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S2B4: MEDI > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Check out this chart! Pick a section & write it down

*spefically remember: medication

A
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2
Q

Check out this fun chart

Write it down

A
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3
Q

What lab results would suggest a genetic underlying cause of hyperlipidemia?

Is genetic testing routinely performed?

Why would diagnosis of genetic underlying cause be beneficial?

A

very high (>95% of normal) LDL

no, genetic testing is not routinely performed

diagnosis of underlying primary cause may aid in prognostic (risk of ASCVD, response to treatment, risks in family members)

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4
Q

What genetic disorders cause hypertriglyceridemia?

Combined hyperlipidemia?

Hypercholesterolemia?

In each of these disorder, also identify the protein defect & elevated lipoproteins

A

** specifically know family hypercholesterolemia

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5
Q

Fill out the provided table

A
  • Pneumonic:
    • One LP, Two LD, Three with E, Four gets more
  • Most important
    • Type 1: pancreatitis
    • Type 2: tenxon xanthomas
    • Type 3: palmar xanthomas
    • Type 4: pancreatitis
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6
Q

How common is the homozygous & heterozygous forms of familial hypercholesterolemia?

Diagnostic criteria for each of these forms?

How is it diagnosed?

What is the relevent biochemisty of this mutation?

A
  • Homozygous- rare
    • total cholesterol 600-1000 mg/dL
    • LDL 550-950 mg/dL
    • Coronary heart disease & aortic stenosis
    • Fatal MI before age 20 if untreated
  • Heterozygous - 1/500
    • total cholesterol 300-600 mg/dL
    • LDL 250-500 mg/dL
    • premature heart disease
  • Typically diagnosed clinically based on values & family history
  • Biochemistry
    • mutation in LDL receptor
    • increased total cholesterol & LDL
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7
Q

What are the imporant clinical considerations of Familial Defective Apolipoprotein B1000?

What is the relevant biochemistry of this mutation?

A
  • Clinical Considerations
    • autosomal dominant in 1/750 caucasions
    • appearance similar to familial hypercholesterolemia but less severe
  • Biochemistry
    • defective Apo B100 causing poor LDL bindign to LDL receptor
    • increased total cholesterol and LDL
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8
Q

What are the important clinical considerations of elevated plasma lipoprotein (a)?

What is the relevant biochemistry to this disorder?

A
  • Clinical Considerations
    • causes premature coronary heart disease
      • 1:14 myocardial infarctions
      • 1:7 aortic valve disease
  • Biochemistry
    • increase in LDL binding to apolipoprotein (a)
    • increased lipprotein (a) (aspecialized form of LDL)
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9
Q

What are the important clinical considerations of familial combined hyperlipoproteinemia?

What is the relevant biochemistry of this disorder?

A
  • Clinical Considerations
    • autosomal dominant polygenic condition affecting 1-2% of the population
    • triglycerides >175, Total cholesterol >250, & HDL <35
  • Biochemistry
    • polygenic causes…
      • increase VLDL production
      • lipoprotein lipase gene defect
    • elecated total cholesterol, LDL, & triglycerides
    • decreased HDL
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10
Q

What are the significant clinical considerations of familial dysbetalipoproteinemia?

What is the relevent biochemistry of this disorder?

A
  • Clinical considerations
    • only a problem when there is another issue…
      • diabetes
      • hypothyroidism
      • alcohol consumption
    • total cholesterol 300-400 mg/dL & Triglycerides 300-400 mg/dL
  • Biochemistry
    • decreased ApoE2 affinity for LDL receptor
    • increased triglycerides, total cholesterol & LDL
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11
Q

What are the significant clinical considerations of lipoprotein lipase deficiency?

What is the relevent biochemistry of this disorder?

A
  • Clinical considerations
    • homozygous: TG> 1,000 mg/dL
    • heterozygous: TG 250-750 mg/dL
    • worse with secondary factors
      • diabetes estrogen therapy
    • clinical presentations
      • pancreatitis
      • hepatosplenomegaly
      • eruptive xanthomas
      • lipemia retinalis (creamy white vessels)
  • Biochemistry
    • lipoprotein lipase (LPL) gene deficiency
    • severely increased triglycerides
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12
Q

What are the significant clinical considerations of apolipoprotein C-II deficiency?

What is the relevent biochemistry of this disorder?

A
  • clinical considerations
    • autosomal recessive
    • rare
  • biochemistry
    • Apo C-II deficiency causing decreaed liporotein lipase activation
    • elevated triglycerides
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13
Q

What are the significant clinical considerations of familial hypertriglyceridemia?

What is the relevent biochemistry of this disorder?

A
  • Clinical considerations
    • autosomal dominant
    • triglycerides 200-500mg/dL
    • HDL <35mg/dL
  • Biochemistry
    • liver overproduces VLDL and increased catabolism of HDL
    • elevated triglycerides & decreased HDL
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14
Q

Fill out the provided table by indicating which conditions cause elevated or reduced LDL?

Also, identify which conditions cause elevated or reduced HDL?

A
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15
Q

Identify the conditions that elevate VLDLs, IDLs, Chylomicrons, and Lp(a)s?

A
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16
Q

Saturated fats have have what impact on lipid levels?

What is the major conern with trans fats?

A
  • Saturated fats increase
    • total cholesterol
    • LDL
    • may or may not effect coronary heart disease
  • Trans fats
    • harmful in regards to cardiovascular health
17
Q

Why can obesity lead to hyperlipidemi?

A

obesity can lead to insulin resistance , which can cause an incerease in liver synthesis of fatty acids & a decrease of lipolysis

decreased HDL and an increased triglycerides

it has a variable effect on LDL

18
Q

Describe the following diseases effects on lipid

hypothyroidism

nephrotic syndrome

diabetes

liver failure

cholestasis

A
  • hypothyroidism
    • due to decrease in LDL receptor synthesis and function
  • nephrotic syndrome
    • comlex, but increased production of LDL and VLDL
  • diabetes
    • increased insulin–> increases HMG CoA reductase
  • liver failure
    • decreased cholesterol and triglycerides
  • cholestasis
    • decreased bile secretion –> increase in total cholesterol
19
Q

Describe the effect of the following substances on lipids

estrogen

thiazides

beta blockers

clozapine & olanzapine

protease inhibitors

A
  • estrogen
    • elevated triglycerides and HDL (can be pronounced)
  • thiazides
    • elevated LDL and triglycerides
  • beta blockers
    • increased triglycerides and decreased HDL
  • clozapine & olanzapine
    • weight gain / obesity / diabetes –> elevated triglycerides
  • protease inhibitors
    • lipodystrophy –> elevated triglycerides
20
Q

In the process of evaluating for hyperlipidemia, what will you be sure to ask about when taking a history?

Whtat will you be looking for during the physical?

What lab tests will you order?

A
  • History
    • family, social, medical (ASCVD, Nephrotic syndrome, diabetes, pancreatitis, etc.)
  • Physical
    • xanthoma (fatty deposits under eyes or on palms)
    • hepatosplenomegaly
  • Lab evaluation
    • lipi panel
    • creatinine
    • urine protein
    • urine protein
    • liver enzymes
    • thyroid stimulating hormone
    • fasting glucose
21
Q

the provided image is an example of what condition?

A

xanthoma

cholesterol rich deposition in the skin

22
Q

What are the AHA screening guidelines for assessing cardiovascular risk?

What clinical findings warrent treatment?

A

assess risk factors for those age >21 every 4-6 years

  • Risk factors
    • smoking, diabetes, hypertension, HDL, total cholesterol
  • Treatment is warrented if
    • triglycerides >500mg/dL
    • LDL-C >190
      • secondary cause
      • if primary cause, screen family
    • unexplained ALT > 3x ULN
23
Q

What is the goal of treating hyperlipidemia?

What are the 2 approaches to treatment?

A
  • Goal
    • reduce the risk of acute pancreatitis
      • ​specifically when high triglycerides
    • prevent coronary heart disease and decrease the risk of heart attack
    • prolong life
  • Approaches
    • therapeutic lifestyle changes
      • decrease saturated fatty acids, trans fatty acids
      • decrease added sugar intake
      • increase exercise
      • increase plant sterols and soluble fiber intake
      • reduce body weight
    • antihyperlipidemic drug therapy
24
Q

What are the Key Points of the ACC / AHA guidelines?

A
  1. Heart healthy lifestyle should be emphasized across all age groups
  2. If patient has ASCVD (i.e. secondary prevention) treat wiht high dose statin theapy - atorvastatin or rosuvastatin (or maximally tolerated statin therapy)
  3. In high risk ASCVD patients, consider additional therapy with statin to goal LDL <70 (specific agents recommended)
  4. If LDL >190 recommend high dose statin therapy (do not need to calculate risk first)
    1. Diabetic patients age 40-75 with LDL >70, treat with moderate or high dose statin (based on risk factors)
  6. Before starting statin for primary prevention in those age 40-75, have a risk/benefit discussion
  7. In patients age 40-75 without DM and with LDL >70 and ADCVD risk score >7.5 start moderate dose statin (if risk/benefit discussion facors)
  8. In patients age 40-75 without DM but ASCVD risk score 7.5-19.9 consider risk factors and if present favor statin therapy
  9. In patients age 40-75 without DM and with LDL 70-160 and ASCVD score 7.5-19.9% but statin decision unclear, get coronary artery calcium measure
  10. Reassess for adherence to statin adn lifestye interventions

S2B4: MEDI (6 decks)

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