MoD: Vascular Diseases Flashcards
What vessels are commonly affected by atheroma?
Bifurcations (sites of turbulent flow) Abdominal aorta Coronary arteries Popliteal arteries Carotid vessels Circle of Willis
What are the 6 stages in the ‘response to injury’ hypothesis of atherosclerosis?
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’)
What is a fatty streak?
The earliest lesion in atherosclerosis.
Composed of lipid filled foamy macrophages.
Components of Virchow’s triad?
1- Endothelial damage (smoking/ hypertension/ surgery)
2- Hypercoagulability (hereditary/ acquired- cancer, obesity, pregnancy)
3- Stasis (immobility, polycythemia)
Differences between Arterial thrombosis and Venous thrombosis… a)mechanism b)location c)composition d)treatment
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)
Differences between a clot and a thrombus?
Clot= platelets not involved, red, gelatinous, not attached to vessel wall. Thrombus= platelets involved, red (venous) pale (arterial), firm, attached to vessel wall.
What is an embolus?
A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin.
How harmful is ischaemic injury?
a) short duration?
b) long duration?
a) cell injury reversible (eg PPI for an MI)
b) irreversible cell damage
What is ischaemia-reperfusion injury?
Tissue reperfusion is not always good, this is when repurfusion generates reactive oxygen species which cause further cell injury.
What are the 2 types of infarction?
1) Red (haemorrhagic)- dual blood supply/ venous infarction.
2) White (anaemic)- single blood supply, hence totally cut off
Why are infarctions usually wedge-shaped?
Because the vascular supply is ‘upstream’ or ‘proximal’ in the tissue, so therefore the entire downstream area will be infarcted.
What type of necrosis is an infarction?
Coagulative necrosis (in the brain it is colliquative necrosis)
What is Shock?
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)
What are the two main things that result in Shock?
- Decreased cardiac output
- Decreased systemic (peripheral) vascular resistance
What are the 3 types of Shock?
1- Hypovolaemic Shock
2- Cardiogenic Shock
3- Distributive Shock
What is hypovolaemic shock?
Intra-vascular fluid loss (blood, plasma etc)
- Decreased venous return to heart (‘pre-load’
- Decreased stroke volume–> decreased cardiac output
What are 2 causes of hypovolaemic shock?
1- Haemorrhage (trauma, GI bleed, ruptured aneurism)
2- Non-haemorrhagic fluid loss (diarrhoea, vomiting, burns. Third spacing)
What is third spacing?
Acute loss of fluid into internal body cavities. Common post-operatively and in intestinal obstruction, pancreatitis or cirrhosis.
What is cardiogenic shock?
Cardiac Pump failure (compensate by increasing the Systemic Vascular Resistance)
What are the 4 causes of cardiogenic shock?
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)
What is distributive shock?
Decreased SVR due to severe vasodilation (compensate by increasing cardiac output= flushed/ bounding heart, warm especially with septic shock)
What are the 4 sub-types of distributive shock?
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)
