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Clinical Pathology > Cardiovascular diseases 2 > Flashcards

Cardiovascular diseases 2 Flashcards

1
Q

What is the pathogenesis behind left-sided (congestive) heart failure?

A

Hypertension = pressure overload

Valvular disease = pressure/volume overload

MI = regional dysfunction with volume overload

All can lead to increase cardiac work = increased wall stress = cell stretch = hypertrophy and/or dilatation

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2
Q

What are the cellular pathological features of heart failure?

A

Increase heart size and mass

Increased protein synthesis

Induction of immediate-early genes

Induction of foetal gene programme

Abnormal proteins

Fibrosis

Inadequate vasculature

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3
Q

What are the characteristics of cardiac dysfunction?

A

Heart failure (systolic/diastolic)

Arrhythmias

Neurohumoral stimulation

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4
Q

What is the impact of low output left heart failure on the kidneys?

A

pre-renal azotemia

Salt and fluid retention

  • renin-aldosterone activation
  • natriuretic peptides
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5
Q

What is the impact of low output left heart failure on the brain?

A

Brain: Irritability, decreased attention, stupor -> coma

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6
Q

What are the general signs and symptoms of left-sided heart failure?

A

Dyspnea

Orthopnea

PND (Paroxysmal Nocturnal Dyspnea)‏

Blood tinged sputum

Cyanosis

Elevated pulmonary “WEDGE” pressure (PCWP) (nl = 2-15 mm Hg)

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7
Q

What is the main cause of the signs/symptoms of left-sided heart failure?

A

Pulmonary congestion and oedema

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8
Q

What is the aetiology of right-sided heart failure?

A

Left-sided heart failure

Cor pulmonale

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9
Q

What is cor pumonale?

A

Abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels.

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10
Q

What are the signs and symptoms of left heart failure?

A

Liver and spleen

  • passive congestion (nutmeg liver)‏
  • congestive splenomegaly
  • ascites

Pleura/Pericardium

  • pleural and pericardial effusions
  • transudates

Peripheral tissues
- Pitting oedema

Fatigue
GI distress
Distention of jugular veins
Elevation of peripheral venous pressure

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11
Q

What might you find in the autopsy of a person with congestive cardiac failure?

A

Cardiomegaly

Chamber Dilatation

Hypertrophy of myocardial fibers, BOXCAR nuclei

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12
Q

What are the two basic types of valvular heart disease

A

Opening problems: Stenosis

Closing problems: Regurgitation or Incompetence or “insufficiency”

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13
Q

Aortic and mitral stenosis account for what percentage of valvular heart defects?

A

70%

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14
Q

What is the aetiology of aortic stenosis?

A

Calcification of a deformed valve

  • “Senile” calcific AS
  • Rheum, Heart Dis.
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15
Q

What is the aetiology of mitral stenosis?

A

Rheumatic heart disease

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16
Q

What is the precursor to rhematic heart disease?

A

Follows a group A strep infection, a few weeks later.

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17
Q

What is pancarditis?

A

Endocarditis
Myocarditis
Pericarditis

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18
Q

What are the features of acute rheumatic heart disease?

A

Inflammation

Aschoff bodies

Anitschkow cells

Pancarditis

Vegetations on chordae tendinae at leaflet junction

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19
Q

What are the features of chronic rheumatic heart disease?

A

Thickened valves

Commisural fusion

Thick, short chordae tendinae

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20
Q

What are the pertinent features of aortic stenosis?

A

2X gradient pressure

LVH (but no hypertension), ischemia

Cardiac decompensation, angina, CHF

50% die in 5 years if angina present

50% die in 2 years if CHF present

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21
Q

What is mitral annular calcification?

A

Calcification of the mitral “skeleton”

Usually NO dysfunction

Regurgitation usually, but Stenosis possible

More common in males

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22
Q

What are the pathological valve regurgitations?

A

Aortic regurgitation

Mitral regurgitation

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23
Q

What are the aetiologies of aortic regurgitation?

A

Rheumatic

Infectious

Aortic dilatations

  • Syphilis
  • Rheumatoid Arthritis
  • Marfan
24
Q

What are the aetiologies of mitral valve regurgitation?

A

Mitral valve prolapse

Infectious

Fen-Phen (drug)

Papillary muscles, chordae tendinae

Calcification of mitral ring (annulus)

25
Q

What are the features of mitral valve prolapse?

A

MYXOMATOUS degeneration (pathological weakening) of the mitral valve

Associated with connective tissue disorders

“Floppy” valve

3% incidence, F»M

Easily seen on echocardiogram

26
Q

What are the clinical features of mitral valve prolapse?

A
  • Usually asymptomatic
  • Mid-systolic “click”
  • Holosystolic murmur if regurg. present
  • Occasional chest pain, dyspnea
  • 97% NO untoward effects
  • 3% Infective endocarditis, mitral insufficiency, arrythmias, sudden death
27
Q

What is the aetiology of congenital heart defects?

A

Faulty embryogenesis (week 3-8)‏

May not be evident till adulthood

Usually monomorphic

28
Q

What is the incidence of congenital heart defects?

A

1% of births

29
Q

What percentage of congenital heart defects are seen with genetic abnormalities?

A

10%

30
Q

Which of the aneuploidies are involved in congenital heart disease?

A

Trisomies 21, 13, 15, 18, XO

31
Q

What environmental factors might contribute to the development of congenital heart disease?

A

Rubella

Teratogens

32
Q

What are the three types of congenital heart disease?

A

L -> R shunts: all “D’s” in their names (VSD, ASD, PDA, AVSD)

  • NO cyanosis
  • Pulmonary hypertension
  • significant pulmonary hypertension is irreversible

R -> L shunts: all “T’s” in their names

  • cyanosi (i.e., “blue” babies)
  • venous emboli become systemic “paradoxical”

OBSTRUCTIONS: aorta or pulmonary artery

33
Q

Are left to right shunts cyanotic or non-cyanotic?

A

Non-cyanotic

34
Q

What is the most feared consequence of left to right shunts?

A

Irreversible pulmonary hypertension

35
Q

What are different kinds of atrial septal defects?

A

SECUNDUM (90%):
- Defective fossa ovalis

PRIMUM (5%):
- Next to AV valves, mitral cleft

SINUS VENOSUS (5%): 
- Next to SVC with anomalous pulmonary veins draining to SVC or RA

Does not include PFO
Usually asymptomatic until adulthood

36
Q

What are the most common congenital heart disease defects?

A

Ventricular septal defects (VSDs)

37
Q

What percentage of ventricular septal defects are isolated?

A

30%

38
Q

What condition are ventricular septal defects often associated with?

A

Tetralogy of Fallot

39
Q

What percentage of VSDs involve the membranous septum?

A

90%

40
Q

What can happen if the muscular septum is involved in VSDs?

A

Can have multiple holes (Swiss cheese septum)

41
Q

What often happens with small VSDs?

A

They close spontaneously

42
Q

What often happens with large VSDs?

A

Often progress to pulmonary hypertension

43
Q

What percentage of patent ductus arteriosus (PDA) are isolated?

A

90%

44
Q

What other conditions are associated with PDA?

A

VSD

Coarctation of aorta

Pulmonary or aortic stenosis

45
Q

What is the pathology of an atrioventricular septal defect?

A

Associated with defective, inadequate AV valves

Can be partial, or complete (all 4 chambers freely communicate)

More than 1/3rd with complete AVSD have Down syndrome‏

46
Q

Which of the congenital heart defects cause a right to left shunt?

A

Tetralogy of Fallot

Transposition of great arteries

Truncus arteriosus

Total anomalous pulmonary venous connection

Tricuspid atresia

  • ALL THE Ts
47
Q

What are the features of Tetralogy of Fallot?

A

1) VSD, large
2) OBSTRUCTION to RV outflow
3) Aorta OVERRIDES the VSD
4) Right Valve Hypertrophy

48
Q

What does survival in Tetraology of Fallot depend on?

A

On severity of subpulmonic stenosis - the greater the onstruction the greater the right to left shunt

49
Q

What is transposition of the great arteries?

A
  • Abnormal formation of truncal and aortopulmonary septa
  • needs a shunt for survival, obviously
    • PDA or PFO (65%), “unstable” shunt
    • VSD (35%), “stable” shunt
    • RV>LV in thickness
    • Fatal in first few months without shunt
    • Surgical “switching”
50
Q

What is truncus arteriosis?

A

Developmental failure of separation of truncus arteriosus - connection between aorta and pulmonary artery

Associated VSD

Produces systemic cyanosis as
well as increased pulmonary blood flow

51
Q

What is tricuspid atresia?

A

Lack of development of the tricuspid valve.

Needs shunt, ASD, VSD ord PDA

Very high mortality

52
Q

What is a Total Anomalous Pulmonary Venous Connection (TAPVC)?

A

Pulmonary veins do not go into LA, but into L. innominate v. or coronary sinus

Needs a PFO or a VSD

Hypoplastic LA

53
Q

What are the obstructive CHDs?

A
  • COARCTATION of aorta
  • Pulmonary stenosis/atresia
  • Aortic stenosis/atresia
54
Q

What chromosomal abnormality is frequently associated with coarctation of the aorta?

A

XO - Turner Syndrome

55
Q

Which form of coarctation of the aorta is serious?

A

Infantile form - with PDA

56
Q

What are the clinical features of pulmonic stenosis/atresia?

A
  • If 100% atretic, hypoplastic RV with ASD

- Clinical severity ~ stenosis severity

57
Q

What are the different types of aortic stenosis/atresia?

A

VALVULAR
- If severe, hypoplastic LVfatal

SUB-valvular (subaortic)‏
- Aortic wall THICK BELOW cusps

SUPRA-valvular
- Aortic wall THICK ABOVE cusps in ascending aorta

Clinical Pathology (65 decks)

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