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Cardiovascular I > Cardiovascula I -patho > Flashcards

Cardiovascula I -patho Flashcards

1
Q

AHA statistics, over 20yo

A

problems increase as we age . Mostly found in ppl>80y

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2
Q

AHA, kids, 12-19 yo

A

healthy diet is the major cause

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3
Q

AHA, adults.20 yo

A

healthy diet score, physical activity and BMI

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4
Q

AHA, over 20yo

A

obesity, which is a modifiable factor is increasing=> increasing cardiovascular problems in men over 35yo and female at 36yo

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5
Q

AHA cost for major cardiovascular disease

A

Heart rate, and HTN, followed by stroke lead the chart

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6
Q

AHA, major cause of deaths

A

Coronary artery disease (47%), other 16.9%, stroke 16.4%, heart failure, HTN, disease of arteries

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7
Q

AHA, CVD (cardiovascular disease) of age group over or less than 85Yo

A
  • under 85yo, the lead is CVD,CA,heart disease

- over 85yo: CA and Alzheimer

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8
Q

CVD trends between sexes

A

1/3 of all deaths is caused by CVD

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9
Q

heart disease and storke statistics-2015 update

A

18% of US have .5 metrics w ideal levels: smoking, physical activity, etc. for ppl over 20yo, caused by poor life style in US and world

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10
Q

Health behaviors causes of death:

A

1 Smoking=2nd leading cause of death/disability; 1/3 of CVD linked to 1ry or 2ry smoking

  1. Physical inactivity=only 50% meet req
  2. Nutrition, 1 out of 8 CVD deaths
  3. Obesity, together w other comorbidities: HTN, high colesterol, DM
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11
Q

Health factors/risk factors- 2015 statistics heart disease and stroke

A
  1. Family genetics= 45-90%
  2. high cholesterol=only 46% have a normal cholesterol level
  3. HTN = 32% mostly Afro Americans
  4. Diabetes Mellitus = 1 in 10 Americans, 90% of adults in DM II, 50% in DM II
  5. Metabolic syndrome = hyperglycemia, increased circ. waist
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12
Q

Risk factors for CV disease

A

Non modifiable: age, gender, race, hormonal status, fam hx
Modifiable: BP, cholesterol, smoking, and others like physical activity, weight, diet, stress, glucose tolerance

1 of THESE FACTORS IS PRESENT IN ALMOST 50% OF CVD DEATHS

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13
Q

hypertension (HTN)-def,

A

high blood pressure against the walls of arteries greater than 140mmhG systolic, greater than 90mmhg diastolic. Systolic pressure in vv when heart is contracting. Diastolic pressure in vv when heart is relaxed between beats.

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14
Q

HTN

A 
primary HTN is idiopathic in 90-95% of cases: related to genetics, smoking, obesity, high cholesterol
- secondarily is a identifiable cause 5-10% of cases related to kidney disease and endocrine disease
I in 3 Americans have HTN
#1 MODIFIABLE risk factor for HEMMORHAGIC and Ischemic strokes, and is 2x more prevalent in Americans than Caucasian
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15
Q

HTN

AHA stats

A

Higher in female over male in ppl. over 75+ yo

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16
Q

HTN risk factors - modifiable

A

Hi Na, Obesity, Insulin resistance, Hi cholesterol, Smoking, Long term alcohol abuse, hi stress, personality, hormonal status in female, and sedentary lifestyle, DM

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17
Q

HTN- non modifiable risk factors:

A

family hx, >55yo,gender,ethnicity

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18
Q

Stages of hypertension

A 
Normal: systolic 160, D:>100
Hypertensive crisis (emergency care needed) S >180, D> 110 mmHg
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19
Q

HTN causes:

A

kidney disease, narrowing of Aorta, narrowing of vasoconstriction of peripheral arteries

  1. Mechanical damage to epithelial lining of arteries: Inflammatory response or proliferation of smooth muscle in arterial wall
  2. Chronic afterload on LV as hyperthrophy or LV failure
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20
Q

HTN: s/s, prevention, dx,tx,px(prognosis)

A

s/s: headache, vertigo, flushed face, blurry vision, nocturnal urinary frequency

prev: PA/exercise, weight control, diet modification
dx: BP, CBC, urinanalysis, serum cholesterol, fasting blood glucose, ECG
tx: ongoing meds, lifestyle modification
px: can lead to ventricular hypertrophy->heart attack.

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21
Q

HTN meds:- combination therapy (tbl 12-6), lifestyle modifications

A

Ace inhibitors, ARB’s , diuretics, Ca channel blockers, L1 -andrenergic blockers, central L2 andrenergic antangonist, peripheral andrenergic blockers, vasodilators, aldosterone receptor blockers, direct renin inhibitors

22
Q

HTN meds:

A
  1. diuretics= decrease plasma volume, decrease K having an effect on kidneys
  2. ACE inhibitors= lower peripheral resistance, SE (side effect) chronic cough
  3. Renin inhibitors= prevent angiotensin from forming
  4. Beta blockers= decrease catecholamine response. Side effect for exercise
  5. Angiotensin receptor blocker= decrease angiotensin to vasoconstrict
  6. Ca- channel blockers= relax coronary smooth msc, vasodilate
23
Q

HTN meds effect on excercise

A

remember to note the pt’s meds, and use the inf to det their effect on BP and possible symptoms

24
Q

Cholesterol

A 
Insoluble, so binds w PROTEINS
- used for cell membrane and hormones
-75% is manufactured by body
LDL = transport cholesterol TO cells
HDL transport FROM body to liver
25
Q

Cholesterol, increased risk for CAD

A 
High LDL (transport cholesterol TO cell)
low LDL (transport From body) to liver
forms plaque between layers of artery wall-> plaque can cause blood clots->CVA, MI
26
Q

Cholesterol stats in adults >20yo

A

form 1988 to 2012, all the levels of cholesterol decreased, but its still high. Between populations mexican americans have the highest levels, followed by white and black ppl.

27
Q

Cholesterol levels:

A

Total cholesterol: 40mg/dl in men and >50 mg in female

Triglyceride (demo atherosclerosis)

28
Q

Smoking

A

pack/year hx
type of smoking
1st hand or 2nd hand
NON smokers exposed to smoke HAVE an increase risk of heart disease up to 25-30%

29
Q

Smoking over 18yo

A

around 23-24% of smoking

30
Q

Smoking effects

A

Carbon monoxide and nicotine
Oxihemoglobine curve: CO binds 250x more to Hgb vs Oxigen = decreased oxygen carrying capacity + increased workload of heart
Chronic HYPOXIA => increased HVT and increased risk of CLOTS
CO (carbon monoxide) damages epithelial lining=> increased permeability tio lipids, smooth muscle into lumen and causes CAD

31
Q

Smoking and Nicotine- vasoconstriction, increased clotting, increased total cholesterol

A

Vasoconstriction: decreased coronary flow at rest and with exercise
Increased clotting: increased in fibrinogen + increased platelet aggregation
Increased total cholesterol

32
Q

Quit smoking effects:

A

after 1yr:- drop heart disease risk by 50%

5-15 y later risk of CVA is the same as of a non smoker

33
Q

Inactivity and obesity -vs exercise

A

exercise can: modify BMI, lower BP, improve insulin secretion, increase HDL + lower LDl, reduce stress, improve endothelial fct, reduce inflammatory markers, reduce homocysteine and improve C REACTIVE PROTEIN = for inflammatory markers

34
Q

AHA dietary recommendation:

A

variety of fruit and vegetables
whole grain, low fat dairy product, skinless poultry and fish, nuts and legumes, non-tropical vegetables oils. Limited saturated fats and TRANS fat, Na, red meat and sweet and sugar sweetened beverages.

35
Q

Diabetes -risk factors

A
  • adults w diabetes have 2-4 X more likely to have CVD or CVA (top 2 killers of those w DM are heart disease and CVA)
  • comorbidities w diabetes: HTN, obesity, abnormal cholesterol level, decreased PA, poor blood glucose level, smoking
36
Q

Non modifiable risk factors:

A

family hx:

37
Q

Aging and CV - pathology

A
  • Reduction in fct: decreased myocytes and cells in conduction tissue, devel of cardiac fct., reduction in Ca transport, lower capillary density, decreased response to B-adrenergic stimulation, impaired autonomic reflex control
  • cholesterol dep. and changes by the age of 30yo
  • increased collagen and Ca deposits=> atherosclerosis plaque.
38
Q

Gender and CV - pathology

A
  • before age of 65 y. ratio of incidence in men vs women is 4:1
    WOMEN: depends on timing + symptoms, Hormones(estrogen increases HDL and decreases clot formation. Estradiol improves vasodilaton), surgery (CABG = more fatalities) , oral contraceptive( including MI and CVA if smoker and >35yo), HTN and cholesterol ( especially after menopause)
39
Q

Coronary artery disease (CAD)+ atherosclerosis - definition

A
  • CAD aa carry O2 to myocardium = creates ischemia and possible infarction when injured at endothelial level
  • Atherosclerosis = formation of plaque that narrows aa. Causes include: 1. High cholesterol and triglycerides
    2. HTN
    3. Smoking
    1st signs is the formation of fatty streak ( lipids, connective tissue, smooth muscle cells and platelets). and it could be stable or not.
40
Q

endothelial layer fct.

A

endothelial layer of artery or the intimal layer makes the vessel permeable to lipoproteins

41
Q

fatty streak

A

is the penetration of lipoproteins into the smooth muscle cells of the intima

42
Q

Atherosclerosis mechanism = lipid hypothesis

A

increased LDL penetrates the arterial wall and the lipids starts to build up in the smooth muscle layer. LDL causes smooth muscle hyperplasia and cells migrate to intima. Sub endothelium is exposed to blood at sites of tears and platelets aggregate => in plaque that will partially or totally block blood flow through the artery.

43
Q

CAD - predictors

A

markers for CAD in pt’s:
serum cholesterol, homocysteine, CRP (inflammation marker), fibrinogen, LP (a) - slows down the breakdown of clots, pulse pressure (

44
Q

Myocardial ischemia

A

happens when:
O2 demand NOT = O2 demand ( exercise activity and psychological stress)
plaque, vasospasm, decreased CO, low O2 levels (lung disease)

45
Q

Angina pectoris- def, s/s

A

cardiac workload > than O2 supply to myocardial tissue => ISCHEMIA => Angina pectoris = 70% or more occlusion of coronary artery. All this will irritate the myocardial fibers and -> ANS (C3-T4) -> Radiation PAIN

Symptoms: last 1-5 min, occlusion up to 20 min: squeezing, burning, pressing, heartburn, indigestion, choking which could mimic: dyspnea, fatique, diaphoresis, pallor

Women: inhale cold air, weakness, lethargy, midthoracic pain, R biceps pain

Angina pectoris can be relieved by NITRATES

46
Q

Angina pectoris causes:

A
  • total occlusion of arteries
  • platelet activation w occlusive thrombus
  • high demand w. limited blood flow
  • vasospasm of diseased artery/pain
47
Q

angina pectoris types:

A
  1. Stable angina = workload precedes ischemia, reduced by rest
  2. Unstable ischemia = lower workload precedes ischemia or lasts longer or different quality esp. in women
48
Q

Zone of hypoxic injury

A

from interior to exterior:

  1. Zone of infarct = necrosis as a weak vulnerable scar for 10-14 days and fibrous scar 6-8 wks
  2. zone of hypoxic injury = may return to normal but susceptible to injury, regain fct. 2-3 wks
  3. zone of ischemia = reversible zone and may have EKG changes nut return to normal as heals.
49
Q

Myocardial infarction ( heart attack) Dx:

A
  • prevalence of symptoms:
    (+) - cardiac enzymes: creatine kinase, homocysteine, LP(a), CRP and (+) ECG changes
  • biochemical markers include: cardiac troponin I and cardiac troponin T
    1. Cardiac catheter
    2. Thallium stress test
    3. Echocardiogram
50
Q

MI -tx

A
  1. Pharmacologic= improve blood flow
  2. Surgical:
    a) PTCA- percutaneous translumen coronary angioplasty = balloon ono obstructed artery and moves the plaque and restores blood flow
    b) STENT = helps keep open artery
    c) CABG - coronary artery bypass graft, internal mammary artery, saphenous vein, brachial artery to graft coronary artery. Bypass to occlusion to return flow.

Cardiovascular I (5 decks)

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