VIVA: Pathology - Cardiovascular system Flashcards

1
Q

What are the risk factors for abdominal aortic aneurysm?

A

Age >60
Male
Smoking
HTN*
Atherosclerosis*
Diabetes mellitus
Family history
Connective tissue disease (e.g. Marfan’s, Ehlers-Danlos)
Vasculitis
Trauma
Congenital
Infection
Inflammation

*needed to pass + two others

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2
Q

Describe the pathogenesis of an aneurysm

A
  • Aneurysms can occur when the structure or function of the connective tissue within the vascular wall is compromised
  • Atherosclerotic plaque in intima compresses media, with degeneration and weakness of the wall and cystic medial degeneration
  • Local inflammation (proteolytic enzymes with collagen degradation, role of matrix metalloproteinases)
  • Loss of vascular smooth muscle cells
  • Inappropriate synthesis of non-elastic ECM
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3
Q

What is the definition of cardiomyopathy?

A

Heterogenous group of diseases of the myocardium that is associated with mechanical and/or electrical dysfunction* that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilation*

Primary cardiomyopathies can be congenital or acquired

Secondary cardiomyopathies have myocardial involvement as a component of a systemic or multisystem disorder

*needed to pass

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4
Q

What are the types of cardiomyopathy? Give a cause of each

A

Hypertrophic *: 75% genetic cause, autosomal dominant HCM
Dilated *: alcohol, myocarditis, idiopathic, peripartum, genetic
Restrictive *: infiltrative (amyloidosis, sarcoidosis), non-infiltrative (idiopathic, scleroderma)

*needed to pass + one example of each

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5
Q

What type of cardiomyopathy is alcoholic cardiomyopathy?

A

Dilated

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6
Q

What are the clinical consequences of an aneurysm?

A
  • Painful/painless mass
  • Rupture* (risk increases with diameter >5cm, modest increase >4cm; retroperitoneal or intraperitoneal with rapid fatal haemorrhage)
  • Obstruction: branch obstruction (e.g. mesenteric, vertebral, renal)
  • Embolism: plaque or thrombus
  • Impingement/compression of adjacent structures (e.g. ureter)
  • Infection (mycotic aneurysm)

*needed to pass + 2 others

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7
Q

Describe the pathogenesis of an aortic dissection

A
  • HTN*: aorta of hypertensive patients have medial hypertrophy of vaso vasorum and degenerative changes in the media
  • Connective tissue disease (inherited or acquired)
  • Both of the above cause weakness in the media*
  • An aortic dissection starts with an intimal tear* and the blood dissects into the media along laminar planes either distally or proximally leading to the formation of a medial haematoma which may then rupture outwards
  • Can subsequently develop cystic medial degeneration

*needed to pass

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8
Q

How are aortic dissections classified?

A

By site of involvement (either classification to pass):
1. Stanford:
- Type A: proximal to L subclavian
- Type B: distal to L subclavian
2. Debakey:
- Type I: ascending and descending aorta
- Type II: ascending only
- Type III: descending only

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9
Q

What are the potential consequences of aortic dissection?

A

3 to pass:
- Rupture back into intima or through adventitia
- Rupture out or into pericardial, pleural or peritoneal cavities
- Cardiac tamponade, aortic insufficiency, MI, distal ischaemia, spinal cord ischaemia
- Death

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10
Q

What are the risk factors for aortic dissection?

A
  • Male
  • Age 40-60
  • HTN*
  • Connective tissue disorders (e.g. Marfans, Ehlers-Danlos)
  • Complication of arterial cannulation (iatrogenic)
  • Trauma
  • Pregnancy

*needed to pass + 1 other

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11
Q

What are the pathological consequences of aortic stenosis?

A
  • Concentric LV hypertrophy*
  • LV outflow obstruction
  • Myocardial ischaemia (coronary artery disease need not be present)
  • Syncope
  • Aortic dissection
  • Heart failure (diastolic or systolic)
  • Endocarditis (uncommon)

*needed to pass + 3 others

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12
Q

What are the most common causes of aortic stenosis?

A

2 to pass:
- Calcific/degenerative
- Bicuspid valve
- Rheumatic heart disease

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13
Q

What clinical signs may differentiate calcific aortic stenosis from rheumatic aortic stenosis?

A
  • Rheumatic disease involves more than one valve (i.e. aortic and mitral)
  • Absence of features of MS/MR
  • Absence of features of AR
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14
Q

What are the predisposing factors for calcific aortic stenosis?

A
  • Age*: normal valve 70-90yrs, bicuspid 50-70yrs
  • Bicuspid valve or other congenital abnormality
  • Wear and tear, chronic injury
  • Hyperlipidaemia
  • HTN
  • Inflammation
  • Other factors associated with atherosclerosis

*needed to pass + 1 other

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15
Q

What are the potential complications of a congenital bicuspid aortic valve?

A
  • Calcification*
  • Stenosis*
  • Regurgitation
  • Infective endocarditis
  • Aortic dilation
  • Dissection

*needed to pass + 2 others

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16
Q

What are the systemic and local factors that lead to atherosclerosis?

A
  • HTN*
  • Hyperlipidaemia*
  • Toxins from cigarette smoke*
  • Homocysteine
  • Infectious agents
  • Inflammatory cytokines (e.g. TNF) can also stimulate pro-atherogenic patterns of endothelial cell gene expression

Two most important causes of endothelial dysfunction are haemodynamic disturbances and hyperlipidaemia*

Local flow disturbances (e.g. turbulence at branch points)* leads to increased susceptibility of certain portions of a vessel wall to plaque formation

*needed to pass

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17
Q

Which arteries are most often affected by atherosclerosis?

A

3/5 to pass:
- Lower abdominal aorta
- Coronary arteries
- Popliteal arteries
- Internal carotid arteries
- Vessels of the circle of Willis

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18
Q

How does an atherosclerotic plaque suddenly cause symptoms?

A

2/5 to pass:
1. Rupture, ulceration or erosion:
- Of the intimal surface of atheromatous plaques exposes the blood to highly thrombogenic substances and induces thrombosis
- Such thrombosis can partially or completely occlude the lumen and lead to downstream ischaemia
2. Haemorrhage into a plaque:
- Rupture of the overlying fibrous cap, or of the thin-walled vessels in the area of neovascularisation, can cause intra-plaque haemorrhage
3. Atheroembolism:
- Plaque rupture can discharge atherosclerotic debris into the bloodstream, producing microemboli
4. Aneurysm formation:
- Atherosclerosis-induced pressure or ischaemic atrophy of the underlying media, with loss of elastic tissue, causes weakness resulting in aneurysmal dilation and potential vessel rupture
5. Occlusion:
- Small vessels can occlude, compromising distal perfusion

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19
Q

Describe the differences between stable and vulnerable atherosclerotic plaque

A
  1. Stable:
    - Dense collagenous and thickened fibrous caps * with minimal inflammation * and small underlying atheromatous * core
  2. Vulnerable:
    - Thin fibrous cap *, large lipid core * and increased inflammation *
    - Prone to rupture

*2/3 for each

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20
Q

Name some causes of dilated cardiomyopathy

A

2/4 to pass:
- Myocarditis (mostly viral)
- Toxins (alcohol, chemotherapeutics, cobalt)
- Congenital
- Pregnancy

21
Q

What are potential pathological consequences of dilated cardiomyopathy?

A

2/5 to pass:
- Valve dysfunction (incompetent mitral/tricuspid)
- Mural thrombi and embolisation
- Lethal arrhythmia
- Atrial fibrillation
- Death from progressive failure

22
Q

What are the causes of acquired cardiomyopathy?

A
  1. Infections*: viral, bacterial, fungal, protozoal
  2. Metabolic*: hyperthyroidism, nutritional
  3. Infiltrative*: sarcoid, carcinoma
  4. Immunological*: autoimmune myocarditis
  5. Drugs/toxins*: alcohol, chemotherapy
  6. Ischaemic
  7. Hypertensive
  8. Valvular

3/5 needed to pass + examples

23
Q

How do dilated and hypertrophic cardiomyopathy differ?

A

Dilated:
- Cardiac dilatation
- Poor LVEF (<40%)*
- Impaired contractility (systolic dysfunction)*

Hypertrophic:
- Myocardial hypertrophy
- Normal or high LVEF*
- Impaired compliance (diastolic dysfunction)*

*needed to pass

24
Q

What is cor pulmonale?

A

R-sided heart failure that is not secondary to L-sided heart failure (pure RHF)*
- Can be acute (e.g. massive PE) or chronic (e.g. chronic lung disease)

*needed to pass

25
Q

What are the common causes of cor pulmonale?

A

Common feature is pulmonary HTN*:
- Diseases of pulmonary parenchyma (e.g. COPD, fibrosis, bronchiectasis)
- Diseases of pulmonary vessels (e.g. primary pulmonary HTN, recurrent PE, extensive pulmonary arteritis e.g. Wegener’s granulomatosis)
- Disorders affecting chest movement (e.g. marked obesity, kyphoscoliosis, neuromuscular)
- Disorders causing pulmonary arterial constriction (e.g. hypoxaemia, metabolic acidosis, chronic sleep apnoea, altitude sickness)

*needed to pass + 3 others

26
Q

What are the major morphological features of cor pulmonale?

A

Pulmonary congestion is minimal whereas engorgement of the systemic and portal venous systems may be pronounced (3 to pass):
- Heart: RV hypertrophy and dilatation, leftward bulging of septum
- Liver / portal system: congestive hepatomegaly, centrilobular necrosis, congestive splenomegaly
- Pleural, pericardial and peritoneal spaces: effusions, ascites
- Subcutaneous tissues: oedema (dependent and peripheral portions of body, anasarca)

27
Q

What factors predispose to infective endocarditis?

A

Cardiac factors*:
- Myxomatous mitral valve
- Calcific aortic stenosis
- Bicuspid aortic valve
- Prosthetic valves
- Rheumatic heart disease

Host factors*:
- Neutropaenia
- Immunodeficiency
- Malignancy
- Therapeutic immunosuppression
- Diabetes
- Alcohol
- IVDU
- Bacteraemia

*2 examples from each to pass

28
Q

Which organisms commonly cause infective endocarditis?

A
  • Streptococcus viridans*
  • Staphylococcus aureus*
  • Staphylococcus epidermidis
  • Enterococci
  • HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
  • Fungi

*needed to pass + 1 other

29
Q

What are the complications of infective endocarditis?

A

Local*:
- Erosion/destruction of underlying cardiac tissue (valve, myocardium)
- Abscess formation

Systemic*:
- Systemic emboli and infarcts (e.g. of brain, kidneys, lung, subcutaneous tissues i.e. Janeway lesions, retina)
- Glomerulonephritis (immunologically mediated)

*1 of each needed to pass

30
Q

What is heart failure?

A

When cardiac function is impaired* and/or the heart is unable to maintain a CO* sufficient for the body’s metabolic needs

*needed to pass

31
Q

Classify the types of heart failure

A
  1. Systolic dysfunction (contractile dysfunction):
    - E.g. myocardial contractile dysfunction secondary to ischaemia, AMI, pressure or volume overload, dilated cardiomyopathy
  2. Diastolic dysfunction (inadequate filling):
    - E.g. LV hypertrophy, myocardial fibrosis, amyloidosis, pericarditis
  3. Others:
    - E.g. arrhythmias, regurgitant flow (MR), outflow obstruction (AS), HOCM
  4. Left heart failure:
    - E.g. IHD, HTN, valvular diseases (AS), rheumatic heart disease, myocardial disease
  5. Right heart failure:
    - E.g. secondary to left heart failure, PE, pulmonary HTN
32
Q

What are the clinical features of heart failure?

A

3/5 to pass:
1. Cardiovascular:
- 3rd heart sound, gallop
- Murmurs
- Displaced apex beat
- JVP elevation
- AF
2. Respiratory:
- Dyspnoea
- Orthopnoea
- PND
- APO
- Pleural effusions
3. Renal:
- Renin-angiotensin-aldosterone system activation
- Fluid retention
- Pedal oedema
- AKI
4. Neurological:
- Confusion secondary to hypoxia
5. Hepatic:
- Engorgement/congestion
- Ascites
- Cirrhosis (late)

33
Q

What are the major causes of heart failure?

A
  • Ischaemic heart disease*
  • Valvular heart disease*
  • HTN*
  • Cardiomyopathy
  • Fluid overload

*2/3 to pass + 1 other

34
Q

What pathological processes can occur in the myocardium in heart failure?

A

2 to pass:
- Infarction
- Ischaemia of myocardium
- Calcification
- Hypertrophy of cardiac myocytes
- Interstitial fibrosis

35
Q

What are the pathological changes in the liver caused by heart failure?

A
  • Nutmeg liver (congestion/oedema)
  • Centrilobular necrosis* (results from central hypoxia)
  • Centrilobular fibrosis* -> cardiac sclerosis (due to longstanding right heart failure)
  • Cardiac cirrhosis in extreme cases

*needed to pass

36
Q

How is hypertension classified?

A

Primary (essential)
Secondary

37
Q

What are the causes of secondary hypertension?

A

6 examples from 3 different systems:
1. Renal:
- Acute glomerulonephritis
- Chronic renal disease
- Polycystic disease
- Renal artery stenosis
- Renal vasculitis
- Renin-producing tumours
2. Endocrine:
- Adrenocortical dysfunction (e.g. Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion)
- Exogenous hormones (e.g. glucocorticoids, oestrogen including pregnancy-induced and OCP, sympathomimetics and tyramine-containing foods, MAOIs)
- Phaeochromocytoma
- Acromegaly
- Hypothyroidism
- Hyperthyroidism
- Pregnancy-induced
3. Cardiovascular:
- Coarctation of aorta
- Polyarteritis nodosa
- Increased intravascular volume
- Increased CO
- Rigidity of the aorta
4. Neurological:
- Raised ICP
- Sleep apnoea
5. Psychogenic:
- Acute stress (including surgery)
- Pain

38
Q

What is an acute coronary syndrome?

A

ACS is a clinical manifestation of ischaemic heart disease, and can present as unstable angina, acute MI (either STEMI or NSTEMI) or sudden cardiac death

39
Q

What are the pathological processes that underlie acute coronary syndrome?

A
  • Typically initiated by an unpredictable and abrupt conversion of a stable atherosclerotic plaque to an unstable and potentially life-threatening atherothrombotic lesion through rupture, superficial erosion, ulceration, fissuring, or deep haemorrhage
  • In most instances, plaque changes (typically associated with intra-lesional inflammation) precipitate the formation of a superimposed thrombus that partially or completely occludes the artery
40
Q

Following acute myocardial infarction, what complications might a patient have?

A

3 to pass:
1. Contractile dysfunction causing hypotension (cardiogenic shock in 10-15%)
2. Arrhythmias (e.g. sinus bradycardia, AF, HB, tachycardia, VT, VF)
3. Myocardial rupture (ventricular free wall rupture 2-7 days post MI, septum rupture, papillary muscle rupture)
4. Ventricular aneurysm
5. Pericarditis (2-3 days post MI) / Dressler’s syndrome / pericardial effusion / tamponade
6. Infarct expansion
7. Papillary muscle dysfunction
8. Progressive heart failure
9. Mural thrombus

41
Q

Describe the pathogenesis of myocardial infarction due to atherosclerosis

A
  1. Acute plaque change*:
    - Rupture/fissuring
    - Erosion/ulceration
    - Haemorrhage into atheroma
  2. Thrombosis*:
    - Platelet adhesion, aggregation and micro-thrombi formation
    - Platelet release of mediators causing vasospasm
    - Activation of coagulation pathway leading to thrombus
  3. Vasoconstriction* stimulated by:
    - Circulating adrenergic agonists
    - Locally released platelet contents
    - Endothelial cell dysfunction causing decreased NO
    - Perivascular inflammatory cell mediators
  4. Vessel occlusion* leading to:
    - Decreased myocardial blood flow
    - Myocyte necrosis

*3/4 needed to pass + understanding

42
Q

What are the main cardiac rupture syndromes?

A

1/3 to pass:
- Free wall -> tamponade (most common; occurs at 1-10 days)
- Septum (causes VSD and L-to-R shunt)
- Papillary muscle dysfunction (causes severe MR)

43
Q

What changes occur in ventricular remodeling?

A

Hypertrophy and dilation * -> increased O2 demand -> ischaemia and depressed cardiac function * -> scar formation * -> stiffening * and hypertrophy

*3 to pass

44
Q

What systemic factors affect infarct healing?

A

3/4 to pass:
- Nutritional: protein, vitamin C
- Metabolic: diabetes
- Circulatory: arterial, venous
- Hormonal: glucocorticoids

45
Q

Describe the time course of myocardial injury after acute coronary artery occlusion

A

Reversible injury:
- Cessation of aerobic metabolism within seconds
- Decreased ATP production and increased lactic acid production (noxious metabolites)
- Loss of contractility within 1 min
- Ultrastructural changes (myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling) within a few mins
- ATP depletion up to 40 mins

Irreversible injury:
- Myocyte injury (defects in sarcolemmal membrane and cell leakage) within 20-40 mins
- Initially subendocardial then transmural myocyte death
- Microvascular injury within 1hr
- Coagulation necrosis after >2hrs (more protracted if collaterals)

46
Q

What are the causes of pericarditis?

A
  1. Infectious:
    - Viral*
    - Pyogenic bacteria
    - TB
    - Fungal
  2. Immune-mediated:
    - Rheumatic fever
    - SLE
    - Scleroderma
    - Post cardiotomy
    - Post MI (Dressler’s)
    - Drug hypersensitivity reaction
    - AMI
    - Uraemia
    - Post cardiac surgery
    - Neoplastic
    - Trauma
    - Radiation

*needed to pass + 1 immune-mediated + 1 other

47
Q

What types of pericardial fluid exudates occur?

A

2/5 to pass:
1. Serous:
- Usually non-infectious inflammation (e.g. RF, SLE) but also viral, uraemia, tumours
2. Fibrinous/serofibrinous:
- Most common
- Post MI, Dressler’s, trauma, post-surgery
- Also as in 1
3. Purulent/suppurative:
- Almost always bacterial
- May be due to invasion from local infection, lymphatic or blood seeding, or from surgery
4. Haemorrhagic
5. Caseous (TB)

48
Q

Describe the characteristic clinical features of pericarditis

A
  • Chest pain* (dull or sharp, pleuritic, positional)
  • Pericardial friction rub* (may be absent if large effusion)*
  • Fever* (chills and rigors if suppurative)
  • Signs of cardiac failure
  • In constrictive pericarditis: distant or muffled heart sounds, elevated JVP, peripheral oedema

*needed to pass