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CPR2 Exam 1 > Cardiac Pathology Part 1 - Dr. Hillard > Flashcards

Cardiac Pathology Part 1 - Dr. Hillard Flashcards

1
Q

leading cause of death in US

A

Coronary Artery Disease

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2
Q

Ischemic Heart Disease (Coronary Artery Disease)

A

Age, male, HTN, hyperlipidemia, DM, smoking

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3
Q

CAD most common cause

A

atherosclerosis

coronary artery emboli, vasculitis, and vessel spasms can also cause it

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4
Q

4 most common sites of coronary artery disease

A
  1. LAD (left anterior descending) = the widow maker
  2. Right coronary artery
  3. Left circumflex
  4. Left coronary artery
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5
Q

how to determine the dominance of a heart

A

the blood supply to the posterior descending artery (most are Right dominance)

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6
Q

left dominated heart what artery supplies the posterior descending artery

A

Circumflex artery

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7
Q

when id knowing dominance of heart important

A
  1. probable site of occlusion in MI
  2. planning coronary artery bypass grafting
  3. in irregular beats or skipping beats = AV block (AV node is supplied by PDA)
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8
Q

MI Sx seen

A
  1. crushing stabbing CP radiating to neck, jaw, arm
  2. SOB : congestion pulmonary
  3. sweating, N/V (usually posterior/ inferior infarct)
  4. 0.25 no sx (usually DM neuropathy)
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9
Q

serum marker for MI

A

Troponin*
CK-MB(creatine kinase-MB)
myoglobin
= regulate Ca mediated contraction of myocardiocytes

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10
Q

irreversible cell injury time

A

20min- 40min = necrosis

microvascular injury happens over 1hr

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11
Q

MI time for loss of function of heart from ATP depletion

A

1-2min

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12
Q

time for neurologic unlikely recovery

A

5min-7min, if 10min severe irreversible damage

during surgery cooling the heart helps prevent cell death as fast

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13
Q

CK-MB
CK-MM
CM-BB

A
  1. MB = cardiac muscle cells
  2. MM = muscles
  3. BB = brain and lung
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14
Q

first biomarker that peaks first

A

myoglobin

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15
Q

CKMB, cTnT and cTnl time to elevate, peak at what time, normalize when

A
  1. 3hr-12hr**
  2. 24hr
  3. CK-MB = 48hr-72hr*
    cTnl, cTnT = >5days
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16
Q

LAD occlusion is what part of the heart

A

APEX, Anterior left ventricle and anterior 2/3 septum

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17
Q

Left circumflex occlusion what part of heart

A

Lateral LEFT VENTRICLE

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18
Q

Right Coronary Artery occlusion what part of the heart

A

right ventricle and left ventricle posterior heart

- posterior 1/3 septum

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19
Q

left dominant heart with circumflex artery occlusion where in the heart

A

the left ventricle lateral, and posterior

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20
Q

2 things that can cause subendocardial infarct

A
  1. reperfusion of transmural infarct (restoring BF fast, a thrombus is dislodged) regional
  2. global hypotension (shock, coronary stenosis)
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21
Q

multifocal microinfarction

A

many small infarcts within smaller intramural vessels

= seen in emboilic disease or drugs like cocaine

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22
Q

how does MI infarction spread

A

from inside =heart to outside (except the thin internal zone that gets perfused by blood passively)

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23
Q

what do you see in histology from 0min-30min

A

myofibrils relaxed, glycogen loss, M swelling

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24
Q

what do you see in histology from 30min - 4hr

A
  • slight waviness of fibers at the border (from sarcolemma disruption)
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25
Q

what do you see in histology from 4hr - 12hr

A
  • very early coagulation necrosis and edema
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26
Q

what do you see in histology from 12hr - 24hr

A
  • increased coagulation necroisis and very developed at 24hr
  • shrink Nuclei (pyknotic)
  • darkly mottled heart (contraction band necrosis)
  • myocytes hypereosinophilic
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27
Q

what do you see in histology from 1day-3days

A
  • a lot of N

- nuclei loss = yellow tan infarct with surrounding mottling

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28
Q

what do you see in histology from 3days - 1 week

A
  • M to phagocytose dead myofibers
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29
Q

what do you see in histology from 1 week - 1.5 weeks

A
  • granulation

- collagen deposition (closer to 2 weeks)

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30
Q

what do you see in histology from 2weeks

A

scar tissue

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31
Q

what do you see in histology from after 2 months

A

scarring is complete and dense scar

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32
Q

when is it easy to see if an MI has happened on gross anatomy and also how to see it

A
  • after 12hrs
  • stain with lactate dehydrogenase stain (triphenyltetrazolium chloride) = this lactate leaks out from dead myocytes and staining turns everything red except scar and necrosis
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33
Q

reperfusion injury

A

when there is irreversible damage to myocytes :

  1. cell membrane disrupted with reperfusion causing influx a Ca = contraction
  2. contraction band necrosis
  3. hemorrhagic looking infarct
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34
Q

moltting

A

uneven patches of color

seen after 1 day

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35
Q

1day to 3days gross anatomy look

A
  • yellow infarct, necrosis hyperemic border
  • many N
  • coagulative necrosis = loss of nuclei
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36
Q

after 2 weeks heart gross anatomy

A

-collagen increases more and more
-fibroblasts
scar is maturing and fully mature at 2mos
- loss of myocytes, inflammation, granulation

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37
Q

complications of an MI : early (within 24hrs)

A
  1. arrhythmias fatal

2. contractile dysfunction from cardio muscle death(can lead to cardiogenic shock)

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38
Q

complications of an MI : intermediate (2-4 days to 2 weeks)

A
  1. rupture of free wall, septum, or papillary muscles
  2. acute pericarditis (inflammation of pericardium) from inflammation N—-> M
  3. acute fibrinous pericarditis + serofibrinous pericarditis
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39
Q

acute fibrinous pericarditis

A

from inflammation a layer of fibrin develops over pericardial surface

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40
Q

serofibrinous pericarditis

A

fibrinous depbri and fluid collection in pericardium

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41
Q

complications of an MI : late (after 2 weeks)

A
  1. immune pericarditis = Dressler syndrome
  2. heart remodeling (fibosis) myocytes are separated in space :
    = aneurysm formation
    = arrhythmias fatal
    = heart failure
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42
Q

most common cause of death from MI

A

fatal arrhythmia from within 1hr onset

= usually Vfib

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43
Q

2nd most common cause of death form MI

A

cardiogenic shock, also within 1hr to even 1day (from contractile dysfunciton = failure to pump) when cells die

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44
Q

intermediate effect of MI : rupture of wall

1. free wall rupture what happens

A

usually when wall weakens form necrosis and inflammation
1 .blood accumulation in pericardial space = prevents heart to open up and fill (DIASTOLE)
= ACUTE PERICARDIAL TAMPONADE —-> hemodynamic collapse

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45
Q

intermediate effect of MI : rupture of wall

2. septal rupture

A
  1. ventricular septal defect (usually in elderly with lower muscle mass), usually during anterior wall MI
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46
Q

intermediate effect of MI : rupture of wall

3. papillary muscle rupture

A
  1. valve incompetence and post infarct regurgitation
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47
Q

PE of pericarditis

A

pain with inspiration

pericardial friction rub heard on auscultation

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48
Q

main thing happening in intermediate MI complication

A
  1. myocardial rupture 2-4days post MI

2. AND acute fibrous or serofibrous pericarditis happening at the same time frame

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49
Q

Dressler syndrome what is it and SX (late so after 2 weeks past MI)

A
  1. fibrous pericarditis from immune reaction to myocardial proteins in the blood from previous MI = anti-heart AB causing inflammation to pericardium
  2. Fever, pleuritic pain, pericardial effusion
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50
Q

Ventricular aneurism + more arrhythmias (other late post 2 weeks MI) happen how

A

from remodeling and scarring (when conducting system is disrupted =arhythmias)

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50
Q

Ventricular aneurism + more arrhythmias (other late post 2 weeks MI) happen how

A

from remodeling and scarring (when conducting system is disrupted =arhythmias)

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51
Q

how to see aneurysm in ventricle

A

CT or angiogram

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52
Q

besides Dressler syndrome and ventricular aneurysm + arrhythmia , what is the last 2 types of late MI (post 2 weeks) complication that can happen

A
  1. Congestive heart Failure

2. Chronic Ischemic Heart Disease —-> CHF

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53
Q

Chronic Ischemic Heart Disease 3 causes

A
  1. healing infarct with fibrosis
  2. V remodeling
  3. hypertrophy
    = fatal arrhymia
    = failure heart , weakened
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54
Q

angina pectoris is what

A

recurrent CP from Myocardial Ischemia (not enough to cause MI)
= can happen with 70% stenosis of coronary A

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55
Q

angina pectoris is what

A

recurrent CP from Myocardial Ischemia = heart does not get enough O2 (not enough to cause MI)
= can happen with 70% stenosis of coronary A

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56
Q

pain from angina is caused by what

A

bradykinin and adenosine released from low O2

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57
Q

2 things that can cause a silent angina

A

DM neuropathy or previous MI

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58
Q

Stable angina
what
improves with
worsens with

A

stenotic occlusion of coronary A

  1. substernal P, sqeezing, burning
  2. Relieved by rest or vasodilators
  3. worse with physical activity, stress (not enough O2 for PE, only enough O2 at rest with the partial occlusion)
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59
Q

Prinzmetal Variant angina
what is it
improves with
worsens with

A

Episodic coronary A spasm
= relieved by vasodilators
= has no dependence on physical activity, BP, or HR

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60
Q

how to test for stable angina

A

exercise stress test, use EKG or echocardiogram and looks for changes during exercise

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61
Q

when does the Prinzmetal variant angina usually happens when, 3 complications that can occur, how often

A 
at rest
1. coronary atherosclerotic disease 
2. V arrhythmia
3. sudden death
(3mo-6mo interval attacks)
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62
Q

vasodilator

A

nitrates

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63
Q

unstable angina

what is it, 2 causes of it

A
  1. Crescendoing pattern = increase severe and duration of pain
    - rupture of plaque , partial non-occlusive thrombus (rest + exercise)**
    - progressive mechanical obstruction (Exercise)**
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64
Q

NSTEMI and STEMI difference in what happens

A
  1. plaque rupture and partial thrombus occlusion, subendocardial infarct
  2. complete occlusion of BV lumen= transmural injury and myocardial infarct
65
Q

NSTEMI and STEMI difference in EKG

A 
1. 
= normal
= inverted T wave
= ST depression 
(same 3 seen in unstable angina)
2.
= hyperacute T wave
= ST elevation
66
Q

unstable angina vs NSTEMI

A

troponin levels elevated only in NSTEMI (cardiomyocytes dying)

67
Q

within 0min -3 hrs what should you do if pt comes with SOB, crushing, stabbing, squeezing CP, radiating to jaw

A

assume STEMI transmural acute MI even with no troponin levels (this takes at least 3hrs to elevate)

68
Q

motor vehicle trauma can cause what 3 heart contusion injuries

A
  1. subendocardial contusion
  2. subepithelial contusion
  3. Transmural contusion —> rupture of wall —-> pericardial blood tamponade = hypotension and death if not fixed
69
Q

motor vehicle trauma other injuries to heart

A
  1. aorta torsion , bending, shearing stress
70
Q

where does the aorta usually tear or bend from MV trauma

A

weak point where it is tethered to the pulmonary artery by LIG ARTERIOSUM
= can cause blood into the adventitia
= life threatening hemorrhage

71
Q

2 most common casues of death from MV accident

A
  1. head trauma
  2. aortic tear or torsion
    (same happens in fall from height)
72
Q

average bpm of SA and AV node

A

SA : 60 -100

AV : 40 - 60 if SA does not work

73
Q

SA node location

A

junction of SVC and atrial appendage

= connected to parasympa and sympa nerves

74
Q

bundle of His location and other name

A

AV bundle

upper V rigth under AV node —–> Purkinje fibers

75
Q

most common cause of arrhythmias **

A

Ischemic heart disease (MI can lead to Vfib) both from early myocyte death and late fibrosis

76
Q

other causes of arrhythmias

A
  1. cardiomyopathies : hypertrophic cardiomyopathy, dialted cardiomyopathy, and restrictive cardiomyopathy
77
Q

restrictive cardiomyopathy

A

infiltrative process such as amyloidosis and sarcodosis

78
Q

reason arrhythmia happens

A

conduction problem, usually from increased spacing between myocytes and then first

79
Q

sick sinus syndrome

A

SA node damage = bradycardia (CHF, Infiltration like sarcodosis and amyloidosis, inflammation like RH disease or infection)
= type of arrhythmia

80
Q

Atrial Fibrillation what is it and what is a complication

A

myocytes depolarize independently and sporadically (atrial dilation) with variable AV node transmission
=irregular HR and beats
= can cause thrombus formation and thromboebolism
= a type of arrhythmia

81
Q

Heart Block

A 
dysfunctional AV node
3 degrees for this
1. prolonger PR 
2. intermittent TR
3. X TR, failure
82
Q

atrial fib 2 causes

A
  1. abnormal firing of SA and conduction in sick sinus syndrome
  2. artrial cavity dilation as myocytes get spaced out (Left V hypertrophy and mitral valve disease = overload and P)
83
Q

thrombus in LA can cause what

A

obstruction of BV in head to CNS

84
Q

hereditary channelopathies

A

inherited defect in ion channels in myocytes = arrhythmia

= LONG QT SYNDROME

84
Q

hereditary channelopathies

A

inherited defect in ion channels in myocytes = arrhythmia

= LONG QT SYNDROME

85
Q

long QT syndrome means

A

increased ventricular depolarization to repolarization

86
Q

long QT syndrome can lead to what

A

ventricular tachy = TORSADES DE POINTES which causes fatal arrhythmias usually during exercise
= from abnormal Na and K channels
= typical pt : strong swimmer drowning unexpectedly from unknown arrhythmia, can happen from low K+ or Ca+ diet

87
Q

TORSADES DE POINTES

A

which causes fatal arrhythmias usually during exercise
= from abnormal Na and K channels
= typical pt : strong swimmer drowning unexpectedly from unknown arrhythmia, can happen from low K+ or Ca+ diet

88
Q

sudden cardiac death most common cause from what

A

coronary artery disease (Stenosis in artery) from ischemia inducing arrhythmia (Vfib or asystole)

89
Q

sudden cardiac death is what and most common causes of it in younger pts

A

no previous sx or death within 24hrs

  1. cocaine and methamphetamines
  2. abnormalities
  3. hypertrophic or dilated heart conditions
  4. myocarditis
  5. mitral valve prolapse + chordae tendineae rupture
90
Q

pathway of blood in the heart

A
  1. SVC + IVC
  2. RA —-> Tricuspid valve
  3. RV —-> Pulmonary valve
  4. Pulmonary A
  5. Lung
  6. Pulmonary Vein
  7. LA —-> mitral valve
  8. LV —-> aortic valve
  9. body through aorta
91
Q

heart changes during HTN

A

heart has to pump harder due to increased peripheral P

= LV hypertrophy

92
Q

LV hypertrophy problems

A
  1. unlike during exercise hypertrophy (with adds capillaries and BS) , no added BS is added = can lead to increased O2 demand and ischemia —-> systolic dysfunction —-> systolic HF (cant pump blood out from heart)
  2. stiff muscle = cant completly relax and lower cavity space —-> Diastolic HF
93
Q

systolic dysfunction

A

cant pump adequately based on peripheral P

= increased O2 demand

94
Q

diastolic dysfunction

A

inability to relax

95
Q

what causes LV hypertrophy

A
  1. HTN

2. stenosis upstream from LV (Aortic stenosis)

96
Q

Dilated heart dysfunction is what

A 
dilated cardiomyopathy
= causes VOLUME OVERLOAD
= walls are dilated and overstretched and weak
= systole dysfunction 
= can cause concentric hypertrophy****
97
Q

dilated cardiomyopathy causes

A 
= excessive alcohol 
= myocarditis
= drugs 
= FE overload
= hereditary and seen during delivery
98
Q

dilated cardiomyopathy causes

A 
= excessive alcohol 
= myocarditis
= drugs 
= FE overload
= hereditary and seen during delivery
99
Q

concentric hypertrophy on LV is seen when

A

HTN

aortic stenosis due to overload happening

100
Q

dilation of ventricle is seen when

A

dilated cardiomyopathies with overload

101
Q

hormone release when atrium is stretched

A

ANP : decreases BP and B volume

102
Q

Congestive Heart Failure is what and what happens

A

pump failure –> not enough O2 delivery (common end stage disease)

  1. X fill ventricles, too stiff (hypertrophy)
  2. X cant contract ventricles (dilated cardiomyopathy)
103
Q

most common type to heart failure

A

LEFT sided = systolic failure and diastolic failure

104
Q

Systolic failure 5 causes

A
  1. Ischemic HD (from hypertrophy) *
  2. HTN *
    3 .Aortic Stenosis *
  3. Dilated cardiomyopathy
  4. regurgitation
    = lower EJECTION FRACTION
105
Q

Diastolic failure 4 causes

A
  1. HTN *
  2. Aortic Stenosis *
  3. Hypertrophic cardiomyopathy
  4. Restrictive cardiomyopathy
    = Normal Ejection fraction
106
Q

2 causes of right sided heart failure

A
  1. left sided induced most common

2. cor pulmonale (lung disease or dysfunction)

107
Q

Left sided CHF sx

A
  1. pulmonary congestion or edema (crackles, sob, wheezing, cough, RR high)
  2. low tissue perfusion
  3. Paroxysmal Nocturnal Dyspnea
  4. orthopnea : dyspnea when laying flat
  5. increased HR
108
Q

3 most common causes of left sided CHF

A
  1. ischemia (including MI)
  2. HTN
  3. Left sided valve problem
109
Q

left sided CHF can eventually cause

A

atrial dilation = atrial fibrillation

which can cause even more loss of pumping and low blood to brain causing confusion, cerebral injury, coma

110
Q

low pumping on left side can lead to

A
  1. cerebral damage : confusion, coma, restlessness

2. azotemia : high cr and urea nitrogen in blood from low BF to kidney

111
Q

left sided CHF imaging

A

CXR
= Kerley B lines (edema in lungs show these parallel lines)
= red blood cells in avleoli —-> M hemosiderin-laden filled (dark brown pigment)

112
Q

right sided CHF most common lung cause

A

parenchymal lung disease

113
Q

right sided CHF signs

A
  1. liver / spleen congestion : hepatosplenomegaly
  2. ascites
  3. distended jugular veins
  4. peritoneal/ pericardial. pleural effusion
  5. leg edema
  6. exertional dyspnea
114
Q

liver in right sided CHF

A

nutmeg liver

if chronic and passive congestion (hemorrhage and necrosis of central vein)

115
Q

2 things that increase the pressure in the lungs

A
  1. emphysema

2. thromboemboli

116
Q

pericardial effusion is what

A

more then 50ml fluid in the pericardium

can accumulate chronically in CHF (serous effusion) or acutely

117
Q

chronic pericardial effusion sx

A

asymptomatic except abnormal heart shadow on cxr (before 500ml)

118
Q

acute pericardial effusion sx

A

within 1 week gets to 200-300ml
= hypotension, death
= cardiac tamponade

119
Q

cause of acute pericardial effusion

A

MVA trauma to chest, hemp[ericardium (blood in pericardial space)
ruptured MI, aortic dissection

119
Q

cause of acute pericardial effusion

A

MVA trauma to chest, hemp[ericardium (blood in pericardial space)
ruptured MI, aortic dissection

120
Q

Pericarditis sx

A
  1. CP : when sitting leaning forward, less when laying down (pleuritic = worse during breathing)
  2. Pericardial friction rub
  3. low fever
  4. pericardial effusion
121
Q

pericarditis EKG

A

elevated ST segment + depression of PR segment

122
Q

Fibrinous / Serofibrinous pericarditis : is what and cause

A 
most common type (fibrous inflammatory exudate)
= Acute MI
= Dressler's Syndrome (post infarction)
= Uremia (CKD high BUN)
= SLE, trauma
123
Q

Serous pericarditis

A

viral or noninfectious inflammatory disease

124
Q

purulent or suppurative pericarditis

A

active infection by microbial invasion

125
Q

Caseous pericarditis

A

TB, can be fungal

126
Q

Hemorrhagic pericarditis

A

spread of malignant neoplasm , or trauma

127
Q

Constrictive pericarditis

A

heart encased in dense, fibrous or fibrocalcific scar (limit diastole + CO) = sx of restrictive cardiomyopathy
= can be cured if resection of scar performed

128
Q

most common malignant tumor of the heart

A

angiosarcoma

129
Q

tumors and the heart

A

80%-90% are benign

130
Q

most common type adult and child heart tumor

A

Adult : myxoma

children : rhabdomyom a

131
Q

Myxoma location and looks like

A

LA (starts in septal region of fossa ovalis

= pedunculated, globular, hard, mottled or gelatenous

132
Q

Myxoma SX

A
  1. ” Ball-valver” obstruction , mechanical valve damage “wrecking ball”, embolization
  2. fever (IL6* from tumor)
  3. auscultation “Plop” form tumor
133
Q

myxoma associated familial syndromes 2

A
  1. McCune - Albright Syndrome

2. Carney complex

134
Q
  1. McCune - Albright Syndrome
A
  1. polyostotic fibrous dysplasia (normal bone replaced by fibro-osseous tissue
  2. cafe au lait spots
  3. endocrine abnormalities
  4. GNAS1 mutation
135
Q

Carney complex

A
  1. skin changes (lentigines)
  2. endocrine dysfunction
  3. PRKAR1A
136
Q

ball and valve type obstruction what happens

A
  1. dyspnea
  2. orthopnea
  3. pulmonary edema
  4. syncope (temporary loss of consciousness)
    - —> this can lead to wrecking ball (valve damage + can embolize
137
Q

Lipoma is what

A

localized mass of mature lobulated fat

subendocardium, subepicardium, myocardium

138
Q

Papillary Fibroelastoma

A

“sea-anemone-like” lesions , usually on the valves (look like lambl excrescence) = increased risk of emboli

139
Q

Rhabdomyoma

A

hamartoma of developing cardiac myocytes
(TSC1 hamartin + TSC2 tuberin mutations)
= spider cells (glycogen filled)

140
Q

Angiosarcoma

A

malignant endothelial neoplasm

older adults

141
Q

associations of rhabdomyomas

A

= tuberous sclerosis causing many benign hamartomas all over the body
= TSC1 and TCS2 mutation

142
Q

metastatic tumor to the heart usually comes from

A

lung carcinoma, melanoma, breast carcinoma

143
Q

tumor to the mediastinum comes from where usually and can do what

A

lymphoma or bronchogenic carcinoma

—-> vascular obstruction leading to superior vena cava syndrome

144
Q

muscin tumors come from what and can cause

A

nonbacterial thrombotic endocarditis =

procoagulation mediators released

145
Q

seratonin mediator release from what tumor

A

carcinoid heart disease

146
Q

high cardiac activity in what tumor

A

pheochromocytoma releasing catecholamine mediators

147
Q

plasma cell neoplasm in what and releases what

A

myeloma

= amyloidosis

148
Q

cellular and antibody mediated rejection of heart transplant happen when

A

months to years after

againts there HLA Ag

149
Q

most significant limitation after heart transplant

A

allograft vasculopathy

150
Q

allograft vasculopathy

A

almost all have it after 10years
= progressive stenosing intimal proliferation of coronary As,
= lead to MI and ischemia
= usually silent MI (due to loss of nerves)

151
Q

common side effect of taking immunosuppressant from heart transplant

A
  1. EBV (T-cell therapy pts)

2. melanoma, BCC, SCC

152
Q

aging heart changes

A

reduction in compliance and elasticity in vessels and heart

see this in increased collagen deposits pts

153
Q

aging heart on the valves

A
  1. fibrous mitral valve –> buckling prolapse during systole —-> A dilation + arrhythmia (Afib)
  2. calcific deposits —-> aortic stenosis
  3. Lambl excrescences
154
Q

aging heart on chambers

A
  1. LV cavity reduced size (esp from HTN)

2. Atrial Dilation (from fibrous mitral valve)

155
Q

aging heart and atherosclerotic changes

A
  1. significant stenosis (MI, aortic dissection if effecting vasa vasorum….)
156
Q

lambl excrescents from what

A

small thrombi or minor endothelial damage (small whister sea urchin looking things on valves)

157
Q

aging heart epicardial and myocardial

A
  1. increase fat epicardial (less muscle)
  2. lipofuscin accumulation (oxidant stress, catabolism product)
  3. Basophilic degeneration (glycoprotein accumulation)
  4. Myocyte loss
  5. Amyloid (transthyretin transporting thyroxine) = stiffens heart
158
Q

amyloid does what to the heart

A

can cause senile cardiac amyloidosis = stiffens heart and thickening of walls = SOB, exercise intolorance, HF eventually

CPR2 Exam 1 (19 decks)

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