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23 General Pathology > 10/23 - Pathology of the Heart > Flashcards

10/23 - Pathology of the Heart Flashcards

1
Q

what is a mechanical organ that generates pulsatile blood? when does it begin?

A

heart - 3 weeks after fertilization

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2
Q

proper development of heart depends on what

A

network of transcription factors regulated by several signaling pathways

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3
Q

many inherited defects of heart involve what genes

A

genes that encode transcription factors

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4
Q

what are abnormalities of heart or greater vessels that are present at birth

A

congenital heart disease

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5
Q

when does congenital heart disease arise

A

Most arise from faulty embryogenesis during gestational week 3 to 8, when major CV structures form and begin to function

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6
Q

what are anomalies of CHD compatible with live birth

A
  1. septal defects
  2. stenotic lesions
  3. outflow tract abnormalities
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7
Q

what CHD is ‘hole in heart’

A

septal defect (ASD or VSD)

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8
Q

what CHD occurs either at level of valves or entire cardiac chamber (hypoplastic left heart syndrome)

A

stenotic lesions

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9
Q

what CHD has inappropriate routing of greater vessels from ventricles

A

outflow tract anomalies

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10
Q

CHD incidence

A

VSD and ASD detected in 5% of live births (most close spontaneously in first year)

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11
Q

T/F: surgical interventions fail to restore complete normalcy or complications arise from prosthetic materials and devices in CHD

A

TRUE

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12
Q

CHD etiology (how does this happen)

A
  1. Environmental exposure (congenital rubella exposure)
  2. Nutritional factors (folate supplementation reduces risk)
  3. Therapeutic drugs
  4. Gestational DM
  5. Genetic factors
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13
Q

modifiable CHD risk factors

A
  1. dietary deficiency
  2. substance abuse
  3. obesity and diabetes
  4. air pollution
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14
Q

non-modifiable CHD risk factors

A
  1. medications (e.g., anti seizure or anti depressants)
  2. infections (e.g., rubella)
  3. rheumatological disorders (e.g., SLE)
  4. race and genetics
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15
Q

what are the two major categories of CHD structural anomalies

A
  1. shunts
  2. obstruction
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16
Q

what is an abnormal communication between chambers of heart of blood vessels of heart

A

shunts

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17
Q

what happens with a CHD shunt

A

Abnormal channels allow blood to flow down pressure gradients from left (systemic) side to the right side (pulmonary) side of circulation or vice versa

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18
Q

what happens in left to right shunt

A
  1. Pressure higher in left side of heart than in right side of heart
  2. No cyanosis initially
  3. Cyanosis develops when shunt reverses following development of pulmonary hypertension
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19
Q

what happens in right to left shunt

A
  1. Pressure higher in right side of heart than in the left side of the heart
  2. Cyanosis initially since blood is shunted away from lungs (reduced oxygenation)
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20
Q

when do you get cyanosis

A

right to left shunt

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21
Q

what is the most common congenital cardiac malformation first diagnosed in adults

A

atrial septal defect

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22
Q

when is there no symptoms of atrial septal defect in childhood

A

flow is left to right

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23
Q

T/F: pulmonary HT may reverse shunt and produce cyanosis

A

TRUE

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24
Q

what is the most common congenital heart disease (CHD) diagnosed at birth

A

ventricular septal defect (VSD)
*most are small and close spontaneously

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25
Q

are atrial septal defects (ASD) more OR less common in adults

A

MORE common

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26
Q

when does patent ductus arteriosus normally close?

A
  • normally closes shortly after birth (1-2 days)
  • usually identified early on and corrected with medication or surgery
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27
Q

what happens if patent ductus arteriosus is not corrected

A

shunt reverses due to pulmonary hypertension and cyanosis develops

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28
Q

what are congenital defects causing right to left shunt

A
  1. Tetralogy of Fallot
  2. Transposition of great arteries

*both give cyanosis since right to left shunt

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29
Q

what happens in right to left shutns

A

blood diverted from pulmonary circulation to systemic circulation thus reducing oxygenation

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30
Q

when is cyanosis characteristic

A

at or near birth

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31
Q

features of Tetraloy of Fallot

A
  1. pulmonary artery stenosis
  2. right ventricular hypertrophy
  3. overriding aorta
  4. ventriculoseptal defect
  5. may have patent ductus which helps oxygenate the blood (some babies)

know word for word PROVe(P)

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32
Q

what is a congenital heart defect where aorta is positioned directly over ventricular septal defect instead of over left ventricle

A

overriding aorta

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33
Q

what is a birth defect of heart in which the two main arteries carrying blood out of the heart, the pulmonary artery and aorta are switched in position (transposed)

A

transposition of great arteries

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34
Q

what is the second leading cause of congenitol cyanosis

A

transposition of great arteries

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35
Q

what congenital diseases are left to right

A

VSD (Ventricular septal defects)
ASD (Atrial septal defects)
PDA (Patent (persistent) ductus arteriosus)

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36
Q

what congenital diseases are right to left

A

Tetralogy of Fallot
Transposition of great arteries

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37
Q

what is main clinical sign of transposition of great arteries

A

cyanosis

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38
Q

what is CHD causing obstructive lesions

A

coarctation of aorta

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39
Q

what is abnormal narrowing of aortic lumen

A

coarctation of aorta

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40
Q

what does coarctation of aorta result in

A
  1. Higher BP in arms than legs
  2. Weak pulses in the lower extremities with signs and symptoms of intermittent claudication (ischemic leg pain)
  3. Enlarged heart
  4. Dissection or rupture of aorta, which can befatal
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41
Q

9/10 with untreated coarctation don’t survive to what age

A

50 years

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42
Q

what does ischemic heart disease (IHD) result from

A
  1. Atherosclerotic lesions in the epicardial coronary artery
  2. Coronary artery emboli
  3. Coronary vessel inflammation
  4. Coronary vascular spasm
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43
Q

atherosclerotic lesions in epicardial coronary artery leads to what

A

leading to myocardial ischemia (an imbalance between myocardial supply (perfusion) and cardiac demands for oxygenation)

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44
Q

ischemic heart disease could also be called what? why?

A

coronary artery disease (since it is the #1 cause of ischemic heart disease)

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45
Q

what is #1 cause of ischemic heart disease

A

plaques in coronary artery (atherosclerotic lesions in epicardial coronary artery)

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46
Q

what are consequences of IHD

A
  1. angina pectoris (ischemia is not severe to cause infarction but can pose infarction risk)
  2. chronic IHD w/ heart failure
  3. myocardial infarction (MI) (ischedmia can cause frank cardiac necrosis)
  4. sudden cardiac death
47
Q

what is temporary chest pain or discomfort caused by inability of diseased coronary arteries to deliver sufficient oxygen-laden blood to heart muscles

A

angina pectoris

48
Q

angina pectoris is a sign of what

A

increased risk of heart attack

49
Q

what can trigger angina pectoris

A
  1. emotional stress
  2. physical exercise
  3. being exposed to very hot or cold temperatures
  4. smoking
  5. eating a heavy meal
50
Q

symptoms of ___ include:
Pressure or pain in the center of the chest that may radiate to the shoulder, arm, back, neck, and jaws

A

angina pectoris

51
Q

what patients have sensations of having indigestion or gas

A

angina pectoris

52
Q

types of angina pectoris

A
  1. stable angina
  2. prinzmetal
  3. unstable angina
53
Q

where does angina pectoris pain radiate

A

center -> shoulder -> arm -> back -> neck -> jaws

54
Q

stable angina pectoris is associated with what?

A

fixed atherosclerotic narrowing of one or more coronary arteries

55
Q

stable angina pectoris symptoms

A

discomfort in chest descibed as deep, poorly localized pressure, squeezing or burning sensation (like indigestion) but unusually as pain

56
Q

what causes stable angina pectoris

A

physical activity, emotional excitement, or physiological stress

57
Q

how to relieve stable angina pectoris pain

A

rest and/or nitroglycerin or calcium channel blockers

58
Q

what is pain in Prinzmetal angina pectoris

A

anginal pain occuring at rest or awakening patient from sleep

59
Q

what is prinzmetal angina pectoris associated with

A

Usually associated with coronary artery
spasm often adjacent to a site of
atherosclerotic plaque

60
Q

mechanism that causes prinzmetal angina pectoris

A

poorly understood

61
Q

what is unstable angina pectoris

A

increased frequency of angina episodes

62
Q

what precipitates unstable angina pectoris

A

progressively less exertion (less emotional trauma like not eating as much)

63
Q

what is unstable angina pectoris pain described as

A

intense pain

64
Q

what is a more intense pain that last longer than “stable angina”? how long does it last?

A

unstable angina pectoris >20 minutes

65
Q

what is induced by acute plaque change w/ superimposed partial thrombosis or vasospasm or both

A

unstable angina pectoris

66
Q

treatment of angina pectoris

A

nicroglycerin (oral medication classified as vasodilater)

67
Q

when do patients take nitroglycerin

A

10 mintues before begin doing activity that will trigger symptoms (of angina pectoris)

68
Q

what is irreversible necrosis of heart muscle (secondary to prolonged ischemia)

A

myocardial infarction

69
Q

etiology of myocardial infarction

A

associated with coronary artery disease

70
Q

common symptoms of myocardial infarction

A
  1. chest discomfort
  2. shortness of breath
  3. discomfort in the upper body
71
Q

when does myocardial NECROSIS begin after infarction?

A

Myocardial necrosis begins within 20-30 minutes of infarction and reaching full size within 3 - 6 hours

72
Q

where does myocardial infarction begin then extend toward?

A

begin: subendocardium
extend toward: epicardium

73
Q

what can limit size of infarct during myocardial infarction

A

thrombolytic agents (tissue plasminogen activator t-PA) may limit size of infarct during time frame

74
Q

what are thrombolytic drugs

A
  1. eminase
  2. retavase
  3. streptase activase
75
Q

is ASPIRIN thromoblytic? explain

A

NO! but may limit clot size- antiplatelet adhesion drug

76
Q

what are clinical complications of acute MI

A
  1. sudden death
  2. cardiogenic shock
  3. cardiac arrythmias
  4. cardiac tamponade due to cardiac rupture
77
Q

what are anatomic complications of MI?

A
  1. Valve insufficiency due to infarcted papillary muscle
  2. Ventricular aneurysms
  3. Mural thrombus giving rise to systemic arterial emboli
  4. Cardiac tamponade due to rupture of the infarcted area of the heart
78
Q

what results due to infarcted papillary muscles (doors are bad)

A

valve insufficiency

79
Q

what giver rise to systemic arterial emoboli?

A

mural thrombus (thrombus in wall of heart)

80
Q

what results due to the rupture of infarcted area of heart

A

cardiac tamponade

81
Q

myocardial infarction treatmetn

A
  1. reperfusion therapy
  2. nitrates
  3. beta-blockers
  4. lipid-lowering treatment (statins)
  5. antithrombotic therapy
82
Q

what is indicated in all patients with symptoms of ischemia of less than 12 hours duration

A

reperfusion therapy

83
Q

what are the more effect nitrates? what does it do?

A

IV nitrates more effective than sublingual nitrates (giving rise to nitric oxygen, which caused vasocilation - nitroglycerin)

84
Q

what doe beta blockers do? example?

A

Beta-blockers (reduces myocardial workload, and thus oxygen demand,, via reduction in heart rate and BP) (olol’s- atenolol, bisoprolol)

85
Q

most common cause of sudden cardiac death

A

ischemic heart disease (sudden death may be initial manifestation of ischemic heart disease

86
Q

what are other causes of sudden cardiac death

A

(1 = ischemic heart disease)
2. Arrhythmias not caused by ischemia
3. Acute cor pulmonale due to massive pulmonary artery thromboembolism

87
Q

what are abonormalities in myocardial conduction that are sustained or sporadic (paroxysmal)

A

arrythmias

88
Q

how are aberrant rhythmias initiated

A

Aberrant rhythms can be initiated anywhere in the conduction system (from SA down to the level of an individual myocyte)

89
Q

in structurally normal heart, what causes arrythmias

A

mutations in ion channels that cause aberrant repolarization and depolarization

90
Q

what is a consequence of increase demands placed on heart by HT

A

pressure overload and ventricular hypertrophy

91
Q

what causes hypertensive heart disease? leads to what?

A

chronically elevated BP; leading cause of illness and death

92
Q

classic example of HT heart disease

A

left ventricular hypertrophy (LVH)

93
Q

progression from HT to LVH is important step on pathway toward what

A

heart failure

94
Q

is HT heart disease chronic or acute?

A

EITHER OR

95
Q

sign and symptoms of HT Heart Disease

A
  1. Shortness of breath with activity or when lying down
  2. Persistent cough or wheezing with white or pink blood-tinged mucus
  3. Rapid or irregular heartbeat
  4. Fatigue and weakness
  5. Reduced ability to exercise
  6. Swelling in the legs, ankles and feet
  7. Swelling of the belly area (abdomen)
  8. Rapid weight gain
96
Q

HT heart disease treatment

A

Individuals are treated with drug therapy that typically includes diuretics and beta-blockers

97
Q

patients with HT heart disease are advised to do what

A
  1. Reduce salt and alcohol in the diet
  2. Abstain from smoking
  3. Lose weight
  4. Exercise regularly
98
Q

what is most prevalent heart valve disorder in developed countries

A

calcific aortic stenosis

99
Q

what is characterized by:

Progressive fibro-calcific remodeling and thickening of the aortic valve leaflets that evolve over years to cause severe obstruction to cardiac outflow; age-related degeneration

A

calcific aortic stenosis

100
Q

what does calcific aortic stenosis result in

A

LEFT ventricular hypertrophy and decreased aortic outflow leads to myocardial ischemia

101
Q

when do patients with calcific aortic stenosis die

A

within 3-4 years unless treated

102
Q

what are new calcific aortic stenosis treatment options

A

balloon valvuloplasty
transcatheter valve replacement

103
Q

what causes mitral regurgitation (Back flow)

A

mitral valve prolapse

104
Q

is mitral valve prolapse common? are most cases sporadic?

A

common (3-5% of population)!
most cases are sporadic!

105
Q

what syndrome could see mitral valve prolapse

A

Marfan syndrome

106
Q

people with mitral valve prolapse are prone to what

A

infective endocarditis, arrythmias and emobli from left atrium

107
Q

T/F: antibiotic prohylaxis is needed prior to dental procedures unless other factors present

A

FALSE!!! no longer recommended!

108
Q

what causes acute, multisystem, immunologically-mediated inflammatory disease usually following group A streptococcal pharyngitis after an interval of a few weeks

A

rheumatic fever causing valve disease

109
Q

is pharyngitis severity related to risk of developing rheumatic fever?

A

no - not related

110
Q

long term consequence of rheumatic fever is related to what

A

induction of permanent cardiac damage

111
Q

rheumatic carditis typically occurs as what

A

pancarditis - involves pericardium, myocardium, and endocardium

112
Q

what is an infection caused by bacteria that enter the bloodstream and settle in the heart lining, a heart valve or a blood vessel

A

infective endocarditis

113
Q

is infective endocarditis common?

A

It is uncommon, but people with some heart conditions have a greater risk of developing it

114
Q

what is an infection of cardiac valves of mural surfaces of endocardium?

A

infective endocarditis

23 General Pathology (24 decks)

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