Cardiac Pathology Part 1 - Dr. Hillard Flashcards
(161 cards)
1
Q
leading cause of death in US
A
Coronary Artery Disease
2
Q
Ischemic Heart Disease (Coronary Artery Disease)
A
Age, male, HTN, hyperlipidemia, DM, smoking
3
Q
CAD most common cause
A
atherosclerosis
coronary artery emboli, vasculitis, and vessel spasms can also cause it
4
Q
4 most common sites of coronary artery disease
A
- LAD (left anterior descending) = the widow maker
- Right coronary artery
- Left circumflex
- Left coronary artery
5
Q
how to determine the dominance of a heart
A
the blood supply to the posterior descending artery (most are Right dominance)
6
Q
left dominated heart what artery supplies the posterior descending artery
A
Circumflex artery
7
Q
when id knowing dominance of heart important
A
- probable site of occlusion in MI
- planning coronary artery bypass grafting
- in irregular beats or skipping beats = AV block (AV node is supplied by PDA)
8
Q
MI Sx seen
A
- crushing stabbing CP radiating to neck, jaw, arm
- SOB : congestion pulmonary
- sweating, N/V (usually posterior/ inferior infarct)
- 0.25 no sx (usually DM neuropathy)
9
Q
serum marker for MI
A
Troponin*
CK-MB(creatine kinase-MB)
myoglobin
= regulate Ca mediated contraction of myocardiocytes
10
Q
irreversible cell injury time
A
20min- 40min = necrosis
microvascular injury happens over 1hr
11
Q
MI time for loss of function of heart from ATP depletion
A
1-2min
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
13
Q
CK-MB
CK-MM
CM-BB
A
- MB = cardiac muscle cells
- MM = muscles
- BB = brain and lung
14
Q
first biomarker that peaks first
A
myoglobin
15
Q
CKMB, cTnT and cTnl time to elevate, peak at what time, normalize when
A
- 3hr-12hr**
- 24hr
- CK-MB = 48hr-72hr*
cTnl, cTnT = >5days
16
Q
LAD occlusion is what part of the heart
A
APEX, Anterior left ventricle and anterior 2/3 septum
17
Q
Left circumflex occlusion what part of heart
A
Lateral LEFT VENTRICLE
18
Q
Right Coronary Artery occlusion what part of the heart
A
right ventricle and left ventricle posterior heart
- posterior 1/3 septum
19
Q
left dominant heart with circumflex artery occlusion where in the heart
A
the left ventricle lateral, and posterior
20
Q
2 things that can cause subendocardial infarct
A
- reperfusion of transmural infarct (restoring BF fast, a thrombus is dislodged) regional
- global hypotension (shock, coronary stenosis)
21
Q
multifocal microinfarction
A
many small infarcts within smaller intramural vessels
= seen in emboilic disease or drugs like cocaine
22
Q
how does MI infarction spread
A
from inside =heart to outside (except the thin internal zone that gets perfused by blood passively)
23
Q
what do you see in histology from 0min-30min
A
myofibrils relaxed, glycogen loss, M swelling
24
Q
what do you see in histology from 30min - 4hr
A
- slight waviness of fibers at the border (from sarcolemma disruption)
25
what do you see in histology from 4hr - 12hr
- very early coagulation necrosis and edema
26
what do you see in histology from 12hr - 24hr
- increased coagulation necroisis and very developed at 24hr
- shrink Nuclei (pyknotic)
- darkly mottled heart (contraction band necrosis)
- myocytes hypereosinophilic
27
what do you see in histology from 1day-3days
- a lot of N
| - nuclei loss = yellow tan infarct with surrounding mottling
28
what do you see in histology from 3days - 1 week
- M to phagocytose dead myofibers
29
what do you see in histology from 1 week - 1.5 weeks
- granulation
| - collagen deposition (closer to 2 weeks)
30
what do you see in histology from 2weeks
scar tissue
31
what do you see in histology from after 2 months
scarring is complete and dense scar
32
when is it easy to see if an MI has happened on gross anatomy and also how to see it
- 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
33
reperfusion injury
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
34
moltting
uneven patches of color
| seen after 1 day
35
1day to 3days gross anatomy look
- yellow infarct, necrosis hyperemic border
- many N
- coagulative necrosis = loss of nuclei
36
after 2 weeks heart gross anatomy
-collagen increases more and more
-fibroblasts
scar is maturing and fully mature at 2mos
- loss of myocytes, inflammation, granulation
37
complications of an MI : early (within 24hrs)
1. arrhythmias fatal
| 2. contractile dysfunction from cardio muscle death(can lead to cardiogenic shock)
38
complications of an MI : intermediate (2-4 days to 2 weeks)
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
39
acute fibrinous pericarditis
from inflammation a layer of fibrin develops over pericardial surface
40
serofibrinous pericarditis
fibrinous depbri and fluid collection in pericardium
41
complications of an MI : late (after 2 weeks)
1. immune pericarditis = Dressler syndrome
2. heart remodeling (fibosis) myocytes are separated in space :
= aneurysm formation
= arrhythmias fatal
= heart failure
42
most common cause of death from MI
fatal arrhythmia from within 1hr onset
| = usually Vfib
43
2nd most common cause of death form MI
cardiogenic shock, also within 1hr to even 1day (from contractile dysfunciton = failure to pump) when cells die
44
intermediate effect of MI : rupture of wall
| 1. free wall rupture what happens
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
45
intermediate effect of MI : rupture of wall
| 2. septal rupture
2. ventricular septal defect (usually in elderly with lower muscle mass), usually during anterior wall MI
46
intermediate effect of MI : rupture of wall
| 3. papillary muscle rupture
3. valve incompetence and post infarct regurgitation
47
PE of pericarditis
pain with inspiration
| pericardial friction rub heard on auscultation
48
main thing happening in intermediate MI complication
1. myocardial rupture 2-4days post MI
| 2. AND acute fibrous or serofibrous pericarditis happening at the same time frame
49
Dressler syndrome what is it and SX (late so after 2 weeks past MI)
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
50
Ventricular aneurism + more arrhythmias (other late post 2 weeks MI) happen how
from remodeling and scarring (when conducting system is disrupted =arhythmias)
50
Ventricular aneurism + more arrhythmias (other late post 2 weeks MI) happen how
from remodeling and scarring (when conducting system is disrupted =arhythmias)
51
how to see aneurysm in ventricle
CT or angiogram
52
besides Dressler syndrome and ventricular aneurysm + arrhythmia , what is the last 2 types of late MI (post 2 weeks) complication that can happen
1. Congestive heart Failure
| 2. Chronic Ischemic Heart Disease ----> CHF
53
Chronic Ischemic Heart Disease 3 causes
1. healing infarct with fibrosis
2. V remodeling
3. hypertrophy
= fatal arrhymia
= failure heart , weakened
54
angina pectoris is what
recurrent CP from Myocardial Ischemia (not enough to cause MI)
= can happen with 70% stenosis of coronary A
55
angina pectoris is what
recurrent CP from Myocardial Ischemia = heart does not get enough O2 (not enough to cause MI)
= can happen with 70% stenosis of coronary A
56
pain from angina is caused by what
bradykinin and adenosine released from low O2
57
2 things that can cause a silent angina
DM neuropathy or previous MI
58
Stable angina
what
improves with
worsens with
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)
59
Prinzmetal Variant angina
what is it
improves with
worsens with
Episodic coronary A spasm
= relieved by vasodilators
= has no dependence on physical activity, BP, or HR
60
how to test for stable angina
exercise stress test, use EKG or echocardiogram and looks for changes during exercise
61
when does the Prinzmetal variant angina usually happens when, 3 complications that can occur, how often
```
at rest
1. coronary atherosclerotic disease
2. V arrhythmia
3. sudden death
(3mo-6mo interval attacks)
```
62
vasodilator
nitrates
63
unstable angina
| what is it, 2 causes of it
1. Crescendoing pattern = increase severe and duration of pain
- rupture of plaque , partial non-occlusive thrombus (rest + exercise)**
- progressive mechanical obstruction (Exercise)**
64
NSTEMI and STEMI difference in what happens
1. plaque rupture and partial thrombus occlusion, subendocardial infarct
2. complete occlusion of BV lumen= transmural injury and myocardial infarct
65
NSTEMI and STEMI difference in EKG
```
1.
= normal
= inverted T wave
= ST depression
(same 3 seen in unstable angina)
2.
= hyperacute T wave
= ST elevation
```
66
unstable angina vs NSTEMI
troponin levels elevated only in NSTEMI (cardiomyocytes dying)
67
within 0min -3 hrs what should you do if pt comes with SOB, crushing, stabbing, squeezing CP, radiating to jaw
assume STEMI transmural acute MI even with no troponin levels (this takes at least 3hrs to elevate)
68
motor vehicle trauma can cause what 3 heart contusion injuries
1. subendocardial contusion
2. subepithelial contusion
3. Transmural contusion ---> rupture of wall ----> pericardial blood tamponade = hypotension and death if not fixed
69
motor vehicle trauma other injuries to heart
1. aorta torsion , bending, shearing stress
70
where does the aorta usually tear or bend from MV trauma
weak point where it is tethered to the pulmonary artery by LIG ARTERIOSUM
= can cause blood into the adventitia
= life threatening hemorrhage
71
2 most common casues of death from MV accident
1. head trauma
2. aortic tear or torsion
(same happens in fall from height)
72
average bpm of SA and AV node
SA : 60 -100
| AV : 40 - 60 if SA does not work
73
SA node location
junction of SVC and atrial appendage
| = connected to parasympa and sympa nerves
74
bundle of His location and other name
AV bundle
| upper V rigth under AV node -----> Purkinje fibers
75
most common cause of arrhythmias **
Ischemic heart disease (MI can lead to Vfib) both from early myocyte death and late fibrosis
76
other causes of arrhythmias
1. cardiomyopathies : hypertrophic cardiomyopathy, dialted cardiomyopathy, and restrictive cardiomyopathy
77
restrictive cardiomyopathy
infiltrative process such as amyloidosis and sarcodosis
78
reason arrhythmia happens
conduction problem, usually from increased spacing between myocytes and then first
79
sick sinus syndrome
SA node damage = bradycardia (CHF, Infiltration like sarcodosis and amyloidosis, inflammation like RH disease or infection)
= type of arrhythmia
80
Atrial Fibrillation what is it and what is a complication
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
Heart Block
```
dysfunctional AV node
3 degrees for this
1. prolonger PR
2. intermittent TR
3. X TR, failure
```
82
atrial fib 2 causes
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
thrombus in LA can cause what
obstruction of BV in head to CNS
84
hereditary channelopathies
inherited defect in ion channels in myocytes = arrhythmia
| = LONG QT SYNDROME
84
hereditary channelopathies
inherited defect in ion channels in myocytes = arrhythmia
| = LONG QT SYNDROME
85
long QT syndrome means
increased ventricular depolarization to repolarization
86
long QT syndrome can lead to what
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
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
88
sudden cardiac death most common cause from what
coronary artery disease (Stenosis in artery) from ischemia inducing arrhythmia (Vfib or asystole)
89
sudden cardiac death is what and most common causes of it in younger pts
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
pathway of blood in the heart
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
heart changes during HTN
heart has to pump harder due to increased peripheral P
| = LV hypertrophy
92
LV hypertrophy problems
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
systolic dysfunction
cant pump adequately based on peripheral P
| = increased O2 demand
94
diastolic dysfunction
inability to relax
95
what causes LV hypertrophy
1. HTN
| 2. stenosis upstream from LV (Aortic stenosis)
96
Dilated heart dysfunction is what
```
dilated cardiomyopathy
= causes VOLUME OVERLOAD
= walls are dilated and overstretched and weak
= systole dysfunction
= can cause concentric hypertrophy****
```
97
dilated cardiomyopathy causes
```
= excessive alcohol
= myocarditis
= drugs
= FE overload
= hereditary and seen during delivery
```
98
dilated cardiomyopathy causes
```
= excessive alcohol
= myocarditis
= drugs
= FE overload
= hereditary and seen during delivery
```
99
concentric hypertrophy on LV is seen when
HTN
| aortic stenosis due to overload happening
100
dilation of ventricle is seen when
dilated cardiomyopathies with overload
101
hormone release when atrium is stretched
ANP : decreases BP and B volume
102
Congestive Heart Failure is what and what happens
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
most common type to heart failure
LEFT sided = systolic failure and diastolic failure
104
Systolic failure 5 causes
1. Ischemic HD (from hypertrophy) *
2. HTN *
3 .Aortic Stenosis *
4. Dilated cardiomyopathy
5. regurgitation
= lower EJECTION FRACTION
105
Diastolic failure 4 causes
1. HTN *
2. Aortic Stenosis *
3. Hypertrophic cardiomyopathy
4. Restrictive cardiomyopathy
= Normal Ejection fraction
106
2 causes of right sided heart failure
1. left sided induced most common
| 2. cor pulmonale (lung disease or dysfunction)
107
Left sided CHF sx
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
3 most common causes of left sided CHF
1. ischemia (including MI)
2. HTN
3. Left sided valve problem
109
left sided CHF can eventually cause
atrial dilation = atrial fibrillation
| which can cause even more loss of pumping and low blood to brain causing confusion, cerebral injury, coma
110
low pumping on left side can lead to
1. cerebral damage : confusion, coma, restlessness
| 2. azotemia : high cr and urea nitrogen in blood from low BF to kidney
111
left sided CHF imaging
CXR
= Kerley B lines (edema in lungs show these parallel lines)
= red blood cells in avleoli ----> M hemosiderin-laden filled (dark brown pigment)
112
right sided CHF most common lung cause
parenchymal lung disease
113
right sided CHF signs
1. liver / spleen congestion : hepatosplenomegaly
2. ascites
3. distended jugular veins
4. peritoneal/ pericardial. pleural effusion
5. leg edema
6. exertional dyspnea
114
liver in right sided CHF
nutmeg liver
| if chronic and passive congestion (hemorrhage and necrosis of central vein)
115
2 things that increase the pressure in the lungs
1. emphysema
| 2. thromboemboli
116
pericardial effusion is what
more then 50ml fluid in the pericardium
| can accumulate chronically in CHF (serous effusion) or acutely
117
chronic pericardial effusion sx
asymptomatic except abnormal heart shadow on cxr (before 500ml)
118
acute pericardial effusion sx
within 1 week gets to 200-300ml
= hypotension, death
= cardiac tamponade
119
cause of acute pericardial effusion
MVA trauma to chest, hemp[ericardium (blood in pericardial space)
ruptured MI, aortic dissection
119
cause of acute pericardial effusion
MVA trauma to chest, hemp[ericardium (blood in pericardial space)
ruptured MI, aortic dissection
120
Pericarditis sx
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
pericarditis EKG
elevated ST segment + depression of PR segment
122
Fibrinous / Serofibrinous pericarditis : is what and cause
```
most common type (fibrous inflammatory exudate)
= Acute MI
= Dressler's Syndrome (post infarction)
= Uremia (CKD high BUN)
= SLE, trauma
```
123
Serous pericarditis
viral or noninfectious inflammatory disease
124
purulent or suppurative pericarditis
active infection by microbial invasion
125
Caseous pericarditis
TB, can be fungal
126
Hemorrhagic pericarditis
spread of malignant neoplasm , or trauma
127
Constrictive pericarditis
heart encased in dense, fibrous or fibrocalcific scar (limit diastole + CO) = sx of restrictive cardiomyopathy
= can be cured if resection of scar performed
128
most common malignant tumor of the heart
angiosarcoma
129
tumors and the heart
80%-90% are benign
130
most common type adult and child heart tumor
Adult : myxoma
| children : rhabdomyom a
131
Myxoma location and looks like
LA (starts in septal region of fossa ovalis
| = pedunculated, globular, hard, mottled or gelatenous
132
Myxoma SX
1. " Ball-valver" obstruction , mechanical valve damage "wrecking ball", embolization
2. fever (IL6* from tumor)
3. auscultation "Plop" form tumor
133
myxoma associated familial syndromes 2
1. McCune - Albright Syndrome
| 2. Carney complex
134
1. McCune - Albright Syndrome
1. polyostotic fibrous dysplasia (normal bone replaced by fibro-osseous tissue
2. cafe au lait spots
3. endocrine abnormalities
4. GNAS1 mutation
135
Carney complex
1. skin changes (lentigines)
2. endocrine dysfunction
3. PRKAR1A
136
ball and valve type obstruction what happens
1. dyspnea
2. orthopnea
3. pulmonary edema
4. syncope (temporary loss of consciousness)
- ---> this can lead to wrecking ball (valve damage + can embolize
137
Lipoma is what
localized mass of mature lobulated fat
| subendocardium, subepicardium, myocardium
138
Papillary Fibroelastoma
"sea-anemone-like" lesions , usually on the valves (look like lambl excrescence) = increased risk of emboli
139
Rhabdomyoma
hamartoma of developing cardiac myocytes
(TSC1 hamartin + TSC2 tuberin mutations)
= spider cells (glycogen filled)
140
Angiosarcoma
malignant endothelial neoplasm
| older adults
141
associations of rhabdomyomas
= tuberous sclerosis causing many benign hamartomas all over the body
= TSC1 and TCS2 mutation
142
metastatic tumor to the heart usually comes from
lung carcinoma, melanoma, breast carcinoma
143
tumor to the mediastinum comes from where usually and can do what
lymphoma or bronchogenic carcinoma
| ----> vascular obstruction leading to superior vena cava syndrome
144
muscin tumors come from what and can cause
nonbacterial thrombotic endocarditis =
| procoagulation mediators released
145
seratonin mediator release from what tumor
carcinoid heart disease
146
high cardiac activity in what tumor
pheochromocytoma releasing catecholamine mediators
147
plasma cell neoplasm in what and releases what
myeloma
| = amyloidosis
148
cellular and antibody mediated rejection of heart transplant happen when
months to years after
| againts there HLA Ag
149
most significant limitation after heart transplant
allograft vasculopathy
150
allograft vasculopathy
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
common side effect of taking immunosuppressant from heart transplant
1. EBV (T-cell therapy pts)
| 2. melanoma, BCC, SCC
152
aging heart changes
reduction in compliance and elasticity in vessels and heart
| see this in increased collagen deposits pts
153
aging heart on the valves
1. fibrous mitral valve --> buckling prolapse during systole ----> A dilation + arrhythmia (Afib)
2. calcific deposits ----> aortic stenosis
3. Lambl excrescences
154
aging heart on chambers
1. LV cavity reduced size (esp from HTN)
| 2. Atrial Dilation (from fibrous mitral valve)
155
aging heart and atherosclerotic changes
1. significant stenosis (MI, aortic dissection if effecting vasa vasorum....)
156
lambl excrescents from what
small thrombi or minor endothelial damage (small whister sea urchin looking things on valves)
157
aging heart epicardial and myocardial
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
amyloid does what to the heart
can cause senile cardiac amyloidosis = stiffens heart and thickening of walls = SOB, exercise intolorance, HF eventually
