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Yr 2 - Clinical Pathology > Cardiovascular Pathology 2 > Flashcards

Cardiovascular Pathology 2 Flashcards

1
Q

Define heart failure

A

Inability of the heart to pump enough blood needed to meet the metabolic demands of the tissue

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2
Q

Causes of heart failure:

A
  • Coronary artery disease
  • Hypertension
  • Cardiomyopathy
  • Arrhythmias
  • Valvular disease
  • Congenital heart disease
  • Anaemia
  • Thyroid disease
  • Alcohol
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3
Q

What is congestive cardiac failure?

A

HF specifically refers to the stage in which fluid builds up within the heart and causes it to pump inefficiently.

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4
Q

CHF can occur over time or acutely. What would cause CHF to occur acutely?

A

Acute haemodynamic stress e.g. fluid overload and large MI

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5
Q

CHF can occur over time. What are the 2 main factors that can cause this to happen?

A

The cumulative effects of chronic workload:

  1. Hypertension and/or
  2. Valve diseases
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6
Q

How does chronic workload lead to CHF?

A
  1. Cardiac myocytes are stretched –> stimulates hypertrophy and sometimes dilatation
  2. LV tries to adapt; thickened left ventricular wall leading to decreased space in left ventricular chamber
  3. Myocytes then overstretch and lose elasticity; thinner ventricular wall and increased space in left ventricular chamber
  4. This leads to heart failure and arrhythmias
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7
Q

As the heart fails, the body tries to compensate.

a) How is HR affected?
b) How is contractility affected?
c) How is fluid volume affected?

A

a) HR is increased via release of noradrenaline
b) Contractility is increased via release of noradrenaline
c) Fluid volume is adjusted via activation of RAAS and release of ANP

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8
Q

What is ANP? Effect?

A

Atrial natriuretic peptide (ANP) is a cardiac hormone that regulates salt-water balance and blood pressure by promoting renal sodium and water excretion and stimulating vasodilation.

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9
Q

Pathogenesis of LS heart failure:

A
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10
Q

What is the Frank-Starling mechanism?

A

Is the description of cardiac hemodynamics as it relates to myocyte stretch and contractility:

Stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction.

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11
Q

Function of this stroke volume adjustment described by Starling’s Law?

A

This allows the cardiac output to be synchronised with the venous return and the arterial blood supply.

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12
Q

The clinical effects of LS heart failure are due to which 3 main factors?

A
  1. Low cardiac output
  2. Hypoperfusion of tissues
  3. Pulmonary congestion
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13
Q

Why can heart failure lead to pulmonary oedema?

A

When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.

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14
Q

What are heart failure cells? Where are they seen?

A
  • WHAT: Macrophages containing hemosiderin generated in the alveoli of patients with left heart failure or chronic pulmonary edema
    • When the high pulmonary blood pressure causes RBCs to pass through the vascular wall where they break down; hemosiderin is one of the breakdown products
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15
Q

What are the respiratory signs and symptoms seen in LS heart failure?

A
  • Oedema
  • Dyspnoea
  • Orthopnoea – ask about pillows!
  • PND (paroxysmal nocturnal dyspnoea) – attack of severe SOB and coughing, generally occurs at night
  • Blood tinged sputum
  • Cyanosis
  • Elevated pulmonary ‘WEDGE’ pressure (PCWP) i.e. pulmonary hypertension
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16
Q

How does LS heart failure affect the kidneys?

A

Reduced renal perfusion

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17
Q

How does heart failure affect the levels of nitrogenous waste products in the blood? What is this condition called?

A

1) Inadequate perfusion to kidney causes body to increase the intraglomerular hydrostatic pressure in an effort to support glomerular function
2) This leads to rise in blood urea nitrogen (BUN) concentration (and serum creatinine)

This is called pre-renal azotemia

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18
Q

How can reduced renal perfusion due to heart failure affect RAAS? What is the effect of this?

A
  • RAAS is activated in patients with heart failure causing salt and fluid retention –> this causes expansion of interstitial and intravascular fluid volume
  • This can can further volume overload a failing system
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19
Q

What neurological effects can advanced cardiac failure lead to?

A
  • Cerebral hypoxia
  • Irritability
  • Restlessness, stupor, coma
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20
Q

What are the 2 major causes of right sided heart failure?

A

1) Left sided heart failure
2) Cor pulmonale

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21
Q

How can LS HF lead to RS HF?

A
  1. LV pumps inefficiently causing a backlog of blood in left side of heart
  2. RV continues to pump blood as normal – blood turns into a traffic jam when it gets to left side of heart
  3. Traffic jam eventually causes blood to back up into the lungs – right side of heart then has to work harder to push blood
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22
Q

What is cor pulmonale?

A

RS HF secondary to pulmonary hypertension; high blood pressure within lungs can cause enlargement of RV

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23
Q

RS HF leads to engorgement of systemic and portal venous systems. This can affect the liver and spleen. What symptoms can show this?

A

Due to portal vein congestion:

  • Passive congestion (nutmeg liver)
  • Congestive splenomegaly
  • Ascites
  • Congestion and oedema of bowel wall
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24
Q

What effects can systemic venous congestion seen in heart failure have on the pleura/pericardium?

A
  • Pleural and pericardial effusions
  • Transudates
  • Oedema of peripheral and dependent parts of body
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25
Q

Does systemic venous congestion lead to the formation of transudates or exudates?

A

Transudates

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26
Q

Valvular heart disease can be divided into opening and closing problems. What are examples of each?

A

Opening; stenosis

Closing; regurgitation, incompetence, insufficiency

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27
Q

What does an ‘opening problem’ in valvular heart disease mean? What can this lead to?

A
  • Failure of valve to open completely, impeding forward flow
  • Leads to pressure overload of the heart
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28
Q

What are opening problems seen in VHD almost always due to?

A

Almost always due to chronic abnormality of valvular leaflet caused by relatively few disorders

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29
Q

What does a ‘closing problem’ in valvular heart disease mean? What can this lead to?

A
  • Failure of valve to close completely allowing reverse flow
  • Leads to volume overload of the heart
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30
Q

What can closing problems in VHD result from?

A
  • Can result from intrinsic disease of the valve cusps or damage to the supporting structures
  • Has many causes and may appear acutely or chronically
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31
Q

Which type of VHD leads to pressure overload?

A

Opening problem; impedes forward flow

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32
Q

Which type of VHD leads to volume overload?

A

Closing problems; allows reverse flow

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33
Q

One of the major forms of VHD is acquired aortic stenosis. What are 3 causes of this?

A
  1. Calcification of a deformed (congenitally bicuspid) valve (50-70y age group)
  2. Senile calcification of anatomically normal aortic valve (>70y age group)
  3. Rheumatic heart disease; a condition in which the heart valves have been permanently damaged by rheumatic fever
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34
Q

What is calcific aortic stenosis (AS)?

A

It is characterised by progressive fibro-calcific remodelling and thickening of the aortic valve leaflets that, over years, evolve to cause severe obstruction to cardiac outflow.

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35
Q

What can acquired AS lead to?

A
  • LVH (not caused by 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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36
Q

What is acquired mitral stenosis (MS) virtually synonymous with?

A

Rheumatic heart disease

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37
Q

What is the most common valvular abnormality?

A

Calcific aortic stenosis

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38
Q

What is calcific aortic stenosis usually the consequence of?

A
  • Age-related wear and tear of normal/bicuspid aortic vale (bicuspid valve undergoes more mechanical stress and so becomes stenotic earlier)
  • Hyperlipidaemia
  • Hypertension
  • Inflammation
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39
Q

is the aortic or mitral valve more often affected by calcification?

A

Aortic valve; mitral valve is generally normal but can be involved by extension of calcific deposits

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40
Q

What are the effects of calcific aortic stenosis?

A
  • Leads to 2x gradient pressure, left heart hypertrophy, ischaemia
  • Long term complications
    • Cardiac decompensation
    • Angina (50% die within 5 years)
    • Congestive heart failure (50% die within 2 years)
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41
Q

What valve does rheumatic heart disease most commonly affect?

A

Mitral valve (70%) but can also affect aortic valve (25%) and tricuspid and pulmonary valves (very rarely)

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42
Q

What does rheumatic heart disease follow?

A

A group A strep (S. pyogenes) infection; anti-strep antibodies cross-react in the heart

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43
Q

What are the subclassifications of rheumatic HD?

A
  • Pancarditis
  • Endocarditis
  • Myocarditis
  • Pericarditis
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44
Q

What acute pathophysiology is seen in mitral stenosis following a group A strep infection?

A
  • Inflammation
  • Aschoff bodies
  • Anitschkow cells
  • Pancarditis
  • Vegetations on chordae tendinae at leaflet junction
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45
Q

What are Aschoff bodies?

A

result from inflammation associated with rheumatic heart disease

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46
Q

What are Anitschkow cells?

A

enlarged macrophages found within granulomas, associated with rheumatic heart disease

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47
Q

What is pancarditis?

A

Pancarditis, also called perimyoendocarditis, is the inflammation of the entire heart: the pericardium, the myocardium and the endocardium.

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48
Q

What chronic pathophysiology is seen in mitral stenosis following a group A strep infection?

A
  • Thickened valves
  • Commissural fusion
  • Thick, short, chordae tendinae
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49
Q

What is commissural fusion?

A

Commissural fusion is the main mechanism of rheumatic MS. Associated lesions are chordal shortening and fusion, and leaflet thickening.

50
Q

By which criteria can acute rheumatic fever be identified?

A

Identified by the Jones criteria

51
Q

What is the Jones criteria?

A

1) Evidence of preceding streptococcal infection2) +2 major manifestations OR 1 major and 2 minor:
* Major manifestations:*

  • Migratory polyarthritis
  • Myocarditis
  • Subcutaneous nodules
  • Erythema marginatum of the skin
  • Sydenham chorea

Minor manifestations:

  • CRP increased
  • Arthralgia
  • Fever
  • Prolonged PR interval
  • Anamnesis of (‘history’ of rheumatism
  • Leucocytosis
52
Q

What are the clinical features of chronic RHD?

A
  • Appears many years after initial episode of rheumatic fever
  • Depends on which cardiac valve is involved
    • Cardiac murmurs
    • Cardiac hypertrophy and dilation
    • Arrhythmias
    • Cardiac failure
    • Thromboembolic complications
    • Infective endocarditis
53
Q

What is valve regurgitation?

A

Regurgitation is the name for leaking heart valves.

54
Q

What are 3 causes of aortic valve regurgitation?

A
  1. Rheumatic fever
  2. Infective endocarditis
  3. Aortic dilatations
55
Q

How can rheumatic fever lead to aortic valve regurgitation?

A

Damages valves

56
Q

What 3 conditions can lead to aortic dilatations which can cause aortic regurgitations?

A
  1. Syphilis; changes elastic properties of aorta and valves, can even cause aortic aneurysms
  2. Rheumatoid arthritis; granulomas can affect aortic valve
  3. Marfan syndrome; can affect valves of heart
57
Q

Mitral valve prolapse is a common cause of mitral valve regurgitation. What conditions can this often be seen in?

A

Marfan Syndrome

58
Q

Other causes of mitral valve regurgitation:

A
  • Infectious endocarditis can affect mitral valve
  • Fen-Phen
  • Papillary muscles; can rupture after MI or infectious endocarditis
  • Chordae tendinae; can tear after infectious endocarditis or rheumatic fever
  • Calcification of mitral ring (annulus)
59
Q

What is Fen-Phen?

A

anti-obesity drug that was shown to cause valve problem

60
Q

How can the calcification of the mitral ring (annulus) lead to regurgitation?

A
  • usually happens with age
  • increased rigidity affects function
  • deep penetration of calcium deposits can also impinge on AV conduction system (sudden death)
61
Q

How can calcification of mitral ring lead to sudden death?

A

deep penetration of calcium deposits can also impinge on AV conduction system (sudden death)

62
Q

What is myxomatous degeneration of the cardiac valves?

A

The non-inflammatory progressive disarray of the valve structure caused by a defect in the mechanical integrity of the leaflet due to the altered synthesis and/or remodeling by type VI collagen

63
Q

What can myxomatous degeneration of the mitral valve lead to?

A

Valve prolapse

64
Q

What is myxomatous degeneration of the mitral valve typically associated with?

A

Associated with connective tissue disorders (Marfan’s syndrome)

65
Q

Clinical features of mitral valve prolapse?

A
  • Usually asymptomatic
  • Mid-systolic ‘click’
  • Holosystolic murmur if regurg. Present
  • Occasional chest pain, dyspnoea
  • 97% NO untoward effects
  • 3% infective endocarditis, mitral insufficiency, arrhythmias, sudden death
66
Q

What is the mitral annulus?

A

The mitral annulus is a fibrous ring that is attached to the mitral valve leaflets.

67
Q

What can mitral annular calcification lead to?

A
  • Regurgitation usually, but stenosis possible
  • Arrhythmias and sudden death due to deep penetration of calcium deposits impinging on the atrioventricular conduction system
  • Increased risk of infective endocarditis and embolic stroke from dislodged overlying thrombi
68
Q

Why can mitral valve calcification increase the risk of embolic stroke?

A

From dislodged overlying thrombi

69
Q

What are ‘congenital’ heart defects?

A

Abnormalities of the heart and great vessels present from birth

70
Q

Embryogenesis of cardiac development:

71
Q

How common are congenital heart defects?

A

Overall incidence 1% of births

72
Q

Different types of cardiac congenital defects:

73
Q

A congenital heart disease can either be cyanotic or acyanotic. How can you distinguish?

A

THINK – does the abnormal blood flow go left –> right (acyanotic) OR right –> left (cyanotic defect)

74
Q

What type of shunt is a cyanotic defect?

A

Right –> left

75
Q

What type of shunt is an acyanotic defect?

A

Left –> right

76
Q

How do left –> right shunts affect lungs?

A

Pulmonary hypertension –> significant pulmonary hypertension is irreversible, named Eisenmenger syndrome or late cyanotic congenital heart disease

77
Q

What 4 defects are acyanotic (i.e. left –> right shunt)?

A
  1. Ventral septal defect (VSD)
  2. Atrial septal defect (ASD)
  3. Patent ductus arteriosus (PDA)
  4. Atrioventricular septal defect (AVSD)
78
Q

Wjhat is an atrial septal defect?

A

Abnormal fixed opening in atrial septum caused by incomplete tissue formation that allows communication of blood between L and R atria N.B. this is NOT a patent foramen ovale

79
Q

Atrial septal defect vs patent foramen ovale?

A

A patent foramen ovale is a special type of hole between the upper chambers of the heart. While an Atrial Septal Defect is always considered a structural abnormality in the heart, everyone at birth has a PFO.

80
Q

How are ASD classified?

A

According to location:

  • Secundum: 90%, defective fossa ovalis (near centre of atrial septum)
  • Primum: 8%, adjacent to AV valves, mitral cleft
  • Sinus venosus: 2%, near entrance of SVC with anomalous pulmonary veins draining to SVC or RA
81
Q

What is a secundum ASD due to?

A

defective fossa ovalis

82
Q

When do ASD typically present?

A

Usually asymptomatic until adulthood

83
Q

Why can an open ASD increase the risk of stroke/ischaemic viscera etc?

A

An open ASD can allow an embolus to enter the systemic circulation from the pulmonary system.

84
Q

What is the most common congenital heart defect?

85
Q

Only 30% of VSDs are isolated. What do the rest occur with?

A

Tetralogy of Fallot

86
Q

VSDs are classified according to size and location. Where are 90% found? Where are the other 10% found?

A
  • 90% involve the membranous septum (membranous VSD); defect occurs at top of septum
  • 10% involved the muscular septum or lie below the pulmonary valve (infundibular VSD)
87
Q

If the muscular septum is invovled in a VSD, how can this appear?

A

Can have multiple holes (swiss-cheese septum)

88
Q

How do small/large VSDs progress?

A
  • Small ones often close spontaneously
  • Large ones progress to pulmonary hypertension
89
Q

What 5 defects are cyanotic (i.e. right –> left shunt)?

A

The 5 T’s:

  1. Tetralogy of Fallot
  2. Transposition of great arteries
  3. Truncus arteriosus
  4. Total anomalous pulmonary venous connection
  5. Tricuspid atresia
90
Q

What is Tetralogy of Fallot?

A

Commonly a combination of 4 congenital heart defects:

  • 1) Large VSD
  • 2) Overriding aorta (sits above VSD)
  • 3) Pulmonary valve stenosis (obstructs RV outflow tract)
  • 4) Right ventricular hypertrophy
91
Q

What is given to neonates at birth with Tetralogy of Fallot? Why?

A

Prostaglandins given to keeps ducts OPEN until surgery

92
Q

What is the cause of Tetralogy of Fallot?

A

Due to anterosuperior displacement of the infundibular septum during embryogenesis

93
Q

What does survival of Tetralogy of Fallot depend on?

A

Survival depends on severity of subpulmonic stenosis

94
Q

What is transposition of the great arteries? Why is it a cyanotic CHD?

A
  • Pulmonary artery and aorta are swapped over
  • Blood flows to the lungs and becomes oxygenated BUT comes back to the lungs instead of the body
  • Blood flowing around body is unable to reach lungs to become oxygenated and just continues circulating –> cyanotic
95
Q

To support life with transposition of the great arteries, what must also be present?

A

To support life; must be patent ASD, VSD or PDA as well

96
Q

What are 4 other types of a cyanotic CHD?

A
  1. Pulmonary atresia
  2. Hypoplastic heart
  3. Coarctation of aorta
  4. Eisenmenger syndrome
97
Q

What are Obstructive Congenital Heart Diseases? What are 3 common defects?

A

Obstructive defects occur when heart valves, arteries, or veins are abnormally narrow or blocked. Common defects include:

  • Pulmonic stenosis/atresia
  • Aortic stenosis/atresia
  • Coarctation of the aorta
98
Q

What is coarctation of the aorta?

A
  • Congenital narrowing of aorta usually where ductus arteriosus inserts
99
Q

What is ductus arteriosus? What is its function?

A
  • Ductus arteriosus is a blood vessel that bridges between trunk of pulmonary artery and the proximal descending aorta
  • Bypass system enables blood to go from the RV straight into the systemic circulation, avoiding the foetus’ fluid filled non-functioning lungs
100
Q

Is coarctation of aorta seen in more men or women? What is the exception to this?

A

M>F (2:1) but females with Turner Syndrome (XO) frequently have it

101
Q

Coarctation of aorta can be divided into what 3 types?

A
  1. Preductal
  2. Ductal
  3. Postductal
102
Q

What does preductal coarctation of aorta involve? How do neonates present?

A
  • Narrowing is BEFORE ductus arteriosus
  • Blood flow distal to coarctation comes via ductus arteriosus (any blood that manages to squeeze through narrowing)
  • Neonates presentation; varying cyanosis in lower body
103
Q

What does ductal coarctation of aorta involve?

A

Narrowing occurs AT LOCATION of ductus arteriosus

104
Q

What does postductal coarctation of aorta involve? How do neonates present?

A
  • Narrowing occurs DISTAL to ductus arteriosus
  • Presentation:
    • Impaired blood flow to lower limbs
    • Will often lead to rib notching; erosions under ribs caused by engorged intercostal arteries that are trying to act as a collateral circulatory pathway
    • Hypertension of upper limbs
    • Weak pulses in lower extremities
105
Q

In which type of coarctation of aorta is rib notching seen?

A

Postductal

106
Q

What is given to a baby born with pulmonary artery stenosis/atresia (either as a singular defect OR as part of Tetralogy of Fallot)?

A

Prostaglandins - given to keeps ducts OPEN until surgery

107
Q

What is aortic atresisa?

A

With aortic atresia, there is no opening from the left ventricle into the aorta. “Atresia” refers to a missing heart structure. The valve cannot open properly, which means the blood can’t move from the left ventricle to the body. The only source of blood flow to the body will be through the ductus ateriosus.

108
Q

What is pulmonary artery atresia?

A

Pulmonary atresia is a birth defect of the heart where the valve that controls blood flow from the heart to the lungs doesn’t form at all. In babies with this defect, blood has trouble flowing to the lungs to pick up oxygen for the body.

109
Q

What are the 3 types of aortic stenosis/atresia?

A
  1. Supravalvular
  2. Valvular
  3. Subaortic
110
Q

What do all 3 types of aortic stenosis/atresia lead to?

A

ALL lead to element of LV outflow obstruction; as obstruction increases, LV shows increasing hypertrophy which can eventually lead to HF

111
Q

What is hypoplastic left heart syndrome?

A
  • Congenital heart defect
  • Aorta and LV are underdeveloped and aortic & mitral valves are either stenosed or atretic
    • Aortic stenosis and aortic atresia are part of the presentation when a neonate has hypoplastic left heart syndrome
112
Q

What does the neonate require when born with hypoplastic left heart syndrome?

A
  1. an ASD to be present for oxygenated & deoxygenated blood to mix
  2. a patent ductus arteriosus to allow blood to reach the aorta and systemic circulation via the RV
113
Q

Complications of hypoplastic left heart syndrome?

A

High pressure on functioning right side leads to lung damage even BEFORE neonate is born

114
Q

Specific gene abnormalities in only 10% of CHD. What are the most common causes?

A

Chromosomal abnormalities; Trisomy 21 (Down’s), 13 (Patau’s), 18 (Edward’s) and XO (Turner syndrome)

115
Q

What CHD are children with Down’s more likely to have?

116
Q

What CHD are children with Edward’s (18) more likely to have?

A

ASD, VSD or Tetralogy of Fallot

117
Q

What CHD are children with Patau’s (13) more likely to have?

A

ASD, VSD or PDA

118
Q

How can gestational diabetes affect risk of congenital HD?

A

Increases risk of cardiac defects

119
Q

TORCH can also predispose to congenital HD. What does TORCH stand for?

A
  • Toxoplasmosis
  • Other (syphilis, parvovirus B19, enterovirus)
  • Rubella à causes the most severe congenital cardiac defects (congenital rubella syndrome)
  • Cytomegalovirus
  • Herpes simplex
120
Q

Which out of TORCH causes the most severe congenital cardiac defects?

A

Rubella; congenital rubella syndrome

121
Q

List of teratogens:

122
Q

What is the most common cause of mitral valve stenosis?

A

Rheumatic fever

Yr 2 - Clinical Pathology (80 decks)

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