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Clin Med - Cardio I > Hyper lipidemia > Flashcards

Hyper lipidemia Flashcards

1
Q

liver produces how much cholesterol

A

75-80%, the rest is from dietary sources like meat, poultry, eggs, fish , and dairy

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2
Q

foods derived from plants contain how much cholesterol

A

none

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3
Q

cholesterol in blood is regulated by

A

liver - after a meal, cholesterol in the diet is absorbed from the small intestine and metabolized and stored in the liver. As body needs it, the liver will secrete it

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4
Q

too much cholesterol results in

A

deposits on artery walls which causes narrowing

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5
Q

prevalence of hyperlipidemia in US

A

1:6

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6
Q

how many people being treated for hyperlipidemia are under good control?

A

1:3

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7
Q

how many pts diagnosed with high cholesterol are receiving tx

A

less than half

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8
Q

risk of hyper lipidemia increases with what

A

age - female onset is delayed by 10-15 years compared to males

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9
Q

roughly what percentage of mena nd women have a total cholesterol >200

A

50%

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10
Q

what is dyslipidemia

A

elevation of plasma cholesterol, TG, or both or increase of LDL

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11
Q

what are the lipoproteins

A

lipids
cholesterol
TG
phospholipids

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12
Q

high cholesterol is a significat risk factor for

A

CV dz

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13
Q

what systems are affected by high cholesterol

A

cardiovascular, endocrin/metabolic

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14
Q

what are chylomicrons

A

lipoprotein formed and absorbed in the SI consisting of digested fats

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15
Q

why is cholesterol good

A

needed as building blocks for cell membranes and hormones

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16
Q

what is VLDL

A

very low density lipoprotein = VERY BAD

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17
Q

what is LDL

A

low density lipoproteins = bad

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18
Q

what is the primary target of therapy/atherogenic

A

LDL

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19
Q

what is HDL

A

high density lipoproteins = good

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20
Q

why is HDL good

A

atheroprotective

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21
Q

the higher the density the _______ the lipid content

A

lower

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22
Q

3 types of triglycerides

A
  1. saturated
  2. monounsaturated
  3. polyunsaturated
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23
Q

what are saturated TGs

A

have the greatest impact on increasing LDL cholesterol

derived from meat products, whole milk, other dairy, some veggies, exotic oils

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24
Q

what are monounsaturated TGs

A

veggie oils

peanuts, avocados

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25
Q

what are polyunsaturated TGs

A

only essential fats
veggie oils
cold water fish

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26
Q

role of HDL

A

transports cholesterol back to the liver, where it is used to synthesize bile salts or excreted

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27
Q

what is the precursor for steroid hormones

A

cholesterol

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28
Q

apoprotein + lipid =

A

lipoprotein

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29
Q

what is the rate limiting step in the synthesis process of cholesterol

A

HMG CoA

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30
Q

2 categories of hyperlipidemia

A

primary & secondary

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31
Q

3 ways to characterize hyperlipidemia

A
  1. increase in cholesterol only
  2. increase in TG only
  3. increase in both
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32
Q

what is primary hyperlipidemia

A

single or multiple genetic mutations that result in over production or defective clearance

  • if found test all family members
  • early lipid lowering has shown beneficial decrease CVD
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33
Q

characterize the following:

  1. familial hypercholesterolemia
  2. familial combined hyperlipidemia
  3. familial hypertriglyceridemia
A
  1. increased LDL
  2. increased LDL, VLDL
  3. increased TGs, autosomal dominant, 50% of pts who have MI under age 60

**all at risk for pancreatitis

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34
Q

type IIa hypercholesterolemia

A 
main cause
affects all ages
TG normal
incr LDL
incr chol
premature vascular dz
xanthomas
thearpy - low fat/low chol diet, meds, intestinal bypass
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35
Q

what is secondary hyperlipidemia

A 
sedentary lifestlye
excessive intake of bad fats andchol
DM or metabolic syndrome
ETOH overuse
tobacco use
chronic kidney dz/nephrosis
hypothyroidism
cholestatic liver dz/biliary
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36
Q

secondary hyperlipidemia meds

A 
thiazides/beta blockers
cyclosporine
retinoids
estrogens/progestins
corticosteroids/anabolic steroids
carbamazepine
protease inhibitors
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37
Q

DM type I and secondary hyperlipidemia

A

significant secondary cause bc pts tend to have an atherogenic combo high TG high LDL fractions, low HDL

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38
Q

type 2 DM and hyperlipidemia

A

-even more risk
-combo of obesity, poor contorl, or both may increase circulating FFAs
–leads to increased liver VLDL production
TG rich VLDL then transfers TG and chol to LDL and HDL
-promotes formation of TG rich, small dense LDL and clearance of TG rich HDL

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39
Q

pathophys of hyperlipidemia

A

deposition of cholesterol in vascular walls creating fatty streaks that become fibrous plaques

  1. initial response is defensive - macrophages sent to consume LDL
  2. foam cells - fatty streaks - grows larger
  3. body protects by covering with fibrous capsule - expands to elastic layer of vessel eventually encroaching the lumen
  4. narrowing, calcium deposits in plaque, stenosis
  5. increased pressure/inflammatory changes can cause damage to outer capsule
  6. inflammatino cuases plaque instability leading to plaque rupture (MI, TIA, CVA)
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40
Q

s/s of hyperlipidemia

A

usually asymptomatic

can be prompted by a family hx

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41
Q

phyiscal assessment for hyperlipidemia

A
  1. calculate BMI
  2. xanthelasma - plaques deposits on eyelids
  3. xanthomas
    - achilles, patella, back of hand
    - eruptive (skin) - esp buttocks
    - usually genetic hyperlipidemia
    - incr VLDL (chylomicrons), TG(>1000mg/dl)
  4. lipidemia retinalis - cream colored blood vessels in the fundus; high TG(>2000mg/dl)
  5. signs of ETOH
  6. signs of DM or metabolic syndrome
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42
Q

lab workup for hyperlipidemia

A 
fasting glucose
LFTs
Chem panel
TSH
urine protein
43
Q

emerging tests to further guide intensity of risk reduction

A

lipoprotein A
homocysteine
PT
CRP

44
Q

definition of metabolic syndrome

A

a cluster of common conditions that increases T2DM and CVD risk

45
Q

insulin resistance drives MS and triggered by

A
  1. post prandial hyperinsulinemia –>fasting hyperinsulinemia
  2. hyperglycemia –>insulin resistance –>MS
46
Q

what are the criteria to diagnose metabolic syndrome?

A 
abdominal obesity
impaired glucose tolerance
decr HDL
incr TG
HTN
(also insulin resistance)
47
Q

how many criteria does someone need to have to be diagnosed with metabolic syndrome

A

> =3

48
Q

what is considered abdominal obesity in males vs females for metabolic syndrome

A

males >40in

females >35in

49
Q

what is considered impaired glucose tolerance in metabolic syndrome

A

fasting plasma glucose >=100mg/dl or on specific med or diagnosed with T2Dm

50
Q

what HTN value is consistent with metabolic syndrome

A

BP >=130mmHg systolic or >= 85mm diatsolic or on a specific med

51
Q

what is considered hypertriglyceridemia in metabolic syndrome

A

TGs >=150mg/dl or on specific med

52
Q

what is considered low HDL cholesterol in metabolic syndrome

A

male

53
Q

what scoring system is used to determine CVD risk in asymptomatic pts within 10 years

A

framingham risk score

low risk: =20%

54
Q

other names for metabolic syndrome alias

A 
dysmetabolic syndrome
hypertriglyceridemc waist
insulin resistance syndrome
obesity syndrome
syndrome X
55
Q

what is in a lipid profile

A 
total chol
HDL
LDL
VLDL
TGs
56
Q

levels of lipids can be affected by

A

acute chronic illnesses including recent infection/MI

dietary intake such as seafood and ETOH within 72 hours can actely affect panel

57
Q

how often should cholesterol be checked in adults >=20yo

A

every 5 years

58
Q

when should total cholesterol and HDL be check every 5 years

A

men >=35
women >=45 if at increased risk for CHD
men ages 20-35 and women 20-45 if increased risk of CHD

59
Q

how often should diabetics be screened for dyslipidemia

A

yearly

60
Q

what is the most important organization regarding lipid screening

A

national cholesterol education program (NCEP)

61
Q

how does the lab calculate lipids?

A

total chol = HDL+VLDL+LDL

VLDL = TG/5

LDL = total-HDL-TG/5

62
Q

how long should pt be fasting before lipid blood work

A

10 hours

63
Q

what level of TG makes it impossible to calculate LDL

A

TG>400-500

64
Q

what ratio can assess risk of developing CVD

A

ratio of total chol to HDL

65
Q

what serum total cholesterol is associated with CHD

A

> 150mg/dL

66
Q

in men with CHD, only what % have high chol (>200) and low HDL (

A

only 20% so now we treat the risk not the lab values

67
Q

classification of cholesterol levels

A

-240 high

68
Q

classification of LDL

A

optimal =190

69
Q

GOAL for drug therapy in decreasing LDL

A

try to achieve a 30-40% reudction in LDL 60% ideal

70
Q

serum TG that is associated with incr CHD risk

A

> 150 mg/dl

71
Q

goals for HDL levels

A

> =60

72
Q

what type of diet should you follow to decrease risk of CVD

A

low total fat, low saturated fat, low cholesterol
emphasize fruits and begetables
emphasize whole grains

73
Q

for every 1% decrease in serum cholesterol level, cardiovascular risk is decreased by

A

2%

74
Q

dietary intake of saturated fat has much more of an influence on _____________ than than dietary cholesterol

A

serum cholesterol

75
Q

decreasing dietary saturated fat intake can decrease serum cholesterol levels by

A

10%

76
Q

replace dietary saturated fat with what reduces serum choesterol levels

A

polyunsaturated

77
Q

keep total fat intake to what % of total calories

A

20-35%

78
Q

examples of polyunsaturated fats and monounsaturated fats

A

fish, nuts, vegetable oils

79
Q

consume less than what % of caloris from saturated fats

A

10%

80
Q

consume less than ____mg/day of cholesterol

A

300

81
Q

HDL is cardio_____

A

protective

82
Q

what nonpharmacologic changes can help keep lipids low

A

exercise
weight loss
modest alcohol use

83
Q

primary goal of tx of hyperlipidemia

A

prevention/reduction of risk factors are primary goals

84
Q

when is bariatric surgery indicated

A

BMI >40kg/m2 or >35mg/m2 with comorbidities

85
Q

what is the glycemic index

A

a measure of the rate of rise in serum glucose fromvarious food sources

86
Q

what is high glycemic load

A

glucose toxicity (post prandial hyperglycemia) results in compensatory hyperinsulinemia and eventually insulin resistance = dyslipidemia = CVD/HTN/thrombus

87
Q

how to determine what statin to put on someone with dyslipidemia (or whether they should be on one)

A

scoring system

> =7.5% in 10 years = high intensity statin

88
Q

all pts >=21 yo with any form of CVD or LDL-C >=190 how to treat

A

high dose statin

89
Q

all pts with diabetes 40-75 with LDL-C 70-189 without any eveidence of CVD should receive what therapy

A

moderate dose statin

consider high dose statin if 10year risk is >7.5%

90
Q

what is the general treatment goal of LDL on dyslipidemia therapy

A
91
Q

LDL goal for T2DM/CVD when on therapy

A
92
Q

4 classes of cholesterol meds

A
  1. HMG CoA reductase inhibitors (STATINS)
  2. Bile acid sequestrants
  3. fibric acids
  4. nicotinic acid
    (zetia & omega 3)
93
Q

1st line drugs for treating dyslipidemia

A

statins
can decr CVD risk by 20-30%
affects LFTs and myopathies

94
Q

2nd line therapy for dyslipidemia

A

Ezetimibe
decr 15-20% LDL
for statin intolerance

95
Q

MOA of statins & advantages

A

inhibit rate limiting enzyme in formation of cholesterol
reduce CAD and total martality
used for primary and secondary prevention

96
Q

what lab values do you want to check for pts on a statin

A

LFTs

CPK - rhabdo

97
Q

s/s of rhabdo

A

muscle pain, tenderness, weakness, brown urine

98
Q

what if someone starts developing muscle pain on statins

A

d/c drug

99
Q

MO of ezetimibe

A

blocks intestinal absorption of dietary and biliary cholesterol (monotherapy or with statin)

100
Q

moa of bile acid binding resins

A

binds bile acids in gut, reducing enterohepatic circulation of bile acids, resulting in increased liver production of bile acids suing hepatic cholesterol

101
Q

affects of bile acid binding resins

A

decresaes LDL 15-25%
no effect on HL
20% reduction in CHD events
only lipid lowering agents considered safe in pregnancy

102
Q

fibric acid derivatives

A

most useful in those with high TG and low HDL
reduce synthesis and incrase breakdown of VLDL, resulting in reduction of LDL, TF, and increase HDL
SE’s cholelithiasis, hepatitis, myositis

103
Q

niacin

A

reduces productino of LDL decreased LDL
raises HDL
decreases TG
decreases homocysteine
reduced long term mortatlity and has optimal effect on lipds BUT poorly tolerated
SE’s flushing can take ASA prior to dosing to preven

104
Q

omega 3 oils

A

decr TG
doesn’t decr mortality or risk of cardiovascular dz/events
preg cat C
d/c if no response after 2mos
SE’s - use cuation in pts with fish/shellfish allergy or sensitivity
if causes GERD recommmend placing capsulse in freezer

Clin Med - Cardio I (7 decks)

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