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Yr 2 - Clinical Pathology > Cardiovascular Pathology 1 > Flashcards

Cardiovascular Pathology 1 Flashcards

1
Q

What is ischaemic heart disease? It results from an imbalance between what?

A

WHAT: Generic designation for a group of syndromes resulting from myocardial ischaemia.

IMBALANCE: An imbalance between demand and supply of oxygenated blood to the heart.

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2
Q

2 major aetiologies of IHD?

A

1) coronary artery atherosclerosis
2) hypertrophy of cardiac muscles (causes increase in demand for oxygenated blood)

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3
Q

What are the 4 major syndromes comprising IHD?

A

1) Myocardial infarction
2) Angina pectoris
3) Chronic IHD with heart failure
4) Sudden cardiac death

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4
Q

How does angina pectoris differ from MI?

A

MI –> Duration and severity of ischaemia causes myocardial death

Angina Pectoris –> Ischaemia is less severe and does not cause myocardial death but instead causes central chest pain

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5
Q

What are the 3 types of angina pectoris?

A
  1. Stable
  2. Unstable
  3. Prinzmetal/Variant
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6
Q

What is Prinzmetal/Variant angina?

A

type of chest pain due to vasospasms and generally tends to be associated with stress

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7
Q

How can chronic IHD lead to heart failure?

A

1) Atherosclerotic changes narrow the coronary arteries
2) This results in a longer duration but less severe form of ischaemia
3) Results in decreased contractility of cardiac myocytes, resulting in heart failure

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8
Q

Pathogenesis behind myocardial ischaemia?

A

Myocardial ischemia is a consequence of reduced blood flow in coronary arteries, due to a combination of fixed vessel narrowing and abnormal vascular tone as a result of atherosclerosis and endothelial dysfunction. This leads to an imbalance between myocardial oxygen supply and demand.

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9
Q

How should blood cholesterol be measured when assessing risk of heart disease?

A

Ratio of total cholesterol to HDL (TC:HDL); high ratio = higher risk of heart disease

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10
Q

Acute coronary syndromes:

A
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11
Q

What is an MI?

A

Death of cardiac muscle from prolonged ischaemia

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12
Q

An MI can be transmural or subendocardial. What does each term mean?

A
  • Subendocardial –> MI tends to begin in the subendocardial layer (the least perfused area of the ventricular wall)
  • Transmural –> MI occurring across the entire wall after prolonged duration
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13
Q

Pathophysiology behind MI?

A
  • 1) Acute plaque changes
  • 2) Platelet aggregation
  • 3) Thrombus formation
  • 4) Occlusion of coronary artery
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14
Q

Describe the myocardium changes during an MI between 24 hours and 3-6 weeks.

A
  • <24h: Normal
  • 1-2dy: Pale, oedema, myocyte necrosis, neutrophils
  • 3-4dy: Yellow with haemorrhagic edge, myocyte necrosis, macrophages
  • 1-3wk: Pale, thin, granulation tissue then fibrosis
  • 3-6wk: Dense fibrous scar
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15
Q

If an MI occurs in the conduction system structures (e.g. SA node, AV node, Bundle of His etc), what are the potential complications?

A
  • Arrhythmias; either directly or by limited perfusion to the conduction system structures
    • This causes contractility dysfunction
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16
Q

How can an MI lead to congestive cardiac failure?

A
  1. Contractility dysfunction (infarcted ventricle)
  2. Papillary muscle (attached to leaflets of valves) infarct causing severe mitral regurgitation
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17
Q

How can an MI lead to thromboembolism?

A

Infarction of LV causing impaired contraction can predispose to thrombus formation which can go on to form emboli

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18
Q

How can an MI lead to pericarditis?

A

acute inflammatory response seen in first 24 hours, if this is limited to the pericardium this can lead to pericarditis

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19
Q

How can an MI lead to an aneurysm?

A

weakened ventricular wall can lead to wall prolapsing to form an aneurysm

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20
Q

How can an MI lead to cardiac tamponade?

A

Transmural infarction and rupture of myocardium can lead to blood leaking out of ventricle and filling the pericardial cavity –> stops heart from being able to pump normally

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21
Q

How can an MI lead to cardiogenic shock?

A

Chronic IHD setting; decreased contractility –> hypotension –> decreases the coronary perfusing of the heart itself –> increased ischaemia –> cardiogenic shock

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22
Q

Complications of MI:

A
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23
Q

What is the major blood marker of IHD?

A

Troponins T&I

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24
Q

What are troponins T&I?

A

proteins released by damaged myocytes

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25
Q

When are troponins detectable?

A

detectable 2 – 3h, peaks at 12h, detectable to 7 days

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26
Q

In which conditions can raised troponins be seen?

A

Raised post MI but also in pulmonary embolism, heart failure, & myocarditis.

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27
Q

What is creatine kinase?

A

enzyme chiefly found in brain, skeletal muscles and heart

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28
Q

What are the 3 isoenzymes of CK? Which isoenzyme is the myocardium the primary source of?

A
  • -BB, -MM and -MB
  • Myocardium is the primary source of CK-MB
29
Q

When is CK-MB detectable?

A

detectable 2 – 3h, peaks at 10-24h, detectable to 3 days

30
Q

What are 3 other blood markers of IHD?

A
  1. Myoglobin
  2. Lactate dehydrogenase isoenzyme 1
  3. Aspartate transaminase
31
Q

Where is myoglobin also released from?

A

Damaged skeletal muscle (as well as damaged cardiac muscle)

32
Q

Why is aspartate transaminase less useful as a marker of myocardial damage?

A

Also present in liver

33
Q

What is hypertension defined as?

A

A sustained diastolic pressure greater than 90 mm Hg or sustained systolic pressure greater than 140 mm Hg.

34
Q

Aetiology of hypertension?

A

The majority of patients (90%) have primary essential hypertension of unknown cause. Can be:

  • Genetics –> insulin resistance, metabolic syndrome (combination of diabetes + hypertension + obesity)
  • Environment –> obesity, alcohol, smoking, stress, Na+ intake
35
Q

What is metabolic syndrome?

A

combination of diabetes + hypertension + obesity

36
Q

What 2 major components regulate blood pressure?

A
  1. cardiac output
  2. peripheral resistance
37
Q

How does RAAS regulate blood pressure?

A

1) Renin is released primarily by the juxtaglomerular apparatus in the kidneys (senses any drop in blood pressure/fluid volume).
2) When renin is released into the blood, it converts circulating angiotensinogen (via proteolytic cleavage) to form angiotensin I
3) Vascular endothelium (particularly in lungs) has an enzyme, angiotensin converting enzyme (ACE), that converts angiotensin I to angiotensin II (AII) by cleaving off 2 amino acids, (although many other tissues in the body also can form AII e.g. heart, brain, vascular)
4) Angiotensin II stimulates the release of aldosterone from the adrenal cortex, which acts on the kidneys to stimulate reabsorption of salt and water

38
Q

Where is renin primarily released from?

A

juxtaglomerular apparatus in the kidneys

39
Q

How does angiontensin II affect:

a) Resistance vessels
b) Sodium transport
c) Adrenal cortex
d) Posterior pituitary
e) Thirst centres
f) Noradrenaline

A

a) Constricts resistance vessels (via AII [AT1] receptors)
b) Stimulates sodium transport (reabsorption) at several renal tubular sites
c) Acts on the adrenal cortex to release aldosterone
d) Stimulates the release of vasopressin (antidiuretic hormone, ADH) from the posterior pituitary –> increases fluid retention by the kidneys
e) Stimulates thirst centres within the brain
f) Facilitates noradrenaline release from sympathetic nerve endings and inhibits noradrenaline re-uptake by nerve endings –> enhancing sympathetic adrenergic function

40
Q

What is a resistance vessel?

A

A resistance artery is small diameter blood vessel in the microcirculation that contributes significantly to the creation of the resistance to flow and regulation of blood flow. Resistance arteries are usually arterioles or end-points of arteries.

41
Q

How does angiontensin II affect cardiac and vascular hypertrophy? WHat is the effect of this?

A

Stimulates cardiac hypertrophy and vascular hypertrophy –> increases cardiac output & peripheral resistance which increases BP

42
Q

What is 2ary hypertension?

A

high blood pressure caused by another disease

43
Q

What are the 4 major endocrine causes of hypertension?

A
  1. Cushing’s Syndrome
  2. Acromegaly
  3. Thyroid Disease
  4. Hyperparathyroidism Disease
44
Q

How can Cushing’s syndrome lead to hypertension?

A

Increased cortisol stimulates sympathetic nervous system & has aldosterone-like effect on kidneys

45
Q

What are the 3 major adrenal causes of 2ary hypertension?

A
  1. Conn’s Disease
  2. Adrenal hyperplasia
  3. Pheochromocytoma
46
Q

What is Conn’s disease?

A

Increased aldosterone release

47
Q

What is a pheochromocytoma?

A

benign tumour in the adrenal gland secreting catecholamines causing hypertension

48
Q

What are the 5 major renal causes of 2ary hypertension?

A
  1. Diabetic nephropathy
  2. Chronic glomerulonephritis
  3. Adult polycystic disease
  4. Chronic tubulointerstitial nephritis
  5. Renal vascular disease
49
Q

What are the 3 major CVS causes of 2ary hypertension?

A
  1. Aortic coarctation
  2. Renal artery stenosis
  3. Polyarteritis nodosa
50
Q

What is aortic coarctation?

A

congenital narrowing of aorta

51
Q

How can renal artery stenosis lead to 2ary hypertension?

A

juxtaglomerular apparatus stimulated to produce renin due to decreased flow

52
Q

What 3 major drugs can cause 2ary hypertension?

A
  1. NSAIDS
  2. Oral contraceptives
  3. Steroids
53
Q

What is ‘malignant’ hypertension defined as?

A

BP >180/120mmHg

54
Q

Malignant hypertension can lead to organ damage if not treated immediately. What are the 3 major types of organ damage that can occur?

A
  1. acute hypertensive encephalopathy
  2. and/or nephropathy
  3. with retinal haemorrhages/papilloedema
55
Q

Hypertension can result in hypertensive renal disease. How does the kidney appear? What is the cause of this appearance?

A

Results in granular surface of kidneys ‘flea bitten kidney’. This is due to pinpoint haemorrhages on surface of kidney due to rupture of arterioles and capillaries.

56
Q

What is hypertensive heart disease? How does it present?

A
  • Hypertensive heart disease refers to heart conditions caused by high blood pressure.
  • Presents as systemic (left-sided) hypertensive heart disease.
57
Q

How can hypertension lead to heart problems?

A

Hypertrophy of the heart is an adaptive response to pressure overload that can lead to myocardial dilation, congestive heart failure and sudden death.

58
Q

What are the 2 criteria for hypertensive heart disease?

A
  1. Left ventricular concentric hypertrophy
  2. History or pathological evidence for hypertension
59
Q

What is ‘cor pulmonale’?

A

Pulmonary (right sided) hypertensive heart disease

60
Q

What is seen in ‘cor pulmonale’?

A

Right ventricular hypertrophy, dilation and potentially heart failure secondary to pulmonary artery hypertension caused by disorders of the lung or pulmonary vasculature.

61
Q

What is right ventricular hypertrophy secondary to?

A

Disease of the left side (congenital causes are generally excluded in the definition)

62
Q

What are the 4 major categories of diseases causing cor pulmonale?

A
  1. Diseases of the pulmonary parenchyma; COPD, diffuse pulmonary interstitial fibrosis, pneumoconiosis, cystic fibrosis, bronchiectasis
  2. Diseases of pulmonary vessels; Recurrent pulmonary thromboembolism; primary pulmonary hypertension; arteritis; drugs; toxins; radiation; tumour microemboli
  3. Disorders affecting chest movement; Kyphoscoliosis; marked obesity (Pickwickian syndrome), Neuromuscular diseases
  4. Disorders inducing pulmonary arterial compression; Metabolic acidosis; Hypoxemia; Chronic altitude sickness; obstruction to major airways
63
Q

What is Pickwickian Syndrome?

A

Obesity hypoventilation syndrome

64
Q

What is an aneurysm?

A

A localised abnormal dilation of a blood vessel or the wall of the heart.

65
Q

What can aneurysms be divided into?

A

True & false

66
Q

What is a ‘true’ aneurysm?

A

In a true aneurysm, the aneurysm is bound by all three layers of the vessel wall (intima, media and adventitia). The wall may be attenuated (thin). The risk of rupture is proportional to the size of the aneurysm.

67
Q

What is a false aneurysm?

A

(Pseudoaneurysm) is a breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space (“pulsating hematoma”)

68
Q

What is a dissection?

A
  • An arterial dissection arises when blood enters the wall of an artery, as a hematoma dissecting between its layers
  • Dissections may, but do not always, arise in aneurysmal arteries
  • Can rupture!
69
Q

What is Marfan Syndrome? What cardiac abnormalities are they most at risk of?

A
  • A genetic disorder that affects the connective tissue.
  • Tend to be tall and thin, with long arms, legs, fingers, and toes.
  • They also typically have overly-flexible joints and scoliosis.
  • Increased risk of mitral valve prolapse and aortic aneurysm.

Yr 2 - Clinical Pathology (80 decks)

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