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
2
Q
foods derived from plants contain how much cholesterol
A
none
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
4
Q
too much cholesterol results in
A
deposits on artery walls which causes narrowing
5
Q
prevalence of hyperlipidemia in US
A
1:6
6
Q
how many people being treated for hyperlipidemia are under good control?
A
1:3
7
Q
how many pts diagnosed with high cholesterol are receiving tx
A
less than half
8
Q
risk of hyper lipidemia increases with what
A
age - female onset is delayed by 10-15 years compared to males
9
Q
roughly what percentage of mena nd women have a total cholesterol >200
A
50%
10
Q
what is dyslipidemia
A
elevation of plasma cholesterol, TG, or both or increase of LDL
11
Q
what are the lipoproteins
A
lipids
cholesterol
TG
phospholipids
12
Q
high cholesterol is a significat risk factor for
A
CV dz
13
Q
what systems are affected by high cholesterol
A
cardiovascular, endocrin/metabolic
14
Q
what are chylomicrons
A
lipoprotein formed and absorbed in the SI consisting of digested fats
15
Q
why is cholesterol good
A
needed as building blocks for cell membranes and hormones
16
Q
what is VLDL
A
very low density lipoprotein = VERY BAD
17
Q
what is LDL
A
low density lipoproteins = bad
18
Q
what is the primary target of therapy/atherogenic
A
LDL
19
Q
what is HDL
A
high density lipoproteins = good
20
Q
why is HDL good
A
atheroprotective
21
Q
the higher the density the _______ the lipid content
A
lower
22
Q
3 types of triglycerides
A
- saturated
- monounsaturated
- polyunsaturated
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
24
Q
what are monounsaturated TGs
A
veggie oils
peanuts, avocados
25
what are polyunsaturated TGs
only essential fats
veggie oils
cold water fish
26
role of HDL
transports cholesterol back to the liver, where it is used to synthesize bile salts or excreted
27
what is the precursor for steroid hormones
cholesterol
28
apoprotein + lipid =
lipoprotein
29
what is the rate limiting step in the synthesis process of cholesterol
HMG CoA
30
2 categories of hyperlipidemia
primary & secondary
31
3 ways to characterize hyperlipidemia
1. increase in cholesterol only
2. increase in TG only
3. increase in both
32
what is primary hyperlipidemia
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
33
characterize the following:
1. familial hypercholesterolemia
2. familial combined hyperlipidemia
3. familial hypertriglyceridemia
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
34
type IIa hypercholesterolemia
```
main cause
affects all ages
TG normal
incr LDL
incr chol
premature vascular dz
xanthomas
thearpy - low fat/low chol diet, meds, intestinal bypass
```
35
what is secondary hyperlipidemia
```
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
```
36
secondary hyperlipidemia meds
```
thiazides/beta blockers
cyclosporine
retinoids
estrogens/progestins
corticosteroids/anabolic steroids
carbamazepine
protease inhibitors
```
37
DM type I and secondary hyperlipidemia
significant secondary cause bc pts tend to have an atherogenic combo high TG high LDL fractions, low HDL
38
type 2 DM and hyperlipidemia
-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
39
pathophys of hyperlipidemia
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)
40
s/s of hyperlipidemia
usually asymptomatic
| can be prompted by a family hx
41
phyiscal assessment for hyperlipidemia
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
42
lab workup for hyperlipidemia
```
fasting glucose
LFTs
Chem panel
TSH
urine protein
```
43
emerging tests to further guide intensity of risk reduction
lipoprotein A
homocysteine
PT
CRP
44
definition of metabolic syndrome
a cluster of common conditions that increases T2DM and CVD risk
45
insulin resistance drives MS and triggered by
1. post prandial hyperinsulinemia -->fasting hyperinsulinemia
2. hyperglycemia -->insulin resistance -->MS
46
what are the criteria to diagnose metabolic syndrome?
```
abdominal obesity
impaired glucose tolerance
decr HDL
incr TG
HTN
(also insulin resistance)
```
47
how many criteria does someone need to have to be diagnosed with metabolic syndrome
>=3
48
what is considered abdominal obesity in males vs females for metabolic syndrome
males >40in
| females >35in
49
what is considered impaired glucose tolerance in metabolic syndrome
fasting plasma glucose >=100mg/dl or on specific med or diagnosed with T2Dm
50
what HTN value is consistent with metabolic syndrome
BP >=130mmHg systolic or >= 85mm diatsolic or on a specific med
51
what is considered hypertriglyceridemia in metabolic syndrome
TGs >=150mg/dl or on specific med
52
what is considered low HDL cholesterol in metabolic syndrome
male
53
what scoring system is used to determine CVD risk in asymptomatic pts within 10 years
framingham risk score
low risk: =20%
54
other names for metabolic syndrome alias
```
dysmetabolic syndrome
hypertriglyceridemc waist
insulin resistance syndrome
obesity syndrome
syndrome X
```
55
what is in a lipid profile
```
total chol
HDL
LDL
VLDL
TGs
```
56
levels of lipids can be affected by
acute chronic illnesses including recent infection/MI
| dietary intake such as seafood and ETOH within 72 hours can actely affect panel
57
how often should cholesterol be checked in adults >=20yo
every 5 years
58
when should total cholesterol and HDL be check every 5 years
men >=35
women >=45 if at increased risk for CHD
men ages 20-35 and women 20-45 if increased risk of CHD
59
how often should diabetics be screened for dyslipidemia
yearly
60
what is the most important organization regarding lipid screening
national cholesterol education program (NCEP)
61
how does the lab calculate lipids?
total chol = HDL+VLDL+LDL
VLDL = TG/5
LDL = total-HDL-TG/5
62
how long should pt be fasting before lipid blood work
10 hours
63
what level of TG makes it impossible to calculate LDL
TG>400-500
64
what ratio can assess risk of developing CVD
ratio of total chol to HDL
65
what serum total cholesterol is associated with CHD
>150mg/dL
66
in men with CHD, only what % have high chol (>200) and low HDL (
only 20% so now we treat the risk not the lab values
67
classification of cholesterol levels
-240 high
68
classification of LDL
optimal =190
69
GOAL for drug therapy in decreasing LDL
try to achieve a 30-40% reudction in LDL 60% ideal
70
serum TG that is associated with incr CHD risk
>150 mg/dl
71
goals for HDL levels
>=60
72
what type of diet should you follow to decrease risk of CVD
low total fat, low saturated fat, low cholesterol
emphasize fruits and begetables
emphasize whole grains
73
for every 1% decrease in serum cholesterol level, cardiovascular risk is decreased by
2%
74
dietary intake of saturated fat has much more of an influence on _____________ than than dietary cholesterol
serum cholesterol
75
decreasing dietary saturated fat intake can decrease serum cholesterol levels by
10%
76
replace dietary saturated fat with what reduces serum choesterol levels
polyunsaturated
77
keep total fat intake to what % of total calories
20-35%
78
examples of polyunsaturated fats and monounsaturated fats
fish, nuts, vegetable oils
79
consume less than what % of caloris from saturated fats
10%
80
consume less than ____mg/day of cholesterol
300
81
HDL is cardio_____
protective
82
what nonpharmacologic changes can help keep lipids low
exercise
weight loss
modest alcohol use
83
primary goal of tx of hyperlipidemia
prevention/reduction of risk factors are primary goals
84
when is bariatric surgery indicated
BMI >40kg/m2 or >35mg/m2 with comorbidities
85
what is the glycemic index
a measure of the rate of rise in serum glucose fromvarious food sources
86
what is high glycemic load
glucose toxicity (post prandial hyperglycemia) results in compensatory hyperinsulinemia and eventually insulin resistance = dyslipidemia = CVD/HTN/thrombus
87
how to determine what statin to put on someone with dyslipidemia (or whether they should be on one)
scoring system
>=7.5% in 10 years = high intensity statin
88
all pts >=21 yo with any form of CVD or LDL-C >=190 how to treat
high dose statin
89
all pts with diabetes 40-75 with LDL-C 70-189 without any eveidence of CVD should receive what therapy
moderate dose statin
| consider high dose statin if 10year risk is >7.5%
90
what is the general treatment goal of LDL on dyslipidemia therapy
91
LDL goal for T2DM/CVD when on therapy
92
4 classes of cholesterol meds
1. HMG CoA reductase inhibitors (STATINS)
2. Bile acid sequestrants
3. fibric acids
4. nicotinic acid
(zetia & omega 3)
93
1st line drugs for treating dyslipidemia
statins
can decr CVD risk by 20-30%
affects LFTs and myopathies
94
2nd line therapy for dyslipidemia
Ezetimibe
decr 15-20% LDL
for statin intolerance
95
MOA of statins & advantages
inhibit rate limiting enzyme in formation of cholesterol
reduce CAD and total martality
used for primary and secondary prevention
96
what lab values do you want to check for pts on a statin
LFTs
| CPK - rhabdo
97
s/s of rhabdo
muscle pain, tenderness, weakness, brown urine
98
what if someone starts developing muscle pain on statins
d/c drug
99
MO of ezetimibe
blocks intestinal absorption of dietary and biliary cholesterol (monotherapy or with statin)
100
moa of bile acid binding resins
binds bile acids in gut, reducing enterohepatic circulation of bile acids, resulting in increased liver production of bile acids suing hepatic cholesterol
101
affects of bile acid binding resins
decresaes LDL 15-25%
no effect on HL
20% reduction in CHD events
only lipid lowering agents considered safe in pregnancy
102
fibric acid derivatives
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
niacin
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
omega 3 oils
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
