Path Fall Ii Endocarditis, Cardiomyopathy

Front 1

what should total cholesterol be
what should LDL be
what should HDL be
what should TAG be


when might you think hypercholesterolemia, what are the vales in kids and adults

Back 1

1. Total: <200
2. LDL <100
3. HDL >45
4. TAG <100

Adult: cholesterol >350, LDL >270
Kid: cholesterol >270 LDL >220

Front 2

should you treat infective endocarditis (IE)

Back 2

hell ya it can be fatal, early tx prevents heart disease

you can get vegetations on the valves

**mitral most commonly infected, Tricuspid infected with IV drug use

Front 3

what is excrescence

Back 3

its the fancy word for vegetation crap on valve from IE (infective endocarditis)

**its chunky cauliflower looking stuff, it can break off and from an arteriole embolis that goes to brain, kideny, bowle, LE, etc

Front 4

what causes IE

Back 4

gram + cocci
gram - bacilli

**can be from dental work, IV drug (tricusp involvement), UTI, trivila breaks in skin

Front 5

what can predispose you to ID

Back 5

1. bad valves (bicuspid aortic) (myxomatous mitral valve) (rheumatic fever)

2. Artificial valves

3. Immunodefciency, DM

4. Drug, EtoH abuse

Front 6

define endocarditis

what are the 2 kinds

Back 6

Acute: rapidly fatal even with tx (s aeurus) normal valves

SUbacute: weeks or months b4 you know you are sick. previously damaged valves. (streptococci). fatal if not treated aggressively

Front 7

Compare/contrast acute bacterial endocarditis
from subacute bacterial endocarditis (SBE).
Include: any predisposing factors or clinical risks;
types of organisms; complications

Back 7

ACUTE: real sick real fast, pretty fatal. previously normal heart valve that develops a NEW murmur. see complications early, rapid onset. caused by staphylococcus aureus


SUBACUTE (SBE): takes weeks/months to feel sick, valves were often previously damaged, caused by low virulence organisms like: Streptococcis viridans, staph epidermidis, strep bovis)
murmer previously seen- MVP, RF,
Microemboli, petecheia, immonological leisions can occur bc we have had time to make AB

Front 8

What are the systemic complications of infective endocarditis related to bacteremia and septic embolization

Back 8

1. embolus (septic embolus, mycotic aneurysm)
2. petechiae
3. splinter hemmorages
4. metastatic infection
5. stroke

bacteremia: osteomylitis, renal abcess, disseminated abcess.

Front 9

whats a roth spot

Back 9

its a leisionin the eye, red with a wite center

Front 10

what are the sx of IE

Back 10

FROM JANE PC

Fever
Roth spot
Oslers Nodes (immune comples, SBE only)
Murmur (new in acute, old in SBE)
Janeway leision (leision on palms and soles)
Anemia
Nail Bed hemmorage (splinter)
Emboli/Ecchymoces
Petechia
Clubbing

Front 11

will you see clubbing in acute IE or SEC? whay about oslars nodes

Back 11

SBE, need time to build them up!

Also SBE, its the immune complex

Front 12

Describe the cardiac morphology and cardiac
complications of infective endocarditis

Back 12

1. vegetations on heart valves- break off and form emboli, really chalky so can make lots of little ones
-found in atrial side of AV valves- mitral most-systemic emboli, TRI in IV drugs-PE

2. heart failure

3. Ring abcess, vlaves fall through

4. artificial valve dihisvence
5. suppurative pericarditis

Front 13

vegetations of the tricuspid will go where? what caused them

Back 13

IV drug use- more acute endo (staph aureus, candida, pseudomonias)

**will go to lungs, PE

Front 14

in IE will fake valves get damages

Back 14

you bet

Front 15

if a pt has a staph auerus IE how might the ventricle get leision

Back 15

aortic valve vegetations that break off and go down coronary

*septic embolization

Front 16

A 32 y/o man presents to the ER c/o high fever
and prostration. A known IV drug abuser, he
admits to use of IV heroin, tobacco and alcohol.
• He reports that a recent HIV test is negative.
• He denies trauma to his hands but “when I’m
high, anything could happen” and didn’t
realize that he had lesions on his hands.
• Lesions are erythematous, petechial to finely
papular. Some are hemorrhagic.

What is the most likely diagnosis? Why?
• What are his skin lesions? How do they arise?
• What is his prognosis

Back 16

Acute endocarditis- IV drug so likely tricuspid involvement

Skin leisions are Janeway leision, septic embolism from vegetations

Prognosis is poor, even with aggressive theraphy. contrast to a subacute with a much better prognosois

Front 17

how is IE dx

Back 17

1. CBC, + blood culture
2. ECHO
3. murmus
4. immunologic leision
5 vascular embolis

Front 18

A 28 y/o female presents with fever, chest pain
and shortness of breath.
There are needle tracts of both antecubital
fossae and urine drug screen reveals opiates.
She admits to regular IV drug use.
Chest radiographs and CT reveal multiple
pulmonary abscesses with air‐fluid levels. In
view of her history, ECHO cardiogram is
performed that reveals vegetations involving the
tricuspid valve. Blood cultures grow MRSA
She is treated with appropriate antibiotics and
remains in intensive care in critical condition for
a number of days. When stable, she is taken to
surgery for replacement of her tricuspid valve
with an oversize porcine graft.
She has no splinter hemorrhages, Janeway
lesions, or Osler nodes. Why?
What is the pathogenesis of IE and pulmonary
abscesses

Back 18

1. splinter hemmorage, janeway- these would be from a mitral valve involvemnt going systemic

osler nodes- immune complex deposition, needs time to make them, not enough time for this in acute. roth is also immune

2. the tricuspid junk broke off and went to the lungs

Front 19

What are the associations of NBTE? Review case
Dan from prior lecture

Back 19

non bacterial thrombic endocarditis- associated with sterile thrombi. vegetations are due to debiliation not infectino

caused by cancer (pancreatic cancer and trousseau syndrome- traveling emboli)

Libman sicks endocarditis

Front 20

A 43 y/o woman presented with an ischemic
3rd toe. A biopsy revealed fibrin thrombus in
an artery w/o vasculitis.
• She subsequently developed ecchymoses of the
trunk and backs of thighs over the next few
weeks. The right index finger became cold and
blue and multiple painful nodules were noted
on
both hands
Serum d‐dimer was 3712 ng/ml (less than 500)
• She described shortness of breath. Hoarseness
developed and tests were consistent with
recurrent laryngeal nerve paralysis.
• A mass is visualized on CT of the chest and
biopsy demonstrates carcinoma of the lung.
• What is the predisposing condition?

What process is occurring in this patient

Back 20

1. multiple sites of embolis- something on heart valve- mitral

increased D dimer means lots of fibrinolysis

2. cancer with multiple emboli- treusseau syndrome

Front 21

whats libman sacks endocarditis

Back 21

non bacterial thrombolytic endocarditis

**associated with SLE and antiphospholipid syndrome

**small sterile vegetations of mitral valve can disform the valve

Front 22

what are the 4 times we see vegetations

Back 22

1. Rheumatic fever, thin leision
2. Infective endocarditis. mounds
3. Nonbacterial thrombotic endocarditis
4. libman sacks endocarditis (autoimmune, SLE, can deform the valve)

Front 23

Describe the cardiac morphology and cause of
carcinoid heart disease. What other substances
are associated with similar morphology

Back 23

caued by increased serotonin from carcinoid tumors. L heart not affected bc lungs metabolize serotonin

5HIAA increased in labs

Carcinoid syndrom is a bund of timgs (flushing, diarrhea, vomit) and cARDIAC leision on R side of heart- tricuspid valve

**thick r vent, thepulmonic and tricuspid vavles have acid mucopolysaccharide on them and we have tricuspid insufficiency

Front 24

Patient saw physician for exertional angina,
shortness of breath and near syncope with
exercise.
• LV hypertrophy; no arrhythmias on EKG.
• Cardiac catheterization: normal coronaries.
• ECHO cardiogram showed heavily thickened,
calcified bicuspid aortic valve with opening
0.8 cm wide.
• Dx: critical aortic stenosis, symptomatic

how do you treat- successful tx and then...

Returns to hospital in 2 wks. c/o severe neck,
shoulder pain.
• CT neg. for PE; pericardial effusion noted.
• Temp. 100.4o, p 112, BP 110/70
• Hb 8.8 gm
• PT 45 sec (~12);
• INR 14.5 (therapeutic 3)
• PTT 46 sec (<32)
• Troponin not elevated
• RBC morphology suggests hemolysis

what ddx

Back 24

syncope with exercise indicated pulm or cardiac problem

aortic valve should be tricuspid

REPLACE THE VALVE: if you choose mechanicla you need anticoagulant

HB is low, he is anemic

Pericarditis, hemmorage

**the guy never got his meds (coumadin) adjusted. he needed to!!!

Front 25

compare bioprosthetic and mechanical valves, who needs anticoagulation

Back 25

1. Bioprosthetic: break down, not immunogenic :)

2. Mechanical: risk for thrombus, needs anticoagulation, risk for IE (staph epidermidis) (great so we are on blood thinners adn then we have embolus- can have hemmorage)

Front 26

Dilated
Hypertrophic


know cause, morphology, clinical

Back 26

**inherent disease of myocardium

Dilated: systolic, most common, low EF, cause: unknown, chagas, EtOH, pregnancy, genetic defect in cytoskeleton

Hypertrophic: Diastolic, decreased compliance. EF is normal

Restrictive: diastolic

Front 27

what is unique regarding the arrhythmogenic RV type of caudiomyopathy

Back 27

familial defect in desmosome

**RV failure most, arrhythemia, sudden death,
**RC is think and has fatty inflitrate

**lots of fibrisis

**die of arrhythemia

Front 28

AG, a 72 year old farmer complains that he no
longer has the strength to lift bales of hay to
feed the cattle. He is increasingly short of breath.
• Past history: unable to feed cows for a period
of 2 days three months earlier due to high
fever and malaise from influenza. On physical examination, there are bilateral
diffuse rales. He has resting tachypnea (30/min).
He has scleral icterus and tender hepatomegaly.
There is bilateral pitting of edema of the legs
and jugular distension with the patient sitting
upright.Chest radiographs revealed cardiomegaly with
pulmonary edema
• Cardiac catheterization is performed. Findings:
‐ Cardiac output : 3.4 L/min (4‐8L/min.)
‐ Ejection fraction 37% (67+ 7)
‐ Right atrial pressure : 12 mmHg (3 mmHg)
‐ Pulmonary arterial pressure : 28 mmHg (9 mmHg)
• The patient continued to suffer from
progressive dyspnea and worsening hypoxia

Describe the morphologic findings of his lungs.
• Why is he dyspneic?
• What is the pathogenesis of this process?
• What is the cause of his liver enzyme elevations?
• What is the pathogenesis of his heart failure?
Describe cardiac morphology

Back 28

1. lung morph: edema, siderophage heart failure cell

2. Dyspneic: (hard to breath): hypoxic, pulm edema, pulm effusion

3. pathogenesis: heart isnt pumping so fluid backs into the lungs

4. in CHF the liver gets backed up, nutmeg liver

5. dilated cardiomyopathy, most common form

Front 29

what does EtOH do to the heart

Back 29

its toxic, can cause dilated myocardial hypertrophy

**can be used to remove excess tissue in HCM

Front 30

what kind of myopathy can you get in pregnancy

Back 30

dilated

Front 31

what does dilated cardiomyopathy look like

Back 31

large globular heart
heart stretches so AV valves get regurg

myocytes hypertrophy and we have subendo fibrosis

Front 32

if the heart has 4 big old chambers what is going on

Back 32

dilated cardiomyopathy

**will have mycardial hypertrophy and increased fibrous tissue

Front 33

what are some clinical findings in dilated cardiomyopathy

Back 33

1. 20-50 yo
progressive CHF, SOB
die due to arrhythemia, 2 mitral regurg
EF is low

tx with transplant

Front 34

tell me about HCM

Back 34

huge heart, in absence of extrinsic stress (exercise)

*EF is normal, but there is impaired compliance, decreased filling, outflow obstruction

Front 35

what myopathy is characterized by a decrease in compliance

Back 35

HCM

Front 36

what is the morphology of HCM

gross
micro

Back 36

1. septal hypertrophy causes banana shaped L vent

Micro:
-myofibir disarray
-myocyte hypertrophy- Extreme
-replacement fibrosis

**septum gets in the way of aortic valve

Front 37

what kind of cardiomyopathy has myofibir disarray at micro

Back 37

HCM

**also has extreme hypertrophy on micro

**the septum gets in the way of the aortic valve
**this is when the septum gets big (L vent also big) and makes a banana shape

Front 38

are cardiomyopathies familial

Back 38

yep, all of them :) get tested if you loved ones goes down!

HCM: always familial
Dilated: can also be caused by myocarditis, peripartum, toxic EtOH. genetics

Front 39

what is the pathogensis of HCM

Back 39

familiar, AD but reduced penetrance so expressed in men more

**mutation that creates abnormal energy transfer in contractile protein. cahnges in sarcomere

Front 40

can dilated cardiomyopathy lead to thrombi

Back 40

yes

Front 41

whats the clinical of HCM

Back 41

impaired diastolic filling of left vent

sudden unexplained death

angina/ischemia (blocked flow due to septum in the way of aorta)

Front 42

The medical examiner’s offices calls to inform
you that they are investigating the sudden death
of one of your patients. He was a 23 y/o recently
evaluated in your office after an episode of syncope
following the funeral of a 21 y/o old cousin who
had died suddenly. Syncope was associated with
mild dyspnea on exertion and palpitations. There
was no associated chest pain. He denied prior
medical illness; murmur or rheumatic feverThere was a forceful systolic heave and apical
precordial impulse displaced far to the left on
the chest wall. The chest x‐ray showed
cardiomegaly with slight atrial enlargement.
An EKG confirmed the presence of LVH. His
liver enzymes were slightly elevated but cardiac
enzymes were negative for myocardial infarction.
He was referred to a cardiologist but had collapsed
suddenly at work and died prior to that visit

The echocardiograph would probably have shown:
• Endomyocardial biopsy would have shown:
• What does the family history indicate about this
disease?

Back 42

1. Echo: HCM, large septum

2. biopsy: extreme hypertrophy and disarray

3. gentic, AD, but penetrance is weird so more common in men

Front 43

we know HCM causes decreased compliance, any others

Back 43

restrictive cardiomyopathy, cant fill vent. no compliance, there is no stretch

Front 44

What are the causes of restrictive
cardiomyopathy

Back 44

caused by amylodisis, infiltrates in the mycardium of improperly folded protein

Front 45

What are the features of
senile cardiac amyloidosis?

Back 45

seen with restrictive cardiomyopathy

**extracellular deposits of misfolded proteion ISOLATED OT HTE HEART!!

Effects old black ppl and the protein is TRANSTHYRETIN,

Front 46

whats transthyretin

Back 46

its amyloid (misfolded protein) that is seen in senile cardiac amyloidosis (isolated ot the heart) and it causes restricted cardiomyopathy

Front 47

A 54 y/o male c/o increasing exercise
intolerance and dependent edema. He has
noted an irregular heart beat.
• Echocardiogram: thickened LV wall, septum
• ECG: Arrhythmia present
Cardiac output decreased on cardiac
catheterization
• An endomyocardial biopsy demonstrated
deposition of amyloid and was + for immunoflurescent stain

What is the diagnosis?
• What type of heart disease is present?
• If this localized to the heart, what material is most
likely to accumulate here

Back 47

1. Dx: restrictive cardiomyopathy


if localized to the heart will ahve transerythretin accumulate (misfolded protein)

Front 48

List 3 uncommon, distinctive causes of
restrictive cardiomyopathy (usually caused by infiltrate in the myocardium)

Back 48

1. endomyocardial fibrosis (kids in africa)
2. loeffler endommyocarditis (eosinophilia)
3. endocardial fibroelastosis (child, cardiac annomolies, thich endo)

Front 49

if the artia are dilated what kind of cardiomyopathy

Back 49

restrictive
**EF is normal
**diastolic dysfx
**ventricles thicken

Front 50

what CM is caused by...

1. various including genetic

2. deposition of amyloid

3. genetic

Back 50

dilation
restrictive, normal EF
HCM, normal EF

Front 51

what is myocarditis, what causes it and whats its characteristic feature

Back 51

inflammation of heart, characterizxed by leukocyte infiltrate, not 2 to ischemia

infections, Immune reactions, sarcoidosis, giant cell myocarditis

Front 52

tell me about coxsackie A/B. what are 5 others that cause myocarditis

Back 52

common cause of myocarditis

hermangina, ulceratinos in back of mouth

1. Lyme disease
2. Diptheriae
3. Trichinosis
4. Toxoplasmosis
5 Chagas
6. viral

Front 53

A 42‐y/o woman presents with a letter stating
that a serologic test of her donated blood was
positive for Chagas' disease.
The patient was born in El Salvador and moved to
the U S when she was 18 years old.
She reports no cardiac or GI symptoms. Her
physical examination is unremarkable.
What are the features of Chagas disease. ECG) shows sinus rhythm at a rate of 72 beats
per minute and p a complete right bundle‐branch
block. Echocardiogram shows mild left
ventricular segmental wall‐motion abnormalities,
but a normal ejection fraction, the characteristic
early cardiac findings of Chaga’s myocarditis
Two serologic tests for Trypanosoma are positive.
She is started on antitrypanosomal therapy to
prevent progression to dilated cardiomyopathy

Back 53

caused by Trypansoma cruzii

causes myocarditis

CHF, dilated cardiomyopathy

Front 54

what are the clinical courses of myocarditis

Back 54

asymptomatic
dilated cardiomyopathy
arrhythemia
sudden death
mitral regurg

Front 55

A 28 y/o male seen in the ER c/o shortness
of breath. He had cough and fever for 2 wks.
He was treated with antibiotics but symptoms
worsened. Hemoptysis and SOB progressed to
dyspnea at rest and orthopnea. There was no
past history of heart or lung disease; he took no
drugs.
• On PE, patient was fit and muscular in moderate
resp. distress. BP 100/70, p155/min, resp. 32/min,
temp. 38.7. O2 86% on room air.Jugular veins were distended to jaw angle
with patient seated. Crackles and ronchi were
present throughout the lung fields. There was
slight pitting edema below the knees.
• ECG showed ST segment elevation in V3 and V4
suggesting acute anterior infarction involving
septal, anterior, and lateral leads. There is marked
left axis deviation indicating anterior fascicular
block.
• Emergency coronary arteriogram was normal.Endomyocardial biopsy showed extensive
lymphocytic infiltrate and necrosis of
myocardium.
• CK rose to 3680 IU/L and troponin I to 92 units
(less than 0.4).
• He was treated with high dose steroids but
progressed to cardiogenic shock and death in
3 days.

What is the diagnosis?
• Why did the ECG and lab work show evidence of
myocardial infarction?
• What is the probable outcome if the patient had
survived the acute illness?
• What is the ultimate treatment for this disease

Back 55

1. myocarditis, viral coxsackie
2. showed infarct bc he had one?
3. outcome: variable, asymptomatic to sudden death
4. transplant

Front 56

what are some cardiotoxic drugs

Back 56

chemo
cocaine

Front 57

what does catecholamine and cocaine do to hart

Back 57

calcium overload, constriction- causes autonomoc stimulation, vasoconstriction occurs even though you need more O2 (coke is a stim- increase HR, ) plaques can rupture

**focal myocyte necrosis, contraction bands, macrophage infiltrate

Front 58

what cardiac pathology is associated with
Fe overload
hyperthyroid
hypothyroid

Back 58

1. hemochomatosis
2. Hyperthyroid: hypertrophy
3. hypothyroidism: myxedema heart, accumulation of mucopolysaccharide

Front 59

What alterations in laboratory tests are seen in
heart failure?

Back 59

Creatanine and BUN increased- poor perfusion to kidney

AST ALT increased bc of hepatic congestrion- nutmeg liver

B natuiretic peptide increased- great predictor of heart failure (releaased from vent in response to stress. causes decreased renin and decreased BP)

Front 60

tell me about B naturetic peptide

Back 60

released from vent when under stress

causes decrease in peripheral Resistance to decrease BP

decreases renin, endothelin

increases natureisis (pee)

Front 61

tell me about pericarditis

1. Serous
2. Purulent
2. fibrinious
4. Caseous

Back 61

1. Serous: noninfectious inflammatory, viral infection.

2. Fibrinious: seen in MI, post infarction syndrome and rheumatic fever. squeaky friction rubs. adhesions are common

3. pululent: due to bacterial infection, adhesions common, mediastinopericarditis or constrictive pericarditis

4. caseous: caused by TB, scarring, fibrocalcific, chronic constrictive pericarditis.

Front 62

can pericarditis cause a pericardial effuction

Back 62

you bet

Front 63

how much fluid can be in the pericardium

Back 63

depends on how fast it gets there

FAST- not so good
SLow accumulation- better

Front 64

what are 3 times you see fibrinious pericarditis

Back 64

1. MI
2. Postintaction syndrome (dresslers syndrome)
3. Rheumatic fever

Front 65

what is adhesive mediastinopericarditis

Back 65

healed pericarditis after suppurative/caseous pericarditis

*parietal pericardium adheres to ehart and results in cardiac hypertrophy/dilation

Front 66

what is constrictive pericarditis

Back 66

pericardium turns into a fibrocalcific scar

diastolic filling is limited, follows TB or supprative infection. BAD

Front 67

A 76y/o female developed cardiac failure
during a febrile illness.
• On PE, there was marked jugular distention
with Kussmaul’s sign (inc. rt. atrial pressure
on inspiration) and edema of legs
• There was mild cardiomegaly on chest x‐ray
with extensive calcifications of ant. and inf.
surfaces of the heart involving both layers of
pericardium.
What is the diagnosis? Likely cause

Back 67

calcific constrictive pericarditis

really thick pericardium