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6. CP - Diseases of the Cardiovascular System > (2) Cardiovascular diseases 2 > Flashcards

(2) Cardiovascular diseases 2 Flashcards

1
Q

Give 3 primary causes of left sided heart failure

A
  • hypertension (pressure overload)
  • valvular disease (pressure and/or volume overload)
  • myocardial infarction (regional dysfunction with volume overload)
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2
Q

Pressure and volume overload are the causes behind left sided heart failure. What are the stages leading to cardiac dysfunction?

A 
Increased pressure/volume overload 
= increased cardiac work
= wall stretch
= cell stretch
= hypertrophy and/or dilation
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3
Q

Hypertrophy and/or dilation in left sided heart failure is characterised by what?

A
  • increased heart size and mass
  • increased protein synthesis
  • induction of immediate-early genes
  • induction of foetal gene programme
  • abnormal proteins
  • fibrosis
  • inadequate volume
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4
Q

Hypertrophy and/or dilation leads to cardiac dysfunction. What is this characterised by?

A
  • heart failure (systolic/diastolic)
  • arrhythmias
  • neurohumoral stimulation
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5
Q

What 2 main things does left sided heart failure cause?

A
  • low output

- congestion

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6
Q

How does low output due to left sided heart failure affect the kidneys?

A
  • pre-renal azotemia
  • RAAS activation
  • salt and fluid retention
  • natriuretic peptides
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7
Q

Pre-renal azotemia may occur in left sided heart failure. What is it?

A

Abnormally high levels of nitrogen-containing compounds (such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds) in the blood.

Related to insufficient or dysfunctional filtering of blood by the kidneys

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8
Q

What are natriuretic peptides?

A

Peptides which induce natriuresis (the discharge of sodium through urine).

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9
Q

How does low output due to left sided heart failure affect the brain?

A
  • irritability
  • decreased attention
  • stupor
  • coma
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10
Q

What is stupor?

A

A state of near-unconsciousness or insensibility

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11
Q

How does congestion due to left heart failure affect the lungs?

A
  • pulmonary congestion and oedema

- heart failure cells

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12
Q

What are heart failure cells?

A

Siderophages generated in the alveoli of patients with left heart failure

High pulmonary blood pressure causes red cells to pass through the vascular wall and encounter macrophages.

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13
Q

What are the symptoms caused by the congestion in left heart failure?

A
  • dyspnoea
  • orthopnoea
  • PND (parxoysmal nocturnal dyspnoea)
  • blood tinged sputum
  • cyanosis
  • elevated pulmonary wedge pressure (PCFP) (nl = 2-15mmHg)
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14
Q

Orthopnoea is a symptom of left heart failure. What is it?

A

Shortness of breath which occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair

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15
Q

PND is a symptom of left heart failure. What is it? (paroxysmal nocturnal dyspnoea)

A

Attacks of severe shortness of breath and coughing that generally occur at night. It usually awakens the person from sleep, and may be quite frightening

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16
Q

What is pulmonary wedge pressure? (elevated in left heart failure)

A

The pressure measured by wedging a pulmonary catheter with an inflated balloon into a small pulmonary arterial branch

Because of the large compliance of the pulmonary circulation, it provides an indirect measure of the left atrial pressure

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17
Q

What is the aetiology of right sided heart failure?

A
  • left heart failure

- cor pulmonale

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18
Q

What is cor pulmonale?

A

Enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or high blood pressure in the lungs

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19
Q

What are the symptoms/signs of right heart failure related to the liver and spleen?

A
  • passive congestion (nutmeg liver)
  • congestive splenomegaly
  • ascites
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20
Q

What is nutmeg liver?

A

Congestive hepatopathy

Sign of right heart failure

Liver dysfunction due to venous congestion

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21
Q

What is ascites?

A

Accumulation of fluid in the peritoneal cavity, causing abdominal swelling

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22
Q

What is congestive splenomegaly?

A

Splenomegaly secondary to portal hypertension, with ascites, anemia, thrombocytopenia, leukopenia, and episodic hemorrhage from the intestinal tract. Called also Banti’s disease.

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23
Q

Which parts of the body are affected by right heart failure?

A
  • liver
  • spleen
  • kidneys
  • pleura/pericardium
  • peripheral tissues
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24
Q

How does right heart failure affect the pleura/pericardium?

A
  • pleural and pericardial effusions

- transudates

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25
Q

What are the general symptoms and signs of right heart failure?

A
  • fatigue
  • dependent oedema
  • distention of the jugular veins
  • liver engorgement
  • ascites
  • anorexia and complaints of GI distress
  • cyanosis
  • elevation in peripheral venous pressure
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26
Q

What are the general autopsy findings in chronic heart failure?

A
  • cardiomegaly
  • chamber dilatation
  • hypertrophy of myocardial fibres
  • boxcar nuclei
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27
Q

What are the 2 main categories of valvular heart disease?

A
  • opening problems (stenosis)

- closing problems (regurgitation, or incompetence of insufficiency)

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28
Q

Which conditions make up 70% of valvular heart disease?

A
  • aortic stenosis

- mitral stenosis

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29
Q

What is aortic stenosis?

A

Calcification of a deformed aortic valve

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30
Q

Why might calcification of the aortic valve occur?

A
  • “senile” calcification (just with old age)

- may be part of rheumatic heart disease

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31
Q

Why might mitral stenosis occur?

A

Rheumatic heart disease

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32
Q

What is rheumatic heart disease?

A

Occurs in cases of rheumatic fever (a serious complication). Follows a group A strep infection (a few weeks later).

Inflammation causes the heart’s valves to become damaged and stiffened

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33
Q

How has the epidemiology of rheumatic heart disease changed?

A

Decrease in developed countries

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34
Q

What are the different types of carditis (inflammation of the heart)?

A

Pancarditis = inflammation of the entire heart

Endocarditis = inflammation of the endocardium

Myocarditis = inflammation of the heart muscle

Pericarditis = inflammation of the pericardium

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35
Q

What are the findings in acute rheumatic heart disease?

A
  • inflammation
  • Aschoff bodies
  • Anitschkow cells
  • pancarditis
  • vegetations on chordae tendinae at leaflet junction
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36
Q

What are Aschoff bodies?

A
  • nodules found in the hearts of individuals with rheumatic fever
  • result from inflammation in the heart muscle
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37
Q

What are Anitschkow cells?

A
  • often associated with rheumatic heart disease

- enlarged macrophages found within granulomas (Aschoff bodies)

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38
Q

What are the findings in chronic rheumatic disease?

A
  • thickened valves
  • commisural fusion
  • thick, short chordae tendinae
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39
Q

What are the clinical features of aortic stenosis?

A
  • 2x gradient pressure
  • left ventricular hypertrophy but no hypertension
  • ischaemia
  • cardiac decompensation
  • angina
  • chronic heart failure
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40
Q

What is the prognosis in aortic stenosis?

A

50% die in 5 years if angina present

50% die in 2 years if chronic heart failure present

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41
Q

What is mitral annular calcification?

A

Calcification of the mitral “skeleton”

Degenerative process involving the fibrous annulus of the mitral valve.

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42
Q

Is mitral annular calcification symptomatic?

A

Usually no dysfunction

Generally an incidental finding associated with ageing

But occasionally prominent enough to cause significant left ventricular inflow obstruction and symptomatic mitral stenosis

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43
Q

Is mitral annular calcification more common in males or females?

A

Females

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44
Q

Does mitral annular calcification cause stenosis or regurgitation?

A

Regurgitation usually, but stenosis is possible

45
Q

What are the different causes of aortic regurgitation?

A
  • rheumatic disease
  • infectious
  • aortic dilatations (syphilis, rheumatoid arthritis, marfan)
46
Q

What are the different causes of mitral regurgitation?

A
  • infectious
  • fen-phen
  • problems with papillary muscles and/or chordae tendinae
  • calcification of the mitral ring (annulus)
47
Q

What is mitral valve prolapse (MVP)?

A

Myxomatous degeneration of the mitral valve

“floppy valve”

Characterised by displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole

48
Q

What is mitral valve prolapse associated with?

A

Connective tissue disorders

49
Q

Describe the incidence of mitral valve prolapse

A

3% incidence. F > M

50
Q

How is metal valve prolapse detected?

A

Easily seen on echocardiogram

51
Q

Mitral valve prolapse involves myxomatous degeneration. What is this?

A

Pathological weakening of connective tissue

52
Q

What are the clinical features of mitral valve prolapse?

A
  • usually asymptomatic
  • mid-systolic “click”
  • holosystolic murmur if regurgitation is present
  • occasional chest pain and dyspnoea
  • 97% no untoward effects
  • 3% infective endocarditis, mitral insufficiency, arrhythmias, sudden death
53
Q

What are congenital heart defects due to?

A

Fault embryogenesis (weeks 3-8)

May not be evident until adult life (coarctation, ASD)

54
Q

Are congenital heart defects usually mono-morphic or dimorphic?

A

Usually mono-morphic eg. single lesion eg. ASD, VSD, hypo-RV, hypo-LV)

55
Q

What is the incidence of congenital heart defects?

A

Overal incidence = 1% of births

56
Q

What makes up the biggest proportion of congenital heart defects?

A

Ventricular septal defect (42%)

57
Q

After ventricular septal defect, what is the next most common congenital heart defect?

A

Atrial septal defect (10%)

58
Q

After ventricular septal defect and atrial septal defect, what are some other relatively common congenital heart defects?

A
  • pulmonary stenosis (8%)
  • patient ductus arteriosus (7%)
  • tetralogy of fallot (5%)
  • coractation of the aorta (5%)
59
Q

Give some of the less common congenital heart defects

A
  • atrioventricular septal defect (4%)
  • aortic stenosis (4%)
  • transposition of great arteries (4%)
  • total anomalous pulmonary venous connection (1%)
  • triscuspid atresia (1%)
60
Q

Which conditions are involved in a left-to-right shunt?

A
  • ventricular septal defect
  • atrial septal defect
  • patient ductus arteriosus
  • atrioventricular septal defect
61
Q

Which conditions are involved in a right-to-left shunt?

A
  • tetralogy of fallot
  • transposition of great arteries
  • truncus arteriosus
  • total anomalous pulmonary venous connection
  • tricuspid atresia
62
Q

Which direction of shunting causes cyanosis (“blue” babes)?

A

Right to left.

blood missing out the lungs and so is reaching the rest of the body without being oxygenated

63
Q

What is tricuspid atresia?

A

Complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic (undersized) or absent right ventricle

Blocks blood flow from the right atrium to the right ventricle

64
Q

What are the 4 components of tetralogy of fallot?

A
  • ventricular septal defect
  • pulmonary stenosis
  • overriding aorta
  • right ventricular hypertrophy
65
Q

In what proportion of congenital heart defects are there gene abnormalities?

66
Q

Trisomies of which chromosomes may contribute to congenital heart defects

A

Trisomies 21, 13, 15, 18, XO

67
Q

Give some examples of genes which encode for transcription factors which mutations of may cause congenital heart defects

A

TBX5 - ASD, VSD

NKX2.5 - ASD

68
Q

Which part of the genome is important in heart development?

A

Region of chromosome 22 (22q11.2)

Deletion - conotruncus, branchial arch, face

69
Q

Name 2 environment factors that play a part in congenital heart defects

A
  • rubella

- teratogens

70
Q

Briefly describe the development of the atrial septum

A
  • septum secundum grows down the right hand side of the septum primum
  • septum has semilunar shape and its border delineates the foramen oval
  • blood may pass from right atrium to left atrium in the foetal period through foramen oval and ostium secundum
71
Q

Briefly describe the development of the aorticopulmonary septum

A
  • septum divides bulbus cordis and truncus into 2 main arterial trunks (aorta and pulmonary artery)
  • has a spiral path that results in final topographical relations of both vessels
72
Q

Name 5 different types of septal defects

A
  • atrial septal defect (ASD)
  • ventricular septal defect (VSD)
  • patent ductus arteriosus (PDA)
  • complete atrioventricular canal defect
  • large VSD with irreversible pulmonary hypertension
73
Q

What are the clinical features of left-to-right shunts? (Ds in the names)

A
  • NO cyanosis
  • pulmonary hypertension
  • significant pulmonary hypertension is irreversible
74
Q

What are the clinical features of right-to-left shunts? (Ts in the names)

A
  • cyanosis (blue babies)

- venous emboli become systemic “paradoxical”

75
Q

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

A

Irreversible pulmonary hypertension

76
Q

What are the different types of atrial septum defect?

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

77
Q

What are the symptoms of ASD?

A

Usually asymptomatic until adulthood

78
Q

Are VSD isolated or associated with other things?

A
  • only 30% are isolated

- often with tetralogy of fallot

79
Q

In VSD, is the membranous or the muscular septum involved?

A

90% involve the membranous septum

If muscular septum is involved, it can have multiple holes (“swiss-cheese” septum)

80
Q

What are the prognoses of VSD depending on size?

A

Small ones often close spontaneously

Large ones progress to pulmonary hypertension

81
Q

Are PDA isolated or associated with other things?

A
  • 90% are isolated

- associated with VSD, coarctation of the aorta, pulmonary and aortic stenosis

82
Q

In PDA, is the shunt left to right or right to left?

A

Left to right

Can become right to left as pulmonary hypertension increases and reaches systemic pressure

83
Q

What is done in the case of PDA?

A

Closing the defect in early life may be life saving in isolated PDA

84
Q

What is used to prevent premature closure of the ductus arteriosus in certain newborns?

A

Prostaglandin E1

85
Q

Why might the ductus arteriosus be needed to be kept patent?

A

In some congenital heart defects eg. transposition of the great vessels) a PDA may need to remain open, as it is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the DA open until surgical correction of the heart defect is completed

86
Q

What kind of murmur do you get in patent ductus arteriosus?

A

Continuous harsh, machinery-like murmur

87
Q

What are the clinical features of AVSD?

A
  • associated with defective, inadequate AV valves
  • can be partial or complete (all 4 chambers freely communicate)
  • more than a 3rd with complete AVSD have Down syndrome
88
Q

Which is the most common condition with right-to-left shunting?

A

Tetralogy of Fallot

89
Q

In tetralogy of Fallot, there is a large VSD, RVH, obstruction to RV outflow and an overriding aorta. What is an overriding aorta?

A

The aorta overrides the ventricular septal defect

90
Q

What does survival depend on in tetralogy of Fallot?

A

Depends on severity of subpulmonic stenosis

91
Q

What is a “pink” tetralogy? (tetralogy of Fallot)

A

When the pulmonic obstruction (pulmonary stenosis) is small, but the greater the obstruction, the greater the right-to-left shunt

92
Q

What is transposition of the great arteries?

A

Group of congenital heart defects involving an abnormal spatial arrangement the pulmonary artery and aorta.

Abnormal formation of the truncal and aortopulmonary septa - needs a shunt for survival

93
Q

Transposition of the great arteries requires a shunt for survival. Which shunts occur?

A
  • PDA or PFO (65%) = unstable shunt

- VSD (35%) = stable shunt

94
Q

What is the difference in thickness of the ventricles in transposition of the great arteries?

A

RV > LV in thickness

95
Q

How is transposition of the great arteries repaired?

A

Surgical “switching”

  • aorta moved from right ventricle to its normal position over left ventricle.
  • pulmonary artery moved from left ventricle to its normal position over the right ventricle

Other defects eg. ASD/VSD/PSA closed

96
Q

If transposition of the great arteries fatal?

A

Fatal in first few months

Requires surgical “switching”

97
Q

What is truncus arteriosus?

A

Single blood vessel (truncus arteriosus) comes out of the right and left ventricles, instead of the normal two vessels (pulmonary artery and aorta)

Developmental failure of separation of truncus arteriosus

98
Q

What are the features of truncus arteriosus?

A
  • aorta and pulmonary artery joined
  • associated VSD
  • produces systemic cyanosis and well as increased pulmonary blood flow
99
Q

What are the clinical features of tricuspid atresia?

A
  • hypoplastic right ventricle (undersized)
  • needs a shunt (ASD/VSD/PDA)
  • high mortality
100
Q

What are the features of total anomalous pulmonary venous connection (TAPVC)?

A
  • pulmonary veins do not go into the left atrium as normal, but go into left innominate vein or coronary sinus
  • needs a PFO or VSD
  • hypoplastic left atrium
101
Q

Name 3 types of OBSTRUCTIVE congenital heart disease

A
  • coarctation of the aorta
  • pulmonary stenosis/atresia
  • aortic stenosis/atresia
102
Q

What are the 2 forms of coarctation of the aorta?

A
  • infantile form (proximal to PDA, serious!)

- adult form (closed ducts - no PDA)

103
Q

What is also present in 50% of cases of coarctation of the aorta?

A

Bicuspid aortic valve

104
Q

Is coarctation more common in males or females?

105
Q

What are the clinical features of pulmonic stenosis/atresia?

A
  • if 100% atretic, hypoplastic right ventricle with ASD

- clinical severity correlated with stenosis severity

106
Q

What are the 3 types of aortic stenosis?

A
  • valvular
  • sub-valvular
  • supra-valvular
107
Q

What happens in valvular aortic stenosis?

A

If severe, you have a hypoplastic left ventricle which can be fatal

108
Q

What is sub-valvular/sub-aortic aortic stenosis?

A

Aortic wall thick below the cusps

109
Q

What is supra-valvular aortic stenosis?

A

Aortic wall thick above the cusps in ascending aorta

6. CP - Diseases of the Cardiovascular System (3 decks)

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