Renal physiology

Question 1

Upper PCT

Answer 1

Sodium with glucose absorption

Question 2

SLGT2

Answer 2

Large capacity, low affinity (target of SLGT2

Question 3

SLGT1

Answer 3

low capacity, high affinity (mops up extra glucose)

Question 4

Lower PCT

Answer 4

Sodium chloride (Cl- transcellularly/paracellularly). Na absorption driven by Na/K/ATPase (basolateral). Water is paracellular, and transcellular via AQP1.
Bicarb reabsorbed by CA (uses basolateral NBCe-1A sodium bicarb pump)
Organic acids secreted (aspirin, penicillin, creatinine, urate).
Protons secreted via sodium/proton antiport, as well as ATPase.
Potassium reabsorbed through solvent drag (lumen becomes more positive).
Ammoniagenesis occurs in PCT.
No net proton gain/bicarb loss (}pH7.4)

Question 5

Diuretic in PCT

Answer 5

CA inhibitor (acetozolomide), blocks bicarb entry and therefore can't be exchanged for proton, which can't be exchanged for sodium. Weak.
SLGT2 inhibitor (blocks sodium glucose symport)

Question 6

DLoH

Answer 6

Water reabsorbed

Urea secreted by UT-A2 transporter

Question 7

Ascending LoH

Answer 7

Active and passive NaCl reabsorption.
Basolateral Na/K ATPase drives apical Na/K/2Cl
Region is impermeable to urea, but NH4+ can sub for K+ and be reabsorbed instead.
K secretion via ROMK

Question 8

Diuretics in LoH

Answer 8

Loop (furosemide)Blocks Na/K/2Cl symport. Normally, reabsorbed K is secreted by ROMK in exchange for paracellular Na/Ca/Mg, therefore reabsorption of these also reduced. ADE: hypokalaemia, hyponatraemia, hypomagnesaemia, rarely photosensitivity and deafness

Question 9

DCT

Answer 9

Active NaCl reabsorption through thiazide sensitive NaCl channel (early DCT), ENaC in late DCT (aldosterone mediated, hactivity of Na/K/ATPase). If aldosterone drives more Na, also drives more K into cell which is excreted through ROMK.
Alpha intercalated cells reabsorb bicarb via apical H+ATPases. Beta intercalated cells absorb protons while secreting K and bicarb.
Ureal reabsorbed through UTA1/UTA2 (under ADH control - high protein diet = high urine conc)

Question 10

DCT diuretics

Answer 10

Thiazides act on Na/Cl symport in DCT (Driven by basolateral Na/K/ATPase. Used as FLT in HT, but also reducing renal calculi recurrance.
ADE: hyponatraemia, photosensitivity, hypokalaemia, hypercalcaemia, reduced glucose tolerance

Question 11

CD

Answer 11

Water reabsorbed though AQP2 channels (ADH acts on V2 receptor). Sodium chloride reabsorbed. Urea reabsorbed. K secreted through ROMK (on principal cell - driven by Na/K/ATPase. High urine flow drives MAXIK K excretion.
Alpha intercalating cells can reabsorb K in hypokalaemia, as well as bicarb.
NH3 secreted into lumen via rhesus (2GP transporters), combines with proton to NH4+ (trapped for secretion)

Question 12

Diuretics in CD

Answer 12

Amiloride (blocks apical sodium channel). Potassium sparing, weak, used in combo to prevent hypokalaemia. 
Aldosterone inhibitor (spironolactone) - potassium sparing, weak. Used in combo, or in ascites. Can cause gynaecomastia in males.
Aquaretic (tolvaptan): ADH V2 inhibitor, prevents ADH AQP2 insertion. Also used in ADPKD to reduce cyst formation with cAMP. Can cause hypernatraemia and LF abnormalities.

Question 13

ADH

Answer 13

Secreted by surpaoptic and paraventricular hypothalamic nuclei, stored in post pit. Released in response to reduce osmolality. Stimulates V2 receptor to trigger AQP2 insertion in DCT. Also stimulates triple co-transporter in ascending LoH to increase Na reabsorption, and increase urea reabsorption via UT-A1 . Can also induced vasocontriction via V1 mediated IP3 increase.

Question 14

Promote AHE

Answer 14

osmoreceptors, atrial stretch, blood volume/pressure sense, hypoxia, pain, stress, emesis, exercise, nausea, hypoglycaemia, morphine , nicotine, angiotensin, beta blockers, PGs

Question 15

ADH inhibition

Answer 15

Alcohol, alpha blockers, glucocoritcoids

Question 16

Hyperkalaemia

Answer 16

Causes Tall, Tented T wave, wide flat P wave. QRS widens as patient heads to cardiac arrest

Question 17

Hypokalaemia

Answer 17

Small, flat T wave, slightly peaked P wave and prominant U wave

Question 18

How does insulin deficiency affect potassium?

Answer 18

Hyperglycaemia causes hyperosmolarity, H2O moves out of cell and brings K too, therefore hyperkalaemia

Question 19

Increased cellular K uptake caused by

Answer 19

insulin (causes skeletal muscle/liver cell uptake), catecholamines/epinephrine (beta 2 adrenoceptor activation)