Hyperlipidemia Flashcards
(101 cards)
1
Q
Where does most cholesterol come from?
A
Made in liver
2
Q
Is atherosclerosis a TYPE of arteriosclerosis (hardening of arteries)?
A
Yes
3
Q
What are the “Ubers” of lipids?
A
Lipoproteins
4
Q
What causes atherosclerosis?
A
Abnormal lipoprotein metabolism
5
Q
What usually causes abnormal lipoprotein metabolism?
A
Genetics!!! (Not diet)
6
Q
What are the 5 types of lipoproteins?
A
Chylomicrons
VLDL
IDL
LDL
HDL
7
Q
What do chylomicrons do?
A
Carry dietary lipids from the intestine to the liver and rest of the body
8
Q
What do VLDLs do?
A
Carry newly made triglycerides from liver to adipose
9
Q
What do LDLs do?
A
Carry CHOLESTEROL from liver to the rest of the body
10
Q
What do HDLs do?
A
Collect cholesterol from the rest of the body (including the vascular endothelium 😀) and return it to the liver for excretion
11
Q
Does the action of HDLs provide a protective effect against heart disease?
A
Yes
12
Q
What should you suspect in anyone with a family history of premature atherosclerotic cardiovascular disease (ASCVD)?
A
An inherited increased lipid disorder
(Familial hypercholesterolemia
Polygenic hypercholesterolemia
Familial combined hyperlipidemia)
13
Q
What are the 3 types of inherited increased lipid disorders discussed in class?
A
Familial hypercholesterolemia
Polygenic hypercholesterolemia
Familial combined hyperlipidemia
14
Q
Is familial hypercholesterolemia monogenic or polygenic?
A
Monogenic
15
Q
How often does familial hypercholesterolemia occur?
A
1 in a million
16
Q
What are the 2 forms of familial hypercholesterolemia?
A
Heterozygotes- 2x normal LDL
Homozygous- 8x normal LDL
17
Q
How do you treat familial hypercholesterolemia?
A
Statin, and consider add-on
18
Q
How do you treat polygenic hypercholesterolemia?
A
Statin, consider add-on
19
Q
How common is familial combined hyperlipidemia?
A
1-2% of general population
20
Q
How do you treat familial combined hyperlipidemia?
A
Statin
Second agent if needed
21
Q
Is familial combined hyperlipidemia monogenic or polygenic?
A
Polygenic
22
Q
What is secondary hyperlipidema?
A
Hyperlipidemia with a NON-lipid etiology
Ex: diabetes, alcoholism, diet, smoking, obesity, hypothyroidism, CKD, liver disease, drugs (steroids)
23
Q
Which is more common: inherited hyperlipidemia or secondary hyperlipidemia?
A
Inherited
24
Q
What are the 4 steps to atherosclerosis?
A
- LDL molecules diffuse through the endothelium at a rate DEPENDENT on concentration of LDL in blood
- Macrophages follow, absorb LDL, and become foam cells. Then they die, release cholesterol, and form deposits
- Body reacts with increased collagen to form a cap
- Cap ruptures and thrombus forms, leading to potential infarct
25
When does UpToDate recommend we screen for familial hyperlipidemia?
Before puberty (9-11 yrs) and
After puberty (17-21 yrs)
(However, there is no established interval. The decision to screen should be based on overal risk of coronary heart disease independent of lipid levels)
26
What are the non-modifiable risk factors for coronary heart disease?
Family history of premature ASCVD
Age (men over 45, women over 55)
Male gender
Symptomatic cardiovascular disease
Chronic kidney disease
27
What are the modifiable risk factors for coronary heart disease?
Hyperlipidemia**
HDL less than 40**
HTN (BP 140/90 or on HTN drugs)
Diabetes
Tobacco
Obesity
28
What level of HDL is a negative risk factor for CHD?
60 or higher
| HDL IS GOOD
29
What is measured in a fasting lipid panel?
Total cholesterol
Triglycerides
LDL
HDL
30
How do you calculate total cholesterol?
HDL+LDL+ (triglycerides/5)
31
How long should you fast before doing a fasting lipid panel, and why?
12 hours
Triglycerides are greatly affected by eating, although cholesterol is not
32
Acutely ill patient may have falsely (high/low) levels in a lipid panel
Low
Cholesterol levels can drop 24-48 hours after a heart attack and can persist for up to 60 days
33
Your patient had a heart attack yesterday and when you checked his fasting lipid panel today, everything was really low! WTF?!
Cholesterol levels drop after a heart attack and may persist for up to 60 days
34
What is a desirable cholesterol level?
Under 200
35
What is a borderline cholesterol level?
200-239
36
What is a high risk cholesterol level
240+
37
What is a desirable triglyceride level?
Under 150
38
What is a borderline triglyceride level?
150-199
39
What is a high risk triglyceride level?
200-499
40
What is a desirable HDL?
60+
41
What is a borderline HDL?
35-45
42
What is a high risk HDL?
Under 35
43
What is a desirable LDL?
60-130
44
What is a borderline LDL?
130-159
45
What is a high risk LDL?
160-189
46
What are plane xanthomas?
Cholesterol-filled, soft yellow plaques that appear in various places (eyelids, palmar creases, etc)
47
What type of hypercholesterolemias do plane xanthomas indicate?
Familial OR secondary causes
48
What are tuberous xanthomas?
Yellow-orange nodules often located on knees, elbows, and tendons
49
What kind of hypercholesterolemia are tuberous xanthomas associated with?
Familial
50
Do eruptive xanthomas happen over time or suddenly all at once?
Suddenly all at once in response to extremely high triglycerides (often over 1500mg)
51
What do eruptive xanthomas look like and where do they show up?
Crops of small red and yellow papules that are most common on buttcheeks and extensor surfaces
52
What type of hyperlipidemia do eruptive xanthomas indicate?
Familial HLD
53
What is a corneal Arcus?
A white or grey ring around the cornea that may be caused by high cholesterol
54
Is a corneal arcus abnormal all the time?
No, it can be normal in pts over 40
55
What is the best diet to manage lipids?
DASH diet (Dietary Approaches to Stop HTN)
- lots of fruits and veggies
- moderate amounts of low-fat dairy
- low animal protein
- lots of plant protein like nuts and legumes
- low sodium
56
Can exercise actually increase HDL cholesterol?
Why yes it can
57
What is the only class of drugs to demonstrate clear inmprovements in overall mortality in preventing heart attacks?
Statins
58
What class of drugs is the focus of the Joint National Committee’s 8 recommendations?
Statins
59
What enzyme is inhibited by statins?
HMG-CoA reductase (an enzyme that makes cholesterol in the liver)
60
As a result of statins inhibiting HMG-CoA reductase and inhibiting cholesterol synthesis, what happens next?
Blood cholesterol levels decrease.
Liver enzymes sense that cholesterol production has decreased, so they increase production of LDL receptors.
Receptors relocate to the liver cell membranes and bind to passing LDL and VLDL.
LDL and VLDL enter the liver and are digested.
61
What are the adverse effects of statins?
- mild GI complaints
- liver toxicity
- muscle pain
- rhabdomyolysis
62
When should a patient take their statin?
At bedtime (most cholesterol is produced at night)
63
What are the ABSOLUTE contraindications of statins?
Active liver disease
Pregnancy
64
In which patients should you use statins “with caution?”
Concomitant use of CYP3A4 inhibitors
Chronic kidney/liver disease
65
What are the 2 types of statin regimens?
High-Intensity
Moderate-Intensity
66
What labs do you need to draw before you start a pt on statins?
Baseline lipid panel
Liver function tests
Creatine kinase
67
After starting statins, how often should you check their lipid panel?
6-8 weeks after starting
Every 6-12 months thereafter
68
How do bile acid sequestrants (resins) work?
Bind bile acids in the intestine and prevent reabsorption
Decreases LDL
(May actually increase triglycerides)
69
Are bile acid sequestrants/resins safe during pregnancy?
Yes
70
How do Bile acid sequestrants (resins) interact with statins?
Synergistically
71
What are the adverse effects of bile acid sequestrants (resins)?
Constipation
Farting
Inhibit fat soluble vitamin absorption
Might affect Warfarin
Can increase triglycerides!!!********
72
What are the contraindications to bile acid sequestrants/resins?
Absolute: Triglycerides over 400
Relative: Triglycerides over 200
73
What 3 drugs are bile acid sequestrants/resins?
Cholestyramine
Colesevelam
Colestipol
(They affect CHOLESTerol in your COLon)
74
What is the effect of Nicotinic Acid/Niacin?
Reduces production of LDL
Increases HDL
May reduce triglycerides
75
What are the adverse effects of Nicotinic acid/niacin?
Flushing and itching**
Liver damage**
May be unsafe when used with statin
76
What are the absolute and relative contraindications to Nicotinic acid/niacin?
Absolute: Active liver disease
Relative:
hyperuricemia
Hyperglycemia
Unstable angina
77
Is Nicotinic acid/niacin safe to use during pregnancy?
NO
78
What are the 3 drugs that are Fibric Acid Derivatives?
Gemfibrozil
Fenofibrate
Bezafibrate
79
What is the best class of drug for lowering triglycerides
Fibric acid derivatives
| May lower TGs up to 50%
80
In addition to lowering the fuck out of your triglycerides, can fibric acid derivatives increase your HDL too?
Yes, up to 25%
81
Do we give fibric acid derivatives to pregnant women?
No
82
What are the adverse effects of fibric acid derivatives?
Gallstones
Hepatitis
Myositis
83
What are the absolute and relative contraindications to fibric acid derivatives?
Absolute:
Gallstones
Taking Simvastatin**
Severe liver/kidney disease
Relative:
Other statin use (risk of myopathy)
On Warfarin
84
Your patient is taking simvastatin. What class of drugs must he absolutely avoid?
Fibric acid derivatives
| Gemfibrozil, fenofibrate, bezafibrate
85
How does ezetimibe/zetia work?
Blocks intestinal absorption of dietary and biliary cholesterol
86
Can you use ezetamibe/Zetia with a statin?
Yes
87
What are the contraindications to ezetamibe/zetia?
Pregnancy
Using it with a statin in someone with liver disease***
88
What effect does Ezetamibe/Zetia have on your lipid panel?
Lowers LDL
89
If your patient is on a statin and you suspect they have myositis (rhabdo), what should you do?
Stop statin and check CK level
90
What effect do PCSK9 Inhibitors have on your lipid panel?
Lower LDL
91
Do we know a lot about PCSK9 inhibitors?
No, it is a very new and expensive injection
92
According to the JNC 8 Recommendations, what should the goal of hyperlipidemia treatment be?
ASCVD risk reduction
NOT target lipid levels
93
According the JNC 8 Recommendations, should we give statins to everyone?
No, only in those who are most likely to benefit
94
What are the 4 statin benefit groups?
1. People with clinical ASCVD (angina, MI, strokes, TIAs, acute coronary syndromes)
2. People with LDL levels 190+
3. 40-75 year old diabetics
4. 10 year ASCVD risk is 7.5% or higher according to the Pooled Cohort calculator
95
What type of therapy should people in Group 1 get?
High intensity statin
BUT if they’re older than 75, do moderate-intensity statin
96
What type of therapy should people in group 2 get?
High intensity statin
97
What type of therapy should people in group 3 get?
Moderate intensity statin
BUT if the calculator said they were over 7.5%, you should do a High-intensity statin
98
What type of therapy should someone in group 4 get?
Moderate to high intensity statin
99
What are some of the other factors you might take into consideration if someone is not in groups 1-4, and the benefit of statin therapy is unclear?
LDL=160 or higher
Family history of premature ASCVD
Hs-CRP = 2 or higher
ABI < 0.9
Elevated lifetime risk of ASCVD according to calculator
100
What is the MOST important contributor to the ASCVD risk calculation?
Age
101
Should you just prescribe statins to everyone and never ask the patient what he thinks?
No, your treatment plan should be a comprehensive approach to risk reduction that incorporates addressing modifiable risk factors and assessing ASCVD risk with the calculator
