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Pharmacology II > Dyslipidemia Part 1 (Exam 3) > Flashcards

Dyslipidemia Part 1 (Exam 3) Flashcards

1
Q

Dietary lipids are broken up to ___ in _____

A

liquid droplets

chyme

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2
Q

Liquid droplets are _____ by bile salts and hydrolyzed by _____ to ______

A

emulsified

pancreatic lipases

mono- and diglycerides in micelles

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3
Q

Mono- and diglycerides are absorbed to form

A

triglycerides packaged into chylomicrons

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4
Q

Major fat in human diet

A

triglycerides

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5
Q

In addition to triglycerides, what is present in foods?

A

phospholipids
cholesterol
cholesterol esters

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6
Q

Phospholipids are hydrolyzed by

A

phospholipase A-2

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7
Q

Cholesterol esters are hydrolyzed by

A

cholesterol esterase

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8
Q

Fatty acids and broken down products are

A

taken up by intestinal mucosa and converted into triacylglycerols

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9
Q

Triacylglycerols are incorporated into chylomicrons with ____ and ____

A

cholesterol

apolipoproteins

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10
Q

Where do dietary fats go for storage?

A

Adipose tissue

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11
Q

___ are poorly absorbed

A

Cholesterols

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12
Q

Which foods prevent cholesterol absorption (decrease blood cholesterol)?

A

Foods high in fiber
They bind bile salts and cholesterol

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13
Q

One third of energy comes out of ___

A

dietary triacylglycerols

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14
Q

Advantage of fats over polysaccharides

A

Carry more energy per carbon
Carry less water

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15
Q

____ and ___ are for short term energy

A

Glucose

Glycogen

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16
Q

____ are for long term energy needs

A

Fats

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17
Q

Triglycerides when feasting

A

stored in adipose tissue

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18
Q

Triglycerides when fasting

A

broken down, releasing fatty acids as energy

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19
Q

Lipoproteins

A

make lipids soluble for transporation

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20
Q

Lipoprotein components

A

triglycerides
cholesterol
phospholipids
proteins

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21
Q

Apo-B containing lipoproteins

A

Chylomicrons
VLDL and LDL (bad)

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22
Q

Chylomicrons

A

transport dietary fatty acids and cholesterol to tissues

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23
Q

VLDL and LDL

A

transport endogenous fat and cholesterol from liver to tissues

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24
Q

Apo-A1 containing lipoproteins

A

HDL (good)

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25
Q

HDL

A

transports cholesterol from tissues to liver

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26
Q

Chylomicrons composition

A

Mainly triglycerides
C, B-48, E, A apolipoproteins

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27
Q

VLDL composition

A

Mainly triglycerides
B-100, C, E apolipoproteins

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28
Q

LDL composition

A

Mainly cholesterol
B-100 apolipoprotein

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29
Q

HDL composition

A

Mainly protein
A, C, E apolipoproteins

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30
Q

Liver produces _____ VLDL

A

triacylglycerol-rich

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31
Q

HDL are essential for

A

removing excess cholesterol from cells

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32
Q

_____ moves cholesterol from cytosolic leaflet to extracellular leaflet

A

Transporter/Flippase

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33
Q

Tangier disease

A

defects in transporter gene causing excess cholesterol in tissues
high risk of heart attack

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34
Q

Synthesis of cholesterol takes places in ____

A

cytosol

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35
Q

Rate-determining step of cholesterol synthesis

A

conversion of HMG-COA to mevalonate

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36
Q

Fate of cholesterol

A

incorporated into cell membrane
precursor of steroid hormone
precursor of bile acids
acylated to form cholesterol ester for storage

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37
Q

Cholesterol pathways

A

Exogenous
Endogenous
Reverse

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38
Q

Exogenous pathway

A

Dietary lipids

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39
Q

Endogenous pathway

A

Synthesized in liver
VLDL –> IDL –> LDL

40
Q

Excess LDL is

A

taken up by vasculature or returned to liver

41
Q

Excess LDL leads to

A

atherosclerosis

42
Q

Reverse pathway

A

HDL removes cholesterol from tissues to liver

43
Q

Dyslipidemia

A

abnormal blood lipid levels

44
Q

Hyperlipidemia

A

increased blood lipid levels

45
Q

Mixed dyslipidemia

A

elevations in LDL and triglycerides
low levels of HDL

46
Q

Atherosclerosis can lead to

A

atherosclerotic cardiovascular disease (ASCVD)

47
Q

ASCVD includes

A

Cerebrovascular disease: stroke or transient ischemic attack
PAD
CAD/IHD –> MI

48
Q

Familial Hypercholesterolemia (FH)

A

generic disorder leading to DLD
autosomal dominant

49
Q

_____ FH is more severe than _____

A

homozygous (HoFH)

heterozygous (HeFH)

50
Q

Primary target for lipid-lowering therapy

51
Q

Drug of choice for dyslipidemia

52
Q

Severe hypertriglyceridema

53
Q

Initiate statin therapy in patients with

A

Clinical ASCVD
LDL > 190
Diabetes (aged 40-75 with LDL >70)
10-year ASCVD risk of >7.5% (aged 40-75 with LDL >70)

54
Q

LDL-C target for plaque progression

A

<100 mg/dL

55
Q

LDL-C target for between plaque progression and ASCVD

56
Q

LDL-C target for ASCVD event

57
Q

Conditions that cause hypertriglyceridemia

A

obesity
uncontrolled diabetes
hypothyroidism
hereditary disorders

58
Q

Drugs that cause hypertriglyceridemia

A

GLUCOCORTICOIDS
estrogens
HIV meds
alcohol

59
Q

Major concern for extreme triglyceride elevation (>1000 mg/dL)

A

acute pancreatitis

60
Q

Symptoms of acute pancreatitis

A

epigastric abdominal pain
nausea
vomiting

61
Q

Tx for fasting TG 175-499 mg/dL

A

lifestyle mods
reassess meds
contain comorbidities

62
Q

Tx for fasting TG >500 mg/dL

A

Statin therapy
TG lowering meds

63
Q

Statins

A

Atorvastatin (Lipitor)
Simvastatin (Zocor)
Rosuvastatin (Crestor)
Lovastatin (Mevacor)
Pravastatin (Pravachol)
Fluvastatin (Lescol)
Pitavastatin (Livalo)

64
Q

Bile Acid Sequestrants

A

Cholestyramine (Questran)
Colestipol (Colestid)
Colesevelam (Welchol)

65
Q

Cholesterol Absorption Inhibitor

A

Ezetimibe (Zetia)

66
Q

PCSK9 Inhibitors

A

Alirocumab (Praluent)
Evolocumab (Repatha)

67
Q

Adensosone triphosphate-citrate lyase (ACL) inhibitor

A

Bempedoic acid (Nexletol)

68
Q

Fibrates (PPARa agonists)

A

Gemfibrozil (Lopid)
Fenofibrate (Tricor)

69
Q

Nicotinic Acid

A

Niacin
ER (Niaspan)
sustained/immediate release (OTC)

70
Q

Omega-3 Fatty Acids

A

Icosapent ethyl (Vascepa)
Omega-3 acid ethyl esters (Lovaza)

71
Q

Inhibitor of Apo B-100 synthesis

A

Mipomersen (Kynamro)

72
Q

Inhibitor of liver microsomal TG transfer protein

A

Lomitapide (Juxtapid)

73
Q

Medications primarily used to lower LDL

A

Statins
Bile Acid Seqestrants
Cholesterol Absorption Inhibitor
PCSK9 Inhibitors
ACL Inhibitors

74
Q

Medications primarily used to lower TG

A

Fibrates (PPAra agonists)
Nicotinic Acid
Omega-3 Fatty acids

75
Q

Meds only approved for HoFH

A

Mipomersen (Kynamro)
Lomitapide (Juxtapid)

76
Q

Statins MOA

A

Competitive inhibition of HMG-CoA reductase

77
Q

HMG-CoA reductase

A

converts HMG-CoA to mevalonic acid which is the rate limiting step

78
Q

When does majority of cholesterol synthesis occur?

A

At night
statins mainly work at night

79
Q

Secondary effect of statins

A

Overexpression of LDL receptors –> enhanced LDL uptake

80
Q

Statins effect on cholesterol levels

A

LDL: 25-60 % decrease
TC: 20-40% decrease
TG: 20-50% decrease
HDL: 5-10% increase

81
Q

High intensity statins

A

LDL lowered by >50%

82
Q

Moderate intensity statins

A

LDL lowered by 30-50%

83
Q

Low intensity statins

A

LDL lowered by <30%

84
Q

Statins ADRs

A

Myalgia
Rhabdomyolosis
Risk of SAMS
Hepatoxicity
Hyperglycemia
Cognitive impairment

85
Q

Inhibition of HMG-CoA reductase leads to _____ due to depletion of _____

A

muscle toxicity

ubiquinone (coenzyme Q10)

86
Q

Prodrugs that undergo hydrolysis in GI tract

A

Simvastatin
Lovastatin

87
Q

Statins that are NOT prodrugs

A

Fluvastatin
Atorvastatin
Rosuvastatin
Pitvastatin
Pravastatin

88
Q

Lipophilicity ranking of statins

A

Simvastain > others > pravastatin and rosuvastatin

89
Q

Lovastatin absorption is increased when

A

taken with food

90
Q

Statin distribution occurs via

A

active uptake by OATP1B1

91
Q

Statins primarily CYP3A4 metabolized

A

Simvastatin
Atorvastatin
Lovastatin

92
Q

Statins primarily CYP2C9 metabolized

A

Fluvastatin
Rosuvastatin
Pitavastatin

93
Q

Half-life of statins are 1-4 hours except

A

Atorvastatin (14h)
Pitavastatin (12h)
Rosuvastatin (19h)

94
Q

Short-acting statin more effective when

A

taken at night

95
Q

Statins are contraindicated in

Pharmacology II (17 decks)

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