Block 2-Reymann (Lipid) Flashcards

Question 1

Q

Lipoproteins

Answer

A

Chylomicrons:
Transport exogenous Trigly from intestine to muscle/Adipose.
Remnants taken up in liver & secreted in bile
Oxidized to bile acids or converted to VLDLs
VLDL: Transport endogenous trigly from liver to Adipose tissue
They are hydrolized in adipose tissue by lipoprotein lipase to IDL-LDL
LDL: transport chelosterol from liver to peripheral tissue
Cleared from plasma via LDL receptors that recogize Apo-B100
HDL: transports cholesterol from tissues back to liver
Cholesterol: Excreted from body by Biliary

Question 2

Q

Atherosclerosis & CVD

Answer

A

Risk is associated w/^{HIGH LDL & LOW HDL}
LDL not taken up by LDL-receptor are oxidized
Oxidized LDL accumulates in macrophages ^{(FOAM CELL)}
Foam cell undergo apoptotic or Necro death = RELEASE of free radicals
Oxidzied LDL triggers LOCAL infammatory response = ^{ATHEROSCLEROSIS}
CVD=_{HIGH LDL }(above 130) & _{LOW HDL} (below 35) & _{HIGH Trigly} (above 150)
Associated w/Alcohol abuse, smoking, hypertension, Type 2 diabetes

Question 3

Q

Dyslipidemia is symptom

Answer

A

Physiological or reactive hyperglyceridema due to excessive^{ alcohol, caloric, or fat INTAKE}
Hypercholesteroemia=excessive fat or cholesterol intake
Secondary causes:
Diabetes
Adipositas (obesity)
Metabolic syndrome
Glucocoticoids
beta-blockers
Thiazides
Oral contracep
4 classes of dyslipedmias:
Hypercholesterolemia
Hypertriglyceridemia
Mixed hyperlipidemia
Disorders of HDL metab

Question 4

Q

Hypercholesterolemia

Answer

A

High TPC (total plasma cholesterol)
HIGH LDL
Triglycerides are normal
Polygenic: No defined genetic cause
Famililal (FH)-Type 2 a Autosomal dom involving defects in LDL receptor
Heterozygote = TPC 275-500
Homozygote = TPC 700-1200 ^{COMPLETE ABSENCE of LDL receptors}
Familial defective ApoB100= Autosomal dominant mutations decrease affinity of LDL for LDL-R

Question 5

Q

Hypertriglceridemia

Answer

A

HIGH Triglyceride (200-500)
Familial hypertri: Type 4 common, autosommal dom
Familial LPL def: caused by absence of LPL, autosomal recessive
Profound hypertriglyceridemia
Infants present w/:
pacreatitis
Eruptive xanthomas
Hepato/splenomegaly
Apoc2 def-RARE

Question 6

Q

Mixed Hyperlipidemia

Answer

A

High cholesterol
High LDL
High Triglyceride
LOW HDL
Familial combined hyperlipidemia (FCH):TYPE 2b common
elevated Trigly & cholesterol BUT reduced HDL
pts present w/features of sedentary lifestyle
Dysbetalipoproteinemia (Type3):
Increased chylomicrons & VLDL rem
Hypertriglyceridemia & Hypercolesterolemia
Symptoms do NOT present in males until 30 & in females not until menopause

Question 7

Q

Disorder of HDL metab

Answer

A

LOW HDL
Defects in
ApoA1 (comp of HDL)
ABCA1 (helps in formation of HDL)
LCAT

Question 8

Q

Antihyperlipidemic Drugs

Answer

A

HMG CoA reductase inhibtiors (statins):
Lovastatin, simvastatin, pravastatin, atorvastatin, Fluvastatin, Rosuvastatin
Niacin (nicotinc acid, B2)
Fibrates (fenofibrate & gemfibrozal)
Bile acid binding agents:
Cholestyramine, colestipol, colesevelam
Cholesterol absorption inhibitors:
Ezetimibe & plant sterols

Question 9

Q

HMG-CoA reductase inhibitors PD&PK

Answer

A

Statins
1st line treatment for elevated LDL ^{(HYPERCHOLESTEROLEMIA)}
PK:
Lovastatin, simvastatin, atorvastatin-P4503A4
Pravastatin & Rosuvastatin NOT metab by CYP-450s
PD:
Inhibit activity of HMG COA reductase
Depelete intracell cholesterol
Increase LDL R expression
Increase LDL uptake
Homozygotes of familial hyperchol NO LDL receptors do NOT respond to statins

Question 10

Q

HMG-CoA reductase inhibitors SEs

Answer

A

SE (monotherapy):
Myopathy & or myositis w/^{RHABDOMYOLYSIS}
Increases transaminase LVLs + liver enzymes
SE (combo therapy):
Drug interaction with cytochrome p-450=^{Metab of other drugs inhibited}
Increased risk of overdose of other drugs
CI:
Pregers/Lactation
Hepatic disease
Mascular disease
Use with Bile acid binding agent or Cholesterol inhibitor =^{ ADDITIVE decrease in LDL}
Use with Niacin = ^{Increase risk of Myopathy}
Fibrates (gemifibrozil) =^{ Increase risk of rhabdomyosis}

Question 11

Q

Inhibitors of bile acid reabsorption PD&PK

Answer

A

Cholestyramine, Colesevelan, Colestipol
Second line treatment for LIPID reduction
PD:
Cationic resins bind to (-) charged bile acids in SI = Prevention of reabsorb
Decreased bile acid reabsorb=Increased conversion of **cholesterol to bile acids **
LDL receptor expression is increased=^{ENHANCING LDL clearance}
PK:
Oral water soluble NOT absorbed/metab
Uncomfortable to ingest-mix with OJ
Completely excrerted in Feces

Question 12

Q

Inhibitors of bile acid reabsorption Use&SEs

Answer

A

Use:
Type 2a & Type 2b hyperlipidemia
Only if isolated increases in LDL
Mainly used for ^{young pts of hypercholesterlemia}
Safe in Pregers
Cholestyramine relieves prutitus caused by accumulation of bile acids w/Bililary obstruction
SE:
GI related-Constipation, Bloating, Farting
Decreased absorb of Fat-sol vit (ADEK) & most drugs (digoxin)
Combo w/ statins OR niacin ADDITIVE reduction of LDL
CI=upreg VLDL & trigly synthesis CAUTION w/pts ^{hypertriglyceridemia}

Question 13

Q

Niacin

Answer

A

Nicotinic acid/Vit B3
PD:
Reduces VLDL, LDL & trigly
In gram doses inhibits lipolysis in adipose
Decrease in FAs = decrease in Trigly synthesis (Required for VLDL-LDL comes from VLDL)
Increases HDL
PK:
Oral & ^{converted to nicotinamide }incorporated into NAD
Excreted in urine
Use: when ^{STATINS are CI}
Familial hyperlipidemias (^{NO LDL-R)}
In combo w/statins for severe Hypercolesterolemias
SE: Cutaneous flush (vasodialator)
Impaired insulin sensitivity - NO diabetics

Question 14

Q

Fibrates

Answer

A

Fenofibrate & Gemifibrozil
_PK: _
Oral & bound to albumin
Excreted as ^{glucoronide conj}
PD:
Reduce VLDLs + TGs W/increase in HDL
Bind to induce PPAR (peroxisome proliferator-activated receptor)-Expressed on heptocytes, muscle, macrophage, heart
USE: Treatment of Hypertriglycerolemias
1st line for ^{dysbetalipoproteinemias}
Se:
Choleithiasis: GOLD gallstones
Interactions: competes w/coumadin for plasma binding shites = ^{+++ anticoag}

Question 15

Q

Cholesterol Absorption Inhibitors

Answer

A

Ezetimibe & Plant Sterols
PD: Reduce LDL
Inhibit intestinal absorption of dietary+biliary cholesterol
reduce LDL inhibiting hepatic production of VLDL
Reduced hepatic cholesterol-UP regs LDL-Receptor
_PK: _
oral & metab in liver/small intest
USE: complimentary to statins & Treat Primary & familial hypercolesterolemia ^{(statin is CI)}
SE: Diarrhea, rash, angioedema
CI: Pregers due to lactation

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Block 2-Reymann (Lipid) Flashcards

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