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

Dyslipidemia Part 1 (Exam 3) Flashcards

(95 cards)

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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 esters
free cholesterol
phospholipids
apolipoproteins

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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
HDL
transports cholesterol from tissues to liver
26
Chylomicrons composition
Mainly triglycerides C, B-48, E, A apolipoproteins
27
VLDL composition
Mainly triglycerides B-100, C, E apolipoproteins
28
LDL composition
Mainly cholesterol B-100 apolipoprotein
29
HDL composition
Mainly protein A, C, E apolipoproteins
30
Liver produces _____ VLDL
triacylglycerol-rich
31
HDL are essential for
removing excess cholesterol from cells
32
_____ moves cholesterol from cytosolic leaflet to extracellular leaflet
Transporter/Flippase
33
Tangier disease
defects in transporter gene causing excess cholesterol in tissues high risk of heart attack
34
Synthesis of cholesterol takes places in ____
cytosol
35
Rate-determining step of cholesterol synthesis
conversion of HMG-COA to mevalonate
36
Fate of cholesterol
incorporated into cell membrane precursor of steroid hormone precursor of bile acids acylated to form cholesterol ester for storage
37
Cholesterol pathways
Exogenous Endogenous Reverse
38
Exogenous pathway
Dietary lipids
39
Endogenous pathway
Synthesized in liver VLDL --> IDL --> LDL
40
Excess LDL is
taken up by vasculature or returned to liver
41
Excess LDL leads to
atherosclerosis
42
Reverse pathway
HDL removes cholesterol from tissues to liver
43
Dyslipidemia
abnormal blood lipid levels
44
Hyperlipidemia
increased blood lipid levels
45
Mixed dyslipidemia
elevations in LDL and triglycerides low levels of HDL
46
Atherosclerosis can lead to
atherosclerotic cardiovascular disease (ASCVD)
47
ASCVD includes
Cerebrovascular disease: stroke or transient ischemic attack PAD CAD/IHD --> MI
48
Familial Hypercholesterolemia (FH)
generic disorder leading to DLD autosomal dominant
49
_____ FH is more severe than _____
homozygous (HoFH) heterozygous (HeFH)
50
Primary target for lipid-lowering therapy
LDL
51
Drug of choice for dyslipidemia
Statins
52
Severe hypertriglyceridema
TG > 500
53
Initiate statin therapy in patients with
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
LDL-C target for plaque progression
<100 mg/dL
55
LDL-C target for between plaque progression and ASCVD
<70 mg/dL
56
LDL-C target for ASCVD event
<55 mg/dL
57
Conditions that cause hypertriglyceridemia
obesity uncontrolled diabetes hypothyroidism hereditary disorders
58
Drugs that cause hypertriglyceridemia
GLUCOCORTICOIDS estrogens HIV meds alcohol
59
Major concern for extreme triglyceride elevation (>1000 mg/dL)
acute pancreatitis
60
Symptoms of acute pancreatitis
epigastric abdominal pain nausea vomiting
61
Tx for fasting TG 175-499 mg/dL
lifestyle mods reassess meds contain comorbidities
62
Tx for fasting TG >500 mg/dL
Statin therapy TG lowering meds
63
Statins
Atorvastatin (Lipitor) Simvastatin (Zocor) Rosuvastatin (Crestor) Lovastatin (Mevacor) Pravastatin (Pravachol) Fluvastatin (Lescol) Pitavastatin (Livalo)
64
Bile Acid Sequestrants
Cholestyramine (Questran) Colestipol (Colestid) Colesevelam (Welchol)
65
Cholesterol Absorption Inhibitor
Ezetimibe (Zetia)
66
PCSK9 Inhibitors
Alirocumab (Praluent) Evolocumab (Repatha)
67
Adensosone triphosphate-citrate lyase (ACL) inhibitor
Bempedoic acid (Nexletol)
68
Fibrates (PPARa agonists)
Gemfibrozil (Lopid) Fenofibrate (Tricor)
69
Nicotinic Acid
Niacin ER (Niaspan) sustained/immediate release (OTC)
70
Omega-3 Fatty Acids
Icosapent ethyl (Vascepa) Omega-3 acid ethyl esters (Lovaza)
71
Inhibitor of Apo B-100 synthesis
Mipomersen (Kynamro)
72
Inhibitor of liver microsomal TG transfer protein
Lomitapide (Juxtapid)
73
Medications primarily used to lower LDL
Statins Bile Acid Seqestrants Cholesterol Absorption Inhibitor PCSK9 Inhibitors ACL Inhibitors
74
Medications primarily used to lower TG
Fibrates (PPAra agonists) Nicotinic Acid Omega-3 Fatty acids
75
Meds only approved for HoFH
Mipomersen (Kynamro) Lomitapide (Juxtapid)
76
Statins MOA
Competitive inhibition of HMG-CoA reductase
77
HMG-CoA reductase
converts HMG-CoA to mevalonic acid which is the rate limiting step
78
When does majority of cholesterol synthesis occur?
At night statins mainly work at night
79
Secondary effect of statins
Overexpression of LDL receptors --> enhanced LDL uptake
80
Statins effect on cholesterol levels
LDL: 25-60 % decrease TC: 20-40% decrease TG: 20-50% decrease HDL: 5-10% increase
81
High intensity statins
LDL lowered by >50%
82
Moderate intensity statins
LDL lowered by 30-50%
83
Low intensity statins
LDL lowered by <30%
84
Statins ADRs
Myalgia Rhabdomyolosis Risk of SAMS Hepatoxicity Hyperglycemia Cognitive impairment
85
Inhibition of HMG-CoA reductase leads to _____ due to depletion of _____
muscle toxicity ubiquinone (coenzyme Q10)
86
Prodrugs that undergo hydrolysis in GI tract
Simvastatin Lovastatin
87
Statins that are NOT prodrugs
Fluvastatin Atorvastatin Rosuvastatin Pitvastatin Pravastatin
88
Lipophilicity ranking of statins
Simvastain > others > pravastatin and rosuvastatin
89
Lovastatin absorption is increased when
taken with food
90
Statin distribution occurs via
active uptake by OATP1B1
91
Statins primarily CYP3A4 metabolized
Simvastatin Atorvastatin Lovastatin
92
Statins primarily CYP2C9 metabolized
Fluvastatin Rosuvastatin Pitavastatin
93
Half-life of statins are 1-4 hours except
Atorvastatin (14h) Pitavastatin (12h) Rosuvastatin (19h)
94
Short-acting statin more effective when
taken at night
95
Statins are contraindicated in
pregnancy

Pharmacology II (18 decks)

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