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54 Cards in this Set
- Front
- Back
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what do contraction bands indicate?
what does MI look like at LM after: 1. 1 day 2. 2-4 days 3. 5-10 days 4. 2 months |
early necrosus, 12-24 hrs seen at LM
**early coag necrosis at 4 hrs 1. Day: 4 hrs, coag necrosis. 12-24 contraction bands 2-4. acute inflammation,-PMN hyperemia (dilated BV). coag nec 5-10 macro eat things up and increased risk for papillary mm rupture, IV septum rupture, tamponade 7 weeks. scar |
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what does an MI look like gross at
1 day 2-4 days 5-10 days 7 weeks |
1. dark molting
2-4. hyperemia- BV dilates 5-10. hyperemic border, with yellow brown soft middle 7 weeks: grey |
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micro after MI
1-2 day 3-4 day 1-2 week |
1-2 contraction bands, no nuclei, some acute inflammation
3-4 days acute inflammation, coag necrosis Macro come in- granulation |
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what 3 things help is make the MI dx
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1. Sx: chest pain, dyspnea, angina, radiates to neck, jaw, L arm (not seen in DM, HTN, elderly)
2. EKG change: st elevation, T inversion 3. Enzymes: CK-MB, Troponin I |
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what are the labs to draw for MI? what is fast, what lasts longer
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1. CKMB- released really fast! peak at 24 hrs, normal by 72
2. Troponin I- remain elevated for 4-7 days |
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if a guys had an MI 3 days ago will you look at CK MB or cTnI
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cTnI- it stays elevated longer
CKBM stays elevated for a day |
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what 4 things cause poor prognosis for MI
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1. DM
2. Female 3. Old 4. Previous MI |
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you are are an old DM female who survived an MI last year what is likely
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you wont survive another
four things with poor outcome female, old, DM, previous MI |
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what is the most common trpe of rupture, when is it most likely to happen after an MI
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vent free wall? leads to hemapericardium and tampanode
**if you dont have hypertrophy you will more likely rupture, not a nice thick wall **rupture will occur at 3-7 days, macro have come in and eaten the junk out |
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what happens whn papillary mm rupture
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mitral regurg
**rupture will occur at about 3-7 days, macro have some in and cleard the junk out and make it weak |
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what are some complications of MI
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1. arrhythemia
2. contractile dysfx- cardiogenic shock 3. rupture 4. extension of infarct/expansion 5. vent aneurysm (late) 6. papillary mm dysfx 7. mural thrombus 8. CHF 9 pericarditis |
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what happens if 3-7 days after MI you have a rupture of the
1. ventricle free wall 2. IV septum 3. Papillary MM |
1. hemopericardium, tampanode
2. L to R shunt 3. Mitral regurg |
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which is not a complication of acute MI
rupture arrhythemia aortic dissection vent aneyrysm pericarditis |
dissection
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what 3 things determine complications/prognosis of an MI
we know that being an old, DM woman who had a previous is BAD for prognosis |
1. Infarct size
2. infarct location- apex is bad 3. transmural extent |
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CIHD (chronic ischemic heart disease) affects what age group, what is the clinical hx, what is the morphology
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1. Elderly
2. Previous MI/CABG 3. enlarged bc of L vent hypertrophy and dilation **also called ischemic cardiomyopathy, insidious onself of CHF as a result of ischemic damage |
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who will get an insidious development of CHF as a result of ischemic damage (ie CIHD)
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old ppl who have had an MI or CABG
they will have a large heart with LV hypertrophy and dilation |
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what is sudden cardiac death
what is the ultimate mech od death? |
death within an hour
lethal arrythemia eventually kills you but can innitiate bc of IHD, myopathy or a whole list of others |
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know these
angina ruptures DVT PE R and L heart failure Age of MI- know in words, micro pic HNT heart Valves **know all of these things Pics: aortic aneurism liver |
angina: chest pain. stable unstable
rupture: DVT PE R/L Heart failure Age of MI HTN heart Valves |
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what are the minimum criteris for dx systemic HTN heart disease, waht does it look like
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MUST have concentric L vent hypertrophy and HTN
**hypertrophy is adaptive but leads to: MI dysfx, sudden death, dilation, CHF |
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the heart with hypertensive disease that has not been decompensated looks like what
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L vent pressure overload concentric hypertrophy- circumferential hypertrophy, no dilation
- the heart is stiff and diastolic filling is decreased **when it get dilated the heart has decompensated |
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when is concentric hypertrophy seen
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in pressure overload, hypertensive heart disease
huge LV, looks like a donut |
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in systemic hypertensive heart disease what happens if we decrease BP
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variable results, may regress
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pulmonary HTN is called what?
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cor pulmonea
R sided hypertensive heart disease **seen when pulm HTN due to lungs/pulm vasculature NOT right sided hypertrophy due to Left dises heart disease |
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what are the 2 types of cor pulmonale
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1. Acute: RV dilation due to PE
2. Chronic: RV hypertrophy/dilation 2 to prolonged pressure overload caused by pulm a obstruction COPD, emphysema, chronic bronchitis |
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what are the 4 things that predispose us to cor pulmonale
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disease of lung tissue itself
disease of pulm vessels disorders the affect chest movement dirorders that cause pulm arterial constriction |
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what are some things that cause chronic pulmonary hypertensive disease
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COPD
Emphysema Chronic Bronchitis **in this case the increased pressure in the lungs will cause R vent hypertrophy with dilation if the heart decompensates |
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Which of the following problems in not correctly matched
with it’s corresponding heart morphology – Pressure overloaded ventricles – concentric hypertrophy – Volume overloaded ventricles – ventricular dilation – Heart hypertrophy – hyperplasia of myocytes – Systemic hypertensive heart disease – ventricular dilation – Systemic hypertensive heart diseases – left atrium dilation |
hyperplasia, we know heart will only hypertrophy
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what is valvular stenosis?
what is valvular insuffiency |
valve wont open completly
regurg, valve wont close completly **can see pure or mixed stenosis or insifficency |
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what are 2 causes of regurgitation
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1. Damage to supporting structure/ Functional: valve isnt closing bc the ventricle is dilated
2. Intrinsic Disease |
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what are the 4 most common valve dysfunction and what causes them
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1. Mitral Stenosis- rheumatic fever (diastolic murmur with opening snap)
2. Mitral Insuffiency- mitral valve prolapse (myxomatous degeneration- change in ECM) (holosystolic murmur) 3. Aortic Stenosis: Calcification of normal or bicuspid valve (systolic murmur, crescendo) MOST COMMON 4. Aortic Insifficiency- dilation of ascending aorta, due to HTN /age (immediate diastolic whistle murmur) |
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whats it associated with?
AAA dilation |
artherosclerosis
HTN |
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what are the most common calcific valvular diseases
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1. calcific aortic stenosis
2. Mitral Annular calcificaiton 3. calcific stenosis of congenitally bicuspid aortic valve |
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what causes
1. Aortic Stenosis 2. Aortic regurg 3. Mitral stenosis 4. Mitral valve prolapse/regurg |
1. calcification due to age
2. dilation of ascending aorta, due to age/HTN 3. rheumatic fever 4. myxomatous degeneration |
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what are the 2 types of calcific aortic stenosis, whats more common
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most common valve abnormality (systolic crescendo/decrescendo)
1. senile calcific arortic stenosis- more common, seen in old ppl 2. Calcification on congenitally bicuspid aorta 2. |
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what is senile calcific aortic stenosis? wat does it look like
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the common stenosis you get bc your old and have calcium deposit on your valves
heaps on nodular masses of calcium within sinuses of Valsalva at the base no commissure fusion |
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whats the differentce btwn an aortic valve that calcifies normally (senile stenosis) and one that calcifies bc its bicuspid
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normal- occurs later in life
congenital- occurs early |
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what happens when you have aortic stenosis
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hard to get blood throuh, L vent hypertrophy- concentric
**angina, syncopre, increased risk of sudden cardiac death, eventual decompensation and CHF |
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wht anatomical cahnge in the heart is associated with mitral valve prolapse
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myxomatous degeneration of mitral valve
**also ppl with marfans or ehlers danlos **midsystolic click with murmur |
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WHO is at risk for MVP
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marfan
ehlers danlos family hx its a myxomatous degenearation |
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what are the serious complications of MVP
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its rare to have complications but they are:
infective endocarditis mitral sufficiency arrhythemia stroke of systemic infarct that form on valve |
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what is the Jones criteria and Labs of acute rheumatic fever of childhood
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she said not on test but... FEVERSS
Fever Erythrema Valvulat Damage/Vegetation ESR increased Red hot joint Subcut nodules Silly dance- chorea dx with strepp infection and some jones criteria -happens after strep, culture is neg, M AB are present and attack self |
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whate does acute rheumatic pancarditis look like
(pan means all) |
Aschoff bodies- collagen surrounded by lymphocytes and fat macros. found in myocardium
Pericardium: fibrinous pericarditis Endocardium: fibrinoid necrosis with small vegetations |
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what is standard practivce when tx Theumatic fever
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prophylatic AB long term
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what are the features of chronic rheumatic heart disease
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valves become fibrotic over time
**rheumatic fever leads to mitral stenosis mostly, sometimes aortic **looks like fishmouth stenosis |
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when might one see fishmouth stenosis
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mitral stenosis caused by rheumatic fever--- chronic rheumatic heart disease
**this picture will be on the test!!! |
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we know rheumatic fever can lead to mitral stenosis, what IS rheumatic fever (aortic is also involed someitmes)
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GABHS can cause it 4-5 weeks after throat infection if not tx with AB
**its an immune inflammartory disease that can cause chronic rheumatic heart disease (mitral stenosis) **the AB made form the strep infection self react with things in ouur joints- joint pain |
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where are aschoff bodies
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in the myocardium of someone with acute pancarditis caused by Rheumatic fever
Myocardium: aschoff bodies Pericardium- fibrinous pericarditis Endo- fibrinoid necrosis with vegetations |
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47‐year‐old woman has noted increasing dyspnea for the past 6 years. A
chest radiograph shows an enlarged cardiac silhouette and bilateral pulmonary edema. Past history reveals that, as a child she suffered recurrent bouts of pharyngitis with group A beta hemolytic streptococcal infections. Which of the following cardiac valves are most likely to be abnormal in this woman? – A Aortic and tricuspid – B Mitral and pulmonic – C Aortic and pulmonic – D Tricuspid and pulmonic – E Mitral and aortic |
E mitral adn aortic
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A 40‐year‐old previously healthy woman dies suddenly
and unexpectedly. At autopsy a diagnosis of mitral valve prolapse is made. What morphologic feature would you see in the mitral valve ? – Myxomatous degeneration – Aschoff bodies – Vegetations – Calcifications – Fibrinous pericarditis |
Myxamatous degeneration
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A 79 year old man presents with episodes of syncope.
Diagnostic workup reveals aortic stenosis with a significantly increased gradient pressure across the valve. The patient receives an aortic valve replacement. What morphologic feature would you see in the removed stenotic valve? • Myxomatous degeneration • Aschoff bodies • Vegetations • Calcifications • Fibrinous pericarditis |
calcium
Myxamatous is associated with MVP Aschoff Bodies as associated with rheumatic fever Fibrinous pericarditis is associated with pancarditis |
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The Dallas County Medical Examiner’s office calls to
inform you that they are investigating the sudden deathof one of your patients. The patient in question was a 55 year old black woman who had been followed for many years in the hypertension clinic. Work‐up at various times had revealed no evidence of renal disease or endocrine abnormalities. On a recent office visit, her BP was measured as 190/10 A few months ago, she was briefly admitted to a hospital after she awakened at night feeling short of breath. Review of hospital notes from that admission shows that she had mild ankle edema, basilar rales and hepatomegaly on initial evaluation. A ches x‐ray showed cardiomegaly and slight atrial enlargement. An EKG confirmed left ventricular hypertrophy Laboratory studies y at that time suggested slight hepatic damage; serial cardiac serum markers were negative for MI, Over the last few years, there had been a steady rise in her serum BUN and creatinine. The medical examiner relates that the patient complained of sudden, severe, sharp chest pain and collapsed at her husband’s softball gameShe was taken to a hospital, where she was noted to be hypotensive with unequal pulses. A chest x‐ray revealed a left pleural effusion and a widened mediastinum. An autopsy is being done to determine whether she died from some catastrophic vascular event related to her hypertension. We see hyperplastic arteriolosclerosis, some hyaline arteriolosclerosis, concentric LV hypertrophy and ultimatly we see... |
aortic dissection
HTN with hyperplastic arteriolosclerosis Abd Aneurysm would be with artherosclerosis |
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70 year old man was brought to the hospital for
evaluation of chest pain. He described feeling weak and dizzy after a walk around the block the morning of his admission. This episode of dizziness was followed by 10‐15 minutes of chest pain that quickly resolved when he rested. He also described a two month history of similar but shorter episodes of chest pain and dizziness after working in his yard. He had been told several years ago that he had a slight heart murmur, but had not been evaluated further.Physical signs and auscultation suggested aortic valve narrowing. His lungs were clear to auscultation. A chest radiograph showed an enlarged heart and a vague area of calcification at the base of the heart in the region of the aortic valve. Cardiac enzymes and other lab tests were normal. An EKG showed atrial fibrillation and LVH. His valve was replaced and he did well for several years. He than began to have signs and symptoms of aortic regurgitation. |
aortic calcification
L vent hypertrophy |
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A ten year old child was brought to a pediatrician
for a mild sore throat. The pediatrician noticed some redness, swabbed the throat, tested for group A Streptococci in the office, sent the blood for anti‐streptolysis O titer, and prescribed treatment. Three weeks later the child returned with fever, painful swelling of the knee joints followed by pain and swelling of the elbow joints. The physical exam revealed a pericardial friction rub and a murmur suggestive of mitral regurgitation. The anti‐streptolysin O titer was elevated over the previous value.The patient recovered and did well over the next several decades. In her thirties the patent began to have dyspnea on exertion, which slowly increased in severity in her forties. In the months prior to her initial hospital admission she had awakened feeling short of breath. There was one fainting spell followed by and episode with temporary loss of vision in one eye. On admission to the hospital she was very short of breath and had coughed up some blood‐tinged sputum. The physical exam and other lab tests suggested narrowin of the mitral valve orifice.Atrial fibrillation was present. X‐ray of the chest showed an enlarged left atrium and pulmonary edema. Cardiac surgery was offered but she refused. She was treated medically for several days and discharged feeling better but with some residual limitation of cardiac function. The week before her second admission she went to a dentist because of tooth pain and underwent a dental extraction. She returned to the hospital with high spiking fevers and overt signs and symptoms of heart failure |
as 10 yo- aschoff bodies in myocardium
stenotic mitral valve aortic stenosis **both valves lead to LV hypertrophy and artial enlargement |
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what are heart ffailure cells
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hemosiderin laden macro in the lungs
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