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Pathology Final Exam > CAD and Risk Factors > Flashcards

CAD and Risk Factors Flashcards

1
Q

What are the two theories of pathophysiology behind CAD?

A
  1. lipid hypothesis

2. Chronic Endothelial Injury Hypothesis

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2
Q

What is the lipid hypothesis?

A

modified LDL’s are absorbed my macrophages damage the endothelium and set up endothelium and intima for lipid deposition

however this evolved into CEIH

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3
Q

What is the chronic endothelial injury hypothesis?

A

loss of endothelium through various processes allows smooth muscle into the intima/media and attract modified LDL

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4
Q

What risk factors can change the adhesive properties or the WBC and inner surface of arterial wall?

A

HTN, high LDL, free radicals from DM, Tobacco

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5
Q

What does a presence of WBC in endothelium lead to?

A

leads to an inflammatory cascade which causes lesion formation

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6
Q

What is epidemiology for CAD?

A

responsible for death of 1/3 of americans under 35

cost U.S healthcare system 444 billion per year

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7
Q

Even if someone lives a healthy lifestyle why can they still get CAD?

A

because genetics can override all of that

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8
Q

What cause the creation of the classic sign of CAD, fatty streaks?

A

due to inflammatory process smooth muscle is pulled from media layer to intima layer, this creates a complex which attracts lipids

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9
Q

What happens if smooth muscle doesn’t relax if ischemic?

A

there is less perfusion during diastole

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10
Q

What is a stenotic lesion?

A

these are generally stable, thick fibrous caps that enclose the lesions, leads to less rupture

smaller lipid cores

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11
Q

What are clinical manifestations of a stenotic lesion?

A

ischemia, angina

slowly advancing system

TX: medical therapy and revascularization

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12
Q

What is a non- stenotic lesion?

A

large lipid cores that usually outnumber stenotic plaques

thin fibrous caps that often rupture and thrombosis

difficult to detect b/c there is no occlusion therefore no decrease in lumen size

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13
Q

What are clinical manifestations of a non- stenotic lesion?

A

infarction

TX: major lifestyle changes

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14
Q

What is the Framingham Heart study?

A

began in 1949 to find out more about heart disease now on 3rd and 4th generation- most of what we know about heart disease is from this study

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15
Q

What are modifiable risk factors for CAD?

A

HTN, HLD, smoking, obesity, stress, DM, inactivity

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16
Q

What compromises metabolic syndrome?

A

HTN, HLD, obesity, DM

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17
Q

What are non modifiable risk factors?

A

age, gender, genetics

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18
Q

Other than CAD what other dz can be caused by HTN?

A

kidney failure

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19
Q

What race is most at risk for HTN?

A

african americans

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20
Q

Why does HTN increase as we age?

A

due to loss of elasticity of arteries

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21
Q

What are the major causes of primary HTN?

A
  • complicated interaction between genetics and environment
  1. unknown exact cause
  2. insulin resistance- type 2 DM
  3. RAAS system- chronic secretion of Renin
  4. SNS dysfunction
  5. chronic inflammation

all lead to vasoconstriction and renal salt/water retention- increases intravascular volume this increasing SBP leading to increased TPR

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22
Q

What is secondary HTN?

A

caused by a systemic disease that increases TPR

  1. CRF
  2. RAS- renal artery stenosis
  3. endocrine dz ( sympathetic nervous system outflow damaged)

mostly reversible if underlying process treated

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23
Q

Why does HTN disrupt endothelium wall?

A

high sbp creates a shearing of the wall and changing permeability of the layer

24
Q

What does HTN do to the smooth muscle of arterial wall?

A

causes smooth muscle hypertrophy in arteries making it more likely to vasoconstrict b/c less dispensibility

25
What part of RAAS has been shown to have same shearing affect?
Angiotensin 2, mere prescence of it
26
What does chronic HTN lead to?
1. chronic elevated afterload 2. left ventricular hypertrophy-----LV failure 3. increased risk of peripheral vascular dz and stroke (#1 cause)
27
When is the first step of HTN tx?
lifestyle mods 1. diet- less salt intake and weight loss 2. aerobic exercise - augments endothelium healing, decreases norepinephrine in bloodstream
28
What are other HTN tx?
meds, smoking cessation, education
29
What are three main areas of cholesterol we as PTs are concerned with?
1. total serum cholesterol 2. low density lipoprotein 3. high density lipoprotein
30
Why are LDL's bad cholesterol?
they are the chief transporter of lipids to body's cells, therefore responsible for depositing lipids on arterial walls after they are damaged or weakened
31
Why are HDL's good cholesterol?
they transport lipids from body to liver for excretion removes cholesterol from smooth muscle in intima blocks action of LDL within layers of arterial walls
32
What happens to cholesterol levels during exercise?
LDL stay the same but HDL increases
33
What are norms for total cholesterol?
under 180- optimal 180-200 borderline over 200- high
34
What are norms for HDL?
under 40 low over 60 high
35
What are norms for LDL?
under 100- optimal 100-129- near optimal 130-159- borderline 160-189 high over 190 high
36
What is the cholesterol ratio?
total cholesterol to HDL less than 5: 1 is good ideal is 3.5 : 1
37
What are triglycerides?
most common type of fat in the body normal under 150 at risk 151-199 high risk 200-499 very high risk over 500
38
Why is fiber in fruits and vegetables important?
this fiber allows for sugar to be absorbed slower in the body
39
What type of exercise is best for hyperlipidemia?
aerobic exercise, benefits come from weight loss and body fat decreases HDL and triglycerides
40
What is the duration needed for a change for exercise?
over 12 weeks of training, 5-6 days of aerobic exercise 75-85% of max HR
41
What are statins?
inhibits cholesterol synthesis and up-regulates LDL receptors in the liver
42
What are the major side effects of statins?
muscle weakness/myopathy (proximal)- may be associated with or without pain liver toxicity- can damage hepatocytes myalgia, helps regulate inflammation
43
What happens to angina signs with DM?
due to autonomic neuropathy- anything weird from chest up thats worse with exercise and better with rest
44
How does metabolic syndrome lead to CAD?
visceral fat accumulates around waist, which triggers release of inflammatory proteins these proteins may trigger a response by certain receptors that cause insulin resistance
45
What is body mass index?
ratio that has standardized values for a given height and weight
46
BMI values?
``` underweight- under 18.5 normal/acceptable- 18.5- 24.9 overweight- 25-29.9 obese class 1- 30-34.9 obese class 2- 35 - 39.9 obese class 3 (morbid)- over 40 ```
47
Body fat analysis?
%BF = (fat mass/ body weight) x 100
48
Healthy ranges of body fat?
Males 12-18% over 25% obese females 18-23% over 30% obese
49
What does smoke contain?
has a high level of carbon monoxide, CO binds to hemoglobin at a much higher infinity than O2 this causes hypoxia which leads to vasoconstriction which raises CO and SBP
50
What does CO do to the bloodstream?
CO damages the endothelial cells, this changes permeability of the arteries and stimulates smooth muscle invasion into the intima
51
What does nicotine do the vessels?
potent vasoconstrictor, increases HTN risk this decreases ischemic threshold leads to increasing myocardial oxygen demand
52
How many hours before a treatment session should a patient not smoke?
4 hours bc smoking increases BP and HR thus increasing myocardial oxygen demand
53
How does stress affect CAD?
stress increases the production of circulating catecholamines which increases BP and myocardial oxygen demand
54
What is the age of manifestation of CAD?
50-51 in men and 60 in women
55
How does gender affect CAD?
premenopausal women have a decreased risk of CAD compared to men post menopausal women have essentially the same risk as men

Pathology Final Exam (4 decks)

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