Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Hyperlipidemia/Dyslipidemia > Flashcards

Hyperlipidemia/Dyslipidemia Flashcards

(55 cards)

Start Studying
1
Q

hypercholesterolemia

A

high LDL, normal TG and HDL

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

mixed or combined dyslipidemia

A

high LDL and TG and possibly low HDL

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

hypertriglyceridemia

A

high TG, normal LDL and possible low HDL

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

where is most cholesterol produced

A

75% in liver

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

what does cholesterol make?

A

hormones
Vit D
bile salts

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

first line conventional tx for hyperlipidemia

A

statins

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

Statins MOA

A

HMG-CoA reductase inhibitors (this enzyme catalyzes the rate-limiting step in cholesterol synthesis) –> liver increases cholesterol uptake from the blood stream by increasing the number of LDL receptors (PCSK9 up regulation)

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

Statin indications

A

first-line therapy for primary and secondary prevention of ASCVD; familial hypercholesterolemia

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

Statin C/I

A

active liver dz (not absolute), pregnancy (category X), or breat feeding

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

Statin s/e

A

myopathy, increase in liver enzymes, nausea, HA

if someone is predisposed to DM, these can make dz more likely

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

Statin pharmacokinetics

A

1) onset: variable, peak effect in a few weeks
2) T1/2 = 1-20 hr
3) metabolism: variable, usu. involves CYP enzyme
4) variable bioavailability

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

How is atorvastatin metabolized?

A

CYP34A

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

How is fluvastatin metabolized?

A

CYP2C9 (major)

CYP34A (20%)

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

How is lovastatin metabolized?

A

CYP3A4

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

How is pitavastatin metabolized?

A

glucoronidation (major)

CYP2C9 and CYP2C8 (minor)

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

How is rosuvastatin metabolized?

A

not extensively metabolized; the major metabolite is formed by CYP2C9 and CYP2C19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is simvastatin metabolized?

A

CYP3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Interactions between statins and natural therapies

A

1) Red yeast rice - duplication of therapy, incr. risk of myopathy
2) Niacin - might interact but is also used purposefully s/t when TG are high or HDL is low
3) Alcohol - hepatotoxicity
4) Grapefruit - CYP3A4 inhibitor, OATP inhibitor
5) Hypericum - CYP3A4 inducer
6) Sweet orange - OATP inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

A person on atorvastatin drinks up to 1 quart of grapefruit juice per day. (1) How might their levels of artorvastatin be effected. (2) What s/e would be of concern? (3) What alternative statins could they take?

A

1) Grapefruit juice inhibits CYP3A4, which metabolizes atorvastatin
2) myalgia; have pt. self monitor b/c juice doesn’t significantly affect all pt.
3) **pravastatin, pitavastatin, rosuvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ezetimibe (Zetia) MOA

A

prevents absorption of dietary and biliary cholesterol –> upregulates LDL receptors in the liver lowering plasma LDL-C

**inhibits cholesterol GI absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ezetimibe (Zetia) indications

A

adjunctive therapy in homozygous familial hypercholesterolemia and primary hyperlipidemia; typically used when statin intolerant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Ezetimibe (Zetia) cautions

A

1) C/I in pregnancy (category C) and breast feeding

2) may incr. liver enzymes; higher likelihood of this when administered w/ statin than as a monotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ezetimibe (Zetia) efficacy

Study These Flashcards
A

on small reduction in ASCVD when used WITH a statin

minor reduction in LDL; even smaller increase in HDL and decrease in TG

24
Q

Ezetimibe (Zetia) pharmacokinetics

Study These Flashcards
A

1) onset = 1 wk
2) T1/2 = 22 hr
3) metabolism = ~30 undergoes glucuronide conjugation in SI and liver, active metabolite; ~80% excreted in feces

25
Ezetimibe (Zetia) interactions with natural products
1) b/c it inhibits sterol absorption in the gut, it will lower effectiveness of green tea, omega-3 FA, sitostanol, and beta-sitosterol 2) numerous meds w/ moderate interactions that effect liver toxicity or drug absorption **no interactions w/ niacin or red yeast rice
26
Fenofibrate (fibric acid) class
fibrate
27
Gemfibrozil class
fibrate
28
Fibrates MOA
lower production and increase clearance of VLDL, increase HDL production ultimately lowers TG and increased HDL, but has variable effect on LDL
29
Fibrates indications
- hypercholesterolemia or mixed dyslipidemia as adjunct therapy or monotherapy in pt. who cannot tolerate statins - hypertriglyceridemia first-line pharmacotherapy (TG > 1000 mg/dL)
30
Fibrates cautions
1) C/I = active liver dz, severe renal impairment or ESRD, pre-existing GB dz, breast feeding 2) s/e = dyspepsia, gallstones, myopathy (incr risk w/ statins, esp. gemfibrozil)
31
Fibrate pharmacokinetics
1) onset = 2-3 days 2) T1/2 = 20 hrs 3) Inactived by glucuronidation in the liver or kidney; ~60% excreted in urine as metabolites
32
Fibrates interactions w/ natural therapies
1) if combined w/ red yeast rice might incr. risk of myopathy 2) niacin might incr. hepatoxicity 3) alcohol - hepatoxicity 4) other meds that cz liver toxicity
33
Gemfibrozil increases the risk for what s/e when used with statin therapy?
myopathy
34
How can we assess severity of myopathy?
creatinine kinase *rarely, pt. can have really high creatinine kinase w/out sx of myalgia, so it might be good to get a baseline and monitor them a few mo. into tx
35
Niacin MOA
somewhat unclear increases lipoprotein lipase (LPL) activity, enhancing removal of TG from plasma; reduces TG synthesis; incr. HDL levels
36
Niacin indications
hypercholesterolemia or mixed dyslipidemia - as adjunct therapy in pt. that don't tolerate fibrates or omega-3 FA - as monotherapy in pt. that don't tolerate statins, BAS, fibrates
37
Niacin cautions
1) C/I = active liver dz (esp. w/ sustained release), gout, or PUD 2) s/e = hepatotoxicity (enhanced SR formulation), hyperglycemia, hyperuricemia, upper GI distress, flushing**, itching
38
Niacin efficacy
studies haven't panned out for using niacin as ASCVD preventative moderate reduction in LDL and TG, moderate incr. in HDL
39
Niacin pharmacokinetics
1) onset = immediate 2) T1/2 = 30 min 3) quickly converted to NAD+ in liver, but pathways become saturated at doses need to tx hyperlipidemia 4) ~70% excreted in urine
40
Niacin interactions with natural therapies
1) Red yeast rice - depends on dose 2) alcohol 3) other meds that increase hepatoxicity
41
Niacin causes flushing, the ER form has less flushing as a s/e. However, it is not used very often because of an increased risk for what s/e?
hepatotoxicity
42
What is the largest benefit of omega-3 FA?
lowering TG
43
What is the therapeutic dose of omega-3 FA?
2-4 grams of EPA + DHA (high!)
44
omega-3 FA MOA
- inhibits release of FA from adipose tissue - inhibits beta oxidation of hepatic FA - inhibits FA synthesis - increased VLDL clearance * *lowers TG and increases HDL
45
omega-3 FA indications
hypertriglyceridemia second-line tx (TG > 1000 mg/dL)
46
omega-3 FA cautions
1) C/I = hypersensitivity to fish oil 2) s/e = eructation, nausea, dyspepsia, taste change 3) may incr. bleeding time (use w/ caution in pt. on anticoagulants and antiplatelets)
47
omega-3 FA efficacy
no benefit in ASCVD risk has been shown small incr. in HDL, 20-50% decease in TG
48
omega-3 FA
1) onset = 2 wks 2) T1/2 = 140 hr 3) 100% bioavailability 4) metabolized by lipid enzymes in liver and tissues **high bioavail. and long T1/2 is impt to consider in terms of bleeding effects
49
Bile acid sequestrants (BAS) MOA
they are resins that bind bile acids in the intestine --> reduces enterohepatic recycling --> increases hepatic conversion of cholesterol to bile acid upregulates LDL receptors on liver
50
Bile acid sequestrants (BAS) indications
hypercholesterolemia for high risk pt. who are statin-intolerant or are on maximal tolerated doses of a statin
51
Bile acid sequestrants (BAS) cautions
1) C/I = TG over 300 mg/dL, complete biliary obstruction 2) s/e = constipation, abdominal discomfort, intestinal gas, dyspepsia, heartburn, diarrhea 3) b/c it's an absorbent, it can bind onto other medications that the pt. is taking
52
Bile acid sequestrants (BAS) pharmacokinetics
1) onset = 21 days to peak effect 2) T1/2 = variable 3) 100% excreted in feces, not absorbed
53
What other drugs shares the intestine as a site of action?
ezemtimibe (Zetia)
54
BAS and Ezetimibe both work to lower GI absorption of cholesterol. What changes occur in the liver to lower LDL?
increased LDL receptors (so that more LDL is taken up from the blood)
55
Bile acid sequestrants (BAS) interactions with natural therapies
1) Niacin absorption might be inhibited | 2) Only moderate interactions, mostly d/t changes in absorption profiles

Pharmacology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions