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Endocrinology > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

Describe how lipids and lipoproteins function as fuel within our bodies

A

Fatty acids break down to form acetyl CoA, NADH, FADh2

- when attached to glycerol, fatty acids are stored as triglycerides

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2
Q

What makes up the lipid cell membrane?

A
  • Phospholpids
  • Glycolipids
  • Cholesterol
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3
Q

What are the lipid-derived steroid hormones?

A
  • Sex hormones
  • Glucocorticoids
  • Mineralocorticoids
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4
Q

Describe the function of bile salts within our bodies, and what is the main bile salt?

A

Function as detergents to emulsify fats

- Glycocholate is the main bile salt

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5
Q

Describe the function of prostaglandins within our bodies

A

Diverse hormone-like fxn

- smooth muscle contraction, platelet aggregation, and inflammatory response

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6
Q

What are the fat-soluble vitamins?

A

A, D, E, K

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7
Q

Lipids combine with what?

A

Carbs: Glycolipids
OR
Protein: Lipoproteins

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8
Q

What is the physiology of cholesterol and triglycerides? and what are they associated with?

A

Both are insoluble in water (hydrophobic core) and must be transported in association w/ protein (ie lipoprotein)

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9
Q

What are the functions/key roles of lipoproteins?

A
  • Absorption and transport of dietary lipids by small intestines
  • Transport of lipids from the liver to peripheral tissues
  • Transport of lipids from the peripheral tissues to the liver (ex: HDL)
  • Transport toxic foreign hydrophobic and amphipathic compounds from areas of invasion and infxn.
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10
Q

The intestines make what particles? and what are they?

A

Chylomicrons: Large triglyceride rich particles

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11
Q

Chylomicrons are involved in what transport?

A

Transport of dietary triglycerides and cholesterol to peripheral tissues and liver

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12
Q

Very Low Density Lipropteins (VLDL) are produced by what? and is rich in what?

A
  • Liver

- Triglyceride rich

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13
Q

VLDL particles contain what? and what it is?

A

Apo B-100: a core structural protein (1 per VLDL particle)

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14
Q

What is Low Density Lipoptroein (LDL)? and what does it carry?

A
  • Bad cholesterol

- Carried the majority of the cholesterol in the circulation.

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15
Q

LDL particles contain what?

A

Apo B-100, each LDL particle has Apo B-100 molecule

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16
Q

Compared to large LDL, small dense LDL are more what?

A

More pro-atherogenic

- longer duration, easily enters the arterial wall, and binds to intraarterial proteoglycans

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17
Q

What is High Density Lipoprotein (HDL)? and what does it enhance?

A
  • Good Cholesterol

- Enhance deposition of cholesterol into the liver vice the blood vessels (reserve cholesterol transport)

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18
Q

What is the potential mechanism of HDL? and how do you increase HDL levels?

A
  • Anti-athrogenic

- Increase via exercise and moderate consumption of alcohol.

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19
Q

What other properties does HDL have that may contribute to their ability to inhibit atherosclerosis?

A
  • Anti-oxidant
  • Anti-inflammatory
  • Anti-thrombotic
  • Anti-apoptotic
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20
Q

What levels of HDL are considered high risk, intermediate, and protective?

A
  • High: <40 mg/dL
  • Intermediate: 40-60 mg/dL
  • Protective “neg CV risk factor”: >60 mg/dL
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21
Q

What are the 4 functions of apolipoproteins (Apo B-48, ApoB-100, Apo E)

A
  • Structural role
  • Acts as a ligand for lipoprotein receptors
  • Guide formation of lipoproteins
  • Serve as activators or inhibitors of enzymes involved in lipoprotein metabolism
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22
Q

Elevated LDL is a major risk factor for what?

A

CAD and cerebrovascular dz

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23
Q

What is the most important and modifiable risk factor for CAD and what does it cause?

A

Hyperlipidemia

- accelerated atherosclerosis

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24
Q

What medication are risk factors for elevated cholesterol?

A
  • Thiazides: increase LDL, TC, TG (VLDL)
  • Beta blockers (Propanolol): increase TG (VLDL) and lower HDL levels
  • Estrogens: increased TG levels in pts w/ hypertriglyceridemia
  • Corticosteriords and HIV protease inhibitors can increase serum lipids
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25
Q

Do you want a high or low total cholesterol to HDL ration?

A

Low, want a ratio of less than 4.5

5.0 is average/standard risk

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26
Q

Xanthelasmas are a severe hyperlipidemia manifestation, what is it?

A

Yellow plaques on eyelids

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27
Q

Xanthomas are a severe hyperlipidemia manifestation, what is it?

A

Hard, yellowish masses found on tendons (finger extensors, Achilles tendon, plantar tendons)

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28
Q

What level of total cholesterol is a high risk for CAD?

A

> 240 mg/dL

normal is <200

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29
Q

What are the normal levels of HDL in males and females?

A

Male: >45
Females: >55

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30
Q

What are normal levels of LDL in pts w/ and w/o DM?

A
  • w/o DM: <100

- w/ DM: <70

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31
Q

What is a normal level of triglycerides?

A

<150 mg/dL

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32
Q

What are the key difference between ATP IV and ATP III?

A
  • Targeting specific cholesterol goals no longer recommended
  • The use of non-statins meds to lower LDL is no longer recommended
  • New risk calculator used to calculate the pts 10-yr risk of ASCVD
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33
Q

What is the recommended caloric intake to lose weight in men and women?

A

Men: 1,500 to 1,800 kcal per day
Women: 1,200 to 1,500 kcal per day

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34
Q

What tx is important before and during statin therapy?

A

Diet!!

- lower fat intake (esp. saturated fat) and increased omega-3 fatty acids

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35
Q

What is the mainstay pharmacologic therapy for hyperlipidemia? and what labs should be checked prior to starting and after starting statins?

A

Statins

- AST and ALT: monitor for hepatoxicity

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36
Q

What are the 4 guidelines for statin therapy?

A
  • > 7.5% risk for ACVD
  • Has ACVD
  • Age 40-75
  • Very high LDL ( >190)
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37
Q

When do you use high intensity statin therapy?

A
  • Has ACVD and age < 75
  • LDL >190
  • Has type 1 or 2 DM (40-75 yr old) and >7.5% risk of ACVD
38
Q

When do you use moderate intensity statin therapy?

A
  • Has ACVD and age >75

- Has type 1 or 2 DM (40-75 yr old) and < 7.5% risk of ACVD

39
Q

When do you use moderate to high statin therapy?

A

Established 10 yr ACVD risk > 7.5% and age 40-75

40
Q

What is the medication effectiveness of high intensity statins?

A

Lowers LDL by about 50%

41
Q

What is the medication effectiveness of moderate intensity statins?

A

Lowers LDL by 30-50%

42
Q

When do you use low intensity statins and what is the effectiveness?

A
  • In pts who cannot tolerate high or moderate dose statins

- Lowes LDL by <30%

43
Q

What is the MOA of the HMG CoA reductase (statins)

A

Rate limiting step in cholesterol synthesis

44
Q

What are the most potent LDL lower agents?

A
  • Pitavastatin
  • Rosuvastatin
  • Atorvastatin
45
Q

What are the intermediate potency agents?

A
  • Simvastatin

- Pravastatin

46
Q

What are the lower potency agents?

A
  • Lovastatin

- Fluvastatin

47
Q

What organ is primarily affected by statins?

A

Liver (marked first pass extraction)

- all hepatically metabolized

48
Q

What are the CI of statins?

A
  • Pregnancy (cat. X)

- cholesterol is an essential component of fetal development, including steroid synthesis and membrane development

49
Q

What are the ASEs of statins?

A
  • Elevated liver enzymes

- Myopathy and rhabdomyolysis

50
Q

If a pt is taking a statin and comes in w/ muscle complaints what should be evaluated?

A

Plasma creatine kinase (CK) levels

51
Q

What is the MOA of Nicotinic Acid (Niacin)?

A
  • At gram dose, strongly inhibits lipolysis in adipose tissue thereby reducing the free fatty acid production
  • renally excreted
52
Q

What are the effects of HDL and triglycerides when taking Nicotinic Acid (Niacin)?

A
  • HDL: most effective agent for increasing HDL

- Triglycerides: lowers by 20-30% at typical dose of 1.5 to 3 grams/day

53
Q

Nicotinic Acid (Niacin) is useful in tx for what?

A
  • Familial hyperlipidemias
  • Lowers plasma level of cholesterol
  • Lowers plasma levels of triglycerides
54
Q

What are the ASEs of Nicotinic Acid (Niacin)?

A
  • Intense cutaneous flushing w/ uncomfortable sensation fo warmth
  • Pruritus
  • Hepaotoxicity
55
Q

What should be taken prior to Nicotinic Acid (Niacin) to decrease flushing sxs?

A

Aspirin, take 30 minutes prior

56
Q

What are the drugs in the Fibric Acid Derivatives?

A

Fenofibrate and Gemfibrizol

- Feno > Gemi in lowering triglycerides

57
Q

What is the MOA of Fibric Acid Derivatives?

A

Binds to PPAR to decrease triglycerides and increase HDL concentration.

58
Q

When would you use a Fibric Acid Derivatives?

A

In tx of hypertriglyceridemias and familial dysbetalipoproteinemia

59
Q

What are the ASEs of Fibric Acid Derivatives?

A
  • Gallstone formation d/t increase biliary cholesterol excretion
60
Q

What 2 drug combo are CI?

A

Gemfibrizol + Simvastatin

61
Q

What drug is apart of the Bile Acid Binding Resin class?

A
  • Cholestyramine
  • Colesevelam
  • Colestipol
62
Q

What is the MOS of Bile Acid Binding Resins?

A

The bound complex is excreted in feces which lowers the bile acid [ ] and causes hepatocytes to increase conversion of cholesterol to bile acids

63
Q

What are the therapeutic use of Bile Acid Binding Resins?

A
  • Treating different types of hyperlipidemias
64
Q

What is the therapeutic use of Cholestyramine?

A

Relieve pruritis related to bile acid accumulation in pts with biliary stasis

65
Q

What is the therapeutic use of Colesevelam?

A

Indicated for DM type 2 d/t glucose lowering effects

66
Q

What are the ASEs of Bile Acid Binding Resins?

A

GI effects: constipation, nausea, and flatulence

67
Q

What drug is apart of the Cholesterol Absorption Inhibitors? and what is the MOA?

A

Ezetimibe

- a selective inhibitor of dietary and biliary cholesterol in small intestine

68
Q

What are the use of omega 3 fatty acids (PUFAs)?

A

Essential fatty acids used mainly for lowering triglyceride levels

69
Q

What is the best tx for lowering LDL?

A

Statins

70
Q

What is the best tx for increasing HDL?

A

Nicotinic acid (Niacin)

71
Q

What is the best tx for lowing triglycerides?

A

Fibrates

72
Q

What is the primary tx for hypertriglyceridemia?

A

Diet and exercise

73
Q

What is the secondary tx for hypertriglyceridemia?

A
  • Fibric acid derivatives (most effective) and Nicotinic acid
  • Omega-3 fatty acids in adequate dose may be beneficial
74
Q

What are the complications of Hyperlipidemias?

A
  • Impotence (good for pt education)
  • MI
  • CVA
  • Retinopathies
  • NEphropathies
  • Rhabdomyolysis and renal failure related to statins
75
Q

What is the primary organ at risk for hypoglycemia?

A

Brain

- unlike other tissues, the brain cannot use free fatty acid as an energy source

76
Q

What usually causes hypoglycemia?

A

An imbalance between insulin and glucagon

77
Q

What is the first line of defense for more severe hypoglycemia? and then what hormone is used to combat hypoglycemia?

A
  • Glucagon is the first line

- Epinephrine is the next hormone

78
Q

What is factitious hypoglycemia?

A

If a pt tool insulin there will be high blood insulin levels and low blood C-peptide level
(exogenous insulin does not contain C-peptide)

79
Q

Ethanol ingestion is a cause of what and why?

A
  • Hypoglycemia
  • Poor nutrition leads to decrease glycogen
  • Metabolism of EtOH lower nicotinamide adenine dinucleotide levels and decreases gluconeogenesis
80
Q

What is reactive (idiopathic) hypoglycemia?

A
  • Sxs that occur 2-4 hrs after a meal

- Rarely indicates a serious underlying disorder

81
Q

What are insulinomas? and what are they associated with?

A
  • Insulin-producing tumor arising from beta cells of the pancreas
  • Usually benign
  • Associated with MEN 1 syndrome
82
Q

Insulinoma can cause what?

A
  • Sympathetic activation

- Neuroglycopenic sxs

83
Q

What are sxs of sympathetic activation?

A
  • Diaphoresis
  • Palpitations
  • Tremors
  • HTN
  • Anxiety
84
Q

What are the Neuroglycopenic sxs?

A
  • HA
  • Visual disturbances
  • Confusion
  • Seizures
  • Coma
85
Q

How do you dx an Insulinoma?

A

72 hr fast
- pt becomes hypoglycemic and insulin does not respond appropriately to hypoglycemia (may increase, decrease or may not change at all)

86
Q

What is the Whipple triad used as a diagnostic tool in a pt with Insulinoma?

A
  • Hypoglycemia sxs brought on by fasting
  • BG <50 mg/dL during symptomatic attack
  • Glucose administration bring relief of symptoms
87
Q

What is the tx of Insulinoma?

A

Surgical resection of tumor

88
Q

What levels of BG usually cause sxs of hypoglycemia?

A

40 to 50 mg/dL

89
Q

What diagnostic tool is used to dx TRUE hypoglycemia?

A

Whipple triad

90
Q

What is the acute tx of hypoglycemia?

A
  • If able to eat: give sugar-containing foods

- if not: administered 1/3 to 3 ampules of D50W IV

91
Q

What is the management of reactive hypoglycemia management?

A

Dietary intervention

92
Q

What is the management of a pt in an alcoholic or suspected alcohol?

A

Give Thiamine before administration of glucose to avoid Wernicke encephalopathy

Endocrinology (18 decks)

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