MoD: Vascular Diseases Flashcards

1
Q

What vessels are commonly affected by atheroma?

A
Bifurcations (sites of turbulent flow)
Abdominal aorta
Coronary arteries
Popliteal arteries
Carotid vessels
Circle of Willis
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2
Q

What are the 6 stages in the ‘response to injury’ hypothesis of atherosclerosis?

A

1- Chronic endothelial injury
2- Accumulation of lipoproteins (oxidised LDL damaged arterial wall)
3- Platelet adhesion
4- Factor release
5- SMC (smooth muscle cell) proliferation and ECM (extra-cellular matrix) production
6- Lipid accumulation (gives rise to ‘fatty streaks’)

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3
Q

What is a fatty streak?

A

The earliest lesion in atherosclerosis.

Composed of lipid filled foamy macrophages.

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4
Q

Components of Virchow’s triad?

A

1- Endothelial damage (smoking/ hypertension/ surgery)
2- Hypercoagulability (hereditary/ acquired- cancer, obesity, pregnancy)
3- Stasis (immobility, polycythemia)

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5
Q

Differences between Arterial thrombosis and Venous thrombosis… a)mechanism b)location c)composition d)treatment

A

a)Arterial= rupture of atheromatous plaque
Venous= combination of factors from Virchow’s triad
b)Arterial= Left heart chambers/ arteries
Venous= venous sinusoids of muscle and valves of veins
c) Arterial= mainly platelets
Venous= mainly fibrin
d) Arterial= anti-platelet agents (clopidogrel)
Venous= anticoagulants (heparin/ warfarin)

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6
Q

Differences between a clot and a thrombus?

A
Clot= platelets not involved, red, gelatinous, not attached to vessel wall.
Thrombus= platelets involved, red (venous) pale (arterial), firm, attached to vessel wall.
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7
Q

What is an embolus?

A

A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin.

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8
Q

How harmful is ischaemic injury?

a) short duration?
b) long duration?

A

a) cell injury reversible (eg PPI for an MI)

b) irreversible cell damage

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9
Q

What is ischaemia-reperfusion injury?

A

Tissue reperfusion is not always good, this is when repurfusion generates reactive oxygen species which cause further cell injury.

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10
Q

What are the 2 types of infarction?

A

1) Red (haemorrhagic)- dual blood supply/ venous infarction.

2) White (anaemic)- single blood supply, hence totally cut off

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11
Q

Why are infarctions usually wedge-shaped?

A

Because the vascular supply is ‘upstream’ or ‘proximal’ in the tissue, so therefore the entire downstream area will be infarcted.

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12
Q

What type of necrosis is an infarction?

A

Coagulative necrosis (in the brain it is colliquative necrosis)

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13
Q

What is Shock?

A

A pathophysiological state of reduced tissue perfusion resulting in decreased oxygen delivery to the tissues.
Leads to cellular hypoxia and derangement of cellular biochemistry (–> end organ dysfunction)

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14
Q

What are the two main things that result in Shock?

A
  • Decreased cardiac output

- Decreased systemic (peripheral) vascular resistance

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15
Q

What are the 3 types of Shock?

A

1- Hypovolaemic Shock
2- Cardiogenic Shock
3- Distributive Shock

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16
Q

What is hypovolaemic shock?

A

Intra-vascular fluid loss (blood, plasma etc)

  • Decreased venous return to heart (‘pre-load’
  • Decreased stroke volume–> decreased cardiac output
17
Q

What are 2 causes of hypovolaemic shock?

A

1- Haemorrhage (trauma, GI bleed, ruptured aneurism)

2- Non-haemorrhagic fluid loss (diarrhoea, vomiting, burns. Third spacing)

18
Q

What is third spacing?

A

Acute loss of fluid into internal body cavities. Common post-operatively and in intestinal obstruction, pancreatitis or cirrhosis.

19
Q

What is cardiogenic shock?

A

Cardiac Pump failure (compensate by increasing the Systemic Vascular Resistance)

20
Q

What are the 4 causes of cardiogenic shock?

A

1- Myopathic (heart muscle failure) from an MI or cardiomyopathies
2- Arrythmia-related (abnormal electrical activity)
3- Mechanical (valvular defects, ventricular septal defects)
4- Extra-cardiac (obstruction to blood outflow, anything outside heart impairing cardiac filling or ejection of blood)

21
Q

What is distributive shock?

A

Decreased SVR due to severe vasodilation (compensate by increasing cardiac output= flushed/ bounding heart, warm especially with septic shock)

22
Q

What are the 4 sub-types of distributive shock?

A

1- Septic shock (systemic infections, increases cytokines/mediators resulting in vasodilation)
2- Anaphylactic shock (severe type 1 hypersensitivity reaction)
3- Neurogenic shock (spinal injury/ anaesthetic accident–> loss of sympathetic vascular tone–> vasodilation)
4- Toxic shock syndrome (S. aureus/ S. pyogenes produce exotoxins. Widespread release of massive amounts of cytokines, reducing systemic vascular resistance)