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Pathology Term 1 > Week 1 - CVS > Flashcards

Week 1 - CVS Flashcards

ARF, RHD, IE, Cong. Heart Disease, CMP

1
Q

Describe septum appearance in Hypertrophyic CMP

A

Irregular thickening of septum –> becomes abnormally large (due to abnormal B-myosin) –> therefore ventricular lumen becomes very narrow (like a BANANA)

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2
Q

What are complications of valve replacement?

A
  1. Tissue Valves –> degeneration requiring a 2nd operation

2. Mechanical Valves –> need for anticoagulant therapy to prevent thrombus formation

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3
Q

What is NBTE?

A

“Non-Bacterial Thrombotic Endocarditis”

  • thrombus formation on valves (hypercoagulable state, DIC, malignancy, etc.)
  • may cause strokes or secondary bacterial infections
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4
Q

What are Libman-Sacks?

A

Sterile immune complex vegetations seen in autoimmune disorders (e.g. SLE)

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5
Q

What are the risk factors and complications for infective endocarditis in RHD?

A

Risk Factors:

  • poor dental hygiene
  • systemic sepsis
  • diabetes
  • immunosuppression
  • trauma/surgery
  • IVDU

Complications:

  • septic embolism
  • septicaemia
  • renal/spleen infarcts
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6
Q

What is the aetiology of mitral valve prolapse?

A
  • MI
  • Primary 3-5% congenital degeneration
  • Marfan’s Syndrome –> fibrillin gene mutation causing abnormal connective tissue
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7
Q

What is the morphology of myocarditis?

A
  • inflammation
  • lymphocytes
  • fibrosis (late)
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8
Q

What are the clinical features of myocarditis?

A
  • pain
  • fever
  • arrhythmias
  • CHF–> sudden death :(
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9
Q

What are the causes of myocarditis?

A

Viral: - enterovirus, CMV, EBV, HIV
Bacterial: - diptheria, leptospirosis, Lyme’s disease
Parasitic: - trypanasoma, toxoplasmosis, trichinosis
Other: - Immune (SLE), ionising radiation, drugs (e.g. doxorubicin)

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10
Q

What type of dysfunction is restrictive CMP?

A

Diastolic dysfunction –> normal sized but impaired diastolic filling due to stiff firm ventricles

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11
Q

What are the gross features of restrictive CMP?

A
  • normal sized ventricles/rarely enlarged

- myocardium is firm/rigid

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12
Q

What are the causes of restrictive CMP?

A
  • idiopathic, iron deposition
  • AMYLOIDOSIS –> amyloid deposition
  • endomyocardial fibrosis –> children, helminths, malnutrition, eosinophilia
  • loeffler endomyocarditis –> adults, mural thrombi, hypereosinophilia?
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13
Q

What type of dysfunction is hypertrophic CMP?

A

Diastolic dysfunction –> rigidity of myocardium results in low stroke volume/cardiac output

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14
Q

What is the cause of hypertrophic CMP?

A

100% genetics - sarcomere dysfunction (autosomal dominant mutation in B-myosin)
-cause of sudden cardiac death in young :(

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15
Q

What is the microscopy of hypertrophic CMP?

A
  • hypertrophy
  • disorientation of myofibres
  • fibrosis
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16
Q

What is ARVC?

A

“Arrhythmogenic Right Ventricular Cardiomyopathy”

  • type of dilated CMP (RARE)
  • inherited, thin, dilated RV with complete loss of muscle (replaced by fibrous wall)
  • arrhythmogenic, VT & fibrillation
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17
Q

What type of dysfunction is dilated CMP?

A

Systolic dysfunction –> heart cannot properly contract and consequently becomes weak due to a structural abnormality (cytoskeleton dystrophin)

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18
Q

What is the main cause of secondary/acquired dilated CMP?

A 
alcohol abuse
(N.B. genetics = 20%)
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19
Q

Describe the gross features of a heart with dilated CMP?

A
  • flabby
  • enlarged
  • 4-chamber dilatation
  • mural thrombi –> can cause a stroke
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20
Q

What happens to the LV ejection fraction in dilated CMP?

A

LVEF < 25% –> slowly progressive CHF

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21
Q

What is cardiomyopathy?

A

intrinsic myocardial dysfunction due to structural or electrical abnormality without significant inflammation (otherwise it would be called myocarditis)

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22
Q

What is Coarctation of aorta? And what are the 2 types?

A

congenital disorder that results in narrowing of the aorta.

  1. Infantile/Pre-ductal
    - narrow aorta with patent ductus arteriosus –> cyanosis of lower half of body and early death :(
  2. Adult/Post-ductal
    - closed PDA, slight aorta narrowing –> upper extremity HTN with lower limb claudication
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23
Q

What is the only instance in which a patient can survive with transposition of the great arteries (TGA)?

A

if there is an associated VSD

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24
Q

What is Eisenmenger’s complex?

A

Reversal of a shunt (i.e. ASD) with cyanosis - from R –> L

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25
Q

What can occur in ASD?

A

asymptomatic till adulthood - usually a small murmur.

-CHF, pulmonary HTN (late/rare) –> RVH can result from pulm HTN

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26
Q

What are the complication of ASD?

A
  • Eisenmenger’s complex

- Infective endocarditis and paradoxical embolisation (thrombus traveling from one side to the other)

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27
Q

What is patent foramen ovale?

A

-lack of fusion of septum primum and spetum secundum
-NOT and ASD
-80% close in first 2yrs of life
20% remain patent after 2yrs –> temporary L-R shunt (increased right sided pressure)

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28
Q

When do congenital heart defects occur in utero?

A

4-9wks gestation (during organogenesis)

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29
Q

What is the etiology of congenital heart diseases?

A
  • 80% = unknown

- 20% = alcohol/drugs, rubella, diabetes, vitamin def.

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30
Q

Outline fetal circulation

A
  • non functional lungs
  • maternal blood –> umbilical veins to right side –> shunt to left by : ductus arteriosus, foramen ovale and ductus venosus (liver)
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31
Q

What are the valve problems that cause:

  1. pan-systolic murmur
  2. mid-diastolic murmur
  3. ejection systolic murmur
  4. early diastolic murmur
A
  1. Mitral regurgitation - often radiates to axilla
  2. Mitral stenosis - opening snap
  3. Aortic stenosis - radiates to carotids; systolic ejection click
  4. Aortic regurgitation - heard best with pt. leaning forward
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32
Q

What are the complications of ARF + RHD?

A

ARF:

  • arrhythmia
  • cardiac hypertrophy
  • heart failure

RHD:

  • arrhythmia
  • AF –> thromboembolism
  • infective endocarditis
  • heart failure
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33
Q

What are mitral facies and why do they occur?

A

butterfly rash over nose and cheeks occurring in mitral stenosis patients
- occurs due to chronic hypoxemia and cutaneous vasodilation

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34
Q

What are gross and microscopic features of ARF?

A

Gross:
-Pancarditis (Pericarditis –> fibrinous; Myocarditis –> T-cell inflamm; Endocarditis –> vegetations)

Micro:
-Aschoff body (fibrinoid necrosis, macrophages/giant cells, t lymphocytes)

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35
Q

Outline pathogenesis of rheumatic fever

A
  1. Susceptible host (ATSI; children 5-15)
  2. Environmental factors –> overcrowding, nutrition, repeated GAS infections
  3. ARF develops 2-3wks following pharyngitis as development of autoimmunity needs time for T-cell proliferation
  4. Molecular mimicry (cross-reactivity with GAS M protein)
  5. T - cell mediated autoimmune response –> deposition of cross-reactive Ab –> vegetations, aschoff bodies, fibrosis
  6. Repeated ARF attacks + fibrosis –> yrs –> chronic RHD!
36
Q

What is rheumatic fever?

A
  • multisystem, autoimmune, inflammatory disorder that affects heart, skin, brain and joints
  • follows a GAS infection
37
Q

What is required clinically for a Dx. of infective endocarditis according to Dukes’ Criteria?

A

2 major OR 1 major + 3 minor OR 5 minor

38
Q

What are the major and minor criteria for Dukes Criteria for infective endocarditis?

A

Major:

    • blood culture for IE
  • evidence of endocardial involvement (+ ECHO)

Minor:

  • predisposition (IVDU/heart condition)
  • fever (>38)
  • vascular phenomena (Janeway’s lesions, arterial emboli)
  • immunologic phenomena (glomerulonephritis, osler’s nodes, roth’s spots)
  • microbiological evidence
  • echocardiographic findings
39
Q

True or False?

Clinical features of myocarditis can mimic those of acute MI

A

True

40
Q

What is the most common cause of myocarditis?

A

Viral infections

-esp. enteroviruses (coxsackie A+B)

41
Q

What is the key feature of syphilic heart disease?

A

Aortitis

42
Q

What is stress (takotsubo) CMP?

A

acute, reversible LV systolic dysfunction

  • caused by severe stress/emotional trauma
  • AKA broken heart syndrome
43
Q

What is Cor Pulmonale?

A

R-sided heart failure secondary to lung disease (i.e. COPD/pulmonary hypertension)

44
Q

How does restrictive CMP cause heart failure?

A

stiff ventricular walls –> decreased ventricular compliance –> restricted ventricular filling –> decreased diastolic volume of one/both ventricles –> diastolic dysfunction –> HEART FAILURE

45
Q

What is the most common cause of cyanosis in infancy?

A

Tetralogy of Fallot

46
Q

What murmur is heard in a VSD?

A

Loud pansystolic murmur + thrill

47
Q

How does dilated CMP cause heart failure?

A

Dilatation of all 4 chambers –> hypertrophy occurs with impaired contraction of LV –> systolic dysfunction –> HEART FAILURE (LVEF < 25%)

48
Q

Clinically, what do endocarditis, myocarditis and pericarditis each give rise to?

A

Endocarditis –> murmurs
Myocarditis –> arrhythmias
Pericarditis –> pericardial rub

49
Q

Why is there shortening/fusion of chordae tendinae in RHD?

A

INFLAMMATION

  • andiogenesis and fibrogenesis factors attracted to valve inflammation cause constant healing and scarring of chordae tendinae which overtime shorten as a result (think of how a scab shortens with time)
  • also the reason why BVs are present in abnormal RHD valves
50
Q

What is the pathognomonic feature of ARF?

A

Aschoff Bodies

51
Q

What is the most characteristic serum finding in ARF?

A

Increased ASO titre (Anti-Streptolysin O)

-Abs against streptolysin O which is a substance produced by GAS bacteria.

52
Q

What is the pathogenesis of SOB in RHD?

A

Mitral stenosis –> backlog of blood from LA to lungs –> increased pulmonary hydrostatic pressure –> fluid in lungs –> SOB

53
Q

True or False?

Cardiac tamponade is a complication of MI

A

True

54
Q

How can mitral stenosis lead to RVH/Heart failure?

A
  • Stenotic valve = decreased blood flow from LA –> LV
  • Therefore increase LA presssure –> increased pulmonary venous pressure –> pulmonary hypertension –> RVH/Heart failure
55
Q

How can mitral stenosis lead to AF?

A

Increased LA pressure due to decreased blood flow from LA to LV –> LA enlargement –> further travel required for impulses which can cause circus impulses –> AF

56
Q

What is the pathogenesis of mitral facies?

A

Dilation of capillaries due to low CO in mitral stenosis

57
Q

How can MI cause mitral regurgitation?

A

Infarct can prevent papillary muscles from contracting and closing the valves properly

58
Q

What axis deviation on an ECG occurs in mitral regurgitation?

A

Right

59
Q

What is a bifid P wave and when is it commonly seen?

A
  • biphasic P wave

- seen in LA enlargement (due to mitral stenosis commonly)

60
Q

What are complications of infective endocarditis?

A
  • septic embolism
  • septicaemia
  • glomerulonephritis
  • splenomegaly
  • arrhythmias
61
Q

Compare the 2 types of endocarditis

A

Acute Endocarditis :(

  • rare, elderly, IVDU
  • occurs on normal valves
  • highly virulent bacteria (S.aureus)
  • necrotising, destructive lesions
  • sudden onset (abrupt fever, fatigue, weakness)
  • poor prognosis
  • increased mortality

Sub-acute Endocarditis :)

  • common, any age
  • occurs on abnormal valves
  • less virulent bacteria (S.viridans)
  • less destructive lesions
  • slow onset (wks –> mths)
  • good prognosis (cure with antibiotics)
  • decreased mortality
62
Q

What additional sound is heard in mitral stenosis?

A

Opening snap

63
Q

When is non-systolic ejection click and systolic ejection click heard?

A

Non-systolic –> mitral valve prolapse

Systolic –> aortic stenosis

64
Q

True or False?

Mitral valve prolapse is more common in males

A

False - females

65
Q

What is the gross appearance of aortic valve calcification?

A

Thick, irregular, fibrosed valve with nodules of calcification

66
Q

What is the etiology of aortic valve calcification and what can result from it?

A
  • progressive age-associated “wear and tear”
  • congenital bicuspid aortic valves increased risk
  • with time can cause LVH and failure
67
Q

What is the most common cause of aortic valve stenosis?

A

Aortic valve calcification

68
Q

What are the 4 components to Tetralogy of Fallot?

A
  1. VSD
  2. RVH (as a result)
  3. Pulmonary stenosis
  4. Overriding aorta

Therfore R–>L shunt with cyanosis and clubbing

69
Q

What is the murmur heard in patent ductus arteriosus?

A

Harsh, machinery-like murmur

70
Q

Which congenital heart defect is the commonest at birth?

A

Ventricular Septal Defect

-BUT –> 50% of cases close without therapy - thus ASDs are the most common congenital defects overall

71
Q

What are Anitschkow cells?

A
  • Activated macrophages found within the aschoff bodies of rheumatic heart fever patients on microscopy.
  • They have a characteristic caterpillar or owl-eyed nuclei appearance
72
Q

Why do patients receive long tern antibiotic Tx. after ARF but not during ARF?

A
  • ARF = autoimmunt disease NOT an infection

- antibiotic treatment given after ARF to prevent RHD developing by stopping recurrent attacks of endocarditis

73
Q

What are MacCallum plaques?

A
  • occur in chronic RHD
  • rough, fibrous plaques in LA caused by regurgitation of jets of blood flow through valve due to mitral stenosis/regurgitation
74
Q

What are the gross features of valves in RHD?

A
  • leaflet thickening
  • commisural fusion (fish-mouth)
  • shortening, thickening and fusion of chordae tendinae
75
Q

Why is ARF incidence increased in children (esp. 5-15yrs)?

A

early exposure to environmental factors

76
Q

What is an Aschoff body?

A

small granulomatous lesions seen in ARF patients consisting of: - fibrinoid necrosis of collagen, macrophages & giant cells, T lymphocytes

77
Q

True or False?

Aschoff bodies are seen in RF but NOT RHD

A

True

78
Q

Which valves are most commonly affected in ARF and why?

A
  • mitral and aortic valves (increased mitral)

- exposed to the highest pressure of all the valves thus increased damage

79
Q

What is the pathogenesis of vegetations/endocarditis in ARF?

A
  • Abs attack collagen which is normally covered by endocardial layer
  • Edges of valves which constantly hit each other begin to form small ulcers which expose underlying collagen allowing Abs to bind
  • Platelet agglutination results at valve border surface
  • Platelets + Ulcers = VEGETATIONS
80
Q

What is the pathogenesis of pericarditis in ARF?

A
  • fibrinogen leaks out of BVs and clots on pericardial surface forming fibrin deposits and threads
  • “Bread and Butter” pericarditis –> pericardial rub as it is no longer smooth
  • result of T cell autoimmunity
  • marked vasodilation and oedema in pericardial sac
81
Q

Describe features of ARF on CXR

A
  • cardiomegaly

- opacities in lungs from pulmonary oedema

82
Q

What are the major and minor criteria for ARF according to Jones’ criteria?

A

Major:

  • pancarditis
  • migratory polyarthritis
  • erythema nodosum
  • sydenham’s chorea
  • subcutaneous nodules

Minor:

  • fever
  • prolonged PR interval
83
Q

What are the diagnostic requirements for ARF?

A
  • 2 major criteria OR 1 major + 2 minor criteria

- PLUS evidence of a preceding GAS infection

84
Q

Describe appearance of normal heart valves compared to RHD valves

A

Normal:

  • avascular
  • transparent
  • thin
  • elastic/flexible

RHD:

  • vascular
  • fibrous/calcification
  • thick
  • scarred
  • stenotic and fixed (MS/MR)
85
Q

What are the 3 etiological factors for rheumatic fever?

A
  1. Genetics –> ? (increased in ATSIs)
  2. Environment –> GAS infection - overcrowding, poor nutrition, poor housing/sanitation, etc.
  3. Autoimmunity –> T-cell; Anti-DNAse B

Pathology Term 1 (6 decks)

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