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CRS > Lecture 13+14 > Flashcards

Lecture 13+14 Flashcards

1
Q

Association of Rheumatic heart disease and IE

A

S pyrogens M protien leads to the creation of Ab’s

there is a cross reaction with organs that host similar organisms such as heart and joints

risk factor for IE

could be after ‘strep throat’
type II sensitivity

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2
Q

enterococcus spp.

A

Can cause both NVE and PVE

Responsible for both community acquired, and healthcare associated IE

features:
members of normal enteric flora

gram positive cocci
diplococci, short to med chains
catalase - and coagulase -
ferments mannitol

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3
Q

E. faecalis

A

Most commonly isolated, and causes 85-90% of
enterococcal infections

Particularly intensive care unit infections

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4
Q

E. faecium

A

Responsible for 5 -10% of enterococcal infections

Displays higher levels of antibiotic resistance

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5
Q

patho of enterococcus (endocarditis)

A

Surface adhesion proteins expressed to attach to
extracellular structures

biofilm formation

are intrinsically resistant to some antibiotics

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6
Q

Staphylococcus aureus

A

coagulase and catalase +

MSA = yellow

beta hemolytic

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7
Q

Staphylococcus epidermidis

A

coagulase -
catalase +

MSA = red

non/gamma hemolytic

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8
Q

Streptococcus sanguinis

A

coagulase and catalase -

MSA = no growth

alpha hemolytic

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9
Q

Enterococcus faecalis

A

coagulase and catalase -

MSA = yellow

non/gamma hemolytic

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10
Q

HACEk organisms

A 
Haemophilus spp.
Aggregatibacter actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella kingae
features: 
• Commensals of the oropharyngeal tract
• Gram-negative coccobacilli bacteria
• Slower growing
• Fastidious
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11
Q

Most common HACEK group organisms to cause IE

A

Haemophilus aphrophilus….Aggregatibacter aphrophilus

commonly found in dental plaque and gingival scrapings

Cases of IE are often associated with dental disease

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12
Q

Aggregatibacter actinomycetemcomitans

A

colonies are star shaped

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13
Q

Culture negative infective endocarditis

A

Antecedent administration of antimicrobial therapy

Fastidious bacteria or non-bacterial pathogens e.g. fungi, parasites

solution:
serology or PCR

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14
Q

myocarditis

A

children:
Viral prodrome common

Respiratory distress, resting tachycardia/ arrhythmias,
dyspnea, syncope, Heart failure symptoms etc.

adult:
Viral prodrome common

Chest pain, palpitations/arrhythmias, heart failure symptoms

DDX: Acute Coronary Syndrome – ECG, cardiac
biomarkers

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15
Q

microbial causes of myocarditis

A

viral causes are most common
bacterial is uncommon

parasites may been seen in low income countries
fungal cases are increasing

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16
Q

viral myocarditis

A

Enterovirus spp. (Coxsackievirus B)

Coxsackievirus B3 is a common cause of primary myocardial disease in humans

Coxsackie virus utilizes the coxsackie-adenovirus receptor (CAR) on the surface of myocytes to gain entry into the cell.

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17
Q

fungal myocarditis

A

Candida and Aspergillus

Most commonly associated with immunocompromised/immunosuppressed patients.

Most cases occur following systemic mycoses -disseminated fungal infections

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18
Q

parasitic myocarditis (Trypanosoma)

A

Intracellular flagellated protozoan parasite
Vector-borne transmission (main)

High grade parasitemia and direct tissue parasitism
Up to 30% of patients develop Chronic Chagas Cardiomyopathy

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19
Q

parasitic myocarditis (toxoplasma)

A

Obligate Intracellular protozoan parasite

Distinct clinical syndromes in immunocompromised individuals

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20
Q

acute pericarditis

A

most common disorder affecting the pericardium
usually only lasts 1-3 weeks

features:
fever
chest pain (sudden, sharp and improves with sitting up)

pericardial friction rub
ECG changes
+/- pericardial effusion

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21
Q

etiological causes of acute pericarditis

A

viruses: Coxsackievirus A and B

bacteria: gram + and - spp.
rarely mycobacterium tuberculosis

fungi (immunocompromised):
Blastomyces dermatitidis
Candida spp.
Histoplasma capsulatum

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22
Q

diagnosis of acute pericarditis

A 
pericardial friction rub 
ECG
cardiac biomarkers 
blood cultures 
chest X-ray 
echocardiogram
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23
Q

hypertensive heart disease progression

A
  1. chronic HTN
  2. increased demand and pressure overload
  3. hypertrophy
  4. maladaptive response over time
  5. dysfunction and ischemia
  6. CHF and death
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24
Q

Systemic left sided hypertensive heart disease

A

Left ventricular hypertrophy in the absence of other cardiovascular pathology

Clinical history or pathologic evidence of hypertension in other organs (e.g., kidney)

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25
Q

Isolated Pulmonary right sided hypertensive heart disease

A

Right ventricular and right atrial hypertrophy

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26
Q

systemic hypertensive heart disease features

A

early stages: asymptomatic

Angina pectoris
Signs and symptoms of left heart failure with
progression

Cerebrovascular accidents (stroke) or renal failure as a
consequence of HTN

Sudden cardiac death

27
Q

pulmonary hypertensive heart disease features

A

Disease of right sided cardiac chambers secondary to pulmonary parenchymal or pulmonary vascular
diseases

excluded:
Pulmonary hypertension due to left heart failure

Pulmonary hypertension due to congenital heart disease

28
Q

systemic hypertensive heart disease histo

A

concentric hypertrophy of LV

enlarged myocytes with large rectangular nuclei

29
Q

acute cor pulmonale (pulmonary hypertensive HD)

A

Pulmonary embolism causing sudden increase in
burden on the right heart

Right ventricle is dilated but no hypertrophy

30
Q

chronic cor pulmonale

A

COPD – Most common cause

Others – Idiopathic pulmonary fibrosis, cystic fibrosis or marked obesity

31
Q

patho of viral myocarditis

A

Direct viral cytotoxicity

Cell mediated immune reactions against infected myocytes

Cytokines released can aggravate myocardial dysfunction

32
Q

clinical of viral myocarditis

A

Varies from asymptomatic to sudden acute heart failure or arrhythmias

Flu-like symptoms
Fatigue, dyspnea, palpitations, chest pain, fever
May mimic acute MI

investigations:
PCR for virus
serology

33
Q

histo of myocarditis

A

Interstitial inflammation mainly lymphocytes and
a few plasma cells

Focal necrosis of myocytes adjacent to
inflammatory cells

34
Q

complications of myocarditis

A
  • Acute heart failure
  • Viral myocarditis may lead to dilated cardiomyopathy→ Chronic CHF
  • Arrhythmias: ventricular arrhythmias are the most dangerous → SCD
35
Q

Trichinella spiralis (Trichinosis) (myocarditis)

A

• Most common helminth associated with
myocarditis.
• Histologically: eosinophils predominance

36
Q

Trypanosoma cruzi (Chagas disease)

A

myocarditis (parasitic)
Endemic in South America.

Myocardium involved in majority of cases.

Parasitization of scattered myofibers by trypanosomes accompanied by a mixed inflammatory infiltrate

37
Q

Toxoplasmosis (Toxoplasma gondii) and myocarditis

A

parasitic

Household cats are the most common vector

Causes myocarditis in immunocompromised

38
Q

histo of fungal myocarditis

A

Morphology is characterized by the presence of mixed inflammatory infiltrate composed of neutrophils, lymphocytes, and plasma cells

39
Q

hypersensitivity myocarditis

A

Methydopa and sulfonamides

Mild and self limiting

Composed of lymphocytes, macrophages and abundant eosinophils

40
Q

giant cell myocarditis

A

idiopathic
associated with SLE, thyrotoxicosis

fatal disease in those 40-50

cause of death is CHF or arrhythmia

41
Q

histology of giant cell myocarditis

A

Granulomatous inflammation with many giant cells, lymphocytes, eosinophils and plasma cells

Focal to extensive necrosis

42
Q

cardiomyopathy

primary vs secondary

A

Associated with mechanical and/or electrical dysfunction
Usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation

Primary cardiomyopathies: involve predominantly the heart → may be genetic or acquired (e.g., viral myocarditis, anthracycline cardiotoxic)

Secondary cardiomyopathies: myocardial involvement as a component of a systemic or multiorgan disorder (e.g. hemochromatosis, amyloidosis

43
Q

Dilated Cardiomyopathy (congestive cardiomyopathy)

A

morphologically and functionally by progressive cardiac dilation and contractile (systolic) dysfunction, usually with concomitant hypertrophy
leads to HF

etiopath:
cause is unknown

more common genetic (auto dom) 
less common (X linked due to dystrophin gene mutation) 
uncommon (mutation of mito proteins)

alcohol is direct cytotoxicity

viral (viral myocarditis) 
nutritional disturbances (thiamine and anemia) 
chemo (doxorubicin) 
stress
peripartum
44
Q

clinical features of DCM

A

Affects mostly individuals between 20-50 year

Fundamental defect is ineffective contraction
Ejection fraction is < 25% (normal 50-65%)

Progressive CHF refractory to therapy, usually end stage by the time of clinical discovery

treatment:
transplantation

45
Q

histology of DCM

A
  • Interstitial and endocardial fibrosis
  • Small subendocardial scars may replace individual cells or groups of cells
  • Most muscle cells are hypertrophied with enlarged nuclei (Some are attenuated, stretched, and irregular)
46
Q

Arrhythmogenic RV Cardiomyopathy

A 
inherited right ventricular cardiomyopathy that classically manifests with right-sided heart failure and rhythm disturbances, which can cause sudden
cardiac death (auto dom)

etio:
Mutations in genes coding for Desmosomal junctional proteins at intercalated disk → plakoglobin

Proteins that interact with desmosome→ intermediate filaments like desmin

47
Q

naxos syndrome

A

Arrhythmogenic right ventricular cardiomyopathy

Hyperkeratosis of plantar and palmar skin surfaces

Associated with plakoglobin mutations

48
Q

histo and gross of Arrhythmogenic RV Cardiomyopathy

A

the RV is major dilated

histo:
the myocardium is replaced by FCT and fat

49
Q

Hypertrophic Cardiomyopathy

A

genetic disorder, auto dom, that leads to myocardial hypertrophy

Leading cause of left ventricular hypertrophy unexplained by other clinical or pathologic causes

Heart is thick-walled, heavy, and hypercontracting
(Primarily diastolic dysfunction)

etiology: 
Missense point mutations in any one of several genes that encode sarcomeric proteins
• β-myosin heavy chain – most common
• Myosin-binding protein C
• Cardiac troponin T
50
Q

patho of hypertrophic cardiomyopathy

A

Gain of function mutation of the sarcomeric proteins → Myocyte hypercontractility → Increase energy use → Intense compensatory hypertrophy (myofiber disarray) and fibroblast proliferation

51
Q

clinical features of hypertrophic cardiomyopathy

A

Massively hypertrophied LV that paradoxically provides markedly reduced stroke volume → Congestive heart failure

Increased demand for oxygen and metabolites by hypertrophied muscle, high left ventricular pressure and compromised intramural coronary arteries leads to
ischemia → Angina

Decreased cardiac output and a secondary increase in pulmonary venous pressure → Exertional dyspnea

Harsh ejection systolic murmur

Sudden death – due to arrhythmias

One of the most common causes of sudden, otherwise unexplained death in young athletes

52
Q

gross and histo of hypertrophic cardiomyopathy

A

gross:
asymmetric septal hypertrophy
massive myocardial hypertrophy

histo:
Marked myocyte hypertrophy – transverse
myocyte diameter is >40 µm (normal 15 µm)

Myofiber disarray - haphazard arrangement of
hypertrophied, abnormally branching myocytes

Interstitial fibrosis

53
Q

Restrictive Cardiomyopathy

A

Primary decrease in ventricular compliance, resulting in impaired ventricular diastolic filling

etiology: 
amyloidosis
sarcoidosis 
radiation induced
tumor 
metabolism disorder  
fibrosis
54
Q

clinical features of RC

morphology?

A
  • Exertional dyspnea
  • Fatigue
  • Chest pain
  • Complications include arrhythmias and congestive heart failure

morph:
• Bi-atrial dilation due to restricted ventricular filling and pressure overloads
• Ventricles approximately normal size (or slightly enlarged)
• Cavities are not dilated
• Myocardium is largely unremarkable

55
Q

endomyocardial fibrosis (EMF)

A
  • A type of restrictive cardiomyopathy
  • Children and young adults
  • Africa and the tropics
  • Dense fibrosis of endocardium and subendocardium from apex to AV valves
  • Reduced volume and compliance of affected chambers
56
Q

Loeffler’s endomyocarditis

A
  • Clinically a restrictive cardiomyopathy
  • Endocardial fibrosis with large mural thrombi
  • Peripheral hypereosinophilia
  • Abnormal degranulated eosinophils
  • Major basic protein (MBP) from granules of eosinophils → endocardial damage, necrosis and fibrosis
57
Q

primary pericarditis

A

uncommon and infection origin

58
Q

Secondary pericarditis

A 
• MI, cardiac surgery
• Uremia – most common systemic disorder associated
with pericarditis.
• Radiation induced
• Rheumatic fever, SLE
• Malignancies
59
Q

fibrinous pericarditis

A
  • Bread and butter- irregular shaggy

* Seen in RHD, uremia, post-MI, post viral

60
Q

fibrinous and hemorrhagic pericarditis

A

seen in malignancy

61
Q

Fibrinopurulent (suppurative) pericarditis

A

seen in pericarditis due to bacteria

62
Q

Caseous pericarditis

A

tuberculosis

63
Q

chronic pericarditis

A

Produces a combination of right sided venous distention and low cardiac output.
Similar to restrictive cardiomyopathy

progresses to chronic:

Usually following caseous and suppurative pericarditis but can be idiopathic
Chronic constrictive pericarditis

morphology:
Delicate adhesions to dense, fibrotic scars that obliterate the pericardial space

Extreme cases – heart is completely encased with dense scar tissue; can not expand – “constrictive” pericarditis

CRS (16 decks)

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