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Y2 Clinical Pathology > Cardiovascular Pathology 1 > Flashcards

Cardiovascular Pathology 1 Flashcards

1
Q

what is meant by cardiovascular disease?

A

It is an umbrella term used to describe all conditions of the heart and blood vessels

it includes congenital and acquired conditions

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2
Q

What is the definition of ischaemic heart disease?

A

Generic designation for a group of syndromes resulting from myocardial ischaemia

(an imbalance between demand and supply of oxygenated blood to the heart)

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3
Q

What is the aetiology of ischaemic heart disease?

A

It is almost always caused by coronary artery atherosclerosis

sometimes due to hypertrophy (increased demand)

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4
Q

What are the 4 ischaemic heart disease syndromes?

A

Myocardial infarction:

  • duration and severity of ischaemia causes myocardial death

angina pectoris:

  • ischaemia is less severe and does not cause myocardial death

chronic IHD with heart failure

sudden cardiac death

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5
Q

What are the 3 different types of angina pectoris?

A

Typical angina is known as stable angina

Prinzmetal angina is variant angina and is due to vasospasm, rather than atherosclerosis

unstable angina is crescendo angina

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6
Q

What are the 3 main features of acute coronary syndrome?

A
  • Myocardial infarction
  • unstable angina
  • sudden cardiac death

these are all IHD syndromes

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7
Q

What is the epidemiology of ischaemic heart disease like?

A

Prevalence of IHD is highest in northern England and scotland

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8
Q

What are the main medical risk factors for IHD?

A
  • High blood pressure
  • lipid profile abnormalities (high blood cholesterol)
  • diabetes
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9
Q

What is a good indicator for risk for CVD?

A

Instead of looking at total cholesterol

high HDL and low TC:HDL ratio are better indicators of risk for CVD

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10
Q

What are the modifiable lifestyle risk factors of IHD?

A
  • Cigarette smoking
  • physical inactivity
  • poor diet
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11
Q

What is the benefit of IHD therapeutic advances?

what are examples of these treatments?

A

Therapeutic advances have allowed earlier, more effective and safer treatments

  • lipid lowering medicines
  • anti-hypertensive medicines
  • antiplatelet medicines
  • antidiabetic medicines
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12
Q

What is the pathogenesis of ischaemic heart disease?

A

Myocardial ischaemia is a consequence of reduced blood flow in coronary arteries

this is 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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13
Q
A
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14
Q

what causes myocardial infarction?

what are the 2 different types?

A

Death of cardiac muscle from prolonged ischaemia

transmural - affects the full thickness

subendocardial - affects the inner one third of the wall (least well perfused)

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15
Q

What is involved in the pathophysiology of myocardial infarction?

A
  • Acute platelet changes
  • platelet aggregation
  • thrombus formation
  • occlusion of coronary artery
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16
Q

When there is a coronary artery thrombus, how does the myocardium change in 6 weeks?

A

< 24 hours:

  • myocardium is normal

1-2 days:

  • pale, oedema, myocyte necrosis, neutrophils

3-4 days:

  • Yellow with haemorrhagic edge
  • myocyte necrosis, macrophages

1-3 weeks:

  • pale, thin, granulation tissue then fibrosis

3-6 weeks:

  • dense fibrous scar
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17
Q

What is shown here?

A

Coronary artery thrombus leading to myocardium changes

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18
Q

What are the complications of myocardial infarction?

A

Arrhythmias:

  • either directly or by limited perfusion to the conduction system structures (e.g. SA node)

congestive cardiac failure:

  • contractility dysfunction or by papillary muscle infarct/severe MR

others:

  • thromboembolism
  • pericarditis
  • ventricular aneurysm
  • cardiac tamponade
  • cardiogenic shock
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19
Q

what is shown here?

A

Myocardial rupture

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20
Q

What is shown here?

A

Haemopericardium

(cardiac tamponade)

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21
Q

What is shown here?

A

Mural thrombus

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22
Q

what is haemopericardium?

what can it cause?

A

Blood in the pericardial sac

depending on the volume and rapidity with which it develops, it may cause cardiac tamponade

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23
Q

What is cardiac tamponade?

A

A clinical syndrome caused by the accumulation of fluid in the pericardial space

this results in reduced ventricular filling and subsequent haemodynamic compromise

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24
Q

what is meant by a mural thrombus?

where do they tend to occur?

A

They are thrombi that adhere to the wall of a blood vessel

they occur in large vessels such as the heart and aorta

they can restrict blood flow, but usually do not block it entirely

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25
Q

What is shown here?

A

Ventricular aneurysm

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26
Q

what is a ventricular aneurysm and what condition is it related to?

A

Ventricular aneurysms are a complication that occurs after a myocardial infarction

it is a bulge or pocketing of the wall or lining of a vessel

it most commonly occurs in the blood vessels at the base of the septum, or within the aorta

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27
Q

What are the main complications of MI?

How do they result from changes in the heart?

A

Impaired contractility:

  • ventricular thrombus leads to stroke (embolism)
  • hypotension causes reduced coronary perfusion and increased ischaemia leading to cardiogenic shock

tissue necrosis:

  • papillary muscle infarction leads to mitral regurgitation and congestive heart failure
  • ventricular wall rupture causes cardiac tamponade

electrical instability:

  • arrhytmias

pericardial inflammation:

  • pericarditis
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28
Q

what are the 5 different blood markers of ischaemic heart disease?

A
  • Troponins T & I
  • creatine kinase MB
  • myoglobin
  • lactate dehydrogenase isoenzyme 1
  • aspartate transaminase
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29
Q

When should troponins T & I be measured?

When are they raised?

A

They are proteins released by damaged myocytes

detectable after 2-3h, peaks at 12h and detectable to 7 days

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

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30
Q

when is creatinine kinase MB detectable?

A

Detectable after 2-3 hours

peaks at 10-24 hours

detectable for up to 3 days

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31
Q

what conditions is a rise in creatinine kinase associated with?

A

It is an enzyme found mainly in the brain, skeletal muscles and heart

an elevated level is seen in heart attacks, when the heart muscle is damaged, or in conditions that cause damage to the skeletal muscles or brain

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32
Q

When is myoglobin detectable?

A

Peaks at 2 hours but is also released from damaged skeletal muscle

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33
Q

when is lactate dehydrogenase isoenzyme 1 detectable?

A

Peaks at 3 days but is detectable up to 14 days

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34
Q

why is aspartate transaminase a less useful marker of myocardial damage?

A

It is also present in the liver

35
Q

what are the different types of hypertension?

A

Primary hypertension can be idiopathic or essential

secondary hypertension

36
Q

What is the definition of hypertension?

A

Blood pressure is considered to be a continuously distributed variable, and essential hypertension is one extreme of this distribution rather than a distinct disease

the detrimental effects of raised BP increase continuously as pressure rises

a sustained diastolic pressure greater than 90 mmHg or a sustained systolic pressure greater than 140 mmHg

37
Q

What is the aetiology of primary hypertension like?

A

The majority of patients (90%) have primary essential hypertension of unknown cause

38
Q

what are the multifactorial, genetic and environmental causes of primary hypertension?

A

multifactorial:

  • involves both genetics and the environment

genetic:

  • insulin resistance (metabolic syndrome)

environmental:

  • obesity
  • smoking
  • alcohol
  • stress
  • high sodium intake
39
Q

what is the epidemiology of hypertension like?

A

Vulnerability to complications increases with age

africans are affected more

40
Q

What is the aetiology of blood pressure?

A

The critical roles of cardiac output and peripheral resistance in blood pressure regulation

41
Q

What are the important roles of the renin-angiotensin-aldosterone system (RAAS)?

A

It plays an important role in regulating blood volume and systemic vascular resistance

together these influence cardiac output and arterial pressure

42
Q

Where is renin released from?

What is its role?

A

It is mainly released by the juxtaglomerular apparatus in the kidneys

it stimulates the formation of angiotensin in blood and tissues

this then stimulates the release of aldosterone from the adrenal cortex

43
Q

What substance does renin act upon?

A

It acts upon angiotensinogen

this undergoes proteolytic cleavage to form the decapeptide, angiotensin I

44
Q

In the RAAS, what happens to angiotensin I?

A

Vascular endothelium (particularly in the lungs) contains angiotensin converting enzyme (ACE)

this cleaves off two amino acids to form the octapeptide angiotensin II

45
Q

what is the role of angiotensin II?

A

It acts on the adrenal gland to stimulate the release of aldosterone

it also acts directly on blood vessels to stimulate vasoconstriction (narrowing)

46
Q

what is the role of aldosterone?

A

It acts on the kidneys to stimulate reabsorption of salt (NaCl) and water

47
Q

How does angiotensin II constrict resistancevessels?

A

It acts via AII [AT1] receptors, thereby increasing systemic vascular resistance and arterial pressure

48
Q

what are other important functions of angiotensin II?

A
  • Stimulates sodium transport (reabsorption) at several renal tubular sites
    • this increases sodium & water retention by the body
  • acts on the adrenal cortex to release aldosterone
    • ​this acts on the kidneys to increase sodium & fluid retention
  • stimulates the release of vasopressin (ADH) from the posterior pituitary gland
    • ​this increases fluid retention by the kidneys
  • stimulates thirst centres within the brain
  • facilitates norepinephrine release from sympathetic nerve endings and inhibits norepinephrine reuptake by nerve endings
    • ​this enhances sympathetic adrenergic function
  • stimulates cardiac hypertrophy and vascular hypertrophy
49
Q

what are the endocrine causes of secondary hypertension?

A
  1. Cushing syndrome
  2. acromegaly
  3. thyroid disease
  4. hyperparathyroid disease
50
Q

what are the adrenal causes of secondary hypertension?

A
  1. Conn’s disease
  2. adrrenal hyperplasia
  3. pheochromocytoma
51
Q

What are renal causes of secondary hypertension?

A
  1. Diabetic nephropathy
  2. chronic glomerulonephritis
  3. adult polycystic disease
  4. chronic tubulointerstitial nephritis
  5. renal vascular disease
52
Q

What are cardiovascular causes of secondary hypertension?

A
  • Aortic coarctation
  • renal artery stenosis
  • polyarteritis nodosa
53
Q

What drugs cause secondary hypertension?

A
  • NSAIDs
  • oral contraceptives
  • steroids
54
Q

why does renal artery stenosis cause secondary hypertension?

A

Juxtaglomerular apparatus stimulated to produce renin

55
Q

What happens in Conn’s disease?

A

Increased aldosterone leads to sodium and water retention

this causes hypertension

56
Q

what is blood pressure like in malignant hypertension?

how is it treated?

A

BP > 180/120 mmHg

it requires urgent treatment to preserve organ function

57
Q

How does malignant hypertension tend to present?

A

Clinical signs and symptoms of organ damage:

  • acute hypertensive encephalopathy
  • and/or nephropathy
  • with retinal haemorrhages / papilloedema
58
Q

What is shown here?

A

Hypertensive renal disease

it is a complication of hypertension where the kidney looks “flea bitten” due to renal cortical scarring

59
Q

what is shown here?

A

Hypertensive cerebrovascular disease

subarachnoid haemorrhage occurs secondary to berry aneurysm rupture

there are lacunar infarcts

60
Q

What are the 2 criteria for hypertensive heart disease?

A
  • Left ventricular concentric hypertrophy
  • history or pathological evidence for hypertension
61
Q

Why does hypertensive heart disease occur?

A

Systemic (left sided) hypertensive heart disease

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

62
Q

What does hypertensive heart disease look like at autopsy?

A

Concentric hypertrophy of the left side and the intraventricular septum

the right side is compressed

63
Q

what is cor pulmonale?

what usually causes it?

A

Pulmonary (right sided) hypertensive heart disease

right ventricular hypertrophy, dilation and potentially heart failure secondary to pulmonary artery hypertension

this is caused by disorders of the lung or pulmonary vasculature

64
Q
A
65
Q

What tends to be excluded from cor pulmonale?

what is common?

A

Right ventricular hypertrophy secondary to diseases of the left side and congenital causes are generally excluded

pulmonary venous hypertension that follows left-sided diseases is quite common

66
Q

What are the 4 categories of causes or cor pulmonale?

A
  • Diseases of the pulmonary parenchyma
  • diseases of pulmonary vessels
  • disorders affecting chest movement
  • Disorders inducing pulmonary arterial compression
67
Q

What are examples of diseases of the pulmonary parenchyma?

A
  • COPD
  • diffuse pulmonary interstitial fibrosis
  • pneumoconiosis
  • cystic fibrosis
  • bronchiectasis
68
Q

What are examples of diseases of pulmonary vessels?

A
  1. Recurrent pulmonary thromboembolism
  2. primary pulmonary hypertension
  3. arteritis
  4. drugs
  5. toxins
  6. radiation
  7. tumour microemboli
69
Q

what are examples of disorders affecting chest movement?

A
  • Kyphoscoliosis
  • marked obesity (pickwickian syndrome)
  • neuromuscular diseases
70
Q

What are examples of disorders inducing pulmonary arterial compression?

A
  • Metabolic acidosis
  • hypoxemia
  • chronic altitude sickness
  • obstruction to major airways
71
Q

What is the definition of an aneurysm?

A

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

it can be a true aneurysm or a false aneurysm (pseudo aneurysm)

72
Q

What is the difference between a true aneurysm and a false aneurysm?

A

True aneurysm:

  • when bounded by arterial wall components or the attenuated wall of the heart

false aneurysm:

  • a breach in the vascular wall leading to an extravascular haematoma that freely communicates with the intravascular space
  • “pulsating haematoma”
73
Q

What is a dissection?

What arteries tend to be affected by them and what is the main danger?

A

An arterial dissection arises when blood enters the wall of an artery, as a hematoma dissecting between its layers

dissections usually (but not always) arise in aneurysmal arteries

Aneurysms and dissections can rupture

74
Q

What is the difference between Type A and Type B dissections?

A

Type A is more common and more serious as it is a proximal lesion involving the ascending aorta

Type B affects the descending aorta alone

75
Q

what is the classification used for dissections?

A

Stanford

76
Q

What is meant by double barrelled aorta in a dissection?

A

it occurs in chronic dissection

a double barrel aorta occurs when a dissection progresses forward, then spontaneously reconnects to the aorta at the distal part of the dissection

77
Q

What is involved in the aetiology of aneurysms?

A
  • Atherosclerosis
  • cystic medial degeneration (common in Marfan syndrome)
  • trauma
  • congenital defects
  • infections (mycotic aneurysms)
78
Q

What is the most common cause of AAA?

What is this?

A

Atherosclerosis and cystic medial degeneration are the most common causes

Abdominal aortic aneurysm is an enlarged area in the lower part of the aorta

79
Q

What is Marfan syndrome?

A

A genetic disorder of connective tissue

the aorta may become enlarged (aortic dilation) or the walls of the aorta may bulge (aortic aneurysm)

the enlarged aorta is at risk for tearing and rupture (aortic dissection)

80
Q

What type of aneurysm is associated with congenital defects?

A

Congenital defects can give rise to berry aneurysms of the brain

these are small aneurysms that occur at the point at which a cerebral artery departs from the circle of Willis at the base of the brain

81
Q

what is a mycotic aneurysm and what is it often secondary to?

A

Mycotic aneurysm can be secondary to infective endocarditis

this is the dilation of an artery due to damage to the vessel wall by an infection

82
Q

What is a syphilitic (leutic) aneurysm and why does it occur?

A

The obliterative endarteritis characteristic of the tertiary stage of syphilis shows a predilection for small vessels with complications especially in the aorta and nervous system

83
Q
A

Y2 Clinical Pathology (76 decks)

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