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Patho Test 2 > Test 2 artherosclerosis > Flashcards

Test 2 artherosclerosis Flashcards

1
Q

Relationship btw HTN & Artherosclerosis

A
  • Pressure exerted traumatizes endothelial lining repair with inflammation – also put down fibrous tissue, calcium, and lipids; occluded this vessel somewhat have to increase pressure to get past occlusion; damages inner wall of vessel = more plague so have to up pressure; vicious circle; High BP means plaque and plague means up the pressure
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2
Q

Risk Factors for Artherosclerosis

A

Cigaretts, Diabetes, Obesity, age (40+),Race (African American), Family, Gender (Post-Menopausal women most likely, Men more likely overall), HTN & Hyperlipidemia

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3
Q

How do Cigarettes effect Artherosclerosis

A

risk seems to be more with number of cigarettes smoked rather than length of time smoked. increase in Carbon Monoxide in tissue, so blood thinks no oxygen is getting to tissue, so heart pumps faster to perfuse with oxygen; nicotine constricts vessels; increases BP

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4
Q

what is a sign of CO2 poisioning

A

– bright cherry, pink color in nail bed Normal is red/purple

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5
Q

How does Diabetes effect Artherosclerosis

A

Type 1 Mostly; high sugar levels damage vessels and trigger the inflammation response like HTN

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6
Q

how does Obesity effect Artherosclerosis

A

Every 10 pounds overweight = 1 extra mile of bv Lose weight=lose bv=lower bp

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7
Q

Ischemia

A

Aerobic metabolism to Anaerobic metabolism= Lactic Acid = ↓pH (acid)=k+up This decreases the ability to repolarize

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8
Q

What do you see on the EKG with Ischemia

A

T wave inversion St Segment depression

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9
Q

What is the point of no return with Ischemia

A

30-45 min then there is irreversible damage to myocardial tissue and it is called a MI

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10
Q

Where is the ischemia most likely to happen in heart?

A

Left Ventricle

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11
Q

Transmural infarction

A

all the way from endocardium to epicardium; full thickness of all myocardial muscle

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12
Q

subendocardial infarction

A

goes about ½ way through myocardial tissue

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13
Q

relationship of enzymes to infarction

A

indirect way of assessing how much tissue is damaged; greater enzyme level, greater tissue damaged

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14
Q

When do you measure for enzymes

A

Blood test q8hrs at least 3 times

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15
Q

ck-mb enzyme

A

indirect way of assessing how much tissue is damaged; greater enzyme level, greater tissue damaged

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16
Q

Troponin

A

Protien that mediates CA, it is not an enzyme, its a protein marker. It rises 4-6 hrs after MI takes 10 days to go down.

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17
Q

CRP

A

elevated CRP r/t MI “there’s a fire, how hot it is, but have no idea where it is.

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18
Q

MI EKG

A

Pronounced Q wave, elevated ST segment, inverted Twave, ST seg and T wave will return to normal.

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19
Q

Congestive heart failure

A

static circulatory situation; things aren’t moving; “congested” traffic or blood; location of congestion depends on which ventricle we’re talking about

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20
Q

Type of Congestive Heart failure in left ventricle

A

pulmonary venous congestion

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21
Q

Type of Congestive Heart failure in right ventricle

A

systemic venous congestion

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22
Q

Cardiogenic Shock

A

greater than 40%loss all at once (can’t perfuse); do get pulmonary venous congestion 80-90%death rate

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23
Q

Ventricular septal defects

A

Complication of an MI. Septum that separates R & L ventricle. If septum gets necrotic b/c of injury pt. will have multiple vessel occlusions.

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24
Q

Septal rupture

A

Pressure difference btw ventricles and L is >. Pressure difference causes hole in septum b/c all that is holding it together is the mesh created in inflammation. These are most common in children.

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25
Q

Most common complication of MI

A

Dysrhythmia 90% Cardiac pt have some degree of dysrhythmia.

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26
Q

how does tachycardia effect CO=HRxSV

A

HR > 150, can’t fill up ventricle before it compresses, compromised because of SV

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27
Q

how does bradycardia effect CO=HRxSV

A

t contract often enough. Not beating fast enoug to keep perfusion

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28
Q

Premature Beat

A

electrical system has been activated from somewhere other than SA node; somewhere in travel another firing fires prematurely before SA firing completely finished its route

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29
Q

Ventricular Fibrillation

A

just quivering, not filling or contracting; defibrillate – turning off electrical activity of heart/shutting down electrical activity;

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30
Q

1-Heart Block

A

prolonged PR interval

31
Q

3-Heart Block

A

none of impulses starting in atria are reaching the ventricles; impulses coming from somewhere else in the conduction system; SA impulses never reach down here; complete heart block;

32
Q

What does EKG look like with 3-Heart Block?

A

will be a P wave, but long period of nothing, then QRS, maybe a T wave, then P wave again;

33
Q

Bundle Branch block

A

impulse not reaching ventricles at the same time bunny ears(QRS) on EKG

34
Q

2 problems produced by diseased valves

A

Regurgitation and stenosis

35
Q

Mitral Regugitation

A

backflow of blood from 1 vent. into atrium b/c of faulty valve

36
Q

acute mitral regurgitation p wave

A

taller and wider

37
Q

chronic mitral regurgitation

A

40% result of rheumatic fever or strep

38
Q

Aortic Stenosis

A

Restrict blood flow from left ventricle into aorta into during ventricular systole causes LVH

39
Q

Aortic Regurgitation

A

backflow of blood from Aorta into Left Ventricle during Ventricular diastole (relaxation); wide QRS 50% result of rheumatic fever

40
Q

Tricuspid Valve Disease

A

Stenosis; Restrict Blood flow from R atrium into R ventricle during diastole b/c its stiff; P wave wider and taller b/c atria takes longer to depolarize

41
Q

Symptoms of Heart Fail

A

Dyspnea, Cough, Rales, Liver enlargement, Edema, low grade fever

42
Q

Cardiac Shock

A

Results when myocardial tissue is not perfused

43
Q

Criteria for Cardiogenic shock

A

<2.1/min

44
Q

Cardiac index

A

CO in L/min/sq. meter of body surface

45
Q

Fusiform aneurysm

A

both sides of artery;typically in aorta; result of some kind of atrophy in middle layer of vessel

46
Q

Saccular Aneurysm

A

One side of artery

47
Q

Thromboembolic venous disease

A

blood clot moving freeing through body; * something that blocks a blood vessel; fat, air, clotted blood, calcium(anything that can obscure a blood vessel

48
Q

3 contributing factors to Thromboembolic venous disease

A

Stasis of blood flow, Endothelial injury, Hypercoagulation

49
Q

Superficial Thrombophlebitis

A

A clot in a vein that is inflammed Superficial=arms and legs Arms most likely d/t IV legs most likely d/t varicose veins

50
Q

Deep Vein Thrombosis

A

Clot in lower extremities

51
Q

3 veins most affected by DVT

A

Popliteal,superficial femoral, ilial femoral

52
Q

Vericose Veins

A

dilation and elongation typically in lower legs; unknown etiology; runs in family; increase incidence in females; nurses at highest risk

53
Q

COPD

A

Increased difficulty to move air in and out of lungs; group of diseases. Chronic Bronchitis, emphyseama, asthma

54
Q

3 reasons to get Asthma

A

Spasm of bronchi, increased mucosal edema, hyper secretion of mucus in bronchi

55
Q

Asthma’s 3 categories

A

Allergic, idiopathic, mixed

56
Q

Allergic Asthma

A

almost exclusively in children

57
Q

idiopathic Asthma

A

> 40 yr. old usually precursor to bronchitis or emphyseama

58
Q

Chronic Bronchitis

A
  • Hypertrophy = increase in number of * goblet cells; produce mucus r/t air polution
59
Q

Centrolobular Emphysema

A

Selectively effects respiratory bronchioles where there are few alvioli. Predominant in Male and smokers

60
Q

Panlobular Emphysema

A

effects everything! Alveoli distortes=less suface area, lose elasticity in lungs leads to barrel chest

61
Q

Bronchiectasis

A

condition characterized by chronic dilation and inflammation of bronchi and bronchioles; inflammation is usually from infection (often times in children) increases risk for pneumonia

62
Q

Cystic Fibrosis

A

genetic condition involving secretions of exocrine glands, sweat glands, liver, lungs; secretions are extremely viscous and thick affects 1:2000 births not A.A population sweat test for CF

63
Q

How does Thoracic cage disorder effect respiratory functioning

A

Lung tissue is fine but pt. will die of respiratory complications ie. OD on drugs

64
Q

Pectus excavatum

A

funnel or caved chest”; born with lower end of sternum physically fused to thoracic spine; chest has caved in appearance; can’t breath up and down seen in Marfans

65
Q

Picwician

A

; people who are extremely obese (like 700lbs) because gravity/can’t move chest and breathe; not exhaling a lot, CO2 levels elevate – feel tired, sleepy All w/ this disease have sleep apnea

66
Q

Pleural effusion

A

excess fluid that accumulates in the pleura, the fluid-filled space that surrounds the lungs

67
Q

Hemothorax

A

Blood in pleural space

68
Q

Pneumothorax

A

air or gas in pleural space

69
Q

Tension Pneumothora

A

accumulation of air under pressure in the pleural space; Happens with an injury to pleural membrane/lung which creates a 1 way door that can bring air into the plural space but with exhalation the door that was created closes and air cannot get out

70
Q

Bacterial Pneumonia

A

exudate (fluid); see fluid on chest film; seeing pus (blood cells), defensive response of lungs

71
Q

Viral Pneumonia

A

No white cell response-no pus. Do not see on chest x-ray

72
Q

Aspiration Pneumonia

A

aspirate vomit into lungs, stomach contents are acidic which are sucked into lungs, kills lung tissue with acid, also pulled bacteria into lungs; gangrenous lung tissue with a lot of bacteria; near drowning in chlorinated pools, chlorine water is very acidic water and can kill lung tissue; same for near river drowning, nasty stuff gets into lungs.

73
Q

Hypostatic Pneumonia

A

occur in lower bases of lungs; see these in patients who are immobile and laying down on their back (nursing home patient); change positions, stretch to airate a large part of lungs; change position often

Patho Test 2 (2 decks)

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