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Clinical Phar_mIDTERMS
Dyslipidemia
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Cards (30)
What is atherosclerosis?
A
chronic
inflammatory condition in arteries characterized by
plaque
formation.
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What triggers the onset of atherosclerosis?
It begins with
endothelial
damage due to
hypertension
, smoking, or high
LDL
cholesterol levels.
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What are the key steps in the pathophysiology of atherosclerosis?
Endothelial dysfunction leads to increased permeability and
leukocyte
adhesion.
LDL
particles accumulate and oxidize, triggering inflammation.
Monocytes
enter the intima, become
macrophages
, and form
foam cells
.
Foam cells aggregate to form a "fatty streak."
Smooth muscle cells migrate, proliferate, and stabilize the plaque.
A
fibrous
cap forms over the plaque, which can rupture.
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What is the role of hypertension in atherosclerosis?
It increases shear stress, damaging the
endothelium
and promoting inflammation.
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How does diabetes contribute to atherosclerosis?
It elevates
pro-inflammatory
cytokines and oxidative stress, disrupting
endothelial
function.
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What effect does smoking have on atherosclerosis?
It contributes to oxidative
LDL
, inflammatory response, and
endothelial
damage.
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What is dyslipidemia's role in atherosclerosis?
High
LDL
and low
HDL
levels enhance lipid accumulation and inflammation in the arterial wall.
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What is LDL known as?
Low-Density Lipoprotein, or "bad" cholesterol.
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What is HDL known as?
High-Density Lipoprotein
, or
"good"
cholesterol.
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What are triglycerides primarily transported in?
Chylomicrons
and
VLDL
.
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What does total cholesterol represent?
The sum of cholesterol across all
lipoproteins
.
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What is non-HDL cholesterol?
Total cholesterol minus HDL, associated with
atherogenic
particles.
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What is Lp(a)?
A genetic marker for
atherosclerosis
risk.
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What is ApoB?
ApoB is found in all
atherogenic
lipoproteins except
HDL
.
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What characterizes familial hypercholesterolemia?
Elevated
LDL
and
total cholesterol
levels.
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What is combined familial hyperlipidemia?
Elevated
triglycerides
and decreased
HDL
levels.
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What are hypolipidemias?
Rare
conditions, except for
low HDL
levels which increase
atherosclerosis
risk.
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What is the difference between primary and secondary dyslipidemia?
Primary is due to
genetic
factors, while secondary is linked to
lifestyle
or diseases.
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What lifestyle changes can help manage dyslipidemia?
Diet: Low in
saturated fats
,
trans fats
, salt, and alcohol.
Physical Activity: Regular exercise to improve lipid profile.
Weight Management: Maintain BMI between 20-25
kg/m²
.
Smoking Cessation: Reduces oxidative
LDL
and inflammation.
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What is the mechanism of statins in treating dyslipidemia?
Statins inhibit
HMG-CoA reductase
, reducing
cholesterol
synthesis and increasing
LDL receptor
expression.
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What are the pleiotropic effects of statins?
They reduce
LDL
oxidation, increase
nitric oxide
, and stabilize plaques.
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What does ezetimibe do?
Ezetimibe
inhibits
dietary cholesterol absorption and is often added to
statins
.
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How do bile acid resins work?
They bind
bile acids
in the intestine, increasing
cholesterol
consumption for bile production.
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What is a caution when using fibrates?
They may increase
triglycerides
in certain patients and have limited effect on
cholesterol
levels.
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What do PCSK9 inhibitors do?
They prevent
LDL
receptor
degradation
, significantly
reducing
LDL levels.
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Who are PCSK9 inhibitors indicated for?
High-risk patients who
can't
achieve
target
LDL
levels with
statins
alone or have statin intolerance.
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What is the role of niacin in dyslipidemia treatment?
Niacin inhibits
lipolysis
, reducing
triglycerides
and mildly lowering
LDL
.
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What is lipoprotein apheresis?
It is the extracorporeal removal of
LDL
,
VLDL
, and
Lp(a)
particles to lower blood lipid levels.
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When is lipoprotein apheresis indicated?
For
high-risk
individuals with
genetic
dyslipidemia or those
unresponsive
to medication.
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What are the recommended lipid levels for low-risk individuals?
Total Cholesterol
: <
200
mg/dL
LDL
: <
100
mg/dL
HDL
: >
40
mg/dL for men, >
50
mg/dL
for women
Triglycerides: <
150
mg/dL fasting, <
200
mg/dL otherwise
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