25 Flashcards

1
Q

describe the difference between High density and low density cholesterol

A
  • High Density = secure, efficient transport (HDL-C)
  • Low density = Insecure, inefficient transport (LDL-C)
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2
Q

describe triglycerides

A
  • calorie transport to and from liver
  • glycerol with 3 long chain fatty acids
  • linked to obesity and atherosclerosis
  • generally inversely proportional to HDL-C
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3
Q

define lipid hypothesis

A
  • LDL-C levels directly relate to ASCVD risk

–> prior: total cholesterol

–> LDL-C

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4
Q

define coronary atherosclerosis

A
  • Presence of raised, yellow, flat plaques in t he endothelial layer of this aorta from the middle-aged man
  • significantly decreased lumen size
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5
Q

define pooled cohort risk assessment

A
  • Estimates 10 year risk for Coronary death or nonfatal myocardial infarction, or fatal or nonfatal stroke
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6
Q

what are major cardiovscular risk factors

A
  • Cigarette smoking
  • hypertension
  • diabetes mellitus
  • family history of premature CAD
  • Age
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7
Q

What are the risk equivalents

A
  • Risk of ASCVD “hard” event = having CAD

–> Diabetes mellitus

–> known ascvd: PAD, AAA, CVA

–> chronic renal disease

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8
Q

describe 4 major statin benefit gorup

A
  • Secondary prevention = ALL INDIVIDUALS with clinical CVD
  • Primary prevention

–> isolated LDL-C (above 190)

–> diabetes mellitis, 40-75years, LDL (70-189)

–> 10 year CVD risk, age 40-75 years and LDL of 70-189

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9
Q

what are some non-drug LDL-lowing therapy

A
  • EDUCATION
  • increase physical activity
  • weight control
  • dietary modification (reduce intake of saturated fat and cholesterol)
  • control of other ASCVD risk factors
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10
Q

describe HMG CoA reductase inhibitors

A
  • DECREASE LDL and TG
  • increas HDL
  • SIDE EFFECTS = myopathy, increase liver enzymes
  • AVOID in liver disease and high grades of HF
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11
Q

describe the demostrated therapeutic benefits of statins

A
  • Reduce

–> major coronary events

–> CAD mortality

–> coronary procedures

–> stroke

–> total mortality

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12
Q

describe bile acid sequestrants

A
  • Actions:

–> reduce LDL

–> INCrease HDL and TG

  • Side effects = gi distress/constipation (decrease absorption of other drugs)
  • Contraindicated: dysbetalipoproteinemia and Raised TG
  • THERAPEUTIC BENEFIT = Reduce major coronary events, and CAD mortility
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13
Q

describe nicotinic acid

A
  • Actions

–> lowers LDL and TG

–> raises HDL

  • Side effects: flushing, hyperglycemia, hepatotoxicity (
  • Aspirin blocks some side effects
  • Contraindicated in liver disease, severe gout, peptic ulcers
  • THERAPEUTIC BENEFITS = reduce major coronary events without statins

–> NO REDUCTION IN TOTAL MORTALITY

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14
Q

Fibric acids

A
  • Major actions

–> Lower LDL, TG

–> raise HDL

  • Side effects = dyspepsia, gallstones, myopathy
  • Contraindicated = severe renal or hepatic disease
  • Thereapeutic benefit: reduce progression of coronary lesions, reduce major coronary events
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15
Q

PCSK9 INhibitors

A
  • Proprotien convertase subtilisin kexin type 9
  • DECREASE LDL by 36-59%
  • TX of familial hypercholesteremia

(genetic variant which DECREASES LIVER LDL RECEPTORS (less LDL is removed from circualtion)

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16
Q

describe teh choice of tx

A
  • Statins are teh drugs of choice for dyslipidemias
  • Intensity of therapy parallels RISK more than Lipid levels (patient oriented medicine)