Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacotherapy II > Hyperlipidemia Hockerman Exam 3 > Flashcards

Hyperlipidemia Hockerman Exam 3 Flashcards

1
Q

What macromolecules are found on the surface of lipoproteins? In the core?

A

Surface: phospholipid, free cholesterol, protein
Core: triglyceride, cholesterol ester

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What lipoprotein is responsible for reverse cholesterol transport?

A

HDL–the good cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What lipoprotein has the highest cholesterol content?

A

LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What lipoprotein is secreted by the liver as a source of triglycerides?

A

VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What lipoprotein transports dietary lipids from gut to liver and adipose tissue?

A

Chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What lipoprotein is simply a triglyceride-depleted VLDL?

A

IDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What apolipoprotein is the seed crystal for HDL and helps with reverse cholesterol transport?

A

ApoA-1 (steak sauce!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What apolipoprotein is produced in the intestine to form chylomicrons?

A

ApoB-48

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What apolipoprotein is produced in the liver and, with HDL, helps with reverse cholesterol transport?

A

ApoE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What apolipoprotein is produced in the liver and is the LDL receptor ligand–helps internalize LDL into the liver?

A

ApoB-100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What apolipoprotein inhibits lipoprotein lipase and interferes with ApoB and ApoE binding to hepatic receptors, preventing triglyceride breakdown and inhibiting LDL internalization?

A

ApoCIII–LOF mutation leads to lower CHD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

IDL + cholesterol from HDL =

A

LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the liver do with chylomicron remnants?

A

Packages them into VLDL, which in turn becomes IDL after capillaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What enzyme is rate-limiting in cholesterol synthesis?

A

HMGCoA reductase–forms mevalonate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

True or false: Limiting dietary intake of cholesterol is the best way to lower blood cholesterol.

A

False–de novo synthesis is the major source of cholesterol, so limiting intake has minor effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What TC/HDL ratio is indicative of increased CVD risk?

A

> 4.5

17
Q

What can hypertriglyceridemia lead to?

A

Pancreatitis, xanthomas (fat in skin). Some association wth increased CHD risk.

18
Q

What are foam cells?

A

Dead macrophages that look foamy due to the high amount of cholesterol they contain. Make up the necrotic pore of the plaque.

19
Q

What is the mechanism of action of cholestyramine (Queastran) and colestipol (Colestid)?

A

These bile acid binding resins inhibit reabsorption of bile acids from the intestine by binding bile acids to form insoluble complex. Inherently decreases cholesterol in body, but also increases excretion of bile acids because loss of negative feedback! They also up-regulate LDL receptors in the liver.

20
Q

What is the clinical effect do the bile acid binding resins have? What side effects?

A

~20% reduction LDL, ~5% increase HDL, may increase TG. Take before meals. High constipation and bloating (eating resin! high fiber diet/water helps), drug interactions.

21
Q

How does ezetimibe function to decrease cholesterol?

A

It inhibits intestinal absorption of cholesterol from dietary sources and bile acid secretion (NPC1L1 transporter).

22
Q

How is ezetimibe primarily used in therapy? What SEs?

A

Usually in conjunction with statins, but lowers LDL 17% by itself. Generally well tolerated, but some liver/skeletal muscle damage.

23
Q

What are the two ways that statins lower LDL?

A

They competetively inhibit HMG-CoA reductase (synthesis) and upregulate LDL receptors in the liver (transcription triggered by low cholesterol levels)

24
Q

What effects do statins have on lipids?

A

All dependent on dose/choice: 20-60% reduction in LDL, 10-33% reduction TG, 5-10% increase HDL.

25
Q

What special instructions should be given to patients about taking their statin?

A

Lovastatin should be taken with evening meal (increased absorption), rosuva/prava/pitava/atorva/fluvaXL/lovaXL any time of day, fluva/lova/simva must be at night.

26
Q

Which statins are strongly metabolized by CYP3A4?

A

Lovastatin, sinvastatin, atorvastatin

27
Q

Which statins are strongly metabolized by CYP2C9?

A

Fluvastatin, rosuvastatin, pitavastatin

28
Q

Which statin is sulfated?

A

Pravastatin

29
Q

What side effects are concerns with statins?

A

Skeletal muscle (rhabdomyolysis, myopathy–monitor CPK), hepatotoxicity (2%, monitor serum transaminase), increased incidence T2DM

30
Q

What two drugs are approved explicitly for homozygous familial hypercholesterolemia? Which one is an oligonucleotide inhibitor of ApoB-100? Which is given PO? Which is injected SC? What side effect do both carry as a black box warning?

A

Juxtapid (Lomatipide) and Mipomersen (Kynamro)
Juxtapid is PO, mipomersen is SC
Mipomersen is antisense oligonucleotide inhibitor
Black box warning for hepatotoxocity

31
Q

What is the mechanism of action for PCSK9 inhibitors? How are they dosed?

A

They inhibit degradation of LDL receptors in the liver, leading to increased degradation of LDL.
Both are dosed SQ every two weeks; evolocumab can be dosed monthly.

32
Q

What is the primary effect of the fibrates? How do they do this?

A

Reduction of serum TG primarily, but also increase HDL and decrease LDL. After bioactivation, they bind PPAR-a to regulate gene transcription (increase ApoA1, decrease ApoCIII).

33
Q

What side effects are associated with fibric acid derivatives?

A

Gallstones, rhabdomyolysis, increase effect of warfarin.

34
Q

How do omega-3 fatty acids like Lovaza (DPA + DHA) work?

A

They reduce synthesis of TG in liver (poor substrates), inhibit esterification of other fatty acids, and inhibit platelet aggregation (prostaglandins made from EPA are worse aggregators).

35
Q

When is Lovaza used? What side effects?

A

Used after failure of lipid lowering diet, in severe hypertriglyceridemia (>500), often in combo with statin. Unfortunately, can increase LDL.

36
Q

How is niacin dosed to reduce serum TG?

A

1-3 g/day

37
Q

How does niacin work to reduce TG?

A

Increase lipase activity, decreases VLDL production (less delivery of FA to liver). Can decrease LDL and increases HDL (big bonus).

38
Q

What are the side effects of high dose niacin?

A

Vasodilation (flushing), itching, tingling, HA (prostaglandins–treat with NSAID), hepatotoxicity

Pharmacotherapy II (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions