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316 Pharmacology > Exam 2: Atherosclerosis > Flashcards

Exam 2: Atherosclerosis Flashcards

1
Q

Tunica intima

A

Endothelium

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2
Q

Tunica media

A

Elastic fibers and smooth muscle

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3
Q

Tunica media is thicker in ____ and thinner in ____

A

Thicker in arteries

Thinner in veins

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4
Q

Tunica extern

A

elastic and collagen fibers (connective tissue)

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5
Q

Tunica extern is thinner than media in ____- but thickest layer in

A

Thinner than media in arteries, but thickest layer in veins

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6
Q

Arteries tend to be ____ than veins

A

Thicker than veins

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7
Q

Arteries contain more

A

Elastic fibers that helps them stretch and recoil during the cardiac cycle

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8
Q

Veins are not designed to

A

Withstand high pressure, but are distensible enough to adapt to variations in the volume and pressure of blood passing through them

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9
Q

Veins have ____ to prevent back flow

A

Valves!

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10
Q

Both arteries and veins are innervated by

A

The SNS

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11
Q

Is the vascular endothelium a simple, single layer of cells lining the heart and blood vessels?

A

No! it is a lot more than that

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12
Q

The vascular endothelium is a

A
  • Metabolic interface between the blood and other tissues

-

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13
Q

The vascular endothelium forms a unique

A

thromboresistant layer between sub endothelial tissue and blood

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14
Q

the vascular endothelium modulates

A

tone, growth, hemostasis, and inflammation throughout the circulatory system

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15
Q

What is an initial step in atherosclerosis

A

Endothelial vasodilator dysfunction

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16
Q

Endothelial vasodilator dysfunction is caused by **

A

loss of endothelium-derived nitric oxide

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17
Q

The body’s endothelial cells account for an area of

A

4,000 - 7,000 sq. miles

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18
Q

Vascular endothelium regulates vasodilation by decorating vasoactive substances like

A

Nitric Oxide
Angiotensin-converting enzyme
Receptors for NE on surfaces of endothelial

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19
Q

What does nitric oxide cause

A

Vasodilation

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20
Q

Angiotensin converting enzyme on the surface of endothelial cells cause

A

Vasoconstriction via RAAS

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21
Q

Vascular endothelium prevents thrombus formation b/c

A

Physiologically thromboresistant

Secretes heparin and other substances that inhibit platelet activity

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22
Q

Arteriosclerosis is a

A

generic term for “hardening of the arteries” (because they become less elastic)

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23
Q

Atherosclerosis is a type of

A

Arteriosclerosis

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24
Q

ATHerosclerosis is a

A

pathologic process involving development of fibrofatty lesions in the intimal lining of cerebral, coronary, and peripheral arteries

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25
Q

Factors that contribute to the pathogenesis of atherosclerosis

A
  • Endothelial dysfunction
  • Dyslipidemia (family history - familial hypercholesterolemia)
  • Inflammation
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26
Q

Atherosclerosis is associated with

A 
Smoking 
Hypertension 
Diabetes 
Gender (male > female premenopausal)
Obesity
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27
Q

Important risk factors for Atherosclerosis and dyslipidemia

A

High levels of low density lipoprotein (LDLs)

Low levels of High density lipoprotein (HDLs)

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28
Q

Atherosclerosis begins with

A

injury to the endothelial cells lining the artery walls

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29
Q

The endothelial injury then progresses to

A

Fatty streak and fibrotic plaque, which leads to complicated lesion

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30
Q

Endothelial damage —>

A

Monocytes and platelets attracted to site

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31
Q

Elevated LDLs alter permeability of endothelial lining allowing

A

Macrophages to migrate under endothelial

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32
Q

Inflammation and endothelial cell dysfunction causes

A

Macrophages release inflammatory cytokines

Endothelial cells cannot make normal amounts of antithrombin and vasodilation substance

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33
Q

Free O2 radicals released by inflammatory process causing

A

Oxidation of LDL (Toxic to endothelium and further damages it)

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34
Q

Macrophages engulf oxidized LDL which causes

A

Foam cells which causes fatty streaks

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35
Q

Macrophages also reales growth factors that stimulate

A

Smooth muscle proliferation which causes smooth muscle and collagen migrate over the fatty streak which causes fibrous plaque

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36
Q

Plaque may

A
  1. calcify and protrude into the lumen or

2. lipids realized from necrotic foam cells from an unstable plaque that may rupture

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37
Q

Fatty streaks are

A

Lesions that can be found in the arterial walls of most people.

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38
Q

Fatty streaks produce

A

Toxic free radicals, recruit T-cells leading to autoimmunity and secrete inflammatory mediators that further damage the vessel walls

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39
Q

Cells in the area begin to proliferate in response to endothelial injury, producing

A

Collagen and cover the fatty streak forming a fibrous plaque

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40
Q

Clinical manifestation of atherosclerosis

A
  • Depends on location and extend of obstruction (Coronary, carotid, cerebral, peripheral)
  • Stenosis, plaque ulceration, and rupture, aneurysm formation, hemorrhage, ischemia, infarction
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41
Q

Lipoproteins are

A

tiny, spherical structures composed of lipids and proteins

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42
Q

Lipoproteins serve as

A

Carriers for transporting lipids (which are insoluble in plasma) in the blood

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43
Q

How do lipoproteins serve as carriers for transporting lipids

A

They have a hydrophilic shell that makes lipids soluble in plasma

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44
Q

lipids are transported to various tissues for

A

Energy utilization
Lipid disposition
Steroid hormon production
bile acid formation

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45
Q

Lipoproteins contain one or more Apolipoproteins that act

A

as recognition sites for cell– surface receptors and enzymatic activity

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46
Q

Lipoproteins are classified by

A

their lipid and protein content (density), apolipoprotein content, and transport function

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47
Q

Density of lipoprotein is determined by

A

Protein and lipid content

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48
Q

Protein is more

A

Dense than lipid

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49
Q

Lipoproteins that have a high % of protein have a

A

relatively higher density

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50
Q

Very low density lipoproteins (VLDLs)

A

Mainly carry triglycerides

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51
Q

Low density lipoproteins (LDLs)

A

Less protein, more fat

52
Q

High density lipoproteins (HDLs)

A

More protein, less fat

53
Q

three classes of lipoproteins relevant to atherosclerosis

A
  • very low density lipoproteins
  • low density lipoproteins
  • high density lipoproteins
54
Q

Desirable level for total serum concentration

A

< 200

55
Q

LDL definitely contributes to

A

Arteriosclerosis

56
Q

LDL cholesterol desirable level

A

< 130

57
Q

HDL cholesterol protects

A

Against atherosclerosis

58
Q

Desirable HDL cholesterol level

A

> or = 40

59
Q

Triglycerides probably contribute

A

to atherosclerosis

60
Q

Desirable levels or triglycerides

A

< 150

61
Q

Divide total cholesterol number by the HDL number: goal ratio below ____ (optimal ratio ___)

A

below 5.1

Optimal ratio 3.5

62
Q

Drug therapy for dyslipidemia are indicated as

A

Adjuncts to lifestyle modifications

63
Q

Dyslipidemia is

A

elevation of plasma cholesterol, triglycerides (TGs), or both, or a low high-density lipoprotein cholesterol level that contributes to the development of atherosclerosis

64
Q

Drug therapy for dyslipidemia are often prescribed

A

In combination

65
Q

Most widely used and most effective drugs for lowering LDL cholesterol levels are

A

HMG-CoA reductase inhibitors (statins)

66
Q

Atorvastastin drug class

A

Antilipemic, HMG-CoA reductase inhibitors (statins)

67
Q

MOA of atorvastatin

A

Inhibits hepatic enzyme HMG C0-A (enzymes involved with cholesterol synthesis)

68
Q

For atorvastatin, increased synthesis of LDL receptors in hepatocytes causes

A

Increased LDL catabolism, which causes decreased LDL cholesterol

69
Q

Atorvastatin increases

A

HDL cholesterol

70
Q

Atorvastatin promotes

A

Plaque stability

71
Q

When is dosing preferred for statins (HMG-CoA reductase inhibitors?)

A

Dosing in the evening to preferred, but may take without regard to time of fay

72
Q

What should be avoided when taking Atorvastatin?

A

Large quantities of grapefruit juice

73
Q

Atorvastatin administration

A

PO only

74
Q

Adverse affects for atorvastatin

A

Hepatotoxicity
Myopathy/rhabdomyolysis (Increased risk if concurrent use of protest inhibitors)
Increase risk of diabetes

75
Q

Atorvastatin is contraindicated in

A

Pregnancy, it is a category X

76
Q

Rhabdomyolysis

A

Striated muscle breakdown

77
Q

Rhabdomyolysis is associated with

A

other toxic or chemical damage; excessive muscular stress, prolonged muscle compression, crushing trauma, ischemia

78
Q

Myoglobin

A

O2 carrying protein important to muscular O2 consumption

79
Q

Release of myoglobin causes

A

Oxidative stress, initiating the inflammatory response

80
Q

What happens when myocytes break down

A

their intracellular contents are released into the plasma

81
Q

Clinical manifestations of rhabdomyolysis

A
  • Fatigue, muscle tenderness, weakness
  • Dark urine (caused by myoglobin in the urine)
  • Renal tubules may eventually be obstructed by myoglobin
82
Q

Labs for rhabdomyolysis

A 
renal function (BUN, Creatinine) 
Intracellular enzymes (CK, LDH, ALT, AST)
Urinalysis
83
Q

Contents of when myocytes break down

A 
Myoglobin
Creatine kinase (CK) 
Lactate dehydrogenase (LDH) 
Aspartate aminotransferase (AST) 
Potassium
84
Q

Treatment for rhabdomyolysis

A

Hydration (normal saline IV)
Correction of electrolyte imbalance
Supportive measures

85
Q

Additional caution with Atorvastatin

A

Diabetics: high blood glucose levels have been reported with HBM- CoA reductase inhibitors
Consume large amounts of ethanol
Liver disease
High potential for cytochrome P450 (CYP)

86
Q

Bile acid sequestrants increase the use of

A

Cholesterol

87
Q

Bile acid sequestrants are often used as

A

Adjuncts to statins to lower LDL cholesterol

88
Q

Bile acide séquestrants are

A 
Biologically Inert (does not initiate a response or interact when introduces to a body tissue)
Insoluable in water 
No GI absorption 
Pass through intestine 
Excreted in feces
89
Q

Cholestyramine resin drug classification

A

Antilipemic agent; bile acid sequestrate

90
Q

Cholestyramine resin MOA

A

Binds to bile acids in the intestinal lumen, which prevent enterohepatic reabsorption of bile salts, which accelerate fecal excretion of LDLs, which in turn LOWERS LDL cholesterol

91
Q

Bile acid sequestrants comes as

A

Powder which is mixed in water or fruit juice

92
Q

Bile acid sequestrants can form

A

complexes with other drugs

93
Q

If a drug is bound to a complex with a bile acid sequestrate,

A

It is not biologically available

94
Q

Drugs known to form complexed with bile acid sequestrants

A

Digoxin, thiazide diuretics, warfarin, some antibiotics

95
Q

How to avoid bile acid sequestrant complex formation

A

Administering PO medications 1 hour before or 4 hours after cholestyramine

96
Q

Bile acid sequestrants decrease absorption of

A

Fat-soluble vitamins
Folic acid
Iron
Calcium

97
Q

Most common adverse effects for bile acid sequestrants

A

GI disturbances

Constipation, nausea, dyspepsia, flatulence

98
Q

Pregnancy category for bile acid sequestrants

A

Risk factor C

99
Q

Enzetimibe drug class

A

Antilipemic agent; Cholesterol absorption inhibitor

100
Q

Enzetimibe administration

A

PO only

101
Q

Enzetimibe MoA

A

Acts on cells of the small intestine (@ brush border) to inhibit cholesterol absorption

102
Q

Enzetimibe decreases

A

Total cholesterol levels, LDL, triglycerides

103
Q

Enzetimibe produces

A

Small increase in HDL

104
Q

Enzetimibe may cause

A

Fatigue, abdominal pain, cholecystitis, myopathy

105
Q

Pregnancy risk factor for ezetimibe

A

Risk factor C

106
Q

Triglyceride levels over 500 are given

A

Fibrates

107
Q

Fibrates are derivative of

A

fabric acid that lower serum triglycerides and increase serum HDL

108
Q

Gemfibrozil drug classifications

A

Antilipemic, fibric acid, fibrate

109
Q

Gemfibrozil moA

A

Decrease serum triglycerides via increase of lipoprotein lipase, which decreases hepatic fatty acid uptake, which decreases hepatic secretions of triglycerides
-ALSO increases serum HDL

110
Q

Lipoprotein lipase

A

Enzyme that breaks down free fatty acids

111
Q

When to administer gemfibrozil

A

PO ONLY

30 minutes prior to breakfast or dinner

112
Q

Adverse effects of gemfibrozil

A

Dyspepsia, abdominal pain, myopathy, rhabdomyolysis, cholelithiasis

113
Q

Pregnancy risk factor for gemfibrozil

A

Risk factor C

114
Q

Examples of PCSK9 inhibitors

A

Alirocumab

Evolocumab

115
Q

PCSK9 is a

A

protein that regulates the lifespan of the cholesterol clearing receptors in the liver

116
Q

PCSK inhibitors promote

A

Modulation of the receptor that clears LDL-C thereby prolonging the receptor activity and promoting the clearance of chloestorl

117
Q

PCSK9 inhibitor significantly lowers

A

LDL cholesterol levels (by 50%)

118
Q

Adverse effects of PCSK9 inhibitors

A

Fairly well tolerated
Muscle pain, diarrhea have been reported
Nasopharyngitis
itching
injection site reactions
Serious allergic reactions have been reported

119
Q

Niacin is a

A

Soluble vitamin, antilipemic agent

120
Q

Niacin decreases ___ and increases _____

A

decreases LDL and increased HDL

121
Q

Niacin administration

A

PO only

122
Q

Niacin MoA

A

Inhibits mobilization of fatty acids from peripheral tissues

123
Q

What happens when there is an inhibition of mobilization of fatty acids from peripheral tissues.

A
  • Causes decrease in hepatic synthesis of triglycerides and VLDL, which leads to a decrease in LDL production.
  • ALSO decreases lipid transfer from HDL to VLDL, leading to an increase of HDL
124
Q

Adverse effects of niacin

A

Flushing (may be decreased by taking NSAID 30-60 minutes before dosing)
Severe cases of hepatotoxicity

125
Q

Niacin begin dose

A

250 mg/day

126
Q

Niacin is contraindicated in

A

Active hepatic disease

127
Q

Caution for niacin in patient

A

who consume substantial amounts of ethanol

316 Pharmacology (19 decks)

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