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Dyslipidemia Flashcards

1
Q

What is dyslipidemia?

A

Presence of one or more of the following:
1. Elevation in total cholesterol
2. Elevation in LDL cholesterol
3. Elevation in triglycerides
4. Low HDL cholesterol

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2
Q

What are the main plasma lipids?

A

Cholesterol, triglycerides, and phospholipids

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3
Q

What is the function of plasma lipids?

A
  1. Essential for cell membrane
  2. Hormone synthesis
  3. Source of free fatty acids
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4
Q

What are the classes of lipoproteins?

A
  1. Chylomicrons
  2. LDL
  3. VLDL
  4. HDL
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5
Q

What is total cholesterol?

A
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6
Q

What is the function of chylomicrons and VLDL?

A

Deliver energy rich triacylglycerol (TAG) to cells in the body -> free fatty acids and monoglycerides

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7
Q

What is the function of just LDL?

A

LDL delivers cholesterol to cells → cholesterol is used in membranes or for the synthe sis of steroid hormones

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8
Q

What is the function of HDL?

A

HDL brings back excess cholesterol to the liver (reverse cholesterol transport)

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9
Q

What are the apolipoprotiens that can be used as lab values?

A

ApoLp(a) and B-100

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10
Q

What are the effects and outcomes of DLD?

A
  1. Excess LDL → atherosclerosis
  2. Excess TG → pancreatitis
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11
Q

What is the function of ApoLp(a)? Where is it located?

A

LDL, HDL

Bound to B100 preventing LDL uptake by B and E receptor

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12
Q

What are the normal functions of vascular endothelium?

A
  1. Control of vascular tone
  2. Maintenance of an antithrombotic surface
  3. Control of inflammatory cell adhesions and diapedesis
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13
Q

What is the function of B100? Where is it located?

A

VDLD, LDL, IDL

Necessary for assembly and secretion of VLVL from the liver

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14
Q

What happens if there is a disruption of vascular endothelium?

A
  1. Inappropriate constriction
  2. Luminal thrombus formation
  3. Abnormal interactions between blood cells (monocytes and platelets)
  4. Activated vascular endothelium
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15
Q

What is an atherosclerotic plaque?

A

Subintimal collections of fat, smooth muscle cells, fibroblasts and intracellular matrix

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16
Q

What is the impact of having atherosclerotic plaques?

A

→ stenosis or rupture → CVD, MI, stroke, PVD, abdominal aortic aneurysm, death

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17
Q

What are the requirements for there to be stenosis?

A
  1. 50% diameter reduction → limitation in ability to meet increased demand
  2. 80% reduction → reduced flow at rest or minimal stress
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18
Q

What is desirable total cholesterol level? High?

A

<200 mg/dL (<5.17 mmol/L)

≥240

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19
Q

What is the optimal LDL level? Very high?

A

<100 mg/dL (<2.59 mmol/L)

≥190

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20
Q

What is considered low HDL? High?

A

<40 mg/dL (<1.03 mmol/L)

≥60

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21
Q

What is considered normal TG levels?

A

<150 mg/dL (<1.70 mmol/L)

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22
Q

What is considered very high TG levels?

A

≥500 mg/dL (≥5.65 mmol/L)

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23
Q

What are clinical signs of heterozygote familial hypercholesterolemia?

A

Development of xanthomas as an adult and vascular disease at 30-50 years

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24
Q

What are clinical signs of homozygote familial hypercholesterolemia?

A

Development of xanthomas as adults and vascular disease in childhood

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25
What are the secondary causes of hypercholesterolemia?
1. Hypothyroidism 2. Obstructive liver disease 3. Nephrotic syndrome 4. Anorexia nervosa 5. Acute intermittent porphyria 6. Drugs
26
What are drugs that can cause secondary hypercholesterolemia?
1. Beta blocker 2. Immunosuppresants (PI, cyclosporine, mirtazapine, sirolimus) 3. GC 4. Progestin 5. Thiazide 6. Isotretinoin
27
What are the clinical signs of familial LPL deficiency?
Pancreatisits
28
What drugs can elevate TG?
1. Alcohol 2. Estrogens 3. Isotretinoin 4. Beta blockers 5. GC 6. Bile acid resins 7. Thiazides
29
What are the causes of lower HDL? Drugs?
1. Malnutrition 2. Obesity Non-ISA beta blockers Anabolic steroids Probucol Isotretinoin Progestins
30
What are causes of hypocholesterolemia?
1. Malnutrition 2. Malabsorption 3. Myeloproliferative diseases 4. Chronic infectious diseases (AIDS, TB) 5. Monoclonal gammopathy 6. Chronic liver disease
31
How should we measure LDL-C and Non-HDL-C
32
How do you use the Friedewald equation?
LDL-C = (TC) – (triglycerides /5) – (HDL-C) Not accurate when TG are over 400 or LDL <70
33
How do you use martin/hopkins equation
LDL-C = TC – HDL-C – TG/novel factor Not accurate when TG are over 400
34
What are the biomarkers of measuring cholesterol?
1. apoB 2. Lp(a)
35
When is apoB used?
HyperTG (>200) >130 is LDL (≥160) Expensive and unreliable
36
When is Lp(a) used?
For family and personal hx of premature ASCVD not explained by major risk factors
37
Why are some cormobidities of lipid abnormality?
1. CVD 2. Secondary causes 3. Xanthomas 4. DM
38
What are atherosclerosis risk factors?
1. Older age >40 2. Cigarette smoking 3. DM 4. DLD (Increased LDL, low HDL) 5. HTN 6. Hyperhomosysteinemia 7. CKD 8. CHF
39
What are ASCVD events?
1. Acute coronary disease (ACS) 2. MI 3. Stable/unstable angina 4. Coronary or revascularization (catheter) 5. Stroke/transient ischemic attack (TIA) 6. Peripheral arterial disease (PAD)
40
The ASCVD risk estimator ____ South Asians while it ____ East Asians
underestimate; overestimate
41
What are ASCVD risk categories?
Low: <5% Borderline: 5-7.4% Intermediate: 7.5-19.9% High: ≥20%
42
What are the clinical presentations of metabolic syndrome?
1. Low HDL 2. High TG 3. Visceral obesity 4. Insulin resistance 5. HTN
43
What are the ASCVD prevention groups?
1. Secondary prevention 2. Severe hypercholesterolemia 3. DM in adults 4. Primary prevention
44
What is secondary ASCVD?
Already had a health incident related to atherosclerosis
45
How falls in secondary prevention?
ASCVD risk
46
What do you always suggest before treating ASCVD?
Non-pharm
47
How do you treat secondary prevention if patients aren't at high risk?
48
What is the LDL goal for secondary prevention?
>70
49
How do you treat secondary prevention if patients are at high risk?
50
What is considered high risk ASCVD?
2 ASCVD events or 1 event and high risk conditions
51
What are the numbers for severe hypercholesterolemia?
≥190
52
What the is schedule for treating severe HCA? When is a PCSK9 used?
53
How do we treat secondary prevention in patients with DM?
54
What are DM-specific risk enhancers for ASCVD?
1. ≥10 yr of DMT2 or ≥20 DMT1 2. Albuminuria (≥30) 3. GFR <60 4. Retinopathy 5. Neuropathy 6. ABI <0.9
55
What is the LDL goal in DM secondary prevention?
<100
56
What is primary ASCVD?
Prevent any occurrence of disease?
57
How do you treat primary prevention based on ASCVD events?
58
How do you treat primary prevention based on age?
59
What are the ASCVD risk enhancers for primary prevention?
1. Family hx of ASCVD 2. LDL ≥160 3. CKD 4. Metabolic syndrome 5. Women 6. Inflammatory disease 7. Ethnicity factors
60
What is coronary artery calcium?
Scan measuring the amount of calcium in the wall of the coronary arteries using a specialized x-ray machine Deposits with plaque buildup
61
What is the scoring for CAC?
CAC score of 0 = low ASCVD 10-year risk (w/o cancelling high risk comorbidities) CAC score of ≥ 100 = 10-year risk of ASCVD ≥ 7.5%
62
What is primary prevention in older adults
1. 75+ with LDL of 70-189 → moderate intensity statin 2. 75+ reasonable to stop stain if risk outweighs benefits 3. 76-80 with LDL of 70-189 → measure CAC (avoid statin if score is 0)
63
What is primary prevention for young adults?
Teach them how to eat healthy Eliminate risk factors Be aware of elevations
64
When should you screen for primary prevention?
1. familial hx of genetic dyslipidemia or early CVD 2. Obesity or metabolic risk 3. screened once between ages 9-11 and then again between 17-21 years
65
What do you do when abnormalities are contributed to obesity? Genetics?
Intense lifestyle therapy Statin initiation
66
What should ASCVD diets consist of? Exclusions?
Veggies, fruit, whole grains, fiber, low fat dairy, protein, veggie oils Sweets, sugary beverages, red meats, saturated fats and cholesterol
67
What type of diet is associated with HLD?
TLC
68
Exercise rec?
150 min/week
69
Statin contraindications?
Pregnancy and nursing
70
High intensity statins? Dosing?
Atorvastatin (Lipitor): 40, 80 mg Rosuvastatin (Crestor): 20, 40 mg
71
Moderate intensity statins? Dosing?
Atorvastatin (Lipitor): 10, 20 Rosuvastatin (Crestor): 5, 10 Simvastatin (Zocor): 20-40 Pravastatin (Pravachol): 40, 80 Lovastatin (Mevachor): 40, 80 Fluvastatin (Lescol): 40 BID
72
Low intensity statin? Dosing?
Pravastatin (Pravachol): 10-20 Lovastatin (Mevachor): 20
73
What are the t1/2 of high intensity statins?
Crestor: 19hr Lipitor: 14hr
74
What statins are metabolized by CYP3A4?
1. Atorvastatin 2. Fluvastatin (minor) 3. Lovastatin 4. Simvastatin
75
What statins are metabolized by CYP2C9?
1. Fluvastatin 2. Pitavastatin 3. Rosuvastatin
76
What are DDIs of statins?
Fenofibrate (less ADR) < Gemfibrozil (rhabdomyolysis)
77
Equivalence of Atovstatin:Rosuvastatin
4:1
78
What is 1st line for all patients with DLD?
Statin
79
What statins can be doses at anytime?
1. Atorvastatin 2. Fluvastatin XL 3. Pitavastatin 4. Rosuvastatin
80
Why are most statins given at night?
Maximum LDL-C reduction
81
Short t1/2 statins?
Fluvastatin, Lovastatin, Pravastatin, Simvastatin
82
What are the major enzymes that metabolize statins?
CYP3A4, 2C9
83
What populations have no sensitivity to statins?
Hispanic, AA
84
How do Asians respond to statins?
1. Higher rosuvastatin plasma levels are seen in Japanese, Chinese, Malay, and Asian Indians as compared with whites → lowering of dose 2. Japanese may be sensitive to statins 3. Caution with titrating up
85
What are the non stain classes?
1. Zetia 2. BAS 3. PCSK9 Inhibitors and Inclisiran 4. Bempedoic Acid
86
What is the second line agent of DLD?
Ezetimibe (Zetia)
87
Effect and ADRs of Zetia?
1. LDL and TG reduction 2. HDL raise Mild GI complaints like diarrhea
88
BAS effect? ADRs? CI?
1. LDL reduction 2. HDL and TG raise 3. Colesevelam is for DMT2 to reduce AIC Constipation and nausea TG>300
89
What is the first line agent for pregnancy?
BAS
90
Counseling point of BAS?
1. binding of other medications → separate administration 1 hr before or 4 hrs after 2. Take w/ food
91
PCSK9? Effects? ADRs? Dosing?
Alirocumab (Praluent), Evolocumab (Repatha) LDL reduction Flu-like symptoms (decrease by room temp before use) Expensive (Not first line for insurance); Bi-weekly or once a month
92
What is Inclisiran?
Leqvio is a siRNA that reduces the production of PCSK9 by inhibiting mRNA LDL reduction Add on to statin, SQ injection
93
What are effects and ADRs of bempendoic acid?
Modest LDL reduction Hyperuricemia and tendon rupture
94
What are the populations at risk for DLD?
1. Ethnicity 2. HyperTG 3. Women 4. CKD 5. Chronic inflammatory disorders and HIV
95
Asian with ASCVD, Lipid, Metabolic Issues?
South asia have increased risk Lower levels of HDL, and higher LDL and TG prevalence Increased MetA with lower waist circumference
96
Hispanic with ASCVD, Lipid, Metabolic Issues?
Women have low HDL DM is disproportionally present
97
AA with ASCVD, Lipid, Metabolic Issues?
Women increases ASCVD risk High levels of HDL and low TG Increased DM and HTN
98
What is the difference between moderate and severe hyperTG?
Moderate: Excess TG are carried in VLDL Severe: Elevated VLDL plus chylomicrons
99
How do you treat hyperTG?
1. 20 or older with hyperTG → lifestyle factors, secondary factors, medications 2. 4-75 moderate and ASCVD 7.5% or higher → favoring initiation or intensification of statin therapy 3. 40-75 sev 4. severe and ASCVD 7.5% or higher → statin therapy 5. Fasting TG ≥1000 → non pharm and vibrate therapy
100
How should women be treated with DKD?
1. No statins for pregnancy 2. Stop statins 1-2 months before pregnancy is attempted
101
CKD recommendations of DLD?
1
102
CKD that is considered elevated risk of ASCVD?
Reduced eGFR (<60) Presence of albuminuria ≥30
103
What is the treatment for chronic inflammatory disorders and HIV?
Lifestyle improvements should be tried for 3-6 months after diagnosis
104
What are statin alternatives?
1. Niacin 2. Fibrates 3. Omega 3 4. Lomitapide 5. Mipomersen
105
Niacin effects? ADRs? Counseling points?
LDL and TG decrease, HDL increase GI intolerance, flushing/itching, lab abnormalities Use of aspirin, taking with meals, and slowly titrating the dose upward may minimize flushing/itching
106
Fibrate effects? ADRs?
Decrease TG and LDL, Raises HDL Dose adjustment for renal dysfunction Gallstones, bleeding risk
107
Omega 3 effects?
Lower TG, raise LDL and HDL
108
Vascepa vs Lovaza?
Viscera supports CV risk reduction
109
ADR of Omega 3?
Fishy burps, Increased bleeding with anti-platelets and coags
110
Lomitapidide?
Only for HoFH → REMS due to hepatotoxicity
111
Mipomersen?
Only for HoFH → REMS due to hepatotoxicity
112
When to monitor efficacy?
1. Follow up about 3-6 months after lifestyle therapy modifications 2. Follow up about 4-12 weeks after pharmacologic therapy initiation or titration 3. Once stable, monitoring is done every 6 months to a year
113
Lab monitoring of DLD toxicity?
1. LFTs 2. Glucose 3. CBC/BMP 4. CK
114
Last line for Primary DLD?
1. Partial ileal bypass 2. Portocaval shunts 3. Plasma exchange 4. LDL-apheresis 5. Liver transplantation
115

Therapeutics I (32 decks)

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