Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

Rate limiting step in cholesterol biosynthesis

A

HMG-CoA reductase

=critical enzyme in the biosynthesis of cholesterol

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

Where is the B-48 adoliportoeins formed?

A
  • Intestine

- Found in chylomicrons and their remnants

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

Where is the B-100 adoliportoeins synthesized? Where is it found?

A
  • Synthesized in liver

- Found in VLDL, LDL, Lp(a) lipoproteins

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

Risk Factors= “FLASH”

A 
F-Family hx of premature CHD
L- Low HDl, <40 mg/dL
A- Age: Men>45, Women> 55
S- Smoking: Cigarettes
H- HTN; CKD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Risk Equivalents to CHD

A
  1. DM
  2. CAD
  3. PAD
  4. AAA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the most common cause for low HDL?

A

Obesity

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

What enzyme converts VLDL to VLDL remnants via lipolysis?

A

Lipoprotein lipase

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

Fibrate MOA

A

unregulates lipoprotein lipase

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

Niacin MOA

A

Decreases both VLDL and LDL levels

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

Bile acid resins MOA

A

Bind bile acids–>increasing the excretion of cholesterol in the stool

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

Statins MOA (2)

A
  1. Inhibits HMG-CoA reductase: directly reduces cholesterol production
  2. LDL receptors unregulated in liver: Lowers LDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ezetimibe MOA

A

Blocks the absorption of cholesterol from the small intestine

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

Statins primary effect?

A

Lowers LDL

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

Statins effect on atherosclerosis?

A

Prevention of atherosclerosis:

  1. Stabilizes/regressionof plaques
  2. Prevents formation of thrombus
  3. Control inflammatory response
  4. Improves endothelial function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How much does high-intensity statins decrease LDL?

A

> or equal to 50%

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

How much does moderate-intensity statins decrease LDL?

A

30-50%

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

How much does low-intensity statins decrease LDL?

A

<30%

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

Low intensity statins and dosage

A

Pravastatin 10-20 mg

Lovastatin 20 mg

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

Which statin is the most potent?

A

Pitavastatin

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

Which drug has the greatest efficacy?

A

Rosuvastatin 40 mg

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

What are the benefits of both Atorvastatin and Rosuvastatin?

A

It doesn’t matter what time of the day you take them

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

What is Atorvastatin metabolized by?

A

Cytochrome 3A4= most common enzyme=more drug interactions compared to Rosuvastatin

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

What is Rosuvastatin metabolized by?

A

Cytochrome 2C9/2C19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the two main differences between Atorvastatin and Rosuvastatin?

A
  1. Different metabolism

2. Different distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Is Atorvastatin and Rosuvastatin lipophilic?
Atorvastatin
26
What is Pitavastatin metabolized by?
UGTIA3/UGT 2B7
27
Severe side effects of Statins
1. Rhabdomylosis-Monitor creatine kinase levels | 2. Hepatic failure-Monitor LFTs
28
Contraindications of Statins
1. Acute liver dz | 2. Pregnancy
29
What is the risk for developing type 2 DM on statins?
approx. 30%
30
What lab values do you want monitor with Statins?
1. LFT's @ baseline 2. Creatine Kinase levels @ baseline if @ increased risk = renal insufficiency, family hx 3.
31
What is the anion transporter is there a genetic variation that is associated with severe myopathy and rhabdo induced by statins?
OATP1B1
32
Atorvastatin drug interaction
3A4 inhibitor and inducer
33
What is red yeast rice associated with?
Lovastatin
34
What statin is affected by grapefruit juice? (increased)
Atorvastatin
35
Rosuvastatin drug interaction
2C9 induces and inhibitor
36
If someone is on Warfarin, what Statin would you recommend? What would you avoid?
Recommend: Atorvastatin Avoid: Rosuvastatin= Vitamin K antagonist
37
What can increase the levels/effects of Rosuvastatin?
Fibric acid derivatives= Gemfibrozil (contraindicated)
38
Cholesterol absorption inhibitor
Ezetimibe
39
Ezetimibe MOA
Inhibits cholesterol absorption in the small intestine, both: - Dietary Cholesterol - Biliary Cholesterol
40
What transport protein does Ezetimibe target?
NPC1L1
41
How much does Ezetimibe reduce LDL by?
18%
42
What statin would you consider combining Ezetimibe with?
Simvastatin
43
Ezetimibe contraindications
1. Active Hepatic Dz | 2. Unexplained persistent elevations in LFTs
44
Drug interactions
Increased levels with fibrates
45
Ezetimibe monitoring
LFTs increased: greater combo with statins
46
Ezetimibe severe side effects
Cholelithiasis: greater in combo with fibrates
47
How is Ezetimibe excreted?
80% through feces
48
List PCSK9 inhibitors
1. Alirocumab | 2. Evolucmab
49
PCSK9 inhibitors MOA
Monoclonal antibodies inhibit PCSK9= Reduce LDL up to 70%
50
Where is PCSK9 found? It's function?
- Protease in Liver | - Degradation of hepatocyte LDL=increases LDL levels
51
Who should we consider PCSK9 inhibitors for?
1. Adults w/ heterozygous familial hypercholesterolemia 2. Primary hyperlipidemia- (Homozygous familial hypercholesterolemia) 3. ADD onto maximal tolerated statin dose and/or exetimibe 4. Intolerance of statins
52
PCSK9 inhibitors adverse reactions
1. URI and flu-like sx's 2. Local runs @ injection site(frequently) 3. Hypersensitivity (rare)
53
How are PCSK9 inhibitors given?
SQ every 2 weeks
54
Why do we want to monitor lipid panels every 4-8 weeks in PCSK9 inhibitors?
Patient adherence
55
Define and list MTP inhibitor
MTP: Microsomal Triglyceride Transfer Protein inhibitor | = Lomitapide
56
MTP inhibitor MOA
1. Binds directly to and inhibits MTP 2. Prevents assembly of apo-B containing lipoproteins 3. Reduced production of chylomicrons and VLDL 4. Reduced plasma LDL
57
MTP inhibitor indication
Homozygous familial hypercholesterolemia
58
Sever side effects
HEPATOTOXICITIY=BLACK BOX WARNING
59
What program are MTP inhibitors through?
JUXTAPID REMS PROGRAM
60
Other MTP inhibitor major side effect
GI upset: Diarrhea=79%
61
PK of MTP inhibitor
1. 99.8% protein bound 2. Hepatic metabolism of CYP3A4-inducer and inhibitors are going to effect level of this drug 3. Renal elimination
62
What drug levels with MTP inhibitor increase?
Lovastatin
63
MTP inhibitor contraindications
1. Pregnancy | 2. Active hepatic dz/impariement
64
What is recommended with MTP inhibitor to avoid GI effects?
Low fat diet, <20%
65
Mipomersen sodium (Kyanamro) MOA
Inhibitor of apoldprotein B-100 synthesis
66
Mipomersen sodium (Kyanamro) major side effect
BLACK BOX WARNING=HEPATOTOXICITY | KYANMOS REMS
67
Fibrates MOA
Upregulates lipoprotein lipase: 1. Increase catabolism of VLDL 2. Elimination of TG-rich particles
68
What is the primary effect of Fibrates?
TG lowering=35-50%
69
What may fibrates potentially increase?
LDLs in pt's with elevated TGs
70
Severe side effects of fibrates?
1. Acute renal failure!!! | 2. Cholelithiasis
71
Fibrate contraindications
1. Severe renal impairment CrCl <30 2. Hepatic dysfunction 3. Breastfeeding
72
Fibrate drug interactions
1. Statins!!!! Increases risk of myopathies--> rhabdo 2. Warfarin 3. Sulfonyluereas- may enhance hypoglycemic effects
73
Nicotnic Acid MOA
Inhibits synthesis and secretion of VLDL-->and therefor LDL
74
Niacin indication
1. High LDL and low HDL | 2. Isolated triglyceridemia
75
Why has Niacin fallen out of favor?
Has not shown to decrease morbidity and mortality
76
What is unique to Nicotinic Acid dosing?
Titration
77
3 main side effects of Nicotinic Acid
1. Flushing 2. Hyperglycemia 3. Hyperuricemia=Increaed risk for gout
78
Nicotinic Acid drug interactions
1. Anticoagulants- May increase bleeding time | 2. Statins-Increase risk of myopathies
79
Caution Nicotinic Acid use with?
1. Diabetics | 2. Renal impairment
80
Bile Acid Sequestrants MOA
- Cholesterol is a precursor to bile acids - Bind with bile acids in intestines-->eliminated via feces - Increased bile acid secretion increased cholesterol catabolism to form more bile acids
81
BASs therapeutic effects
Decrease LDL 15-30% | Minimal effect on HDL and TG
82
Severe side effects of BASs
Bleeding with chronic use | =affects Vitamin K absorption
83
BASs drug interactions
All bind with other medications, absorbant!!!
84
Omega-3 Acid Ethyl Esters (O3FAs)
Lovaza
85
O3FAs drug interactions
Inhibit platelet aggregation and cause bleeding

Pharmacology (9 decks)

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