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z S1: Module > Lipids > Flashcards

Lipids Flashcards

1
Q

Cholesterol is a steroidal compound with C___

A

27

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2
Q

What enzyme is cholsterol synthesized from

A

acetyl coenzyme A

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3
Q

How does HMG CoA go to Mevalonic Acid

A

by HMG CoA reductase

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4
Q

What molecules are triglycerides formed from

A

glycerol-3-phosphate

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5
Q

What are the 4 classifications of major plasma lipoproteins

A

very low density lipoproteins
intermediate-density lipoproteins
low-density lipoproteins
high-density lipoproteins

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6
Q

Statins are inhibitors of HMG-CoA reductase and they lower plasma cholesterol levels by what three mechanisms

A

inhibition of cholesterol biosynthesis
enhancement of receptor-mediated LDL uptake
reduction of VLDL precursors

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7
Q

What is the pharmacophore of HMG-CoA reductase inhibitors

A

7 ring system dihydroxyheptanoic acid

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8
Q

The decalin ring is essential for anchoring the drug to the enzyme _______ _____

A

active site

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9
Q

Does a beta hydroxyl group increase or decrease hydrophilicity

A

increase (may improve cellular specificity)

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10
Q

What statin is the most hydrophilic and therefore has minimal penetration into lipophilic membrances, better selectivity for hepatic tissues and reduction in side effects

A

Pravastatin

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11
Q

All HMGRIs in active form contain a carboxylic acid that is primarily ________ at physiological pH

A

ionized

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12
Q

What CYP enzyme metabolizes HMGRIs

A

CYP34A

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13
Q

When should statins be administered

A

at night because it counteracts the peak cholesterol synthesis that occurs in the morning

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14
Q

Cholesterol Absorption Inhibitor MOA (ezetimbie)

A

-inhibits the absorption of cholesterol at the brush border of the small intestine
-competitively binds to sterol transporter

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15
Q

Ezetimibe is selective and does not interfere with the absorption of what molecules

A

triglycerides
lipid soluble vitamines

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16
Q

In Cholesterol Absorption Inhibitors the hydrolysis or expansion of the beta-lactam ring produces an ________ compound

A

inactive

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17
Q

Why is the secondary alcohol of ezetimibe not as important as the phenolic alcohol

A

The drug can conjugate to become active at the phenolic site

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18
Q

Bile Acid Sequestrants act by what MOA

A

binding to major bile acids, glycocholic acid and taurocholic acid, and greatly increase their fecal excretion

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19
Q

Bile acid sequestrants do not bind to specific receptors but bind to _______ charged atoms or functional groups on drug molecules

A

negatively

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20
Q

Since bile salts contain numerous positive charges they are more likely to bind to ________ compounds or nonelectrolytes

A

acidic

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21
Q

Impaired lipolysis by nicotinic acid ________ the mobilization of free fatty acids which reduce their plasma levels and their delivery to the liver

A

decreases

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22
Q

Nicotinic acid does not have any effects on what two things

A

cholesterol catabolism or biosynthesis

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23
Q

Fibrate MOA

A

-decrease plasma triglyceride levels more than cholesterol levels
-help lipoprotein metabolism by activation of peroxisome proliferator-activated receptors (alpha)

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24
Q

Which group in fibrates are essential for activity

A

isobutyric acid and the phenoxy ring

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25
Q

The extra space in gemfibrozil enhances _____ solubility which allows the drug to be absorbed through the GI membrane without the need of an ester prodrug

A

lipid

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26
Q

What functional group is important for fibrate binding and activity

A

carboxylic acid

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27
Q

Fenofibrate is a ______ that undergoes rapid hydrolysis to produce fenofibric acid active metabolite

A

prodrug

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28
Q

Dyslipidemia

A

Levels of lipids or lipoproteins in the blood that are outside or normal boundaries and have adverse effects

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29
Q

Hyperlipidemia

A

elevated levels of lipids or lipoproteins in the blood (mainly family)

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30
Q

Hyperlipidemia and ASCVD are associated with a general inflammatory state that contribute to ___________________ disorders

A

neurodegenerative

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31
Q

Primary risk factors of hyperlipidemia

A

reduce clearance that cause overproduction of LDLs or triglycerides
increase clearance that cause underproduction of HDLs

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32
Q

Secondary risk factors of hyperlipidemia

A

diet
sedentary life
obesity
diabetes
excessive alcohol
CKD
hypothroidism
liver dieases

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33
Q

Risk factors of low HDL

A

SMOKING
anabolic steroid use
HIV infection
nephrotic syndrome

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34
Q

What are chylomicrons synthesized from

A

synthesized from dietary triglycerides, cholesterol, and lipid-soluble vitamins in small intestine

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35
Q

Synthesized intestinal cholesterol and plant sterol absorption by what

A

niemann-pick c1-like protein 1 (NPC1L1)

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36
Q

ATP-binding cassette transporters pump what back into intestinal lumen

A

plant sterols

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37
Q

What is diagylcerol transferase transferred by

A

microsomal triglyceride transfer protein (MTP) to newly forming chylomicrons

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38
Q

What is ApoB-48

A

organizes newly forming chylomicrons

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39
Q

Type 2 isozyme of acyl-coenzyme A; __________ _________ esterifies dietary cholesterol, regulates cholesterol absorption

A

cholesterol acyltransferase (ACAT2)

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40
Q

________ enter the lymphatic system, pass to circulation via thoracic duct

A

chylomicrons

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41
Q

Chylomicronemia syndrome is genetic impairment of _____ or _______, impair chylomicron function

A

LPL
apoC-II
(cause severe hypertriglyceridemia, pancreatitis)

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42
Q

Chylomicron remanants are remanants after __________ from chylomicrons

A

triglycerides

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43
Q

What are the different chylomicron remanants

A

endothelial fenestres
ApoE
Hepatic lipase (HL)
LDL receptor or LDL receptor-related protein

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44
Q

What is LDL

A

-produced in liver, large, can cause plasma turbidity
-production is stimulated by triglycerides released from chylomicrons

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45
Q

What is IDL

A

triglycerides in VLDL metabolized by LPL to form IDL
released from capillary beds into circulation

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46
Q

How is LDL cleared

A

ApoB100/LDL receptor interaction in hepatocytes

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47
Q

Atherosclerosis is a syndrome in which atherosclerotic _________ develop in arteries, producing narrowing of the arterial passage and thickening of the arterial wall

A

plaques

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48
Q

How are plaques formed in atherosclerosis

A

oxidized LDL is taken up by macrophages

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49
Q

HDL is produced by liver and intestine and form chylomicron ___________ and VLDL

A

remnants

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50
Q

Pre-beta1 HDL primarily mediates transport of __________ to and from other cells

A

cholesterol

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51
Q

Lecithin is cholesterol acetyltransferase that esterifies cholesterol in what

A

pre beta1 HDL
HDL
HDL2
HDL3

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52
Q

In reverse cholesterol transport ____ absorb cholesterol from peripheral cells/macrophages

A

HDL

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53
Q

HDL2 and HDL1 exchanges cholesterol in liver excreted in bile _____ with bile _______

A

ducts
salts

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54
Q

In exogenous lipid transport ____ hydrolyzes triglycerides; free fatty acids absorbed by tissues

A

LPL

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55
Q

In exogenous lipid transport LPL releases free fatty acids to form _____

A

IDL

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56
Q

Cholesterol synthesis: long metabolic pathway, begins with transport of _________ from mitochondrial stores

A

acetyl-coA

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57
Q

3-hydroxy-3-methylgutaryl-CoA synthesized from acetyl-CoA and acetoacetyl-CoA by what

A

HMG-CoA reductase

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58
Q

Drugs that treat hypercholesterolemia

A

statins
ezetimibe
bile acid-binding agents
PsK9 inhibitors

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59
Q

Drugs that treat hypertriglyceridemia

A

fibrates
omega-3 fatty acids
niacin

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60
Q

What is the rate limiting step in cholesterol synthesis

A

HMG-CoA reductase

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61
Q

Statin inhibit HMG-CoA reductase which reduce endogenous ________ _________

A

cholesterol synthesis

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62
Q

What are the two natural statins

A

mevastatin
lovastatin

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63
Q

What are the two synthetic statins

A

pravastatin
simvastatin
fluvastatin
atorvastatin
rosivastatin
pitavastatin

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64
Q

All statins contain a _______ acid side chain that is a structural analog of an HMG-CoA intermediate

A

heptanoic

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65
Q

Membrane-bound (sterol regulatory element bring protein) is cleaved by a protease and SRE translocates to the ______

A

nucleus

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66
Q

SRE increases expression of ______ gene

A

LDLR

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67
Q

Statins increase the removal of LDL from the blood __________ LDL-C

A

lowering

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68
Q

Where are statins absorbed

A

small intestine

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69
Q

Where are statins distributed

A

most in liver
low levels in plasma
mostly protein-bound

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70
Q

How are statins metabolized/excreted

A

metabolized in liver and excreted in feces

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71
Q

What is rhabdomyolysis

A

toxic muscle protein products in serum

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72
Q

Carriers of PCSK9 cause a loss of function allele which _____ MI

A

decreases

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73
Q

Fibrates are what kind of agonist

A

peroxisome proliferator-activated receptor alpha (PPARalpha)

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74
Q

Fibrates reduce triglyceride levels by how much percent

A

30-50%

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75
Q

What are the two main fibrate drugs

A

gemfibrozil
fenofibrate

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76
Q

Omega 3 fatty acids are peroxisome proliferator-activated receptor _____ and ______

A

alpha
gamma

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77
Q

Cholesterol uptake inhibitor drug

A

ezetimibe (zetia)

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78
Q

Ezetimibe inhibit luminal cholesterol absorption via ________ by jejunal enterocytes

A

NPC1L1

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79
Q

NPC1L1 recruits free cholesterol creating a ___________ mechanism

A

raft-like

80
Q

Ezetimibe is metabolized by ___________ (intestinal wall)

A

glucuronidation

81
Q

Ezetimibe absorption limited to enterohepatic circulation which causes a limited ________ exposure

A

systemic

82
Q

Dual therapy with ezetimibe cause exacerbated ______ associated adverse effects

A

statin

83
Q

Primary bile acid synthesized by ________ from cholesterol

A

hepatocytes

84
Q

Secondary bile acids are synthesized in ___ by bacteria

A

gut

85
Q

What are bile salts

A

they are bile acids conjugated with taurine or glycine secreted into bile ducts

86
Q

Bile salts reduce ____ globules to smaller emulsified droplets

A

fat

87
Q

Bile salts increase effectiveness of _________ _________ freeing more fatty acids for absorption

A

pancreatic lipase

88
Q

What is niacin

A

water soluble B complex vitamin
source of NAD or NADP
improves all lipid parameters

89
Q

Niacin acts at ______ and senses energy metabolites in adipose tissues

A

HCA2 (hydroxycarboxylic acid receptor 2)

90
Q

In the liver Niacin inhibits __________ which decreases triglyceride synthesis/triglyceride esterification

A

diacylglycerol acyltransferase-2

91
Q

Adverse side effects of Niacin

A

Dyspepsia
Hepatic Toxicity
Flushing/pruritus

92
Q

Niacin exacerbates statin-induced _______

A

myopathy

93
Q

Cholesterol absorption and transportation

A

-cholesterol from food and bile enters the intestine
-micelles bind cholesterol and transport to enterocyte
-fatty acids synthesized to TGs
-TF and cholesterol esters from chylomicrons
-chylomicrons released into lymphatic system then transport to liver

94
Q

ILDL can promote growth of ______

A

atheroma (ASCVD risk)

95
Q

What is the main component of atheromatous plaque (ASCVD risk)

A

LDL

96
Q

How to calculate LDL-C

A

TC - (TG/5) - HDL

97
Q

If TG are greater then 400 mg/dL what happens

A

do not use equation and cannot calculate

98
Q

The equation is not as accurate if LDL is very low. What level is considered low

A

<70 mg/dL

99
Q

Is fasting needed to collect a lipid pannel

A

no

100
Q

What are the 4 ASCVD risks

A

coronary artery disease
stroke
aortic aneurysm
peripheral vascular disease

101
Q

What is CAD

A

Angina
MI (revascularization)
-stent or balloon
-CAD

102
Q

Carotid artery stenosis is a common cause of what

A

strokes

103
Q

Is this primary or secondary ASCVD:
genetic defects
-hypertiglyceridemia
-homozygous familial hypercholesterolemia
-heterozygous familial hypwecholesterolemia

A

primary (familial)

104
Q

Is this primary or secondary ASCVD:
-diet/lifestyle
-drugs
-disorders/defects
-diseases/comorbidities

A

secondary (acquired)

105
Q

What are the diet etiology

A

excessive alcohol intake
anorexia or weight gains
excessive carb intake

106
Q

What are the drugs etiology

A

atypical antipsychotics
beta-blockers/diuretics
glucorticoids
estrogen

107
Q

What are the diseases etiology

A

renal failure
pregnancy
hypothyroidism
uncontrolled diabetes

108
Q

Symptoms related to ASCVD events

A

chest pain
palpitations
sweating
anxiety
SOB
loss of consciousness
difficulty speaking/moving

109
Q

Signs of ASCVD

A

pancreatitis
eruptive xanthomas
peripheral neuropathy

110
Q

Labs of ASCVD

A

elevated: TC, LDL, TG, CRP, Apo-B
decreased: HDL, Apo-A

111
Q

What are the 4 diagnostics of ASCVD

A

carotid ultrasound (carotid artery stenosis)
coronary calcium score (CAD/stroke)
Ankle-brachial index (PVD)
Left heart catheterization (CAD)

112
Q

Primary prevention of ASCVD

A

before an ASCVD event occurs
No active disease
Prevent dyslipidemia or future ASCVD event

113
Q

Secondary prevention of ASCVD

A

after an ASCVD event occurs
Active disease
prevent another future ASCVD event

114
Q

ASCVD risk stratification:
Low
Borderline
Intermediate
High

A

Low: <5%
Borderline: 5-7.4%
Intermediate: 7.5-19.9%
High: >20%

115
Q

What are premature ASCVD for males and females

A

male: <55
female: <65

116
Q

What age to start screening for ASCVD

A

20 yo

117
Q

Ages 0-39 are generally low risk but what are the exceptions

A

familial hypercholesterolemia
premature ASCVD in family and LDL >160 mg/dL
LDL > 190mg/dL

118
Q

Ages 4-75 yo: risk varies
who benefits from statin

A

LDL >190 mg/dL
DM

119
Q

ASCVD risk enhancers

A

family history
LDL >160 mg/dL
CKD
metabolic syndrome
women preeclampsia, premature menopause
inflammatory diseases (arthritis, HIV)
Ethnicity (African American)

120
Q

What are the 5 indicators in metabolic syndrome and how many do you need to be considered to have it

A

3/5
-HTN
-waist >40 male, >35 females
-blood glucose >100 mg/dL
-TG >175 mg/dL
-Low HDL <40 male, <50 female

121
Q

What is CAC

A

computed tomography (CT) scan
provides imaging of calcium deposits in coronary arteries

122
Q

CAC Agatston score

A

0: low risk
1-10 low risk <10% ASCVD
11-100: low risk, consider meds if >55 yo
101-400: moderate plaque, high risk, start statin
>400: large plaque, very high risk, start statin

123
Q

What are the 4 statin benefit groups

A

clinical ASCVD
LDL >190 mg/dL
Age 40-75 yo & DM
40-75 with ASCVD >7.5%

124
Q

Following a low-cholesterol diet can lead to how much of a reduction in LDL

A

20-30%

125
Q

How long can you trial a lifestyle change in patients to lower their LDL

A

12 weeks

126
Q

Comorbidities of dyslipidemia

A

hypothyroidism
obstructive liver disease
renal disease
DM
pregnancy

127
Q

Statins

A

HMG-CoA reductase inhibitors
block conversion of HMG-CoA to mevalonic acid
rate-limiting step in cholesterol production
mainstay of LDL-lowering therapies
most effective oral medication for lowering LDL levels

128
Q

Why should some statins be taken at night

A

Medications with short half-lives should be taken at night because that is when cholesterol is the highest

129
Q

What are the three statins that should be taken at night

A

lovastatin
fluvastatin
simvastatin

130
Q

What are the two hydrophilic statins

A

rosuvastatin
pravastatin

131
Q

Drug interactions with gemfibrozil

A

all statins
increased risk of rhabdo

132
Q

Drug interactions with amiodarone

A

inhibit 3A4 and 2C9
max simvastatin 20 mg
max lovastatin 40 mg

133
Q

Drug interactions with amlodipine

A

inhibit 3A4
max simvastatin 20 mg

134
Q

Drug interactions with diltiazem

A

inhibit 3A4
max simvastatin 10 mg
max lovastatin 20 mg

135
Q

Drug interactions with fenofibrates

A

all statins
increased risk of rhabdo

136
Q

Common ADRs with statins

A

diarrhea
arthralgias
nasopharyngitis
nausea

137
Q

SAMS: myalgias

A

muscle pain
no CK elevation

138
Q

SAMS: myopathy

A

muscle pain
CK >10x ULN

139
Q

SAMS: rhabdomyolsis

A

muscle pain
CK >40x ULN
often with acute renal failure

140
Q

SAMS: immune-mediated necrotizing myopathy (IMNM)

A

muscle pain
elevated CK
HMG-CoA antibodies

141
Q

Non-modifiable risk factors of SAMS

A

first year of therapy
>75 yo
hypothyroidism
preexisting muscle disease
females
surgery
Asians
Renal/hepatic dysfunction

142
Q

Modifiable risk factors of SAMS

A

drug interactions
low body mass index
heavy exercise
higher doses of statins
lipophilic statins

143
Q

Management of SAMS

A

assess for history of current muscle pains
obtain a baseline CK levels
assess for muscle complaints at every patient encounter
assess for any non-statin causes of muscle pain

144
Q

Management of SAMS if discontinue statin and symptoms resolve within 2 weeks

A

not statin
resume as same or reduced dose

145
Q

Management of SAMS if discontinue statin and symptoms resolve 2-4 weeks

A

statin related
resume at reduced dose or change statin

146
Q

Management of SAMS if discontinue statin and symptoms do not resolve >4 weeks

A

not statin
hold until aches resolve, resume at same dose or reduced dose

147
Q

Other statin strategies

A

change to hydrophilic statin
every other day dosing
M, W, F dosing
once weekly dosing

148
Q

Should you use Coenzyme Q10 to help with SAMS

A

no
there is no evidence

149
Q

Statin contraindications

A

active liver failure
decompensated cirrhosis
lactation

150
Q

Baseline labs for statins

A

lipid pannel
AST/ALT
CK

151
Q

Follow-up labs for statins

A

repeat lipid pannel in 4-12 weeks and then every 12 months after LDL at goal

152
Q

Cholesterol reuptake inhibitors MOA

A

-inhibit absorption of cholesterol at brush border of small intestine
-block sterol transporter (NPC1L1)
-leads to decreased delivery of cholesterol to the liver

153
Q

Adverse effects and contraindications of ezetimibe

A

AE: increase serum transaminase, myalgias, myopathy, rhabdo
Contra: pregnancy and breastfeeding

154
Q

Bile acid sequstrants MOA

A

-binds biles acids in the intestinal lumen
-interrupts enterohepatic circulation of bile acids
-increased excretion of acidic steroids in the feces
-increased conversion of hepatic cholesterol into bile acids occurs to replenish the bile acid supply

155
Q

BAS medications are to avoid if TG are above what

A

300 mg/dL

156
Q

When to place someone on a BAS

A

-consider when patients are unable to take statins
-can add in patients who do not have >50% LDL-C reduction on a statin and ezetimibe
-safe in pregnancy since no systemic absorption

157
Q

BAS adverse effects

A

GI upset
Constipation
Contraindications
Decreased vitamin absorption

158
Q

When taking BAS they should be taken __ hours before or __ hours after other meds with drug interactions

A

1
4

159
Q

BAS monitoring

A

baseline lipid pannel (repeat 4-12 wks)
Monitor triglyceride levels

160
Q

PCSK9 inhibitors MOA

A

-MABs
-inhibition of PCSK9 leads to LDL-R recycling to cell surface
-increases LDL clearance from circulation

161
Q

ADE of PCSK9 inhibitors

A

injection site reactions
angioedemia
headache
flu-like symptoms

162
Q

Adenosine Triphosphate-Citrate Lyase Inhibitors (ACL) MOA

A

-ACL is an enzyme responsible for generating acetyl CoA
-Acetyl CoA is needed for synthesis of fatty acids and cholesterol in the liver
-ACL inhibitors prevent cholesterol production upstreams of statins

163
Q

Adverse side effects of ACLs

A

gout
hyperuricemia
ab distress
tendon rupture

164
Q

Fredrickson Classification of hyperlipdemia

A

-Primarily for research / genetic screening
-Blood sample is centrifuged
-NMR spectroscopy performed for lipoproteinsubfraction analysis

165
Q

What is the Associated Clinical Disorder and genetic defect for LDLs

A

ACD: Familial hypercholesterolemia, familial combined hyperlipidemia
Genetic: LDL receptor deficiency

166
Q

What is the Associated Clinical Disorder and genetic defect for LDL, VLDL

A

ACD: Familial combined hyperlipidemia
genetic:LDL receptor deficiency

167
Q

What is the Associated Clinical Disorder and genetic defect for VLDL

A

ACD: familial hypertriglyceridemia and familial combined hyperlipidemia
genetic: Increased VLDL production/synthesis

168
Q

What is the Associated Clinical Disorder and genetic defect in chylomicrons and VLDL

A

ACD: Familial combined hyperlipidemia
genetic: Increased VLDL production and decreased LPL

169
Q

Atherosclerosis is “ramped up” = ________ risk of premature ASCVD

A

higher

170
Q

Familial Hypercholesterolemia

A

Deficit of LDL-receptors
Elevation of LDL due to lack of LDL degradation
24X higher risk of an MI before the age of 40 yo

171
Q

HoFH is MORE severe form

A

Early appearance of xanthomas
Essentially no LDL receptors
TC: 650-1000 mg/dL
Fatal CV event before 20 years old

172
Q

HeFH is LESS severe form

A

Later appearance of xanthomas
Half the normal number of LDL receptors
TC: 300-600 mg/dL
CV events in 30 and 40 years of age

173
Q

Xanthomas

A

Foam cells (plaque) build up in tendons/organs

174
Q

Atheromas

A

Foam cells (plaque) build up in arteries

175
Q

Familial HypercholesterolemiaTreatment

A

-Usually requires a lipid specialist
-Multiple lipid lowering agents required (statin, ezetimibe, PCSK9i, bempedoic acid)
-LDL apheresis

176
Q

Familial Hypertriglyceridemia

A

TGs elevated: 200-500 mg/dL (can be >1000)
Fasting TG >500 mg/dL is usually due to a genetic defect (not just lifestyle/comorbidities) Elevated TG can cause eruptive xanthomas
can cause pancreatitis

177
Q

Hypertriglycerdemia treatment if level is 150-499

A

Lifestyle modifications
Address secondary causes

178
Q

Hypertriglyceridemia treatment if level is over 500

A

Consider adding statin first if ASCVD risk is >7.5

179
Q

Hypertriglycerdemia treatment if level is above 500 and ASCVD is below 7.5%

A

Add omega 3 polyunsaturated fatty acid and then fibrate if necessary

180
Q

What is acute pancreatitis

A

-Most clinically relevant complication of hypertriglyceridemia
>500 risk may be increased
>1000 increased risk in all patients
>2000 medical emergency

181
Q

What are the disease states the acute pancreatitis can lead to

A

pseudocyst
pancreatic necrosis
infection
sepsis/death

182
Q

Fibric Acid Derivatives MOA

A

-Activated peroxisome proliferator-activated receptor type alpha (PPARalpa)
-Increase lipolysis and elimination of trig-rich particles
-Increase synthesis of apoproteins A1 and A2
-decrease VLDL, LDL, increase HDL

183
Q

What are the two fibric acid derivatives

A

fenofibrate (cause renal dysfunction)
gemfibrozil (dont use with statin)

184
Q

When TG >500 mg/dL to reduce risk of acute pancreatitis what medicine is used

A

fibric acid

184
Q

ADE of fibric acids

A

GI discomfort
increase risk for gallstones
elevations in transaminase levels
myalgias
increase serum statin concentrations

185
Q

Omega-3-polyunsaturated fatty acids MOA

A

EPA prevents LDL oxidation and promotes LDL clearance
High doses needed (2-4 g/d) to reduce TG and VLDL by 20-50%

186
Q

Lovaza

A

Omega-3-polyunsaturated fatty acids
4 g qd or 2 g bid
generic

187
Q

Lcosapent ethyl/vascepa

A

2 g bid
EPA only
not generic

188
Q

ADEs of omega-3-PUFA

A

GI
ab pain
fishy burps (refrigerate capsules)

189
Q

Niacin MOA

A

-increase HDL
-decrease TG/LDL
-inhibit lipolysis, decrease FFA in plasma and decrease hepatic esterification of TG
-reduce HDL catabolism and decrease hepatic removal
-reduce synthesis of VLDL

190
Q

ADE niacin

A

flushing
itching
elevate LFT
hyperuricemia
hyperglycemia

191
Q

Contraindication of niacin

A

acute liver disease
gout flare
active peptic ulcer disease

192
Q

Low HDL cholesterol treatment

A

Men <40mg/dL
Women <50 mg/dL
No HDL raising goals
Recommendations is smoking cessation, physical activity, diet

193
Q

Dietary supplements: fiber

A

-increase soluble fiber intake through bran, pectins, psyllium products
-decrease LDL only
-decrease absorption of cholesterol

194
Q

Dietary supplements: fish oils

A

decrease ASCVD and CV deaths
reduce TG and VLDL
need high doses

195
Q

Dietary supplements: phytosterols

A

reduce LDL levels
2 g qd
decrease cholesterol uptake
Avoid in sitosterolemia

196
Q

Dietary supplements: red yeast rice

A

identical to lovastatin
NO recommendations

z S1: Module (8 decks)

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