CSIM 1.64: Cardiovascular Disease 3 Flashcards

1
Q

What are the types of ischaemia?

A
  • Arterial ischaemia
    • Capillary ischaemia
    • Venous ischaemia
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2
Q

What are the aetiologies of arterial ischaemia

A
  • Atheroma, thromboses and embolism
    • Vasculitis (inflammation of blood vessels - these tend to thrombose)
    • Hypertension (causing arteriolar changes)
    • Spasm
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3
Q

What is Reynaud’s disease and which type of ischaemia is it likely to cause?

A

Vasospasms due to cold or emotional stress causing peripheral loss of flow
• Spasms arterial ischaemia

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4
Q

What increases susceptibility to arterial ischaemia?

A
  • Lower adequacy of organ function and perfusion prior to ischaemia
    • Single arterial supply as opposed to dual supply
    • Sudden/fast onset as opposed to gradual (where collaterals have time to develop)
    • Tissue susceptibility (brain and heart highly susceptible)
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5
Q

Which common clinical syndromes are caused by arterial ischaemia?

A
  • Angina
    • Hypertensive renal disease
    • Claudication (brain infarct or gangrene)
    • Ischaemic colitis
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6
Q

Describe capillary ischaemia and give some examples of the common syndromes caused by this.

A

Blocked or damaged capillaries leading to very localised ischaemia
• Frostbite
• Cryoglobulinaemia
• Disseminated intravascular coagulation
• Diabetic microangiopathy

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7
Q

What is a strangulated hernia, and what type of ischaemia does it lead to?

What other pathology of the gut can cause venous ischaemia?

A

Intestines herniate, which strangulates the venous return from this section of intestine. This causes retrograde pressure increase and flow cessation.
–> VENOUS ISCHAEMIA

Volvulus of the gut - a loop of gut twists around its mesenteric base, obstructing venous return

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8
Q

Describe chronic ischaemic cardiopathy

A

Myocyte atrophy and fibrosis following an infarct of the heart (silent or clinical). This results in myocardial degeneration and ultimately death by cardiac failure.

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9
Q

What is cardiac sudden death?

What causes it?

A

Unexpected death due to heart problems occurring

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10
Q

What is the alternative name for angina and what causes it?

A

Angor Pectoris

• Paroxysmal and recurrent chest discomfort caused by transient myocardial ISCHAEMIA which fails to induce necrosis

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11
Q

What are the types of angina?

A

Stable angina
• Atherosclerosis with 50% stenosis
• Occurs at rest

Unstable crescendo angina
• Progressively increasing frequency of pain with less effort
• Disruption of plaque with superimposed partial thrombus (type 6)

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12
Q

What are the ACUTE coronary syndromes?

A

Unstable crescendo angina:
• No elevation of biomarkers of myocardial necrosis

Non-ST-segment elevation MI (NSTEMI):
• Elevation of biomarkers of myocardial necrosis
• Q waves absent
• ST segment not elevated
• Due to partial-thickness MI
• Partial thrombotic occlusion over plaque

ST-segment elevation MI (STEMI):
  •  Elevation of biomarkers of myocardial necrosis
  •  Q waves present
  •  ST segment elevated
  •  Due to transmural MI
  •  Complete thrombotic occlusion

IMG 156 and 157

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13
Q

What can be observed using imaging when looking for aspects of MI?

A
  • Reduction of loss of tissue perfusion (using contrasts)

* Cardiac wall motion abnormalities

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14
Q

What are the patterns of pathogenesis of MI

A

Transmural MI
• 90%
• Affects the whole thickness of the myocardium
• Caused by a thrombosis over an unstable atheromatous plaque

Subendocardial MI
• 10%
• Multiple foci of necrosis found in the subendocardial layer
• Caused by diffuse atherosclerosis

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15
Q

Describe the macroscopic appearances of a heart infarct

A
4 hours (histological)
  •  Wavy fibres at border
18 hours (histological)
  •  Coagulation necrosis
  •  Loss of cross striations
  •  Polymorphonuclear infiltration
24 hours
  •  Pallor of myocardium
  •  Contraction bands and nuclear pyknosis histologically
72 hours 
  •  Pallor with hyperemia
  •  Total loss of nuclei
7 days
  •  Mononuclear infiltration
  •  Central yellowing as fibrovascular response begins
  •  Hyperemic border
21 days
  •  Maximally yellow and soft
  •  Prominent granulation tissue from fibrovascular reponse
  •  Vascular margins
7 weeks
  •  White fibrosis

IMG 158

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16
Q

How can MI be detected after 24 hours with immunohistochemistry?

A

By assessing C9 complement fraction

IMG 159

17
Q

Describe where coronary arteries typically become occluded, and what each of these typically supplies.

A

Left coronary artery
OCCLUSION: Anterolateral MI (LAD & LCx)

LCA: Anterior descending (LAD)
OCCLUSION: Anteroseptal MI
• Anterior left ventricle
• Anterior 2/3 of the inter-ventricular septum

LCA: Left circumflex (LCx)
OCCLUSION: Lateral MI
• Lateral wall of left ventricle

Right coronary artery
OCCLUSION: POSTERIOR INF MI
• Posterior left ventricle
• Posterior 1/3 of inter-ventricular septum

IMG 160

18
Q

What are the complications of MI?

A
Early phase complications 2-10 days
  •  Reinfarction
  •  Arrhythmia 
  •  Cardiac rupture
  •  Acute ventricular aneurysm 

Late phase complications 10+ days
• Chronic ventricular aneurysm
• Chronic cardiac failure
• Dressler syndrome

19
Q

What is Dressler syndrome?

A

Pericarditis 2-10 months after an MI due to immunological pathogenesis. Indicated by elevated ESR.

20
Q

What is the most common arrhythmia that results from MI?

A

• Ventricular fibrillation

21
Q

What cardiac rupture can occur as an early phase complication post MI?

What does each result in?

A

Free wall rupture
• Haemopericardium
• Cardiac tamponade

Papillary muscle rupture
• Acute severe mitral regurgitation

Intra-ventricular septum rupture
• Left-to-right shunt