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MBBS IV - Teaching Clinics, Data Interpretation, Interactive Tutorials > Block A - Medicine - Endocrine Teaching Clinic - Lipid disorders > Flashcards

Block A - Medicine - Endocrine Teaching Clinic - Lipid disorders Flashcards

1
Q

Calculated LDL- C formula

A

Friedewald Formula: LDL-C = TC – HDL-C – (TG/2.2)

Does not apply if TG>4.5 mmol/l

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2
Q

Cut-offs for LDL- C, HCL-C and TC

A
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3
Q

Causes of secondary hyperlipidemia

A
  1. Diabetes mellitus type II
  2. Alcohol abuse
  3. Hypothyroidism (LDL receptors are downregulated)
  4. Chronic renal failure
  5. Nephrotic syndrome (liver synthesizes protein to compensate)
  6. Cholestatic liver disease (jaundice)
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4
Q

Ddx secondary hyperlipidemia: Isolated increase Triglyceride

A
  1. Type II Diabetes mellitus
  2. Alcohol abuse
  3. Chronic Renal Failure
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5
Q

Ddx secondary hyperlipidaemia:

Isolated high cholesterol

A

Hypothyroidism

Cholestatic liver disease

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6
Q

Ddx secondary hyperlipidaemia:

Both increase TG and Cholesterol

A

Nephrotic syndrome

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7
Q

Types of Primary Hyperlipidemia

A

Common (polygenic) hypercholesterolaemia

Familial combined hyperlipidaemia

Familial hypercholesterolaemia

Remnant hyperlipidaemia

Chylomicronaemia syndrome

Familial hypertriglyceridaemia

HDL hypercholesterolaemia

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8
Q

Ddx primary hyperlipidemia associated with pancreatitis

A

Remnant hyperlipidaemia
Chylomicronaemia syndrome **
Familial hypertriglyceridaemia **

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9
Q

Ddx primary hyperlipidemia with high CVD risk

A

Common (polygenic) hypercholesterolaemia
Familial combined hyperlipidaemia
Familial hypercholesterolaemia **
Remnant hyperlipidaemia **

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10
Q

LDL level that indicates genetic forms of hypercholesterolemia

A

LDL-C ≧190 mg/dL (4.9 mmol/L)

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11
Q

Familial hypercholesterolaemia

  • Inheritance
  • Pathophysiology
  • Clinical manifestations
A

Inheritance: Autosomal dominant (chromosome 19, 4
classes of mutations)

Pathophysiology: Defective function of LDL receptors, cannot clear LDL

Clinical manifestations:

  • Corneal arcus
  • Xanthelasma
    • Tendon Xanthomata
  • Cutaneous xanthomata, Tuberous/ Palmar/ Planar
  • Myocardial infarction, Angina, Sudden cardiac death
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12
Q

Treatment of familial hypercholesterolemia

A

Lifestyle modification: control CVD risk factors and diet

Drugs:
 HMG CoA reductase inhibitor + cholesterol absorption inhibitor (2nd)
 Resins, fibrates, nicotinic acid
 PCSK9 inhibitor

Last-line:
 LDL apheresis, liver transplant, gene therapy (homozygous FH)
 Partial ileal bypass vena-caval shunt

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13
Q

List CVD risk factors

A
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14
Q

How to assess 10-year CVD risk

A

For patients with multiple (2+) risk factors: perform 10-year risk assessment

o Framingham Risk Chart
o PROCAM Risk Chart
o European Coronary Risk Chart
o Joint British Societies Coronary Prediction Risk Chart
o New Zealand Cardiovascular Risk Prediction Chart

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15
Q

Systemic approach to the treatment of primary dyslipidemias

A
  1. Make an accurate diagnosis: baseline lipid levels, repeat testing
  2. Identify and control other CVD risk factors, 10-year CVD risk
  3. Initiate therapeutic lifestyle modifications changes ± lipid lowering drugs
  4. Monitor drug efficacy, side effects, combination
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16
Q

Outline diet modifications for primary dyslipidemia

A

 All fats are high in calories, aim to reduce

 Replace saturated fats (animal products) with monounsaturated or polyunsaturated fats (plant products)
 Increase fruits, vegetables, whole-grain foods
 Limit alcohol intake

Macro:

Total fat 25-35% of total calories

Carbohydrate 50-60% of total calories

Cholesterol <200 mg/day

17
Q

LDL-C goals for patients with/ without CVD

A

LDL-C <2.6mmol/L - Without CVD

LDL-C <1.8mmol/L - With CVD

18
Q

Outline the tiers of treatment for primary dyslipidemia

A

Primary: Monotherapy with high-intensity statin (Rosuvastatin or atorvastatin)

Secondary: Rosuvastatin/ Atorvastatin + Ezetimibe

Tertiary: Rosuvastatin/ Atorvastatin + Ezetimibe + PCSK9 inhibitor/ Fibrates/ Resins/ Niacin

19
Q

List first-line, second-line and combination therapy for hypercholesterolemia

A

1st = Statin

2nd = Resin/ Fibrate

Combo = Statin + Resin/ Fibrate

20
Q

List first-line, second-line and combination therapy for combined hyperlipidemia

A

1st = Fibrate/ Statin

2nd = Resins

Combo = Fibrate + Statin/ Fibrate + Resin

21
Q

List first-line, second-line and combination therapy for hypertriglyceridemia

A

1st = Fibrate

2nd = Statin, Omega-3 oil, Nicotinic acid

Combo = Fibrate + fish oil/ nicotinic acid

22
Q

Interpret following lipid profile:

M/17 178cm 55kg (ideal: 78-100kg) BMI 17.4

  1. Total cholesterol 14.7
  2. TG 1.09
  3. LDL 13.4
  4. HDL 0.9
A
23
Q

One major GI condition a/w dyslipidemia

A

Pancreatitis

24
Q

One endocrine disorder a/w dyslipidemia

A

hyperlipidemia secondary to hypothyroidism

Causes Isolated hypercholesterolemia, predominantly LDL

25
Q

Statins

  • Examples
  • Effect on lipid profile, efficacy
  • Indication
  • MoA
  • S/E and C/I
A

Statins = HMG- CoA reductase inhibitors

Examples: Lovastatin, Simvastatin, Atorvastatin…

Effect: Lower LDL-C, lower TG, Increase HDL

Indications: Hypercholesterolemia; lower CHD mortality, CVD intervention, stroke rate…

MoA: Upregulate LDLr on hepatocytes, lower cholesterol synthesis, increase LDL catabolism

S/E: GI disturbance, Rash, Myopathy, Fatigue, Headache

C/I: Liver diseases

26
Q

Fibrates

  • Examples
  • Effect on lipid profile, efficacy
  • Indication
  • MoA
  • S/E and C/I
A

Fibrates = Fibric acid derivatives

Examples: Fenofibrate, Gemfibrozil, Ciprofibrate…

Effect: Lowers TG and IDL-C, Increase HDL-C

Indication: Familial hypertriglyceridemia, Familial Combined Hyperlipidemia

MoA: Increase lipoprotein lipase, Increase fecal sterol excretion, Lower liver VLDL synthesis, Lower hormone-sensitive lipase

S/E: Dyspepsia, Gallstone, Myopathy, Low libido, Hair loss

C/I: Renal or liver failure

27
Q

Cholesterol absorption agent

  • Examples
  • Effect on lipid profile, efficacy
  • Indication
  • MoA
  • S/E and C/I
A

Cholesterol absorption agent

Example: Ezetimibe (only one)

Effect: Lower LDL-C, Increase HDL-C

MoA: Block NPC1L1 >> inhibit dietary and biliary cholesterol absorption at intestines + Decrease hepatic cholesterol storage, increase cholesterol clearance from blood

S/E: headache, abdominal pain, diarrhea

C/I: Liver failure

28
Q

Resins

  • Examples
  • Effect on lipid profile, efficacy
  • Indication
  • MoA
  • S/E and C/I
A

Resins = Bile acid sequestrants

Examples: Cholestyramine, Colestipol

Effect: Lower LDL-C, Increase HDL-C

Indications: FH, FCH

MoA: Stops enterohepatic bile acid recycling + increase LDLr expression

S/E: Constipation, GI disturbance

C/I: Dys-Beta-Liproproteinemia, high TG

29
Q

Niacin

  • Examples
  • Effect on lipid profile, efficacy
  • Indication
  • MoA
  • S/E and C/I
A

Niacin = nicotinic acid

Examples: immediate/ sustained/ extended release formulas

Effect: Lower TG, VLDL-C, IDL-C, LDL-C; Increase HDL-C

Indication: All hyperlipoproteinemia (except type I)

MoA: Antilipolytic, decrease liver cholesterol synthesis, Increase catabolism of chylomicrons, VLDL, LDL

S/E: Flushing, Dry itchy skin, Duodenal ulcer, Gout, Hyperglycemia, Hepatotoxic

C/I: Peptic ulcer, gout, liver disease

30
Q

PCSK9 inhibitor

  • Examples
  • Effect on lipid profile, efficacy
  • Indication
  • MoA
  • S/E and C/I
A

Examples: Alirocumab, Evolocumab

Effect: Lower LDL-C, apoB100

MoA: PCSK9 inhibited >> cannot bind to LDLr >> LDLr not internalized in liver >> Increase overall LDLr expression >> Lower LDL

S/E: Nasopharyngitis, Injection site reaction, Arthralgia and back pain

MBBS IV - Teaching Clinics, Data Interpretation, Interactive Tutorials (8 decks)

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