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Mary's Tests - Spring 2016 > Last Patho Exam > Flashcards

Last Patho Exam Flashcards

1
Q

Preload

A

Stretch of LV myocardial fibers at end of diastole

Fills the volume of the heart

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2
Q

Preload is mainly determined by

A

venous return

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3
Q

Frank Starling Law

A

the greater the strech the greater the force of contraction

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4
Q

As preload increases

A

SV and CO increase

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5
Q

There is an increase in preload if..

A

increased blood volume occurs as in fluid volume deficit and heart valve regurg/ septal defects

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6
Q

There is a decrease in preload if

A

decrease in blood volume as in dehydration

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7
Q

Afterload

A

resistance to ventricular ejection; the pressure the ventricle must overcome to pump out blood

EX: pushing

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8
Q

What is afterload largely determined by

A

BP- total peripheral resistance and resistance to pulmonary flow

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9
Q

As afterload increases,

A

there is a decrease in SV and CO

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10
Q

hypertension and high peripheral resistance can cause

A

increased afterload

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11
Q

decreased afterload results in what condition

A

arteriolar dilation

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12
Q

Systole

A

period of ventricular contraction and ejection of blood

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13
Q

at the end of systole

A

ventricles relax causing inraventricular pressure to fall

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14
Q

end systolic volume should be what ml

A

50

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15
Q

Diatole

A

period of ventricular relaxation and filing

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16
Q

end diastolic volume amount of blood in ml

A

120

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17
Q

CHD

A

coronary heart disease: occurs mainly from impaired blood flow in the coronaries

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18
Q

main cause of CHD

A

atherosclerosis

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19
Q

CHD includes:(5)

A

angina, MI, dysrhythmias, heart failure, sudden death

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20
Q

Two main coronary arteries

A

left and right that arise from aortic arch

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21
Q

Left coronary artery splits to become:

A
  1. Left anterior desceding to supply LV and portion of septum and papillary muscle.
  2. circumflex- to supply the left lateral wall of LV
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22
Q

Right coronary artery supplies what? and ext3ends to where

A

SA node and RV

extends to back of the heart

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23
Q

coronary arteries are mainly perfused during

A

diastole

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24
Q

coronary circulation is affected by..

A

aortic pressure- autoregulation allows constant blood flow to coronary arteries at mean arterial pressure of 60-180

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25
Q

metabolic control of coronary circulation

A

heart needs aerobic metabolism and fatty acids for energy

blood flow is regulated by O2 needs of myocardium

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26
Q

metabolic mediators for coronary circulation and how is it released..

A

K, lactic acid, CO2, adenosine-

released from myocardial cells in response to decreased O2 supply R/T demand and cause of vasodilation

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27
Q

endothelial cells that line coronary artieries secrete factors that..

A

affect blood flow.

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28
Q

vasodilating factors: endothelial control

A

nitric oxid- released when endothelium comes in contact with aggregating platelets, thrombin, products of mast cells, increased shear force

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29
Q

vasoconstricting factors: endothelial control

A

endothelin release stimulated by thrombin, epi and vasopressin

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30
Q

anti-thrombinogenic factors: endothelial control

A

imhibits platelet aggregation and clot formation

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31
Q

as larger arteries occlude,

A

smaller ones increase in size

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32
Q

What is atherosclerosis

A

the major cause of CHD, narrowing of coronary arteries due to buildup of plaque

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33
Q

people with atherosclerosis can do really well until what percentage of blockage

A

75

34
Q

Atheromas/ Plaques in the heart, brain and peripheral arteries cause

A

angina in the heart
TIA in the brain
intermittent claudication in the peripherals

35
Q

Two types of artherosclerotic lesions

A
  1. ) Fixed-stable, obstructs blood flow

2. ) Unstable- rupture spontaneously due to stress or presure

36
Q

Risk factors for atherosclerosis

A

hemodynamic changes- BP, HR, increase in SNS activity, force of contraction, coronary blood flow

Diurnal changes- rupture first thing in the morning due to stress

37
Q

In atherosclerosis, the lipid core provides,,

A

stimulus for platelet aggregation and thrombus formation

38
Q

White platelet containing thrombi

A

found in patients with unstable angina

39
Q

Red fibrin containing thrombi

A

found in vessel occlusion in Mi

40
Q

CHD can occur in normal arteries, TRUE or FALSE

A

TRUE

41
Q

CHD is due to an increase in what and a decrease in what..

A

increase in heart muscle demand, decrease in perfusion pressure (aortic stenosis)

Commonly occurs in those who have increased metabolic demands (hyperthyroidism, pregnancy, severe exertion, sepsis.

42
Q

Chronic ischemic heart disease: CHD

A

stable angina, variant angina, silent MI

43
Q

Acute coronary syndrome: CHD

A

unstable angina, MI (STEMI and NONSTEMI)

44
Q

What is angina

A

chest pain or pressure associated with transient myocardial ischemia

45
Q

anginal pain lasts for how long

A

2-10 min and is relieved with rest or NITRO

46
Q

Where is angina pain typically felt

A

in the pericardial and substernal area of chest, radiating to shoulder, jaw, arm, epigastrum or back

47
Q

Atypical presentation of angina

A

common with women and elderly: fatigue, SOB, heartburn, nausea, weakness, dizziness, faintness, confusion

48
Q

Angina can be silent. and is due to

A

sedentary lifestyle, development of adequate collateral circulation or inability to perceive pain (diabetes)

49
Q

Stable Angina

A

short lived, lasting 2-10 minutes, relieved by rest, occurs during exertion, cold, or stress.

50
Q

Stable angina is caused by

A

fixed obstruction due to atherosclerosis resulting in disparity between supply and demand

51
Q

Unstable Angina

A

unpredictable, may occur at rest and is prolonged.

no relieved by rest or NITRO

New onset (

52
Q

unstable angina is caused by

A

atherosclerotic plaque disruption (ruptured plaque)

53
Q

Variant Angina/ Vasospastic angina is caused by and may be associated with

A

vasospasms rather than atherosclerotic plaque.

May be associated with coronary stenosis but can occur without presence of disease

54
Q

Variant Angina/ Vasospastic angina

A

occurs at rest, during sleep, with minimal exercise or stress. Pain follows a cyclic pattern and happens that the same time every day.

55
Q

Variant/ Vasospastic angina is treated with

A

calcium antagonists

56
Q

STEMI

A

ST elevation Myocardial Infarction

tramural/ Q wave- involves FULL THICKNESS of ventricular wall, most common with obstruction of single coronary artery.

Most MI’s are transmural and involve LV

57
Q

NON-STEMI

A

NON-ST elevation MI

subendocaredial/non-Q wave- involves inner 1/3 or 1/2 of ventricular wall, most common when arteries are severely narrowed but still patent

58
Q

Pathophysiology of ischemia/ MI

A

loss of blood flow= anaerobic metabolism

cell dysfunction and contractile function decrease within a minute of onset

59
Q

Cell changes start within minutes with irreversible cell death after…

A

20-40 minutes

60
Q

microvascular injury occurs in about how many minutes

A

60

61
Q

reestablish blood flow within an hour of infarct leads to..

A

minimal cell death

62
Q

reestablish blood flow within 6-12 hours of onset of symptoms decreases

A

mortality and morbidity

63
Q

where does ischemic necrosis begin

A

subendothelial area and progresses through the muscle wall

64
Q

Area of injury

A

surrounding area has some blood flow and some cells will recover

65
Q

iIshcemic zone

A

if blood flow is reestablished this area can be salvaged so there will be no cell death

66
Q

Acute inflammatory response can occur within

A

the first 3 days

67
Q

Macrophages remove..

A

necrotic tissue in the inflammatory response

68
Q

Whe is the center of the infarct area soft/weak and can rupture

A

4-7 days post MI

69
Q

In 6-8 weeks, necrotic tissue is replaced wtih

A

scar tissue

70
Q

Anginal pain versus MI pain

A

angina is short lived.

71
Q

12 Lead EKG

A

detects dysrhythmias due to ischemia
provides evidence about a previous MI
identifies pattern changes with ischemia, injury and infarction (ST elevation or depression)
used for STEMI
In Non-stemi patients this may appear normal

72
Q

In a 12-lead EKG, ischemia alters ..

A

myocardial repolarization (T wave changes), no polarization from necrotic tissue (Q Waves)

73
Q

Cardiac Catheterization

A

insert the cath into a vein if viewing the rt heart, or an artery if viewing the left heart and thread into pulmonary capillaries or coronary arteries

Inject dye to visualize obstructions

Can measure pressures and o2 sats

74
Q

what electrolytes should be monitored

A

K and Mg

75
Q

Main way to diagnose a non-ST segment elevation is by

A

assessing cardiac markers (Troponin)

76
Q

what are cardiac markers

A

they are enzymes and muscle proteins that are released from myocardial cells as they die

77
Q

Creatine Kinase (CK): begins to rise, peak and return to normal in…

where is it found

A

rise- 4-8 hours
peak- 12-24 hours
return to normal- 2-4 days

found in the brain, heart and skeletal muscle cells

78
Q

CK-MB (isoenzyme): begins to rise, peak, and return to normal in..

found in

A

rise- 4-8 hours
peak- 12-24 hours
return to normal- 2-3 days

found in heart

79
Q

myoglobin: begins to rise, peak, return to normal

found in

A

rise- 1-2 hours… RISES EARLY
peak-4-8 hours
return to normal- 24-36 hours

found in heart, skeletal muscle

80
Q

Troponin T versus Troponin I

A

Troponin T- rises in 2-6 hours, peaks in 12-24 hours, returns to normal in several weeks

Troponin I- rise in 2-6 hours, peaks in 12-36 hours, returns to normal in 7-10 days

both found in heart muscle and increase in MI

Mary's Tests - Spring 2016 (10 decks)

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