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102 Cards in this Set

  • Front
  • Back
atherosclerotic plaque is a result of what
causes lipids to accumulate by passing through dysfunctional endothelium at the site of the artery wall
is instability of plaque related to plaque size
no - thin capsules that are friable and increase the risk of breaking off
what is the major vasodialator in the body
nitric oxide
what are the three lipid groups
cholesterol, triglyceride, phospholipids
what is cholesterol function
manufacture and repair the cell membrane
used for adrenal and gonadal steriods - base of hormones
synthesis of bile acids in liver -why fatty liver is common
atherosclerotic plaque is a result of what
causes lipids to accumulate by passing through dysfunctional endothelium at the site of the artery wall
how is cholesterol synthesized
in most tissue, by HMGCoA
major core lipid of LDL and HDL
is instability of plaque related to plaque size
no - thin capsules that are friable and increase the risk of breaking off
what is the major vasodialator in the body
nitric oxide
what is TG function
used to serve as energy substrates in liver and muscles

excess is stored in adipose tissue
central obesity increases visceral fat which is fat around organs - bad!!
what are the three lipid groups
cholesterol, triglyceride, phospholipids
how is TG synthesized
small intestines and liver, its a glycerol backbone with three fatty acids
visceral easily gets into bloodstream
what is the function of lipoprotiens
transport cholester and TG from sites of absorption and synthesis to sites of utilization
what is cholesterol function
manufacture and repair the cell membrane
used for adrenal and gonadal steriods - base of hormones
synthesis of bile acids in liver -why fatty liver is common
what is the make up of lipoprotiens
lipid portion is TG, cholesterol and phospholipids
protien portion - apolipoprotiens - transports cholesterol and TG from sits of absorption to utilization
how is cholesterol synthesized
in most tissue, by HMGCoA
major core lipid of LDL and HDL
what is TG function
used to serve as energy substrates in liver and muscles

excess is stored in adipose tissue
central obesity increases visceral fat which is fat around organs - bad!!
how is TG synthesized
small intestines and liver, its a glycerol backbone with three fatty acids
visceral easily gets into bloodstream
what is the function of lipoprotiens
transport cholester and TG from sites of absorption and synthesis to sites of utilization
what is the make up of lipoprotiens
lipid portion is TG, cholesterol and phospholipids
protien portion - apolipoprotiens - transports cholesterol and TG from sits of absorption to utilization
what are the six classifcations of lipoprotiens
LDL
HDL
VLDL
IDL
Chylomicrons
Lp(a)
What are apolipoprotiens
provide structural stability
act as cofactors to specific enzymes
serve as ligands to receptors involved in lipoprotien metabolism
what is pattern B LDL
are small dense LDL, cholesterol carrying particle that is prone to oxidation and endothelial uptake
most atherogenic
if present high risk of elevated LDL - usually with DM - why DM is CV risk
what is the size difference in LDL
small dense B LDL can easily invade the arterial wall

large pattern A LDL carry a lot of cholesterol but do not invade the artery wall, the liver disposes the cholesterol
Pattern B Particles are likely present with what TG and HDL
TG 180 - 200 and HDL under 35 or women under 45
what is Lipoprotien A
modified LDL partical with an apoprotien attached
this is abnormal
thrombosis is encouraged with this
what level do you want lipoprotien A under
20
why would you check a lipoprotien a level
strong family history of CV disease, young patient with HL
what medication lowers lipoprotien A
Niacin
what non-lipid causes endothelial dysfunction
homocystiene
fibrinogen
smoking
chronic infections
what is homocystiene
independent RF for atherosclerosis
famililal
amino acid byproduct
promotes atherothrombosis by injuring the endothelium and promotes thrombosis
what level should homocystiene be under
less than 10
this marker is thought to play a role in the progression of plaque and acute cardiac events
independent RF for atherothrombotic event
fibrinogen
this is an inflammatory marker
inflamed plaque are the more vulnerable to rupture
strong independent risk factor for CVD
CRP - HS
aspirin decreases which markers
fibrinogen and CRP
should you given HRT for women who have CV risk factors
not unless it is as soon as they start menopause, it will increase CRP
will increase thrombus event
what are some secondary causes of HL
DM
nephrotic syndrome
hypothyroidism
toxins - ETOH, Dioxin
Liver disease - cannot metabolize cholesterol
Meds - steroids, thiazides, BB
what is the lifetime risk of CHD by total cholesterol in men verses women based on age
lower in women until menopause then will catch up to men.
women have different symptoms: fatigue, neck pain and do not think of cardiac issue
what percent of patients have less than 50% occlusion with MI
50
why is intravascular US better then angio
plaque builds up in wall of artery but may not always look narrowed by angio

angio and stress test cannot detect non-obstuctive atherosclerosis
what stenosis is the majority of MIs caused by
under 50%
what percent of stenosis causes CP or ischemia
over 70% which 86% of MIs are less than 70% and 64% have under 50% stenosis
is cholesterol a good predictor of heart disease risk
no - 80% have same levels as those who never develop CAD
who to treat for atherosclerosis
personal history of known MI, DM, HTN or smoker

family history
PE - bruit
Framingham score 10 yrs over 20%
what signs and symptoms are with atherosclerosis
history of MI CVA or angioplasty
has aortic knob calcification
Bruits
decreased pedal pulses - PAD
retinal changes
has intimal thickening or plaque on carotid US
what are the atherosclerosis RF
smoker
HTN
HDL under 40
Family History of premature CHD
Age Men over 45 and women over 55
what is the 10 year risk of CHD with 0-1 risk factors
10%
what is the LDL goal for low risk of 0-1 RF
160
what is the 10 year risk for CHD in moderate high risk
10-20%
what is the target LDL for moderate risk
130
what is the target LDL for moderate high risk
130
what is the target LDL for High risk
100
what is the target LDL for very high risk
70
what are the criteria for metabolic syndrome
over 3:
waist circ over 102cm
TG >150
HDL <50
BP >135/85
glucose >110
what is the prevelence of metabolic syndrome for age and race
even amoung races, increases with age
what is xanthomas
thickened nuckles and cartilage areas meaning increased TG
check Lp (a)
what is the goal of cholesterol
under 200
what is borderline and high cholesterol
200 - 239
over 240
what is the goal of TG
under 150
what is borderline TG
150-199
what strategies lower TG
lower simple surgars and carbs
increase fiber
limit fat
avoid alcohol
fish oil 1gram BID
what is the goal of HDL
over 60, under 40 is low
what is optimal LDL
under 100
what is the TLC diet
sat under 7
poly under 10
mono under 20
carbs 50-60
fiber 20-30g
protien 15
cholesterol under 200
what lifestyle changes can decrease cholesterol
BMI <28
smoking cessation
plant based fat
moderate ETOH use
moderate physical activity 30 minutes 5x per week
how much omega 3s needed to treat TG
2-4 grams
what foots have omega 3s
olive oil
walnuts
canola oil
flaxseed
what do plant sterols reduce
LDL by 10-15%
what are the benefits of dietary fiber
reduce LDL
glucose control
reduce BP
what are solube fiber foods
oatmeal
psyllium
what medications are best for elevated LDL and TG - pattern B
statin
niacin
gemfibrozil or fenofibrate
omega 3s
what factors would you treat with medications LDL for primary prevention
LDL >150
LDL >140 with 1 - 2 RF
LDL >130 >2 RF
Any HDL <40
what factors would you treat with medications for secondary prevention - LDL
LDL >130
Any pattern B LDL
HDL <40
How do Bile Acid Resins reduce cholesterol
LDL 15-30%
HDL increase 3-5%
when would you avoid resin medications
TG >200 because it increases VLDL
if a patient is on a bile acid sequestrant how would you teach to take the medication
one hour before or two hours after other medications because it will decrease the absorption of others
what is the affect of cholesterol absorption blockers and what is an exampl
Zetia
decreased LDL 18% with monotherapy
has no affect on vasculature, does not reduce CV risk
what are the benefits of statin medications
best at lowering LDL 18-60%
increase HDL 5-15%
decrease TG 7-30%
does statins convert pattern b LDL to pattern a
no
what medications convert pattern b LDL to pattern a
Niacin
Firbrates - Tricor, Triglide, Antara
TZDs - which have a lot of SE
Metformin
Also lifestyle changes and decrease saturated fat
which statin medications need to be adjusted based on GFR under 30
all but lipitor and pravastatin, zocor only on 5mg
when is the full effect of statins seen
3-4 weeks
what are the major SE of statins
HA, insomnia, muscle pain, myopathy and eleveated LFTs
this is defined as muscle ache or weakness without CK elevation
myalgia
this is defined as muscle symptoms with increased CK
myopathy
this is defined as muscle symptoms with marked CK elevation, and creatnine elevation with brown urine and urine myoglobin
rhabdo
what factors will increase the risk of myopathy with statin medicatons
increased age
RI
hepatic dysfunction
hypothyroidism
Diet high in grapefruit
polypharmacy
which statin has the lowest and highest risk of myopathy
lowest - lipitor, safe at any doese
highest - zocor and is dose dependent
CYP3A4 inhibitors (azoles) are now contraindicated in this statin
zocor
how does niacin affect cholesterol
blocks VLDL synthesis and release of lipoprotien lipase
decrease LDL 15-25%
decrease TG 25-35%
increase HDL 15-30%
Best for Lp(A)
what are the major SE of niacin
flushing, reduced with NSAID, will go away after 2 weeks - use ER tab or start at low dose

abdominal cramping, nausea, diarrhea, dry skin, high glucose, itching
what is niacin contraindicated in
gout, liver dysfunction, DM, high uric acid, PUD
how do Fibrates lower cholesterol
reduce TG 25-40%
stimulate lipoprotein lipase which decreases VLDL
revert pattern B to pattern A
if a patient is on a statin, when would you consider combination therapy
HDL <35/ 45 in females
TG >150 in primary prevention
TG >100 in secondary prevention or DM
if pattern B LDL present
what combination therapy should be started on pattern B LDL
statin and niacin/fibrate/or zetia
Niacin alone
Fibrate or gemfibrozil
add metformin or TZD if DM
What is ther EBP treatment for atherosclerosis
ASA
Plavix for secondary prevention
vitamin E
strick BP control
strict glucose control - metformin
aggressive lipid control
a 56 year old male presents with no hisotry of atherosclerosis or DM
He is a non smoker
FMH of father with MI age 45
BMO 28
BP 128/82 on ACE and HCTZ
Lipid panel:
TC 196;LDL 133; HDL 42; TG 110.
What other questions would you ask
What is your plan
Is this primary or secondary prevention
Ask: Dietary habit, ever see a nutritionist
Plan: discuss ways to increase HDL
Start lipitor 10mg for goal LDL <100
Primary prevention
If a women in her 30s presents with no PMH but has a FMH of mother with MI at 45 years, LDL 132 what is your plan
lifestyle modification for 3-6 months, hold off on statin as long as child bearing if you can
47 year old women with PMH of DM taking metformin BID
Last HgA1C 7.2%
BP 135/80 on ACE and Diuretic
nonsmoker
mother died at 54 from MI
Does not exercise
BMI 33
Lipid panel:
TC 189
LDL 118
HDL 38
TF 165
What is your plan and is this primary or secondary prevention
secondary prevention
Plan:
refer to nutrition, encourage exercise and diet
weight loss goal
HgA1C elevated, may increase metformin which will lower TG
start on statin
goal LDL <100
76 year old man with PMH of HTN, previous MI, HL
on exam:
BMI 25
BP 120/85 HR 50
BMI 28
Labs:
LDL 112
HDL 44
TG 160
on lipitor 20 enalapril 10, metoprolol 50mg, ASA 325
what is your plan
secondary prevention
increase lipitor to 40
check BMP - may be pre-DM
increase enalipril
goal LDL <70
48 year old male with previous MI, HTN and smoker
PE
144/90 HR 50
BMI 28
Labs:
LDL 143
HDL 36
TG 190
fasting glucose 120
what is your plan for this patient
meds:
lipitor 40
enalipril 10
metoprolol 50
ASA 325
rule out metabolic syndrome, get HgA1C - if over 6.5 - DM
start metformin
Niacin to lower LDL and TG and increase HDL or double lipitor to 80
Diet and exercise
start on amlodipine/lipitor combo or diuretic
67 year old women with CHD afib HTN and mother died from MI at 48 years old
PE 122/80 HR 70
BMI 28
murmur
Labs:
LDL 88
TG 90
HDL 49
INR 2.5
Meds:
Warafin 7
Lipitor 40
Lisinopril 40
HCTZ 50
Atenolol 50
what is your plan
continue regimen,
encourage diet and exercise for HDL >50
LDL <70