Brainscape's Knowledge GenomeTM

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


See full index

Primary care of adults 2 > Hyperlipidemia (5 questions) > Flashcards

Hyperlipidemia (5 questions) Flashcards

1
Q

Approximately ____ % of adults in the US-a total cholesterol of ≥240mg/dL; _____% of all U.S. -a total cholesterol > 200mg/dL.

A

25~ 30% - ≥240mg/dL

>50% - > 200mg/dL.

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

Types of lipoproteins

A
  • Chylomicrons
  • Very low density lipoprotein (VLDL)
  • Intermediate density lipoprotein (IDL)
  • Low density lipoprotein cholesterol (LDL-C)
  • High density lipoprotein cholesterol (HDL-C) (cardioprotective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Composition of lipoproteins

A
  • a lipid core containing cholesterol ester and triglycerides
  • An outer layer of phospholipids and apo-proteins is wrapped around the core
  • One molecule of Apo B is present for each LDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Significance of Apo B

A
  • One molecule of Apo B is present for each LDL
  • This allows lipoproteins to travel in the blood
  • They are very small particles and are more atherogenic than normal size

(We don’t routinely measure Apo B)

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

Explain the exogenous pathway

A
  • Cholesterol and TG from diet travel through GI system to small intestine and are packaged into Chylomicrons
  • These are transported and deposited in muscle and fat tissue
  • Some break down into free fatty acid for energy
  • Others are taken to the liver where they bind to LDL receptor (most LDL receptors in liver – genetic probs, consider)
  • The liver metabolizes cholesterol into bile for elimination in feces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain the endogenous pathway

A
  • In the liver, cholesterol & TG are made into VLDL, transported to muscle and fat tissue and broken down for energy and storage
  • VLDLs break down into IDL
  • Some IDL return to liver, others break down into fat and muscle tissues to form LDL
  • LDL binds to LDL receptor and is taken into cells for cell wall synthesis
  • Excessive LDL goes int oblood
  • macrophages – foam cells - plaque*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

5 atheroprotective roles of HDL

A
  1. Reverse Cholesterol Transport
  2. Antioxidant property
  3. Maintenance of endothelial function
  4. Protection against thrombosis
  5. Low blood viscosity via permitting red cell deformability (high blood viscosity related to inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ATP III: when should adults begin getting lipid profile screening, and how often?

A

over age 20- lipid profile every 5 years

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

Who should get screened for lipids regardless of age?

A
  • Atherosclerosis, other CHD, DM, Metabolic syndromes or HTN regardless of age
  • FHx of premature CVD
  • Clinical hyperlipidemia (Xanthomas, Acanthosis nigrans, Arcus corneus)
  • CRF, Erectile dysfunction, HIV infection with HAART tx, autoimmune diz (lupus, RA, psoriasis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When should we start screening lipids in children of patients w/ severe dyslipidemia?

A

start at the age of 10

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

Goal of dyslipidemia management

A

prevent future ASCVD

  • Definition: Clinical ASCVD (acute coronary syndrome, hx of MI, stable or unstable angina, coronary or other arterial revascularization, stroke , TIA or peripheral arterial disease based on RCT inclusion criteria)
  • Primary and secondary prevention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examples of primary, secondary, and tertiary prevention in the context of ASCVD

A
  • Primary: diet. For anyone w/history of CAD, checking lipids for screening
  • Secondary: had MI last year and you are treating them
  • Tertiary: full blown symptoms, trying to slow progression/stop symptoms

normally think prmary prevents dz, secondary detects and cures while asymptomatic, tertiary reduces complications

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

When did ATP III come out?

A

2001

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

What is involved in ATP III screening?

A
  1. Determine lipoprotein levels using a 9-12 hour fast (most require 12)
  2. Identify presence of clinical atherosclerotic disease that confer high risk for CHD or equivalent
  3. Determine the presence of major risk factors
  4. If 2+ risk factors (other than LDL) are present w/o CHD or CHD equivalent, assess 10-yr risk
  5. Determine risk category
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is a fasting lipid panel recommended?

A

TGs increase after food–

new evidence shows may not change >10%, so not so important

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

Secondary causes of elevated LDL and TG

A

Diet, medications, comorbid conditions, disordered/altered metabolism

altered metabolism is most common

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

ATP III Guidelines: Total cholesterol (mg/dL)

Optimal/desirable, near optimal, borderline high, high

A
  • Optimal/desirable:
  • borderline high: 200-239
  • high: > 240
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ATP III Guidelines: LDL cholesterol (mg/dL)

Optimal/desirable, near optimal, borderline high, high

A
  • Optimal/desirable:
  • near optimal:
  • borderline high: 130-159
  • high: 160-189
  • very high: _>_190
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ATP III Guidelines: TGs (mg/dL)

Optimal/desirable, borderline high, high

A
  • Optimal/desirable:
  • near optimal
  • borderline high: 150-199
  • high: _>_200
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ATP III Guidelines: HDL Cholesterol (mg/dL)

Optimal/desirable, near optimal

A
  • Optimal/desirable: > 60
  • Low: < 40 men, < 50 women
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ATP III Guidelines

A

Former guidelines based on risk factors

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

2013 ACC/AHA Guidelines

A
  • Replaced ATP III
  • no longer to Tx LDL chol targets
  • Non statin therpay discouraged in most cases
  • Lifestyle modification rec’d for all pts
  • 10yr ASCVD risk calculator - risk category determines what level of statin therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Presence of clinical atherosclerotic disease that confer high risk for CHD or equivalent (ATP III)

A
  • Clinical CHD
  • Symptomatic carotid artery disease
  • Peripheral arterial disease
  • Abdominal aortic aneurysm.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Major risk factors for ACVD (ATP III)

A
  • Cigarette smoking
  • HTN (BP > 140/90 or on antiHTN med
  • Low HDL (<40mg/dL)
  • FH premature CHD (CHD in male 1st degree relative <55yo, CHD in female first degree relative <65yo)
  • Age (men > 45yo, women > 55yo)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How many major risk factors need to be present in order to assess 10 year risk? (ATP III)

A

If 2+ risk factors (other than LDL) are present w/o CHD or CHD equivalent, assess 10-yr risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is a negative risk factor? (ATP III)

A

HDL > 6omg/dL counts as a “negative” risk factor. Its presence removes one risk factor from the total count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is a CHD risk equivalent? (ATP III)

A

A CHD risk equivalent is a condition that carries an absolute 10-year risk for developing new CHD e_qual to the risk for having recurrent CHD events in persons with established CHD,_ i.e., >20% per 10 years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

10 year risk intervals (ATP III)

A
  • >20% — CHD risk equivalent
  • 10-20%
  • <10%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ATP III Risk categories

A
  • CHD or CHD Risk equivalents (10 yr risk >20%)
  • 2+ risk factors (10 year risk < 20%)
  • 0-1 risk factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

ATP III goal if CHD or CHD Risk equivalents (10 yr risk >20%)

A
  • LDL Goal <100 mg/dL (<70 optional)
  • LDL level at which to initiate TLC: > 100 mg/dL
  • LDL Level at which to consider drug therapy: > 130 mg/dL (100-129 mg/dL: drug optional)

most important: risk is >20%. No matter how many risk factors, if risk is >20%, these are goals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

ATP III Goal if 2+ risk factors (10 year risk < 20%)

A
  • LDL Goal <130 mg/dL
  • LDL level at which to initiate TLC: > 130 mg/dL
  • LDL Level at which to consider drug therapy:
    • 10yr risk 10-20%: > 130 mg/dL
    • 10yr risk <10%: > 160mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

ATP III Goal if 0-1 risk factors

A
  • LDL Goal <160 mg/dL
  • LDL level at which to initiate TLC: > 160 mg/dL
  • LDL Level at which to consider drug therapy: > 190 mg/dL (160-189 mg/dL: LDL lowering drug optional)

(almost all have 10yr risk <10%, so 10yr risk assessment not necessary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

CHD Risk equivalents: Diabetes Mellitus

A
  • calculate pt specific risks w/calculator. If cannot
    • men >40yo w/DMII and any other risk factor
    • men >50yo w/DMII
    • women >45yo w/DMII and any other risk factor
    • women >55yo
    • men & women of any age w/DMI or DMII for >20yrs w/another risk factor
    • men & women of any age w/DMI or DMII for >25yrs

UpToDate, class notes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

CHD RIsk equivalents other than DM

A
  • symptomatic carotid artery disease
  • PAD
  • AAA
  • Multiple risk factors that confer a 10yr risk of CHD >20%
  • CKD w/Cr >1.5mg/dL [133 umol/L] or eGFR <60 mL/min per 1.73m2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Components of physical exam for dyslipidemia

A
  • Vital signs
  • Cardiovascular
  • Waist measurements
  • Skin
  • Eye
  • PV
  • Thyroid

some clinics do body fat measure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Dyslipidemia PE: what are you looking for on the skin

A

xanthomas, skin tags, acanthosis nigrans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Dyslipidemia PE: what are you looking for in the eye exam

A

corneal arcus, AV nicking, papilledema, hemorrhages, exudates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Dyslipidemia PE: what are you looking for in the PV exam?

A

Peripheral pulses, ABI (should be close to 1. Higher good, lower bad)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q
A

Corneal arcus, aka arcus senilis

More present in strong family history of hyperlipidemia

common in older adults w/o being a predictor of CV risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q
A

Acanthosis nigrans

insulin resistance – often coexists w/high cholesterol (metabolic syndrome), diabetes, pcos, cushings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q
A

Xanthomas

can be anywhere in body, but usually elbow, joint, knee, tendon, buttock. Specific to hyperlipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q
A

Eruptive xanthoma

Specific to hyperlipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Secondary causes of lipid abnormalities

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Secondary causes of increased TGs

A

obesity, DM, etoh use, CKD, OCPs, diuretics*

*short term effects only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Secondary causes of decreased HDL

A

obesity, sedentary lifestyle, BB*s

*short term effects only; BBs w/intrinsic sympathomimetic activity, e.g., pindolol and acebutolol, do not affect lipid levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Secondary causes of increased HDL

A

etoh use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Secondary causes of increased total cholesterol

A

DM, hypothyroidism, nephrotic syndrome, CKD, obstructive liver disease, Cushing Dz, corticosteroid use, OCPs, Diuretics*, BBs*

*short term effects only; BBs w/intrinsic sympathomimetic activity, e.g., pindolol and acebutolol, do not affect lipid levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Secondary causes of decreased total cholesterol

A

hyperthyroidism, liver dz (cirrhosis), malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is significant about TGL >500

A

needs to be treated. Affects accurate reading of LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How can you calculate LDL Cholesterol?

A

Total chol - VLDL (or 1/5 TG) - HDL

*validity depends on TGs <400mg/dL

*Measured directly if patients have profound ­TG
*Errors in TC, HDL, and TG can affect values

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How can you calculate Non-HDL Cholesterol?

A

TC – HDL-C

All cholesterol in atherogenic lipoproteins including LDL, Lipoprotein a, IDL, VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Therapeutic lifestyle changes for high cholesterol: how long a trial is appropriate before introducing pharm therapy?

A

Can do a 12 week trial unless high risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe therapeutic lifestyle changes for high cholesterol

A
  • Reduce saturated fat to <7% of total calories (teach to read nutr label) Reduce fats & carbs!
  • Add plants and fiber
  • Lose weight
  • Increase physical activity. “

Time frame to give another try – 3-6 mths.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

TLC for dyslipidemia: how can you help patients understand intensity of physical activity?

A

This table!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are some lipid lowering dietary sources/ supplements?

Overall a combination diet with multiple cholesterol-lowering agents causes much more significant LDL reductions

A
  • Fish oil, Flaxseed/oil, canola oil, soybean oil, nuts-omega 3 fatty acids-salmon
  • Soy
  • Red yeast rice
  • Garlic
  • fiber, green tea
56
Q

Effect on lipids of fish oil, Flaxseed/oil, canola oil, soybean oil, nuts-omega 3 fatty acids-salmon

A

Reduction in TG, minimal effect on HDL

57
Q

Considerations for recommending or Rxing fish oil

A
  • Pill form
  • Be careful to choose one without mercury and additives; Prescription strength EPA plus DHA 1-6 g daily for high TGL (oily fish)
  • undesirable GI side effects
58
Q

how many servings of fish recommended per week (lipids)

A

2 servings of fish/week recommended

59
Q

Lipid lowering: considerations with SOY

A
  • Source of phytoestrogens inhibiting LDL oxidation
  • Mixed result :25-50 g/day reduce LDL by 4-8%; isoflavone supplements do not appear to be of benefit (not be taken with a goal of lowering lipid and lowring CVD risk)
60
Q

Lipid lowering: considerations with RED YEAST RICE

A
  • Chemically equivalent to lovastatin (20-40 mg);
  • Manufacturing process unregulated: Dose is 1.2-2.4g;ADR: myalgias, High LFTs
  • so don’t prescribe statin with! Must know what they’re taking.
61
Q

Lipid lowering: considerations with GARLIC

A
  • Mixed results of clinical trials
  • In combination with fish oil and large doses (900-7.2 g/d), decreases in LDL observed
62
Q

By how much do HMG-CoA Reductase Inhibitors (Statins) lower LDL-C?

A

18-55%

63
Q

Statins: MOA

A

Inhibits HMG-CoA reductase from converting HMG-CoA to cholesterol,

thereby reducing cholesterol synthesis.

Up-regulates LDL receptors on hepatocytes.

64
Q

Statins: ADRs

A

hepatic dysfunction and myalgia (AST and ALT elevated)

65
Q

Statin metabolism: important consideration

A

Metabolized via CYP450 enzymes - use with caution!

66
Q

Statins: baseline tests

A

hyroid, renal, hepatic function, CPK (CK)

67
Q

Statins: C/Is

A

active or chronic liver disease

68
Q

What should you do if someone is on statins and wants to get pregnant?

A

D/C statins 3 months prior to conception attempt

69
Q

Which statins do not require renal dosing?

A

Atorvastatin & Fluvastatin

70
Q

Which statins should be used in chronic liver disease?

A

Pravastatin or rosuvastatin

71
Q

Which statins have fewer drug interactions?

A

Pravastatin, fluvastatin, rosuvastatin (not metabolized via CYP3A4)

72
Q

Which statins have less muscle toxicity?

A

Pravastatin & Fluvastatin

73
Q

Biggest to lowest effect on serum cholesterol & LDL for 6 available statins?

(at highest doses)

A

Rosuvastatin (Crestor)

Atorvastatin (Lipitor)

Simvastatin (Zocor)

Lovastatin (Mevacor)

Pravastatin (Pravachol)

Fluvastatin (Lescol)

74
Q

Comparative efficacy of lipid lowering agents

A
75
Q

Statins: what is considered “myopathy”?

A

Any pain, weakness, stiffness

76
Q

Statins: when does myopathy begin?

A

Few weeks-4 months onset

77
Q

Statins & myopathy: what are you looking for after D/Cing?

A

Symptoms and CPK should normalize over days to one month after d/c

78
Q

Who is at increased risk for myopathies on statins?

A
  • ARF/CRF
  • Obstructive liver disease
  • Hypothyroidism
  • Concomittant use of drugs interfering with CYP3A4?? Antidepressants, antibiotics, seizure meds. Famous for interactions
  • Gemfibrozil combined therapy
79
Q

How common are myalgias with statins?

A

(2-11%): common

they don’t always know. Ask if feeling weak, trouble climbing stairs, etc.

80
Q

How common is myositis with statins?

A

(0.5%): uncommon

81
Q

How common is rhabdomyolysis with statins?

A

<0.1%:

82
Q

Statins: difference between myalgias, myositis, rhabdomyolysis

A
  • Myalgias: without physical finding, or lab evidence of muscle dysfunction
  • Myositis: Moderate muscle sx and ­ CPK >5-10 x ULN
  • Rhabdomyolysis:
    • Severe muscle Sx (weakness ) and ­­­ CPK, and myoglobinuria and acute renal failure (usually)
83
Q

Statins: what to do if CPK 10x ULN?

A
  • D/C drug, regardless of symptoms
  • CPK returns to nl within 1 month
84
Q

Statins: very athletic and CPK

A

sometimes very athletic have high cpk - take into consideration

85
Q

Statins: hepatic side effects - how common is aminotransferase elevation and what should you expect?

A

0.5 to 5% persistent elevations in amino-transferases in first 3 months (dose-dependent), asymptomatic and resolves spontaneously.

86
Q

Statins: aminotransferase elevation: when to intervene

A

Tx should be d/c if elevation exceed 3x the upper limit of normal of pt has Sxs (eg.,fatigue, wt loss)

87
Q

Statins: FDA recommendations for monitoring LFTs

A
  • FDA indicates if baseline LFTs are normal, further hepatic monitoring is not needed.
    • Not true – we check every 12 weeks (3mths)
88
Q

Benefits of Nicotinic Acid (Niacin)

A

Benefits LDL, HDL, TGL, most powerful HDL raising agent.

89
Q

Nicotinic Acid: formulations and dosing

A
  • Immediate release (crystalline): 100 mg TID and titrated to tolerance
  • Sustained release - most common d/t fewer side effects
    • Niacor
    • Niaspan: 500 mg QHS x one month and then titrated to 1000 mg usually given daily after evening meal
90
Q

Nicotinic Acid (Niacin): ADRs

A

flushing, pruritus, GI (nausea, gas) (e.g., man complains of hot flashes)

Can raise blood glucose & uric acid

91
Q

Nicotinic Acid (Niacin): baseline tests

A

Obtain baseline LFTs, A1C, uric acid, and again during titration to a maintenance dose and q 6 month thereafter

92
Q

Niacin & flushing/hot flashes: how to reduce

A

325mg aspirin

93
Q

Dyslipidemia: how do Fibrates (fibric acid) work?

A
  • Works by lowering TG (20-50%) and ­increasing HDL (10-20% for HDL, not as effective as niacin) 1st line for TGs
94
Q

Fibrates (fibric acid): agents

A

Gemfibrozil, fenofibrate

(dyslipidemia)

95
Q

Gemfibrozil: dosing and effect

A

600 mg po BID (11% raise in HDL). Modest LDL reduction but little effect in combined hyperlipidemia. Can increase LDL in pure hypertriglyderidemia

(Fibrates/fibric acids)

96
Q

Fenofibrate: dosing and effect

A

200 mg capsules or iii caps 67 mg QD (renal dosing and can decrease Cyclosporin levels). Better for LDL lowering

97
Q

Fibrates: ADRs

A

Gallstone formation, Dyspepsia, diarrhea, nausea, vomiting, abdominal pain, eczema, rash, vertigo and myalgias

98
Q

Fibrates: important drug interactions

A
  • Use cautiously with statins: ­ risk of myopathy (is prescribed, in which case monitor closely)
  • decreases warfarin by 30%
99
Q

Fibrates: contraindications

A

GB disease, severe liver or kidney disease (eGFR<30ml/min)

100
Q

Bile Acid Sequestrants (Resins): MOA

A

¯lower LDL (15-30%), ­ increase HDL slightly, may raise TG

101
Q

Bile Acid Sequestrants (Resins): agents and dosing

A
  • Cholestyramine 8 grams/day. 24-30 grams/day can lower LDL up to 24%
  • Colestipol 10 grams/day
  • Colesevelam 1.5-4.5 grams/day
102
Q

Bile Acid Sequestrants (Resins): ADRs

A

GI (Indigestion, bloating, constipation, abdominal pain, flatulence, nausea)

makes compliance difficult

103
Q

Which bile acid sequestrant has the least problem w/GI ADRs?

A

Colesevelam

104
Q

Drug interactions with Bile Acid Sequestrants

A

Digoxin, warfarin, and fat soluble vitamins (give 1 hr before or 4 hrs after bile acid sequestrant)

105
Q

Cholesterol Absorption Inhibitors: Agents

A

Ezetimbe (Zetia)

106
Q

Ezetimbe (Zetia): MOA & effect on lipids

A

Blocks absorption of dietary and biliary cholesterol

decreases LDL (15-20%), decreases TGL (slightly), ­ increases HDL slightly

107
Q

Ezetimibe (Zetia) + statins: effect

A

Enhances reduction of LDL when used with statin, but ­increased incidence of myopathy and ­increased transaminases when co-administered with a statin

108
Q

Ezetimibe (Zetia): effect on clinical events

A
  • Currently no evidence that LDL lowering with ezetimbe provides a corresponding reduction in clinical events.
109
Q

NIacin: absolute and relative C/Is

A

Absolute: chronic liver dz, severe gout

Relative: diabetes, hyperuricemia, PUD

110
Q

Hypertriglyceridemia: prioritizing when high LDL

A

The 1st aim is to reaching LDL goal then lowering TG

111
Q

Mgmt if TGs 150-200 mg/dL

A
  • Intensify wt management
  • Increase physical activity
112
Q

Mgmt if TGs 200-499 mg/dL

A
  • Intensify wt management
  • Increase physical activity
  • Add nicotinic acid or fibrate to further lower VLDL
113
Q

Mgmt if TGs > 500 mg/dL

A

Prevention of pancreatitis!!

  • Intensify wt management
  • Increase physical activity
  • Very low-fat diet (<15% calories from fat)
  • Fibrate or nicotinic acid, fish oils
114
Q

4 Major Statin benefit groups

A
  1. Individuals with clinical ASCVD
  2. Individuals with primary elevations of LDL–C ≥190 mg/dL
  3. Individuals 40 to 75 years of age with diabetes with LDL-C 70-189 mg/dL and without clinical ASCVD
  4. Individuals without clinical ASCVD or diabetes who are 40 to 75 years of age with LDL-C 70-189 mg/dL and an estimated 10-year ASCVD risk of 7.5% or higher
115
Q

High, moderate, and low intensity statin therapy. How much should a daily dose of each lower LDL-C?

A

High Intensity: > 50%

Moderate intensity: 30 to < 50%

Low-intensity: <30%

past: you’d add more agents to meet the target and the patient gets side effects. Now if you reduce by 50%, even if not at target goal, it’s good – don’t need to add more and more. Evidence shows percentage reduction associated w/reduced CVD event risk

116
Q

High intensity statins

A

Atorvastatin/Lipitor: (>40) to 80mg

Rosuvastatin/Crestor: 20 (40) mg

117
Q

Low intensity statins

A

Simvastatin 10mg

Pravastatin 10-20mg

Lovastatin 20mg

Fluvastatin 20-40mg

Pitavastatin 1mg

118
Q

Adolescents: can begin treating at what age?

A

8yo and older

119
Q

LDL thresholds for adolescents

A
  • LDL thresholds different from adults
    • >190 with no other risk factors
    • >160 in the context of obesity and HTN, premature family history of CVD
    • >130 for children with diabetes
120
Q

Pharm therapy for adolescents

A
  • statins (over 8) watch LFTs, CPK
  • Bile acid resins poorly tolerated, no niacin, ? fibrates
121
Q

Other methods used to determine cholesterol risk: not used on daily basis but perhaps in future

A
  • Total/HDL cholesterol ratio
  • Non-HDL cholesterol (Total-HDL)
  • Apo-lipoprotein measurement
  • Hs-CRP (high sensitivity CRP)
122
Q

Total/HDL cholesterol ratio: what is recommended? Why?

A
  • Ratio <4.0 advocated by the Canadian guidelines
  • Better epidemiologic predictor of CV events than LDL , however no trials based on this ratio
123
Q

Non-HDL cholesterol: what is included in measurement?

A

Includes all atherogenic cholesterol (LDL, lipoprotein a, IDL, VLDL)

124
Q

Non-HDL cholesterol: why use this measurment? What is the target?

A
  • Lipid Research clinics program showed slightly stronger predictor of CVD than LDL
  • Secondary target in pts with high triglycerides >200 mg/Dl (ATP III)
  • Goal 30 above LDL goal
125
Q

Apolipoprotein measurement: why use it? Why not use it?

A
  • Apo B/ Apo A-I found to be a better predictor of events than LDL and total/HDL in AMORIS study; best predictor of events on statins in AFCAPS/TexCAPS study
  • Most useful in the hypertriglyceridemic patient (elevated apoB levels)
  • Not universally available and much more expensive
  • Needs more cost-benefit analysis before routine use
126
Q

Hs-CRP (High sensitivity CRP): why use it? Why not?

A
  • Intensity of atherosclerotic process
  • Recommendation of AHA, should be measured in the patient with intermediate Framingham risk (10-20%) with LDL below the cutoff point for tx
  • Questionable correlation with LDL levels
127
Q

What must be done before prescribing anti-dyslipidemic meds?

A

LFT, CPK (A1c, uric acid?) should be done

128
Q

What is the most effective drug to lower LDLs?

A

Statin

129
Q

Most effective drug to lower TGs?

A

Fibric acid and niacin

130
Q

Most effective drug to increase HDL?

A

niacin (then fibrate)

131
Q

When do statins kick in? When to expect max effect?

A

starts after 1 week and its maximum effect after 4-6 weeks

132
Q

When to d/c statin or give alternative?

A

If CPK >10x, LFT >3x, or pt with statin Tx comes w/ muscle pain- d/c statin and give alternative (ie.,other statin, fibrates or niacin)

133
Q

If on pharm mgmt for lipids, when to F/U?

A

every 3 months to check lipid, LFT, CPK,…then 6-12months when pt stable

134
Q

Stance of new guidelines for dyslipidemia on agents other than statins

A

New guideline does not support niacin, fibric acid, fish oils etc due to lack of effectiveness but use your clinical judgment for subgroup of pt

135
Q

What are the new guidelines for cholesterol/obesity/htn?

A
  • Cholesterol Guideline Update (2013ACC/AHA)
  • Hypertension Guideline Update (JNC 8)
  • Obesity Guideline (2013 AHA/ACC/TOS)
  • Lifestyle guideline (2013 AHA/ACC)

Primary care of adults 2 (15 decks)

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