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Pathophysiology > Final Exam- 4 Cardiovascular > Flashcards

Final Exam- 4 Cardiovascular Flashcards

1
Q

chronic thickening/hardening of blood vessel walls

A

arteriosclerosis

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2
Q

What is the mechanism process of the arteriosclerosis

A

damage to tunica intima
smooth muscle cells and collagen move into it
now becomes stiffened/thickened

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3
Q

disease where walls thicken due to plaque development

A

atherosclerosis

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4
Q

What is the mechanism process of atherosclerosis

A

accumulated LDL macrophages are in artery walls
lesions form

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5
Q

What is the leading cause coronary artery disease and cerebrovascular disease

A

atherosclerosis

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6
Q

Causes of atherosclerosis

A

high fat diet, diabetes, hypertension

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7
Q

How do you classify hypertension

A

elevated BP 140+/90+

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8
Q

What is the most significant cause of organ damage

A

hypertension

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9
Q

What are hypertension risk factors

A

female 70+ years
male 55+ years
black
obesity
cigarettes
alcohol abuse

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10
Q

What are the mechanisms of hypertension

A

increased cardiac output (increases HR & stroke volume)
increased peripheral resistance (increases blood viscosity & vasoconstricts)

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11
Q

Manifestations of hypertension

A

no symptoms early on
angina pectoris
severe headache
vision changes

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12
Q

hypertension due to genetics, overactive sympathetic nervous system, and inflammation

A

primary hypertension

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13
Q

hypertension due to a systemic disease that increases peripheral vascular resistance or/and cardiac output

A

secondary hypertension

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14
Q

hypertension that rapidly progresses, diastolic over 140, and possibility of encephalopathy

A

malignant hypertension crisis

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15
Q

condition where the systolic/diastolic decreases by 20/10 when standing

A

orthostatic postural hypertension

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16
Q

What is the mechanism process of orthostatic hypertension

A

cardiac output overly decreases due to reduced venous return or reduced sympathetic adrenergic vasoconstriction

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17
Q

Manifestations of orthostatic postural hypertension

A

lightheadedness, dizziness, blurry vision

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18
Q

Difference between primary and secondary orthostatic postural hypotension

A

volume depletion (POTS) vs cardiac valvular disease

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19
Q

equation for cardiac output

A

stroke volume x HR

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20
Q

What is stroke volume

A

available blood in vessels

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21
Q

What is the relationship between heart rate and volume

A

heart beats faster if volume is lost (vice versa)

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22
Q

condition where local dilation or out pouching of vessel wall occurs

A

aneurysm

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23
Q

Causes of an aneurysm

A

atherosclerosis, hypertension, collagen/elastin disorders

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24
Q

What is the mechanism process of an aneurysm

A

forms due to damage that weakens the artery walls

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25
Q

Type of aneurysm that involves all three arterial wall layers

A

true aneurysm

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26
Q

Type of aneurysm where an extravascular hematoma moves to intravascular space (blood pores in)

A

False aneurysm

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27
Q

Where do false aneurysms typically occur

A

thoracic or abdominal aorta

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28
Q

What is the mechanism process of arterial thrombus formation

A

atherosclerosis damges tunica intima –> plaque cap ruptures –> coagulation starts –> blood clot forms around ruptured plaque cap

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29
Q

condition for when a blood clot that stays attached to artery wall

A

arterial thrombus

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30
Q

What are possible complications of arterial thrombus

A

grow large enough to block artery= tissue ischemia
detaches from vessel wall & travels = tissue ischemia

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31
Q

condition where bolus of matter moves in blood stream but eventually gets stuck and occludes blood flow leading to ischemia

A

embolism

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32
Q

What is the cause of an embolism

A

starts in heart–>endocarditis or dysrhythmia (A-fib)

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33
Q

Type of embolism where a dislodged thrombus leads to an obstructed vessel

A

thromboembolism

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34
Q

Type of embolism where room air enters the body circulation

A

air embolism

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35
Q

Type of embolism where amniotic fluid gets forced into mom’s bloodstream

A

amniotic fluid

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36
Q

Type of embolism resulting from infectious endocarditis

A

bacterial embolism

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37
Q

Type of embolism due to a trauma on long bones leading to formation of fat globs in the blood

A

fat embolism

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38
Q

Type of embolism when something enters the blood during a trauma or from an IV line

A

Foreign matter embolism

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39
Q

Manifestations of peripheral artery disease

A

intermittent claudication (pain on back of legs when walking)
loss of pulses
skin color changes

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40
Q

Condition where there of episodes of vasospasming in the arterioles of the fingers

A

Raynaud’s disease

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41
Q

condition where there is vasospasming in the finger arterioles due to a systemic disease, malignancy, long term cold exposure, or vibrating machinery

A

Raynaud’s phenomenon

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42
Q

What are risk factors for Raynaud’s disease

A

young and female
brief cold exposure
emotional stress

43
Q

Manifestations of Raynaud’s disease/phenomenon

A

change in skin color on skin (not symmetrical)
paresthesias

44
Q

VLDL; what it makes up

A

very low density lipoproteins
triglycerides + lipoproteins

45
Q

LDL (definition/function)

A

cholesterol + carrier protein
delivers cholesterol to tissues

46
Q

HDL (definition/function)

A

phospholipids + carrier protein
returns excess cholesterol to liver
eliminated as bile or turned into cholesterol containing steroids

47
Q

What is Virchow’s triad

A

increases risk of deep vein thrombosis
1) venous stasis
2) venous epithelial damage
3) hyper coagulable state

48
Q

What is the severe risk of deep vein thrombosis

A

can detach and become a pulmonary emboli

49
Q

term for the degree of ventricular stretch before the next contraction

A

preload

50
Q

term for resistance the heart overcomes to eject blood during systole

A

afterload

51
Q

What are some factors affecting preload

A

length of diastole (longer=increased stretch)
increased venous return= increases stretch
condition of the myocardium affects the ability to stretch
condition of kidneys (failure can lead to water retention)

52
Q

What is the #1 source of increased after load

A

hypertension

53
Q

What does increase after load lead to

A

overworking of ventricle
ventricular remodeling

54
Q

Characteristics of NSTEMI myocardial infarction

A

non ST elevation (partial occlusion and less severe)

55
Q

Characteristics of STEMI myocardial infarction

A

ST elevation (no blood flow)

56
Q

type of angina with predictable chest pain but resolves with rest

A

Stable angina

57
Q

type of chest pain the doesn’t resolve with rest; can usually resolve with meds or percutaneous intervention

A

unstable angina

58
Q

type of angina that occurs unpredictably at night; related to sympathetic nervous system hyperactivity

A

prinzmetal angina

59
Q

What are manifestations of myocardial infarction

A

radiating chest pain (arm/back)
EKG changes (look at ST)
elevated troponin level
diaphoresis
confusion (w/ STEMI)
feeling of dying

60
Q

functional change after myocardial infarction where there is temporary loss of contractile function hours to days once perfusion is restored

A

myocardial stunning

61
Q

structural change after myocardial infarction where persistently ischemic tissue has metabolic changes to prolong survival

A

hibernating myocardium

62
Q

functional change after myocardial infarction where tissue changes occur in the myocardium as a result of inflammation; becomes not as effective for pumping

A

myocardial remodeling

63
Q

How does Angiotensin II is affected by myocardial infarction

A

body senses a drop in cardiac output from the MI
produces angiotensin II

64
Q

Systemic effects of Angiotensin II after MI

A

peripheral vasoconstriction
fluid retention
work of myocardial increases–> contractility is overworked

65
Q

Local effects of Angiotensin II after MI

A

growth factor in heart leads to release of catecholamine
leads to coronary artery spasms

66
Q

How angiotensin II after an MI causes myocardial remodeling

A

tissue no longer able to pump effectively (loss of contractile function); change in functionality

67
Q

Complications of MI

A

death
arrhythmia
rupture
tamponade
heart failure
valve disease
aneurysm of ventricle
Dressler’s syndrome
embolism
reoccurrence

68
Q

What is cardiac tamponade

A

fluid accumulates in the sac around the heart–> difficulty pumping

69
Q

Dressler’s syndrome

A

pericarditis from the MI
vessels leak fluid
inflammation from WBCs

70
Q

acute or chronic inflammation of pericardium

A

pericarditis

71
Q

causes of pericarditis

A

MI, infection, radiation therapy

72
Q

What is the mechanism process of pericarditis

A

cardiac tamponade leaks fluid between inner & outer layers

73
Q

Manifestations of pericarditis

A

precordial pain
pericardial friction rub at 2nd-4th intercostal spaces
ST elevate/T wave flattening
pericardial effusion (fluid collection)

74
Q

diverse group of diseases that affects myocardium leading to remodeling

A

cardiomyopathies

75
Q

type of cardiomyopathy that leads to dilation of heart

A

dilated cardiomyopathy

76
Q

Manifestations of dilated cardiomyopathy

A

dyspnea, palpitations, dizziness

77
Q

Type of cardiomyopathy that thickens myocardium

A

hypertrophic cardiomyopathy

78
Q

Manifestations of hypertrophic cardiomyopathy

A

angina
dyspnea
fatigue

79
Q

type of cardiomyopathy where myocardium becomes rigid/noncompliant related to autoimmune disorders

A

restrict myocardium

80
Q

What is the mechanism process of restrictive cardiomyopathy

A

impedes ventricular filling –> raises filling pressure –> R. sided heart failure

81
Q

a congenital or acquired dysfunction of one of four heart valves

A

valvular dysfunction

82
Q

Valvular stenosis

A

valve constricted/narrowed leads to blood backing up in chambers; hardening of valves

83
Q

Valvular regurgitation

A

valve doesn’t shut completely (incompetence)
too much blood moves forward during systole
blood moves backward during diastole (back in atria)

84
Q

Where can valvular stenosis occur

A

aortic and mitral

85
Q

Where can valvular regurgitation occur

A

aortic
mitral
tricuspid

86
Q

Manifestations of valvular disorders

A

characteristic heart sounds (extra sounds)
cardiac murmurs

87
Q

How does rheumatic fever occur

A

delayed immune response to a strep infection

88
Q

What is the diagnostic test for rheumatic fever

A

transesophageal echocardiogram (TEE) to better visualize heart valves

89
Q

Term for infectious lesion on the heart valves

A

vegetations

90
Q

What are risk factors for infective endocarditis

A

IV drug use
rheumatic fever

91
Q

What are the common pathogens for infective endocarditis

A

staph aureus
strep

92
Q

Manifestations of infective endocarditis

A

positive blood cultures even with antibiotics
septic emboli (lesions on palms & soles)

93
Q

condition for structural/functional disorders that impairs ventricle to fill or eject blood; heart can’t pump enough for metabolic demands

A

heart failure

94
Q

heart failure that back into SVC/IVC
increased peripheral venous pressure
enlarged liver & spleen
distended jugular veins
dependent edema

A

right sided heart failure

95
Q

What does cor pulmonale

A

right sided heart failure related to the lungs

96
Q

heart failure that increases pulmonary pressure
backs into lungs
dyspnea, cough of frothy sputum, orthopnea

A

left sided heart failure

97
Q

Normal electrical pathway in heart

A

SA node –> AV node –> Bundle of HIS/Perkinje

98
Q

Process of depolarization

A

Na+ ions rush into cells= contraction

99
Q

Process of repolarization

A

Na+ closes and K channel opens
K ions leave cells
cells now relax= negative charge

100
Q

term for small changes in normal heart rhythm leading to extra or skipped beats

A

ectopy

101
Q

abnormal cardiac rhythms

A

dysrhythmia

102
Q

What occurs in the P wave

A

atrial depolarization

103
Q

What occurs in QRS complex

A

ventricular depolarization
atrial repolarization

104
Q

What occurs in T wave

A

ventricular repolarization

Pathophysiology (6 decks)

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