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PHARMA > BLOOD-GOUT 3 > Flashcards

BLOOD-GOUT 3 Flashcards

1
Q

Total cholesterol is the sum of

A

LDL-C + VLDL-C + HDL-C

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2
Q

Is the primary goal of cholesterol-lowering therapy.

A

Reduction of LDL-C

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3
Q

Treatment options for Hypercholesterolemia.

A
  • lifestyle changes

- HMG CoA reductase inhibitors (statins)

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4
Q

Treatment includes diet and exercise, niacin and fibric acid derivatives, omega-3 fatty acids and statins.

A

Hypertriglyceridemia

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5
Q

TYPE OF HYPERLIPOPROTEINEMIA

  • Serum conc. of IDL are increased, resulting in increased TG and cholesterol levels
  • cause is either overproduction or underutilization of IDL due to mutant apolipoprotein E
  • Xanthomas and accelerated vascular disease develop in pt by middle age
  • Tx: diet. Drug therapy incluudes niacin and fenofibrate or a statin.
A

TYPE III (Familial Dysbetalipoproteinemia)

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6
Q

TYPE OF HYPERLIPOPROTEINEMIA

  • Massive fasting hyperchylomicronemia, even ff normal dietary fat intake, resulting in greatly elevated serum TG levels.
  • Deficiency of lipoprotein lipase or deficiency of normal apolipoprotein CII (rare)
  • is not associated w/ an increase in CHD.
  • Tx: low fat diet. No drug therapy is effective
A

Type I (Familial Hyperchylomicronemia)

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7
Q

TYPE OF HYPERLIPOPROTEINEMIA

  • Similar to Type IIA except that VLDL is also increased, resulting in elevated serum TG as well as cholesterol levels
  • caused by overproduction of VLDL by the liver
  • relatively common
  • Tx: diet. drug therapy is similar to that for Type IIA.
A

TYpe IIB (Familial Combined (Mixed) Hyperlipidemia)

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8
Q

TYPE OF HYPERLIPOPROTEINEMIA

  • VLDL levels are increased, wherease LDL levels are normal or decreased, resulting in normal to elevated cholesterol, and greatly elevated circulating TG levels.
  • Cause is overproduction and/or decreased removal of VLDL and TG in serum
  • This is a relatively common disease. It has a few clinical manifestations other than accelerated ischemic heart disease. Px w/ this disorder are frequently obese, diabetic,m hyperuricemic.
  • Tx: diet. If necessary, drug therapy includes niacin and/or fenofibrate.
A

Type IV (Familial Hypertriglyceridemia)

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9
Q

TYPE OF HYPERLIPOPROTEINEMIA

  • Elevated LDL with normal VLDL levels due to a block in LDL degradation, This results in increased serum cholesterol but normal TG levels.
  • Caused by defects in the synthesis or processing of LDL receptors
  • Ischemic heart disease is greatly accelerated.
  • Tx: Diet. heterozygotes: cholestyramine and niacin (statin)
A

Type IIA (Familial Hypercholesterolemia)

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10
Q

TYPE OF HYPERLIPOPROTEINEMIA

  • Serum VLDL and chylomicrons are elevated. LDL is normal or decreased. This results in elevated cholesterol and greatly elevated TG levels.
  • cause is either increased production or decreased clearance of VLDL & chylomicrons. Usually, it is a genetic defect.
  • occurs most commonly in adults who are obese and/or diabetic.
  • Tx: Diet. If necessary drug therapy includes niacin and/or fenofibrate or statin.
A

Type V (Familial ixed Hypertriglyceridemia)

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11
Q

Most effective drugs at lowering LDL cholesterol.

A
  • HMG- CoA reductase inhibitors
  • Resins
  • Ezetimibe
  • Niacine
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12
Q

Drugs most effective at lowering triglyceride and VLDL and raising HDL.

A
  • Fibric acid derivative (gemfibrozil)
  • Niacin
  • Marine omega-3 fatty acids
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13
Q

Have direct anti-atherosclerotic effects and have been shown to prevent bone loss.

A

Statins (HMG-CoA Reductase inhibitors

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14
Q

Most potent LDL cholesterol-lowering statins

A
  • pitavastatin
  • rosuvastatin
  • atorvastatin
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15
Q

Least potent LDL cholesterol loweing statins.

A
  • lovastatin

- fluvastatin

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16
Q

Adverse effect of HMG- CoA reductase inhibitors (statins)

A
  • Liver failure
  • mild elevations of serum aminotransferases - common
  • myopathy and rhabdomyolysis
  • teratogenic
  • contraindicated in pregnancy
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17
Q

The most effective agent for increasing HDL-C and also lowers triglycerides. Strongly inhibits lipolysis in adipose tissue.

A

Niacin (Nicotinic Acid)

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18
Q

Toxicity of Niacin

A
  • intense cutaneous flush (accompanied by an uncomfortable feeling of warmth)
  • pruritus (aspirin)
  • moderate elevations of liver enzymes
  • severe hepatotoxicity
  • hyperuricemia
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19
Q

Receptors that regulates transcription of genes involved in lipid metabolism in Fibric acid derivatives.

A

PPAR- alpha protein

20
Q

Where fibrates stimulates fatty acid oxidation that limits the supply or triglycerides and decreases VLDL synthesis.

A

liver

21
Q

In most px, fibrate have ___ or ___ effect on LDL conc.

A

little or no

22
Q

Fibric acid derivatives is used to treat

A

hypertriglyceridemia

23
Q

Toxicity of FIbric Acid derivatives

A
  • nausea - most common
  • skin rashes - common with gemfibrozil
  • increased risk of cholesterol gallstones
  • use of gemfibrozil is contraindicated with simvastatin
24
Q

Increased serum levels of which of the ff is associated with a decreased risk of atherosclerosis?

A

HDL

25
Q

A 35 y.o woman appears to have familial combined hyperlipidemia. Her serum conc of total cholesterol, LDL cholesterol and triglyceride are elevated. Her serum conc of HDL cholesterol is somewhat reduced.

The px is started on gemfibrozil. W/c of the ff is a major mechanism of gemfibrozil’s action?

A. Increased exretion of bile acid salts
B. Increased expression of high-affinity LDL recpetors
C. Increased secretion of VLDL by the liver
D. Increase triglyceride hydrolysis by lipoprotein lipase
E. reduced uptake of dietary cholesterol

A

Increase triglyceride hydrolysis by lipoprotein lipase

26
Q

W.c of the ff is a major toxicity associated w/ gemfibrozil therapy?

A

Cholelithiasis (gallstone formation)

27
Q

Is a complex response to cell injury that primarily occurs in vascularized connective tissue and often involves the immune response.

A

inflammation

28
Q

often effective in controlling inflammatory pain

A

aspirin

29
Q

Have moderate effectiveness in inflammation

A
  • ibuprofen

- naproxen

30
Q

prototype of the salicyates and other NSAIDs

A

aspirin

31
Q

has greater anti-inflammatory effectiveness

A

indomethacin

32
Q

has greater analgesic effectiveness

A

Ketorolac

33
Q

was the 1st member of a newer NSAID subgroup and has higher incidence of cardiovascular thrombotic events that nonselective drugs

A

Celecoxib

34
Q

2 Isoforms of Cyclooxygenase.

A
  • COX 1- noniflammatory cells

- COX-2 activated lympocytes, PMNs, other inflammatory cells

35
Q

Inhibit both cyclooxygenase isoforms and thereby decrease prostaglandins and thromboxane synthesis throughout the body.

A

aspirin and nonselective NSAIDs

36
Q

Acetylates and thereby irreversibly inhibits cyclooxygenase

A

Aspirin

37
Q

The inhibition produced by other NSAIDs is

A

reversible

38
Q

Reduce the manifestations of inflammation, and reduces fever by suppressing the prostaglandins synthesis in the CNS (antipyretic action.)

A

clycooxygenase

39
Q

Effect of NSAIDs in kidney disease.

A
  • reduce the blood flow to the kidneys
  • induce full blown nephrotic syndrome
  • negative impact on the glomerular filtration rate
  • leading cause of acute kidney injury
  • inflammation and swelling of the space in between the kidney tubules (acute interstitial nephritis)
40
Q

3 therapeutic dose ranges of Aspirin.

  • low range:
  • intermediate doses:
  • high doses:
A
  • low range: (<300mg/d)- reduce platelet aggregation
  • intermediate doses: 300-2400mg/d- antipyretic and analgesic effects
  • high doses: (2400- 400mg/d)- anti-inflammatory effect
41
Q

Other NSAIDs (ibuprofen, naproxen, piroxicam) is used for

A
  • mild to moderate pain (musculoskeletal inflammation: arthritis and gout)
  • dysmenorrhea, headache, & patent ductus arteriosus in premature infants
42
Q

Used mainly as a systemic analgesic and the only NSAID available in a parenteral formulation.

A

Ketorolac

43
Q

Toxicity of Aspirin

A
  • tinnitus
  • vertigo
  • hyperventilation
  • respi alkalosis
  • Reye’s syndrome (children w/ viral infections)
44
Q

Toxicity of Nonselective NSAIDs

A
  • gastrointestinal disturbance
  • risk of renal damage
  • parenteral ketorolac (restricted to 72h)
45
Q

Toxicity of COX-2-selective inhibitors (Celecoxib, rofecoxib, valdecoxib)

A
  • reduced risk of gastrointestinal effects
  • risk of renal damage
  • risk of MI and stroke
  • risk of arterial thrombosis

PHARMA (26 decks)

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