RENAL Flashcards
Angiotensin effect on arteriolar resistance
Constricts efferent >afferent arteriole (AT1 receptor)
Afferent arteriole dilators
Prostaglandin
NO
Dopamine (low dose)
Afferent arteriole constrictors
Adenosine
Noradrenaline (SNS)
Vasopressin
Endothelin
AT2 receptor action
Vasodilatation
Renal autoregulatin response
Via changes in afferent arteriole tone
> Prostaglandin and NO causing dilation
> Adenosine causing constriction
Angiotensin II action
Increases SNS Increases aldosterone secretion from adrenals Arteriole vasoconstrictor ADH production Increases tubular Na/Cl reabsoorption
Tubule segment that is not permeable to water
Ascending thin and thick loops
distal convoluted tubule
Tubule segment that is not permeable to sodium
descending thin loop of henle
ADH receptor
G coupled receptor on basolateral membrane. Leads to aquaporin-2 insertion on apical membrane and aquaporin-3 on basolataeral
Tubule segment associated with complete resorption of glucose, amino acids, majority of bicarbonate and phosphate
Proximal tubule
Sodium transporter in the loop of henle (Thick ascending limb)
NKCCT (Na x1 K x1 Cl x2)
Blocked by frusemide
Sodium transporter in the distal tubule
Na-chloride cotransporter on apical membrae, Na-K-ATPase in basolateral membrane
Na-Cl CTP blocked by Thiazide diuretics
Electrolyte effects thiazide
Hypokalaemia
Hyponatraemia
Metabolic Alkalosis
Hypercalcaemia
Sodium transporters in the proximal tubule
Organic molecules co transporter (eg Na-glucose, Na-amino acids)
Na/H exchanger
Sodium transporter in the collecting duct
Na/K-ATPase in basolateral membrane of principal cells
Aldosterone action
Acts on receptors on basolateral membrane
in distal tubule, increases mRNA synthesis in the nucleus leading to increases Na-K ATPase
Results in Na reabsorption and K excretion
Due to effect of increased K in duct, results in Hydrogen excretion
The action of Type A intercalated cell
Excretion of H+
Action of Type B intercalcated call
Excretion of HCO3-
Amiloride action
Blocks apical Na channels (ENac) in principal cells
Site of hypoosmotic tubular contents
Thick ascending loop (impermeable to water)
Tubular site of PTH for calcium reabsorption
Thick ascending limb and distal tubules
Role of FGF-23
Decrease serum PO4
Acts on FGF receptor and coreceptor klotho in proximal tubule, decreasing PO4 reabsorption
Decreases calcitriol, in turn reducing phosphate GI absorption
High FGF-23 levels
Early marker of CKD-MBD
Increase CVD mortality risk, causes LVH
Barter syndrome
Defect in NaCl resorption in ascending thick limb
Hypokalaemia
Metabolic alkalosis
Hypercalcaemia
Barter syndrome Type 3
Affects basolateral Cl channel CIC-Kb impacting on NKCCT
Barter syndrome Type 5
Affects Calcium sensing receptor Hypocalcaemia Hypokalaemia Metabolic alkalosis Hypomagnesaemia
Drug class leading to barter type 5 effect
Aminoglycosides
Gitelman syndrome
Hypokalaemia
Metabolic alkalsosis
Hypomagnesaemia
Hypocalcaemia
Liddle’s
EnaC function increased Hypokalaemia Hypertension Metabolic alkalosis Treated with amilioride
Minimal obligatory urinary loss volume
430ml
Insensible daily losses
500ml
Site of K reabsoroption
proximal tubule
Drug that inhibits ADH
Alcohol
NAGMA
Chloride excess
Addissons
GI
Extra - RTA
HAGMA
Ketoacidosis Lactic acidosis Ethalene/methanol salicyclic acid Uraemia Metformin CO
Type 1 RTA (Distal tubule)
H+ secretion is defective
NAGMA
Alkalotic urine (>5.5)
Hypercalcaemia