Rhabdomyo

Angio-edema.

42
Q

MECHANISM OF ACTION of NIACIN
It works in _______ and in the _____

A

In Adipose

In Liver

43
Q

MECHANISM OF ACTION of NIACIN

In Adipose

Bind and block __________ in adipose tissue thereby Decreases _______________

A

HORMONE-SENSITIVE LIPASE

break of triglyceride into plasma Fatty acid

44
Q

MECHANISM OF ACTION of NIACIN

In Liver

Inhibits the __________ of ______ , thereby Reducing _________

A

ESTERIFICATION of Fatty acid

Triglyceride synthesis

45
Q

Niacin lead to reduction in ___________

A

VLDL and LDL

46
Q

Niacin leads to
____-___ % ↓ TG
___-___% ↑ HDL-C
___-___% ↓ LDL-C

A

35–45

30–40

20–30

47
Q

ADVERSE EFFECT of NIACIN

Flushing

Heart _____

________ distress

Skin _______

A

Palpitations

Gastrointestinal

Itching(Pruritus)

48
Q

ADVERSE EFFECT of NIACIN

Flushing

Elevated ______

_______toxicity

Hyper_______

A

Liver enzymes

Hepato

uricemia

49
Q

EXAMPLES of FIBRATES

??

A

Bezafibrate
Ciprofibrate
Gemfibrozil
Fenofibrate
Clofibrate

50
Q

MECHANISM OF ACTION of FIBRATES

Activates _____________ which Increase __________ for _________ and _____

A

PEROXISOME PROLIFERATOR
ACTIVATED RECEPTOR-ALPHA (PPARα)

transcription of the genes

Lipoprotein lipase and Apo A1 and A5.

51
Q

Fibrates lead to decrease ______ levels.

52
Q

____________________ (PPARα)

A

PEROXISOME PROLIFERATOR
ACTIVATED RECEPTOR-ALPHA

53
Q

Flushing noticed after taking ______ is associated with production of ____ and is reduced by taking the dose 30 minutes after _____

A

NIACIN

PGD2

aspirin

54
Q

Fibrates leads to
____% ↓ TG
____% ↓ LDL-C
_____% ↑ HDL-C

55
Q

ADVERSE EFFECT of FIBRATES

Nausea, Rash

______

Muscle _______(_____)

A

Gallstones

Infection; Myositis

56
Q

ADVERSE EFFECT of FIBRATES

__________

________uria

______________ failure

A

Rhabdomyolysis

Myoglobin

Acute renal

57
Q

BILE ACID BINDING RESIN

List 3 examples

A

Cholestyramine

Colestipol

Colesevelam

58
Q

MECHANISM OF ACTION of BILE ACID BINDING RESIN

It ________ bile acids in the intestine and prevent ______________

A

Sequesters

their reabsorption and enterohepatic recirculation

59
Q

Bile acid binding resin leads to reduction in ____________

A

Total Cholesterol

60
Q

ADVERSE EFFECT Of BILE ACID BINDING RESIN

Bloating, Constipation

Unpleasant _____

Impaired ___________

A

gritty taste

lipid soluble Vitamin absorption

61
Q

ADVERSE EFFECT Of BILE ACID BINDING RESIN

Impaired drug absorption

_____,_____,_____

A

Thiazide diuretics

Warfarin

Statin

62
Q

MECHANISM OF ACTION of EZETIMIBE

Bind and blocks _______ in the ______ of the small intestine

This leads to inhibition of __________

A

NPC1L1 transport

brush border; intestinal cholesterol absorption

63
Q

Ezetimide leads to the reduction in ______

A

Total Cholesterol

64
Q

FISH OIL DERIVATIVE Reduce __________ but increase _______

A

plasma triglyceride concentrations

cholesterol.

65
Q

_____________ (PUFA)

A

n-3 polyunsaturated fatty acids

66
Q

Dietary supplementation with n-3 polyunsaturated fatty acids (PUFA) improves survival in patients who have recently had a myocardial infarction.

T/F

67
Q

Cardiovascular disease is a leading cause of morbidity and mortality in the developed countries.

T/F

68
Q

Numerous epidemiological studies have demonstrated that cardiovascular risk increases significantly as low-density lipoprotein cholesterol (LDL-C) ______eases.

69
Q

Hypercholesterolaemia: A state of _____________ in the plasma.

• Dyslipidemia: a state of ______in the levels of plasma _______ and _______

A

elevated levels of cholesterol

abnormalities

lipids and lipoproteins.

70
Q

Treatment Strategies
Lifestyle Modifications

• This has been shown to lower serum cholesterol levels, with the most notable benefits coming from ______ and ______

A

diet and weight loss.

71
Q

Treatment Strategies
Lifestyle Modifications

Dietary strategies include reducing cholesterol intake to <_____ mg daily and reducing total fat intake to <____ % of total caloric intake.

72
Q

Treatment Strategies
Lifestyle Modifications

• Inclusion of dietary soluble fibre, phytosterol esters, soy isoflavones, and nuts have all been shown to _________

A

reduce LDL-C

73
Q

________ are the mainstay of treatment for elevated LDL-C levels

74
Q

______ are the most commonly prescribed pharmacological agent used to lower LDL-C.

75
Q

Cholestyramine and colestipol bind drugs like ______,_______,______, and ______ . Therefore, there is need to space drugs and resin administration by ______

A

digoxin, tetracycline, statins and thiazide diuretics

3-4 hours.

76
Q

Examples of bile acid resins

______,________,_______

A

Cholestyramine, colestipol, and cholesevelam

77
Q

Inhibitors of intestinal absorption of cholesterol

• Examples: ___________ and ________

A

Plant stanol esters and Ezetimibe

78
Q

Plant stanol esters (present in food products like ________)

79
Q

Plant stanol esters ___________________.

Ezetimibe reduces _______________ by inhibiting the intestinal and hepatic _______________ protein, thereby _________________

A

block the absorption of dietary cholesterol

dietary and biliary cholesterol absorption

Niemann-Pick C1-Like 1

lowering total cholesterol and LDL-C levels.

80
Q

PCSK9 Inhibitors
• PCSK9 acts by ___________, thereby ____________.

Inhibition of PCSK9 leads to _____eased LDL receptor breakdown, thereby ___easing hepatic uptake of LDL, and (lower or higher?) serum LDL levels.

A

degrading LDL receptors

reducing the hepatic uptake of LDL

decr; incr

Lower

81
Q

PCSK9 Inhibitors

• Examples:____________ and _________

A

Alirocumab and evolocumab

82
Q

______________________________ (PCSK9)

A

Proprotein convertase subtilisin/kexin type 9

83
Q

Novel Agents

• One pharmacological therapy targets ___________(CETP), which normally works to facilitate the transfer of ________ from _____ to ______ .

CETP inhibition has been shown to lead to ____eases in HDL-C and ____eases in LDL-C and lipoprotein(a) levels.

A

cholesterylester transfer protein

cholesteryl esters and triglycerides

HDL to lipoproteins

incr; decr

84
Q

Novel Agents

• Example: __________

A

Anacetrapib

House Pharmacology (50 decks)

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