Pathology of Ischaemic Heart Disease and Hypertension Flashcards

1
Q

How does a thrombus form in a blood vessel?

A

If there is damage to the endothelial cells lining the blood vessel, they lift up.

Platelets are attracted to collagen under the endothelial cells.

Positive feedback loop where platelets then release chemicals which attract more platelets which will all stick to each other.

Blood clotting mechanisms are then turned on too so that fibrinogen polymerises into fibrin - which holds together the RBCs and platelets.

This forms a thrombus

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2
Q

What 3 factors can precipitate thrombosis in BVs?

A
  • change in vessel wall
  • change in blood flow (normal flow is laminar flow)
  • change in blood constituents (some people have too many platelets)
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3
Q

What are the causes of ischaemic heart disease (lack of blood to the heart)? (3)

A
  • Atherosclerosis - disease of arterial BVs
  • Myocardial hypertrophy - increase in size of heart muscle due to increase in cell size
  • Small vessel disease (e.g. arterioles)
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4
Q

What are the risk factors for developing atherosclerosis? (5)

A
  • Areas of deprivation
  • Smoking
  • Hypertension
  • Uncontrolled diabetes
  • Hyperlipidaemia
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5
Q

What may make atherosclerotic plaque increase in size even faster?

A

Haemorrhage within the plaque

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6
Q

How can LVH cause ischaemic heart disease?

A

The blood supply remains unchanged, even though in LVH the ventricular muscle is much bigger - more difficult to supply

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7
Q

What happens during small vessel changes?

What causes it?

A

Inappropriate vasoconstriction

Caused by: Reduced production of nitric oxide or increased destruction of nitric oxide

Nitric oxide aims to keep the BVs open so if there isnt enough of it they wont stay open

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8
Q

What does ischaemic heart disease look like?

A

Regional transmural myocardial infarction

Subendocardial myocardial infarction

Chronic ischaemia - goes on for a long time without the heart muscle actually dying

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9
Q

What is the most common type of MI?

A

Regional transmural MI.

Chunk of heart muscle has died which is the full thickness of the wall of the heart. Due to a blockage in a coronary artery.

Acute occluding event in one of three main coronary arteries

Lack of collateral circulation for blood to flow via a different route.

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10
Q

What happens in a subendocardial MI?

A

The inner part of the ventricle dies off which is furthest from the blood supply. Not the full thickness of the wall.

Tends to occur with severe coronary artery atherosclerosis in all three main coronary arteries.

Some sudden reduction in blood flow, e.g. hypotension during an operative procedure - occurs in hospital more

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11
Q

What symptom is given by chronic ischaemia?

A

Fixed atherosclerotic lesions.

Pt gets angina on exertion.

Myocardial fibrosis / hibernating myocardium / stunned myocardium

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12
Q

What are the complications of myocardial infarction?

A
  • sudden death
  • arrhythmias
  • cardiac failure - loss of myocardium so reduced pump function
  • mitral incompetence - rupture/necrosis of papillary muscles
  • pericarditis
  • cardiac rupture - weakening of wall due to muscle necrosis and acute inflammation (3-7days after infarction)
  • mural thrombosis - thrombosis on the abnormal endothelial surface following infarction
  • ventricular aneurysm
  • pulmonary embolism
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13
Q

What is the bad thing about having hypertension?

A

You dont know you’ve got it - no symptoms

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14
Q

What is the clinical importance of hypertension?

What is it a major risk factor for?

A

Commonest cause of heart failure in most countries

Major risk factor for atherosclerosis

Major risk factor for cerebral haemorrhage

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15
Q

What is the one year survival rate for heart failure?

A

60%

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16
Q

What is the standard blood pressure reading? (systolic/diastolic)

A

120/80

17
Q

What is the cause of primary hypertension? (3 factors)

A

No definitely identified cause

Must involve sodium control (higher sodium levels may retain more water = higher BP)

Involves adrenaline too - this causes smooth muscles to contract to increase BP

And the renin angiotensin aldosterone system in the kidneys

18
Q

What is the cause of secondary hypertension?

A
  • renal - renin dependent, salt and water overload
  • endocrine - Cushings, Conns, phaeochromocytoma
  • coarctation of aorta (stenosis in aorta)
  • drug therapy - corticosteroids, NSAIDs
19
Q

What is the clinicopathological classification of hypertension?

A

benign (most common)

  • long asymptomatic period
  • increased frequency of complications later

malignant

  • markedly raised diastolic pressure
  • symptomatic
  • rapidly fatal if untreated
20
Q

What are the effects of hypertension? (3)

What do these effects then cause on the body? (3)

A
  • accelerated atherosclerosis
  • sclerosis of smaller vessels
  • microaneurysms and haemorrhages in the brain
  • heart failure
  • kidney failure
  • cerebral haemorrhages (strokes)