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UF COM GI > Dyslipidemias GI Exam 2 > Flashcards

Dyslipidemias GI Exam 2 Flashcards

1
Q

Cholesterol ___ makes up 20% of total cholesterol and the other 80% is ____.

A

Cholesterol from the diet makes up 20% of total cholesterol and the other 80% is syntesized in the liver.

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2
Q

chylomicrons and VLDL are ______ rich whereas LDL and HDL are _____ rich

A

chylomicrons and VLDL are triglyceride rich whereas LDL and HDL are cholesterol rich

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3
Q

——–and ———-produce a cloudy plasma because they bounce around light. If you leave them in a test tube at 4-degrees, ______form a beige layer on top.

A

chylomicrons and VLDL produce a cloudy plasma because they bounce around light. If you leave them in a test tube at 4-degrees, chylomicrons form a beige layer on top.

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4
Q

______ LDL binds to LDL scavenger receptors more readily that _______ LDL. The scavenger receptors are on macrophages creating foam cells. This is the theoretical basis for _______ being anti-atherogenic

A

oxidized LDL binds to LDL scavenger receptors more readily that unoxidized LDL. The scavenger receptors are on macrophages creating foam cells. This is the theoretical basis for antioxidants being anti-atherogenic

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5
Q

___ and ___ are small enough to traverse the endothelium of blood vessels to be taken up by macrophages which makes them atherogenic

A

IDL and LDL are small enough to traverse the endothelium of blood vessels to be taken up by macrophages which makes them atherogenic

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6
Q

IDL and LDL are small enough to traverse the endothelium of blood vessels to be taken up by macrophages which makes them _____

A

IDL and LDL are small enough to traverse the endothelium of blood vessels to be taken up by macrophages which makes them atherogenic

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7
Q

____ and _____ are too large to make it through the endothelium of blood vessel and so are not atherogenic

A

VLDLs and Chylomicrons are too large to make it through the endothelium of blood vessel and so are not atherogenic

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8
Q

_______________ is an LDL variant that is particularly atherogenic. Levels are strictly ________ determined (not ____!) and very hard to alter. It has _____ on its surface.

A

Lipoprotein a is an LDL variant that is particularly atherogenic. Levels are strictly genetically determined (not diet!) and very hard to alter. It has Apo(a) on its surface.

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9
Q

Lipoprotein(a) has been associated with increased risk of ____ and ______.

A

Lipoprotein(a) has been associated with increased risk of stroke and coronary artery disease.

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10
Q

___ is a lipoprotein with ApoA1 on it’s surface. The enzyme LCAT incorporates cholesterol from tissues and other lipoproteins into ___. This cholesterol scavenging accounts for ___’s anti-atherogenic properties.

A

HDL is a lipoprotein with ApoA1 on it’s surface. The enzyme LCAT incorporates cholesterol from tissues and other lipoproteins into HDL. This cholesterol scavenging accounts for HDL’s anti-atherogenic properties.

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11
Q

HDL is a lipoprotein with ____ on it’s surface. The enzyme ____ incorporates cholesterol from tissues and other lipoproteins into HDL. This cholesterol scavenging accounts for HDL’s anti-atherogenic properties.

A

HDL is a lipoprotein with ApoA1 on it’s surface. The enzyme LCAT incorporates cholesterol from tissues and other lipoproteins into HDL. This cholesterol scavenging accounts for HDL’s anti-atherogenic properties.

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12
Q

A chylothorax can result from injury to the _____. If you tap the fluid, you will find ____ fluid in the pleural space rich in ______ and ______

A

A chylothorax can result from injury to the thoracic duct. If you tap the fluid, you will find turbid fluid in the pleural space rich in leukocytes and triglycerides

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13
Q

______ are packages of lipid containing surface proteins termed apolipoproteins

A

Lipoproteins are packages of lipid containing surface proteins termed apolipoproteins

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14
Q

______ and ____ are triglyceride transporters. __ transport TG from the intestine, while ____ transport TG from the liver

A

Chylomicrons and VLDL are triglyceride transporters. CM transport TG from the intestine, while VLDL transport TG from the liver

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15
Q

Chylomicrons and VLDL are _______ transporters. CM transport __ from the intestine, while VLDL transport __ from the liver

A

Chylomicrons and VLDL are triglyceride transporters. CM transport TG from the intestine, while VLDL transport TG from the liver

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16
Q

___________ in tissues removes much of the triglyceride by hydrolysis and leaves remnant lipoproteins (from chylomicrons) or IDLs (from VLDL).

A

Lipoprotein lipase in tissues removes much of the triglyceride by hydrolysis and leaves remnant lipoproteins or IDLs.

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17
Q

Lipoprotein lipase in tissues removes much of the _____ by hydrolysis and leaves remnant lipoproteins (from chylomicrons) or IDLs (frmo VLDL).

A

Lipoprotein lipase in tissues removes much of the triglyceride by hydrolysis and leaves remnant lipoproteins (from chylomicrons) or IDLs (frmo VLDL).

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18
Q

The _______ is responsible for cholesterol uptake into hepatocytes and steroidogenictissue

A

The LDL receptor is responsible for cholesterol uptake into hepatocytes and steroidogenictissue

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19
Q

Dietary triglycerides are hydrolyzed in the intestinal lumen by _______ into _______ and ______

A

Dietary triglycerides are hydrolyzed in the intestinal lumen by pancreatic lipase into free fatty acids and monoglyceride

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20
Q

_______ and _________ in the intestinal lumen are absorbed by enterocytes and then reassembled into triglycerides in the cytosol.

A

free fatty acids and monoglycerides in the intestinal lumen are absorbed by enterocytes and then reassembled into triglycerides in the cytosol.

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21
Q

An enzyme called ____ packages triglycerides and cholesterol esters into ______ in the cytoplasm of enterocytes

A

An enzyme called ACAT packages triglycerides and cholesterol esters into chylomicrons in the cytoplasm of enterocytes

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22
Q

___ and ___ cooperate to help cholymicrons escape enterocytes into the chyle.

A

ApoB and microsomal triglyceride transfer protein (MTP) cooperate to help cholymicrons escape enterocytes into the chyle.

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23
Q

______ have Apo proteins E, CII, and B48 on their surface. Apo___ helps _____ bind to the lipoprotein lipases on the endothelial cells that line the small blood vessels of skeletal muscle and adipose tissue.

A

Chylomicrons have Apo proteins E, CII, and B48 on their surface. ApoCII helps chylomicrons bind to the lipoprotein lipases on the endothelial cells that line the small blood vessels of skeletal muscle and adipose tissue.

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24
Q

Chylomicrons have Apo proteins ___, ___, and ___ on their surface. ApoCII helps chylomicrons bind to the ______ on the endothelial cells that line the small blood vessels of ______ and _______.

A

Chylomicrons have Apo proteins E, CII, and B48 on their surface. ApoCII helps chylomicrons bind to the lipoprotein lipases on the endothelial cells that line the small blood vessels of skeletal muscle and adipose tissue.

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25
Q

______ enter the lymph system via _____ within vili of the small intestines.

A

Chylomicrons enter the lymph system via lacteals within vili of the small intestines.

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26
Q

Lipoprotein lipase is attached to the endothelial cells lining the small vessels of skeletal muscle and adipose by the anchoring protein ______.

A

Lipoprotein lipase is attached to the endothelial cells lining the small vessels of skeletal muscle and adipose by the anchoring protein GPIHBP1

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27
Q

Once lipoproteins are cleaved by lipoprotein lipase, the ____ are used as energy by skeletal muscle and stored in adipocytes and the _______ continue on the blood sans ApoCII.

A

Once lipoproteins are cleaved by lipoprotein lipase, the free fatty acids are used as energy by skeletal muscle and stored in adipocytes and the IDL/lipoprotein remnants continue on the blood sans ApoCII.

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28
Q

____s are synthesized in the liver. The have Apo proteins E, CII, and B100

A

VLDLs are synthesized in the liver. The have Apo proteins E, CII, and B100

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29
Q

VLDLs are synthesized in the liver. The have Apo proteins __. __, and ___

A

VLDLs are synthesized in the liver. The have Apo proteins E, CII, and B100

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30
Q

____ and ____ travel in the blood stream where they are taken up by the liver

A

Chylomicron remnant an IDL travel in the blood stream where they are taken up by the liver

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31
Q

___ can bind only IDL and LDL

___ can bind IDL and chylomicron remnants

A

LDL-receptor can bind only IDL and LDL

LRP1 can bind IDL and chylomicron remnants

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32
Q

LDL-receptor can bind ____

LRP1 can bind ____

A

LDL-receptor can bind IDL and LDL only

LRP1 can bind IDL and chylomicron remnants

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33
Q

Hepatic lipase further digests ___ into ___. The lipoprotein loses Apo_ in the process.

A

Hepatic lipase further digests IDL into LDL. The lipoprotein loses ApoE in the process.

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34
Q

______ further digests IDL into LDL. The lipoprotein loses ApoE in the process.

A

Hepatic lipase further digests IDL into LDL. The lipoprotein loses ApoE in the process.

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35
Q

___ induces LDL receptor degradation. Thus, increased ___activity increases LDL in the blood.

A

PSCK9 induces LDL receptor degradation. Thus, increased PSCK9 activity increases LDL in the blood.

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36
Q

PSCK9 induces ___ degradation. Thus, increased PSCK9 activity increases ___ in the blood.

A

PSCK9 induces LDL receptor degradation. Thus, increased PSCK9 activity increases LDL in the blood.

37
Q

____ mediates positioning of the LDL receptor in coated pits. Mutations in the gene for ____ cause autosomal recessive hypercholesterolemia.

A

LDLRAP1 mediates positioning of the LDL receptor in coated pits. Mutations in the gene for LDLRAP1 cause autosomal recessive hypercholesterolemia.

38
Q

Hyperlipidemia may be the result of _____, ____ and/or ______

A

Hyperlipidemia may be the result of excess VLDL production by the liver, decreased action of lipolipase on triglyceride-rich mlcs, and/or decreased uptake of ApoB protein lipoproteins

39
Q

Severe hypertriglyceridemia may be seen in defects of ______ or ___

A

Severe hypertriglyceridemia may be seen in defects of lipoprotein lipase or apoCII

40
Q

Classic familial hypercholesterolemia is due to a defect in the _________

A

Classic familial hypercholesterolemia is due to a defect in the LDL receptor

41
Q

Familial hypercholesterolemia may be due to a defective ___ or a gain-of-function of ____

A

Familial hypercholesterolemia may be due to a defective apoB100 or a gain-of-function of PSKC9

42
Q

The hyperlipidemias that result from lipid overproduction can be ____ or ____.

A

The hyperlipidemias that result from lipid overproduction can be genetic (e.g. familial combined hyperlipidemia) or acquired

43
Q

________ and _________ can lead to hyperlipidemia

A

Hypothyroidism and uncontrolled diabetes mellitus can lead to hyperlipidemia

44
Q

___ or ___ will significantly affect lipid studies. Very low lipids may be encountered in ____ patients.

A

Recent illness or current hospitalization will significantly affect lipid studies. Very low lipids may be encountered in critically ill patients.

45
Q

Clinical lipid studies tell you 4 things:

A

Clinical lipid studies tell you 4 things:

  1. Total cholesteral
  2. HDL-C
  3. LDL-C (sometimes this is calculated)
  4. Triglycerides
46
Q

The report “LDL cholesterol is 120 mg/dL” means
“_____________”

A

The report “LDL cholesterol is 120 mg/dL” means
“The concentration of cholesterol derived from the LDL particles is 120 mg/dL”
(Does not mean that the concentration of LDL lipoprotein particles is 120 mg/dL)

47
Q

Having high ____ and ____ increases atherosclerotic risk. High HDL-C decreases risk.

A

Having high LDL-C and high triglycerides increases atherosclerotic risk. High HDL-C decreases risk.

48
Q

“______” includes LDL-C and HDL-C

“______” includes VLDL, IDL, CM

A

“total cholesterol” includes LDL-C and HDL-C

“triglycerides” includes VLDL, IDL, CM

49
Q

“total cholesterol” includes ____ and ____

“triglycerides” includes ____, ___, ___

A

“total cholesterol” includes LDL-C and HDL-C

“triglycerides” includes VLDL, IDL, CM

50
Q

Friedwald Calculation

A

LDL = total cholesterol - HDL - trglycerides/5

51
Q

The Frieldwald calculation can only be used…

  1. ???
  2. ???
A

The Frieldwald calculation can only be used…

  1. If the patient is fasting
  2. If plasma triglycerides are <400 mg/dL
52
Q

wat dis?

A

xanthomas. deposits of lipids in skin or tendons

53
Q

Familial Combined Hyperlipidemia

  • is a genetic cause of ______.
  • It is a ____genic trait.
  • Labs on these patients will show high ______.
  • Among people with CAD before age __, 20% of FCHL
A

Familial Combined Hyperlipidemia

  • is a genetic cause of VLDL over production.
  • It is a polygenic trait.
  • Labs on these patients will show high VLDL, LDL, total cholesterol, and triglycerides.
  • Among people with CAD before age 60, 20% of FCHL
54
Q

The Metabolic syndrome

  • is an acquired cause of ______
  • Pts will have large abd girth, HTN, hyperinsulinemia, glucose intolerance, hyperlipidemia
  • Labs will show high _______
A

The Metabolic syndrome

  • is an acquired cause of VLDL over production
  • Pts will have large abd girth, HTN, hyperinsulinemia, glucose intolerance, hyperlipidemia
  • Labs will show high triglycerides, so high LDL, but low HDL
55
Q

Other than the metabolic syndrome, 3 other acquired causes of hyperlipidemia are…

A
  1. A high carb diet that upregulates fatty acid synthesis
  2. Alcohol use which inhibits oxidation of fatty acids and upregulates triglyceride synthesis
  3. Nephrotic syndrome. The increased lipolipid production is a compensatory response to the decreased oncotic pressure caused by hypoalbuminemia.
56
Q

_______ is a genetic cause of decreased lipolipase action. It can result from lipolipase enzyme deficiency or from ApoCII deficiency.

A

Familial chylomicronemia is a genetic cause of decreased lipolipase action. It can result from lipolipase enzyme deficiency or from ApoCII deficiency.

57
Q

Familial chylomicronemia is a (genetic, acquired) cause of decreased lipolipase action. It can result from ____ enzyme deficiency or from Apo___ deficiency.

A

Familial chylomicronemia is a genetic cause of decreased lipolipase action. It can result from lipolipase enzyme deficiency or from ApoCII deficiency.

58
Q

VIC tris

A

VLDL, IDL, CMs all cause increase in triglycerides

59
Q

Familial Chylomicronemia

  • genetic cause of super high ______
  • pts have vvv high ___ only mildly elevated ___
  • blood in vacutainer at 4-deg will have ____
  • Patients are at risk for _____ because ______________ (not _________)
A

Familial Chylomicronemia

  • genetic cause of super high triglycerides (10,000-25,000)
  • pts have vvv high CMs only mildly elevated VLDL
  • blood in vacutainer at 4-deg will have thick cream layer on top
  • Patients are at risk for pancreatitis because chylomicrons obstruct tiny vessels (not atherosclerosis)
60
Q

___ is an acquired cause of deficient lipolipase activity that leads to high triglycerides.

A

DKA is an acquired cause of deficient lipolipase activity that leads to high triglycerides.

occurs in pts with DM-I. insulin helps lipoprotein lipase function.

61
Q

There are 5 genetic causes of deficient uptake of ApoB containing lipoproteins:

  1. ?
  2. ?
  3. ?
  4. ?
  5. ?
A

There are 5 genetic causes of deficient uptake of ApoB containing lipoproteins:

  1. Familial Hypercholesterolemia
  2. Familial Defective ApoB100
  3. PSCK9 Mutation
  4. Autosomal Recessive Hypercholesterolemia
  5. Dysbetalipoproteinemia/Type III Hyperlipoproteinemia
62
Q

Familial Hypercholesterolemia

  • cause: ??
  • pathology: ??
  • FH: ??
  • Clinical presentation/outcomes: ??
A

Familial Hypercholesterolemia

  • cause: genetic, autosomal dominant
  • pathology: defective LDL receptor, LDL-C can reach 400 mg/dL with craaaazy high cholesterol
  • FH: patients will have FH of early CAD disease
  • Clinical presentation/outcomes: untreated, men are at increased risk of heart attack by age 50, women by age 60. Homozygous form can be fatal in early childhood.
63
Q

Familial Defective ApoB100

Cause: ??

Pathology: ??

FH: ??

Effect: ??

A

Familial Defective ApoB100

Cause: genetic, autosomal dominant

Pathology: defective ApoB100 can’t bind to LDL receptor

FH: same as Familial Hypercholesterolemia

Effect: same as Familial Hypercholesterolemia

64
Q

PSCK9 Mutation

cause: ??
pathogenesis: ??

Effect: ??

A

PSCK9 Mutation

cause: genetic, autosomal dominant gain of function mutation in PSCK9 gene
pathogenesis: Upregulated PSCK9 degrades LDL receptor.

Effect: elevated LDL-C. Clinically indistinguishable from Familial Hypercholesterolemia.

65
Q

Autosomal Recessive Hypercholesterolemia

cause: ??
pathogenesis: ??

FH: ??

Effect: ??

A

Autosomal Recessive Hypercholesterolemia

cause: genetic, autosomal recessive defect in the LDLRAP1 protein; vvv rare
pathogenesis: LDL no longer positioned appropriately in coated pit

FH: parents will have normal cholesterol. Founder effect in Sardinia

Effect: phenotype similar to Familial Hypercholesterolemia

66
Q

Dysbetalipoproteinemia/Type III Hyperlipoproteinemia

cause: ??
pathogenesis: ??

Clinical effect: ??

A

Dysbetalipoproteinemia/Type III Hyperlipoproteinemia

cause: homozygous for ApoE2 PLUS liver dz, renal dz, diabetes, or alcoholism
pathogenesis: Chylomicron remnants and IDL can’t bind LDL receptor - “remnant disease”.

Clinical effect: increased risk of CAD and peripheral vascular disease because remnants are atherogenic. Palmar crease xanthomas

67
Q

Both ____ and ___ are acquired causes of defective uptakes of ApoB containing lipoproteins

A

Both hypothyroidism and CKD are acquired causes of defective uptakes of ApoB containing lipoproteins

68
Q

“non-HDL cholesterol” is the (formula). This number is meaningful because (lipoproteins) are atherogenic. It is a better prdictor of (clinically meaningful end point) and is _______ as opposed to Frieldwald calculation

A

“non-HDL cholesterol” is the total cholesterol - HDL. This number is meaningful because LDL, IDL, and VLDL are atherogenic. It is a better prdictor of cardiovascular disease than LDL-C alone and is measured directly as opposed to Frieldwald calculation

jury is out on VLDL

69
Q

Major lipolipid classes an be further subdivided into ____. For example, ____ LDL is more atherogenic than l____ LDL.

A

Major lipolipid classes an be further subdivided into subfactions based on density. For example, small dense LDL is more atherogenic than large, bouyant LDL.

70
Q

Both LDL receptor deficiency and defective apo B100 produce elevations in ___. In addition, LDL receptor deficiency may also cause elevated ___ in addition to elevated ___. Defective apo B100 does not produce elevations in ___

A

Both LDL receptor deficiency and defective apo B100 produce elevations in LDL. In addition, LDL receptor deficiency may also cause elevated VLDL in addition to elevated LDL. Defective apo B100 does not produce elevations in VLDL

VLDL has ApoE to help bind LDLR. LDL only has B100. If B100 is defective, LDL has nothing

71
Q

If diet and exercise don’t work, patient can treat their high LDL with (drug). Unless the pt also has liver disease, then use (drug) because it’s the only drug w/o liver side effects.

A

If diet and exercise don’t work, patient can treat their high LDL with a statin drug. Unless the pt also has liver disease, then use a bile-acid binding resin because it’s the only drug w/o liver side effects.

72
Q

___ or ___ can both cause hyperchylomicronemia. However, ___ is not, in general, as severe as ___ and often presents at a later age.

A

LPL deficiency or apo CII loss-of-function mutations can both cause hyperchylomicronemia. However, apo CII deficiency is not, in general, as severe as LPL deficiency and often presents at a later age.

73
Q

___ and ___ can present with abdominal pain and low fever. In vitro, pt’s blood wil appear turbid and a cream layer will form on top if refrigerated. Triglycerides will be crazy high and cholesterol will be elevated. This makes sense because ___ degrades chylomicrons. Treat with dietary fat restriction

A

LPL deficiency and ApoCII deficiency can present with abdominal pain and low fever. In vitro, pt’s blood wil appear turbid and a cream layer will form on top if refrigerated. Triglycerides will be crazy high and cholesterol will be elevated. This makes sense because LPL degrades chylomicrons. Treat with dietary fat restriction

74
Q

LPL deficiency and ApoCII deficiency can present with ____ and ____. In vitro, pt’s blood wil appear ____ and a ____ will form on top if refrigerated. ______ will be crazy high and ____ will be elevated. This makes sense because LPL degrades _____. Treat with _____

A

LPL deficiency and ApoCII deficiency can present with abdominal pain and low fever. In vitro, pt’s blood wil appear turbid and a cream layer will form on top if refrigerated. Triglycerides will be crazy high and cholesterol will be elevated. This makes sense because LPL degrades chylomicrons. Treat with dietary fat restriction

75
Q

The presentation of Familial Combined Hyperlipidemia is like Familial Hypercholesterolemia except total cholesterol and triglycerides are _____. In FH, ___>>> ___

A

The presentation of Familial Combined Hyperlipidemia is like Familial Hypercholesterolemia except total cholesterol and triglycerides are similarly elevated. In FH, cholesterol >>> triglycerides

76
Q

Xanthomas on knees and elbows? Think this disease…

A

Familial Hypercholesterolemia

77
Q

Familial Hypercholesterolemia is treated with (pharmacotherapy) and (therapy). It can be cured entired with ______

A

Familial Hypercholesterolemia is treated with triple drug therapy (statin, bile-acid binding resin, niacin/ezitamide) and LDL-apheresis. It can be cured entired with a liver transplant so they’ll have working LDL receptors

78
Q

Xanthomas in the palmar creases are seen in (disease)

A

Xanthomas in the palmar creases are seen in Familial Dysbetalipoproteinemia

79
Q

A young patient presents with high triglycerides, hyperchylomicronemia, and multiple small red/yellow papules that appeared suddenly. What’s his diagnosis?

A

Lipoprotein lipase deficiency.

The papules are eruptive xanthomas classic to LPL deficiency

80
Q

A man in his 40s presents with angina pectoralis, vvvv high cholesterol w/ moderately elevated triglycerides, and nodules on his knees, elbows, and buttocks. He also has nodules in his tendons. What’s is diagnosis?

A

Familial Hypercholesterolemia. Nodules are tuberous xanthomas.

caused by defective LDL receptor

81
Q

tendonous xanthomas are seen in what disease?

A

Familial Hypercholesterolemia.

Tendonous and Tuberous

82
Q

Planar xanthomas near the eyes called xanthelasma can occur in lots of hyperlipidemic states or ___ individuals. They are not specific

A

Planar xanthomas near the eyes called xanthelasma can occur in lots of hyperlipidemic states or normal individuals. They are not specific

83
Q

Pictured blow, arcus senilis is due to cholesterol deposition. It is ____with aging, but should prompt work up in patient <__ y.o.

A

Pictured blow, arcus senilis is due to cholesterol deposition. It is normal with aging, but should prompt work up in patient <50 y.o.

84
Q

True or False: LDL receptor decrease with age

A

True

85
Q

Cholesterol removal from _____ may be responsible for antiathrogenic effects of HDL

A

Cholesterol removal from arterial cells may be responsible for antiathrogenic effects of HDL

86
Q

The enzyme ____ esterifies HDL cholesterol. Cholesterol esters are the transferred from HDL to ___ to be taken back up by the liver.

A

The enzyme LCAT esterifies HDL cholesterol. Cholesterol esters are the transferred from HDL to LDL to be taken back up by the liver.

87
Q

The two classes of lipid-lowering drugs that affect warfarin action the most are _____ and _____, though all drugs that affect lipoprotein levels will affect the action of warfarin. You will probably have to tweak their anti-coag dose.

A

The two classes of lipid-lowering drugs that affect warfarin action the most are fibric acid derivatives and bile-acid binding agents, though all drugs that affect lipoprotein levels will affect the action of warfarin. You will probably have to tweak their anti-coag dose.

88
Q

The statins, Lovastatin and Atorvastatin, are HMG-CoA Reductase inhibitors.

A

The statins, Lovastatin and Atorvastatin, are HMG-CoA Reductase inhibitors.

UF COM GI (4 decks)

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