Bromley Emergency

Answer.

1.

Explanation.

Potassium is readily filtered by the glomerulus with around 7-8% of this filtered potassium load ultimately excreted by the kidney. Of the remainder, the majority (70%) is re-absorbed in the proximal tubule (K+-CL- symport and K+-H+ exchanger) and a smaller amount (20%) in the ascending loop of Henle (Na+-K+-2Cl co-transporter) while the distal tubule and collecting ducts can either reabsorb or secrete potassium and are the main point of control of potassium balance.

Influences over the absorption or secretion of K+ in the distal tubule and collecting duct include:

1. Aldosterone increases K+ secretion by increasing both numbers and activity of Na+/K+ ATPase in the distal tubule and collecting ducts. These reabsorb Na+ in exchange for pumping out K+ into tubular fluid. Aldosterone secretion from the adrenal cortex is stimulated by rising plasma [K+].
2. Secretion of K+ is into tubular fluid also occurs by passive diffusion, and is therefore proportional to the flow rate of tubular fluid; increasing flow causes increased K+ secretion.
3. A rise in serum [H+] (acidaemia) causes an increase in K+ reabsorption. The H+-K+ antiporter in the proximal tubule and H+/K+ ATPase of the intercalating cells of the collecting duct both reciprocally pump H+ out into the tubular fluid in exchange for K+ into the cell for reabsorption. Upregulation of these transporters to secrete more H+ in acid excess will cause a reciprocal increase in K+ reabsorption. This in one of the mechanisms through which metabolic acidosis and hyperkalaemia are linked.

    

Of the diuretics, the loop and thiazides will increase K+ excretion through increasing distal tubular flow rates (and both have the complication of hypokalaemia), while spironolactone increases potassium reabsorption through its effect as an aldosterone antagonist (hence known as a potassium sparing diuretic). ACE inhibitors suppress the renin-angiotensin-aldosterone system and so reduce aldosterone secretion and lead to greater potassium reabsorption.

Answer.

4.

Explanation.

The brain is metabolically very active and under normal condition, cerebral oxygen consumption is about 20% of total body oxygen consumption.

Glucose is the source of 90% of energy of brain in normal conditions. This energy is required for maintaining electrical gradient across cell membrane and transmission of electrical impulses. Rest of energy comes from ketone bodies and other small energy metabolites but very little from fatty acids.

Cerebral blood flow is closely autoregulated and kept constant for mean arterial pressures (MAP) between around 60-150mmHg. Typically, cerebral blood flow is about 750ml per minute or round 15% of cardiac output.

Cerebral autoregulation relies on

1. Vasomotor reflex. Increased sympathetic tone moderates blood flow through cerebral arteries at higher blood pressures
2. Local metabolites produced when a region of brain tissue becomes more active (e.g. CO₂, ADP, K⁺, H⁺) cause vasodilatation of local arterioles, thereby increasing blood flow to that region. Occurring throughout the brain this mechanism matches cerebral blood flow to demand both at the local level and for the brain as a whole.
3. While marked hypoxia (pO2 < 6-8KPa) will stimulate cerebral arteriolar vasodilatation to increase blood flow to the brain, throughout the physiological range of arterial pO2 (8-15Kpa) cerebral arterioles are largely insensitive to oxygen. Furthermore, supplemental oxygen above this level, if anything, tends to cause vasoconstriction of cerebral arterioles and reduced blood flow.