Ischaemic stroke

Question 1

What is the Oxford-Bamford classification of stroke?

Answer 1

Total anterior circulation stroke: all 3 of the following: unilateral weakness of the face, arm or leg; homonymous hemianopia, higher cerebral dysfunction.
Partial anterior circulation stroke 2 of the following: Unilateral weakness of the face, arm and leg; homonymous hemianopia, higher cerebral dysfunction.
Lacunar infarct: one of the following: pure sensory, pure motor, sensori-motor, ataxic hemiparesis.
Posterior circulation syndrome: one of the following: cranial nerve palsy and a contralateral motor/sensory deficit; bilateral motor/sensory deficit; conjugate eye movement disorder; cerebellar dysfunction; isolated homonymous hemianopia or cortical blindness

Question 2

What is the MOA of rivaroxaban?

Answer 2

Inhibits both factor 10 in the free and bound state within the prothrombinase complex

Question 3

What is the MOA of digoxin?

Answer 3

 Digoxin’s primary mechanism of action involves inhibition of the sodium potassium adenosine triphosphatase (Na+/K+ ATPase), mainly in the myocardium. This inhibition causes an increase in intracellular sodium levels, resulting in decreased activity of the sodium-calcium exchanger, which normally imports three extracellular sodium ions into the cell and transports one intracellular calcium ion out of the cell. The inaction of this exchanger causes an increase in the intracellular calcium concentration that is available to the contractile proteins. Increased intracellular calcium lengthens phase 4 and phase 0 of the cardiac action potential, which leads to a decrease in heart rate.

Question 4

What is the MOA of furosemide?

Answer 4

Furosemide, like other loop diuretics, acts by inhibiting the luminal Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus causing sodium, chloride, and potassium loss in urine.

Question 5

What is clauss fibrinogen?

Answer 5

o The final stage in the molecular co-operation of the procoagulant participants of secondary haemostasis is the conversion of soluble fibrinogen monomers to insoluble, cross-linked fibrin polymers to stabilise the blood clot. Fibrinogen is a large, symmetrical dimeric glycoprotein composed of two identical sub-units, each of which is comprised of three non-identical polypeptide chains. It is present in plasma at a high concentration and is also contained in platelet α-granules. Fibrin is formed by thrombin cleavage of the small fibrinopeptides A & B from intact fibrinogen molecules that exposes donor sites which interlock with complementary unshielded acceptor sites on adjacent molecules to promote polymerisation.

Question 6

What is the scoring system for stroke risk? What does it take into account? What is a significant score?

Answer 6

CHA2DS2-VASc
CHF or LVEF <40% (1)
HTN (1)
Age>75 (2)
diabetes (1)
stroke (2)
vascular disease (1)
65-74 (1)
female (1)
Anyone who scores 2 or above should be started on oral anticoagulation

Question 7

What is the course of the MCA?

Answer 7

The MCA arises from the internal carotid and continues into the lateral sulcus where it then branches and projects to many parts of the lateral cerebral cortex.

Question 8

What is the MOA of alteplase?

Answer 8

Alteplase binds to fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain. The protease domain then cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action.