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Pharmacology > 1-6 and 7 > Flashcards

1-6 and 7 Flashcards

1
Q

What type of patient should NOT be prescribed resins (bile acid sequestrants)?

A

Patient with severe hypertriglyceridemia

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2
Q

There is a DDI between resins and what three other drug classes?

A

Beta blockers, Loop Diuretics, and Thiazide Diuretics

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3
Q

What drug class works via charge based interaction?

A

Bile Acid Sequestrants

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4
Q

Bile acid sequestrants are ___ charged while bile acids are ___ charged. Given this, bile-resin complex is eliminated from body via stool.

A

Bile acid sequestrants are positively charged
Bile acids are negatively charged

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5
Q

What compensation occurs due to bile acid sequestrants?

A

-Increase in LDL receptors

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6
Q

What are the three bile acid sequestrants?
(coles in a pool, cole saved a lamb, coles tyrin me out)

A

1) Colesevelam
2) Colestipol
3) Cholestyramine

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7
Q

True or False: Depletion of bile acid is accompanied by a decrease in new bile acid synthesis in the liver

A

False - Depletion of bile acid is accompanied by an INCREASE in new bile acid synthesis in the liver

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8
Q

How does increasing bile synthesis affect hepatic cholesterol content?

A

Increasing bile synthesis DECREASES hepatic cholesterol content

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9
Q

True or False: Colestipol increases hepatic LDL receptor membrane localization and enhances LDL clearance from circulation

A

True

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10
Q

Simvastatin and Atrorvastatin belong to which drug class?

A

Statins (HMG-CoA Reductase inhibitors)

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11
Q

True or False: Simvastatin and Lovastatin are inactive lactones that need to be converted to active forms

A

True -
Their active forms are simvastatin hydroxy acid and lovastatin hydrox acid

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12
Q

Which drug class has extensive first pass metabolism and is regulated by OATP1B1?

A

Statins (HMG-CoA Reductase Inhibitors)

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13
Q

Why is myopathy an AE of statins?

A

Statins can induce reduction in CoQ10 synthesis

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14
Q

Rhabdomyolysis (rapid muscle damage) is an AE associated with which drug class?

What increases one’s risk of developing this?

A

Statins
Consuming grapefruit (furanocoumarins in grapefruit inhibits CYP, preventing statin metabolism, increasing systemic presence and leading to toxicity)

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15
Q

True or False: statins have role in anti-inflammatio/anti-coagulation, decreasing LDL-C levels, and improving endothelial function

A

True

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16
Q

Inhibition of HMG CoA results in increased expression of which gene?

A

LDL receptor gene

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17
Q

Statins cause reduced synthesis of cholesterol within cells. As a result of this, __ proteins (found in ER and Golgi) are cleaved by ___, leading proteins to be translocated into the nucleus.

A

SREBP (sterol responsive element binding protein)

Site Proteases (S1P, S2P)

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18
Q

How does the presence of SREBP in the nucleus affect LDL receptor gene?

A

Leads to increase in LDL receptor genes, thereby causing more LDL receptors on surface of cell, which aid in removing LDL cholesterol from blood

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19
Q

Prior to being secreted into the plasma, where is Apo-A1 made?

A

Liver

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20
Q

When ApoA-I and phospholipid interact with each other (via RCT), they form what two HDL molecules?

A

1) Nascent HDL (Pre-B1-HDL)
2) Nascent Discoidal HDL (ndHDL)

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21
Q

In reverse cholesterol transport, cholesterol is effluxed by receptors like ___, ___, or ___

A

ABCA1, ABCG1, SR-B1

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22
Q

In reverse cholesterol transport, the nascent HDL absorbs free cholesterol in circulation and converts them to cholesterol esters via ____, and enzyme.

A

LCAT (lectin-cholesterol acetyltransferase)

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23
Q

As nascent LDH accumulates more cholesterol ester, it grows in sizes and matures, becoming ___ and ___ particles (also known as a1-4 particles)

A

HDL 3 and HDL 2 particles

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24
Q

Which enzyme is the rate limiting one involved in the step of Reverse Cholesterol Transport whereby HDL size increases?

A

PLTP (Phospholipid transfer protein)

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25
Q

LCAT converts pre-B-1 (nascent LDH) to ___
PLTP converts HDL3 to ___

A

HDL3; HDL2

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26
Q

True or False: As ApoA1 containing particles mature, they try to intake as many TG particles as possible

A

True

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27
Q

Which protein helps in the exchange of cholesterol ester (CE) and triglyceride particles (TG) between HDL and ApoB100 (VLDL and LDL) containing lipoprotein particles?

A

CETP (cholesterol ester transfer protein)

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28
Q

Once cholesterol esters are taken up by VLDL and LDL, they are transferred back to the liver via ___ receptor. Cholesterol esters will be broken down and made to make bile.

A

LDL - receptor

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29
Q

____: pathway that transports cholesterol from extrahepatic tissues (vessel wall) to the liver and intestines for recycling and excretion

A

Reverse Cholesterol Transfer

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30
Q

What are the two principal mediators for reverse cholesterol transport?

A

HDL (high density lipoprotein)
ApoA-I (the apoprotein associated with HDL)

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31
Q

True or False: HDL levels in body can help assess efficiency of RCT and cholesterol efflux out of vessel walls

A

True

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32
Q

True or False: LDL is primarily involved with removing cholesterol from atherosclerotic plaques, back into the liver, and finally into bile

A

False - primarily mediated by HDL

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33
Q

Why is HDL considered ‘good’ cholesterol?
Why is LDL considered ‘bad’ cholesterol?

A

HDL: REMOVES cholesterol from blood/artery walls

LDL: DEPOSITS cholesterol between layers in artery wall and STARTS process of atherosclerosis

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34
Q

_____is formed by bridging of Apo B 100 (containing LDL) and Apo A via: disulfide bond and is a NOVEL BIOMARKER FOR CV DISEASE AND ATHEROSCLEROSIS

A

Lipoprotein (a)
(levels greater than 75 nmol/L are considered risk factors)

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35
Q

What gene mutation can lead to hyperlipidemia?

A

Mutation in LPL (lipoprotein lipase) in infancy or childhood

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36
Q

HDL is a ___ containing lipoprotein

A

Apo A

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37
Q

Liver derived VLDL and LDL lipoproteins are ____ containing lipoproteins

A

Apo B-100

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38
Q

Diet or gut derived lipoproteins are chylomicron ______ containing lipoproteins

A

Apo B-48

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39
Q

What happens if apoprotein (acts as ligand) is not located on lipoprotein surface, as it normally is?

A

Particles are not taken up by liver

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40
Q

What is found within a lipoprotein?

A

1) Triglycerides
2) Cholesterol esters

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41
Q

What is found on surface of lipoprotein?

A

1) Apoprotein
2) Cholesterol

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42
Q

Chylomicrons are lipoproteins formed in the ____ following dietary fat intake

A

intestine

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43
Q

VLDL is the lipoprotein produced from the __

A

liver

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44
Q

True or False: Both VLDL and chylomicrons contain triglycerides that undergo breakdown with aid of LPL (lipoprotein lipase) and HL (hepatic lipase) to release free fatty acids

A

True

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45
Q

The breakdown products or remnants of lipoprotein particles are taken up by the liver through mediation of ___ and ___, which act as ligands

A

Apo B and Apo E

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46
Q

Exogenous dietary lipids are processed by the intestine to ___ particles

Endogenouos lipoproteins are synthesized by the ___ in the form of ____ particles

A

Exogenous - chylomicron particles
Endogenous - liver; VLDL

47
Q

Cholesterol Synthesis Pathway is also known as ___ Pathway

A

Mevalonate Pathway

48
Q

_____ is the rate limiting enzyme for cholesterol synthesis in the Mevalonate Pathway

A

HMG-CoA Reductase

49
Q

___ is also known as pyridine-3-carboxylic acid

A

Niacin

50
Q

True or False: Niacin belongs to the water soluble B-complex vit family and posses vitamin property only in carboxyl form

A

False - only in amide form

51
Q

True or False: Niacin shows anti-hyperlipidemic effects only at lower doses

A

False - Niacin shows anti-hyperlipidemic effects only at HIGHER doses

52
Q

How does Niacin affect: LDL-C, HDL-C, and triglycerides?

A

LDL-C, cholesterol: Decreases
HDL-C: Increases

53
Q

Niacin acts through the niacin 1/2 receptor, also known as the hydroxycarboxylic acid receptor or GPR ___ A and B

A

GPR 109 A/B

54
Q

True or False: Niacin belongs to GPCR family

A

True

55
Q

How does niacin (nicotinic acid) prevent TG (adipose) from being converted to free fatty acids in the liver?

(hint: what enzyme is inhibited?)

A

Inhibits HSL (hormone sensitive lipase) in adipose tissue

-thereby: blocking conversation of TF to FFA in the liver

56
Q

True or False: As a result of niacin, there is decrease breakdown of TG to free fatty acids

A

True

57
Q

What enzyme does Niacin inhibit?

A

HSL (hormone sensitive lipase)

58
Q

How does Niacin promote clearance of chylomicrons and VLDL triglycerides?

A

Enhances LPL activity

59
Q

How does Niacin affect Apo AI content in plasma?

A

Niacin increases Apo-A-1 content within the plasma

60
Q

True or False: In monocytes/macrophages, niacin enhances the cholesterol efflux process by up-regulating efflux transporter (e.g ABCA1)

A

True

61
Q

Flushing and dyspepsia are an AE associated with which anti-hyperlipidemic drug?

What worsens flushing?

A

Niacin
-Caffeine use + Niacin

62
Q

The most important and serious AE with niacin use is ____, as observed with elevated AST/ALT

A

hepatotoxicity

63
Q

Niacin can increase hepatic gluconeogenesis, leading to the _____, an AE.

A

hyperglycemia

64
Q

Mechanism for flushing AE in niacin use?

A

1) The niacin receptor mediates the release of arachidonic acid, produces PGE2/PGD2
2) PGE2 and PGD2 acts on DP1/EP2/EP4 receptors in VSM
3) Vasodilation and redness

65
Q

Contraindication for niacin use?

A

Diabetic

66
Q

What is the major niacin metabolite?

A

Nicotinuric acid (non-toxic metabolite of nicotinic acid)

67
Q

What class of anti-hyperlipidemic drugs do fenofibrate and gemfibrozil belong to?

A

The Fibrates (PPAR alpha agonists)

68
Q

What receptors to the Fibrates act on?

A

PPAR’s (Peroxisome Proliferator-Activated Receptors)

69
Q

Where do Fibrates act?

A

Liver and Adipose Tissue

70
Q

When a fibrate binds to PPAR, it promotes heterodimerization of PPAR (nuclear receptor) with ____. This leads the heterodimer complex to bind to the ____, changing gene regulation

A

RXR (retinoid x receptor)
PPRE (responsive element)

71
Q

What three genes do PPAR alpha agonists (fibrates) upregulate?

A

1) LDL receptor
2) Apo CII
3) Apo A1

72
Q

When two genes do PPAR alpha agonists down regulate?

A

1) Apo C111 (inhibits LPL)
2) IL-6

73
Q

Gemfibrozil has major interaction with which drug class?

A

Statins
- prevents uptake of statins in liver
- interferes with OATP1B1 transporter mediated statin uptake

74
Q

Statins/gemfibrozil compete for same enzyme, _____, for metabolism

A

Glucoronosyl transferase

75
Q

If gemofibrozil is given with statins, both of their plasma levels will increase. Elevated statin level can lead to the AE of ___

A

myopathy

76
Q

True or False: Both Gemofibrozil and Fenofibrate have major drug interactions with statins

A

False - Fenofibrate has NO major drug interactions with statins (no myopathy)

77
Q

True or False: Fibrates are ok for kids to take

A

False - NOT ok

78
Q

Where is PCSK9 (proprotein convertase subtilisin/kexin 9) highly expressed/formed prior to being secreted into bloodstream?

A

Kidney, liver, intestine

79
Q

True or False: PCSK9 is localized intracellularly

A

False - PCSK9 is localized EXTRACELLULARLY

80
Q

____ are antibodies and inhibit PCSK9 activity

A

PCSK9 Inhibitors

81
Q

What are the two PCSK9 inhibitors?
(hint: evolution and ally rows + -cumab)

A

1) Evolocumab
2) Alirocumab

82
Q

How do PCSK9 inhibitors increase LDL receptors in membrane?

A

Inhibiting PCSK9 prevents PCSK9 mediated LDL receptor degradation in lysosomal system

83
Q

True or False: PCSK9 Inhibitors increase membrane LDL receptors and increase LDL-C clearance from plasma

A

True

84
Q

___ is a siRNA targeting PCSK9 mRNA, resulting in degradation of PCSK9 mRNA and limiting PCSK9 protein synthesis

A

Inclisiran

85
Q

Which drug inhibits dietary cholesterol uptake?

A

Ezetimibe

86
Q

Where does Ezetimibe act?

A

Intestinal lumen

87
Q

How does Ezetimibe inhibit luminal cholesterol uptake by jejunal enterocytes?
(hint: what receptor does it block)

A

Blocks NPC1L1 - cholesterol transport protein

88
Q

True or False: Ezetimibe reduces 1) cholesterol content for intestinal chylomicron synthesis and 2) delivery of cholesterol load into liver as chylomicron remnants

A

True

89
Q

What is a secondary benefit of Ezetimibe?

A

As cholesterol delivery to liver decreases, liver makes more LDL receptors

90
Q

___ blocks NPC1L1 present in enterocytes of intestine (mostly jejenum)

A

Ezetimibe

91
Q

What drug class does Lomitapide belong to?

A

MMTP (microsomal triglyceride transfer protein) Inhibitors

92
Q

Lomitapide binds to ____ in the ER, preventing packaging/assembly of ___ containing lipoprotein bodies, which include both ___ (enterocytes) and VLDL-C____(hepatocytes)

A

MTTP; ApoB; ApoB48 (enterocytes);
VLDL-C-ApoB100 (hepatocytes)

93
Q

Major AE with MTTP Inhibitors?

A

Hepatic toxicity

94
Q

What are the active ingredients in omega-3 fatt acid?

A

EPA and DHA (Lovaza, Omytrg)

95
Q

How does omega-3 act as a anti-inflammatory drug?

A

Prevents formation of AA

96
Q

The DHA (omtryg) component in omega 3 supplements are known to increase ___ levels

A

LDL-C levels

97
Q

Vascepa contains only one of the active ingredients in omega-3 fatt acids - which one?

A

Vascepa contains EPA component only

98
Q

What are the benefit of using vascepta?

A

Since it only contains EPA (active ingredient in omega 3 fatty acids) - it does NOT increase LDL-C (as DHA component does)

99
Q

True or False: Vascepa/Icosapent Ethyl prevents plaque formation/inflammatory responses, improves endothelial function, and inhibits platelet aggregation

A

True

100
Q

What is a newer agent for treating hyperlipidemia?

A

1) Bempedoic Acid
2) Evinacumab

101
Q

How does Bempedoic Acid, a newer agent for treating hyperlipidemia, decrease cellular cholesterol synthesis?

A

Inhibits ATP Citrate Lyase, the enzyme involved in synthesizing Acetyl-CoA

102
Q

True or False: Bempedoic Acid is a prodrug that needs to be activated in hepatic tissue

A

True

103
Q

Clinical indication for Bempedoic Acid use?

A

Heterozygous Familial Hypercholesterolemia or persistent, long term atherosclerotic CVD

104
Q

True or False: Bempedoic Acid is very effective at lowering blood LDL-C levels

A

True

105
Q

True or False: Bempedoic Acid can be used as an adjunct to diet and max. tolerated statin therapy

A

True

106
Q

There is a DDI with Bempedoic Acid and ___, leading to higher incidences of ___

A

statins; myopathy

107
Q

More than _ mg of Simvastatin and _ mg of Pravastatin should be avoided

A

20 mg ; 40 mg

108
Q

What anti-hyperlipidemia drug causes a rise in blood uric acid levels?

A

Bempedoic Acid

109
Q

____ can be administered in combination with Ezetimibe

A

Bempedoic Acid

109
Q

____ is a recombinant IgG4 monoclonal antibody that targets antiopoietin-like protein 3 (ANGPTL3)

A

Evinacumab

110
Q

What drug is approved to be an adjunctive therapy for homozygous familial hypercholesterolemia (HoFH)

A

Evinacumab

111
Q

Evinacumab bind and blocks_____, an angiopoietan-like protein, thereby sparing LPL/EL activity, improving triglyceride breakdown, and reducing LDL-C levels

A

ANGPTL3

112
Q
A

Pharmacology (53 decks)

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