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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
COMPLICATIONS of DYSLIPIDEMIA State which is attributed to cholesterol and which is to triglycerides Ischemic cerebrovascular disease/ Stroke Peripheral vascular disease Pancreatitis
cholesterol triglycerides
26
DIAGNOSIS of DYSLIPIDEMIA Lipid Profile: _______ _________ _________ ___________
Total Cholesterol LDL Cholesterol HDL Cholesterol Triglyceride
27
Target cholesterol levels Total cholesterol - less than ______mg/dL LDL - less than ______mg/dL HDL- _____ mg /dL or higher Triglycerides-less than ______mg/dL
200 100 60 150
28
Non-Pharmacological TREATMENT of DYSLIPIDEMIA _____ modification ________ ________ restriction
Dietary Exercise Alcohol
29
Non-Pharmacological TREATMENT of DYSLIPIDEMIA Dietary modification such as _______ , _____,——— etc
Low calories Low saturated fats High fiber
30
Anti-Dyslipidemic agents Includes _________ _________ _________ _________ _________ _________
STATINS FIBRATES NIACIN BILE ACID RESIN EZETIMIBE FISH OIL DERIVATIVES.
31
STATIN EXAMPLES ???
Simvastatin Lovastatin Pravastatin Fluvastatin Rosuvastatin Atovastatin
32
MECHANISM OF ACTION of STATIN Inhibit the _________ of _______ in the ____
endogenous synthesis ; cholesterol; Liver
33
MECHANISM OF ACTION of STATIN Bind and block ________________________ in the _____ pathway.
3-HYDROXY-3- METHYLGLUTARYL COENZYME A (HMG- COA) REDUCTASE Cholesterol
34
Statins lead to reduction in _____
LDL
35
The rate-limiting enzyme in cholesterol synthesis is _________, which catalyzes the conversion of ________ to ________
HMG-CoA reductase HMG-CoA to mevalonic acid.
36
Statins In response to the reduced free cholesterol content within hepatocytes, synthesis of ______ is increased and their degradation is reduced.
LDLreceptors
37
Statins also can reduce LDLlevels by _________________ and by _______________
enhancing the removal of LDLprecursors (VLDL and IDL) decreasing hepatic VLDL production.
38
Statins have a triglyceride-lowering effect T/F If T, how? If F, why?
T By decreasing hepatic VLDL production.
39
Statins lead to ___%-___% ↓LDL-C, __% ↓ TG __%-____% ↑ HDL-C
20; 50 5 5; 15
40
ADVERSE EFFECT of STATINS ______ pain _____ Distress Elevated _________ Insomnia
Muscle (Myalgia) GI liver enzymes
41
ADVERSE EFFECT of STATINS Insomnia ________. _________lysis __________
Rash Rhabdomyo Angio-edema.
42
MECHANISM OF ACTION of NIACIN It works in _______ and in the _____
In Adipose In Liver
43
MECHANISM OF ACTION of NIACIN In Adipose Bind and block __________ in adipose tissue thereby Decreases _______________
HORMONE-SENSITIVE LIPASE break of triglyceride into plasma Fatty acid
44
MECHANISM OF ACTION of NIACIN In Liver Inhibits the __________ of ______ , thereby Reducing _________
ESTERIFICATION of Fatty acid Triglyceride synthesis
45
Niacin lead to reduction in ___________
VLDL and LDL
46
Niacin leads to ____-___ % ↓ TG ___-___% ↑ HDL-C ___-___% ↓ LDL-C
35–45 30–40 20–30
47
ADVERSE EFFECT of NIACIN Flushing Heart _____ ________ distress Skin _______
Palpitations Gastrointestinal Itching(Pruritus)
48
ADVERSE EFFECT of NIACIN Flushing Elevated ______ _______toxicity Hyper_______
Liver enzymes Hepato uricemia
49
EXAMPLES of FIBRATES ??
Bezafibrate Ciprofibrate Gemfibrozil Fenofibrate Clofibrate
50
MECHANISM OF ACTION of FIBRATES Activates _____________ which Increase __________ for _________ and _____
PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR-ALPHA (PPARα) transcription of the genes Lipoprotein lipase and Apo A1 and A5.
51
Fibrates lead to decrease ______ levels.
VLDL
52
____________________ (PPARα)
PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR-ALPHA
53
Flushing noticed after taking ______ is associated with production of ____ and is reduced by taking the dose 30 minutes after _____
NIACIN PGD2 aspirin
54
Fibrates leads to ____% ↓ TG ____% ↓ LDL-C _____% ↑ HDL-C
50 10 15
55
ADVERSE EFFECT of FIBRATES Nausea, Rash ______ Muscle _______(_____)
Gallstones Infection; Myositis
56
ADVERSE EFFECT of FIBRATES __________ ________uria ______________ failure
Rhabdomyolysis Myoglobin Acute renal
57
BILE ACID BINDING RESIN List 3 examples
Cholestyramine Colestipol Colesevelam
58
MECHANISM OF ACTION of BILE ACID BINDING RESIN It ________ bile acids in the intestine and prevent ______________
Sequesters their reabsorption and enterohepatic recirculation
59
Bile acid binding resin leads to reduction in ____________
Total Cholesterol
60
ADVERSE EFFECT Of BILE ACID BINDING RESIN Bloating, Constipation Unpleasant _____ Impaired ___________
gritty taste lipid soluble Vitamin absorption
61
ADVERSE EFFECT Of BILE ACID BINDING RESIN Impaired drug absorption _____,_____,_____
Thiazide diuretics Warfarin Statin
62
MECHANISM OF ACTION of EZETIMIBE Bind and blocks _______ in the ______ of the small intestine This leads to inhibition of __________
NPC1L1 transport brush border; intestinal cholesterol absorption
63
Ezetimide leads to the reduction in ______
Total Cholesterol
64
FISH OIL DERIVATIVE Reduce __________ but increase _______
plasma triglyceride concentrations cholesterol.
65
_____________ (PUFA)
n-3 polyunsaturated fatty acids
66
Dietary supplementation with n-3 polyunsaturated fatty acids (PUFA) improves survival in patients who have recently had a myocardial infarction. T/F
T
67
Cardiovascular disease is a leading cause of morbidity and mortality in the developed countries. T/F
T
68
Numerous epidemiological studies have demonstrated that cardiovascular risk increases significantly as low-density lipoprotein cholesterol (LDL-C) ______eases.
incr
69
Hypercholesterolaemia: A state of _____________ in the plasma. • Dyslipidemia: a state of ______in the levels of plasma _______ and _______
elevated levels of cholesterol abnormalities lipids and lipoproteins.
70
Treatment Strategies Lifestyle Modifications • This has been shown to lower serum cholesterol levels, with the most notable benefits coming from ______ and ______
diet and weight loss.
71
Treatment Strategies Lifestyle Modifications Dietary strategies include reducing cholesterol intake to <_____ mg daily and reducing total fat intake to <____ % of total caloric intake.
200 20
72
Treatment Strategies Lifestyle Modifications • Inclusion of dietary soluble fibre, phytosterol esters, soy isoflavones, and nuts have all been shown to _________
reduce LDL-C
73
________ are the mainstay of treatment for elevated LDL-C levels
Statins
74
______ are the most commonly prescribed pharmacological agent used to lower LDL-C.
Statins
75
Cholestyramine and colestipol bind drugs like ______,_______,______, and ______ . Therefore, there is need to space drugs and resin administration by ______
digoxin, tetracycline, statins and thiazide diuretics 3-4 hours.
76
Examples of bile acid resins ______,________,_______
Cholestyramine, colestipol, and cholesevelam
77
Inhibitors of intestinal absorption of cholesterol • Examples: ___________ and ________
Plant stanol esters and Ezetimibe
78
Plant stanol esters (present in food products like ________)
margarine
79
Plant stanol esters ___________________. Ezetimibe reduces _______________ by inhibiting the intestinal and hepatic _______________ protein, thereby _________________
block the absorption of dietary cholesterol dietary and biliary cholesterol absorption Niemann-Pick C1-Like 1 lowering total cholesterol and LDL-C levels.
80
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.
degrading LDL receptors reducing the hepatic uptake of LDL decr; incr Lower
81
PCSK9 Inhibitors • Examples:____________ and _________
Alirocumab and evolocumab
82
______________________________ (PCSK9)
Proprotein convertase subtilisin/kexin type 9
83
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.
cholesterylester transfer protein cholesteryl esters and triglycerides HDL to lipoproteins incr; decr
84
Novel Agents • Example: __________
Anacetrapib

House Pharmacology (50 decks)

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