Urinary Flashcards
Course of ureters
cross pelvic brim at bifurcation of common iliac. Runs along lateral pelvic wall. Turns obliquely at level of ischial spine and ends bladder posteriolaterally
renal blood supply
renal to 3x segmental to interlobar to arcuate to interlobular to afferent
where is bladder anatomically
posterior to pubic symphysis
how does horseshoe kidney occur
kidneys ascend in development and can fuse and get stuck on IMA
what is patent urachus
urine from umbilicus
what is a common fistula of the bladder
exstrophy of bladder through abdo wall
give anatomy of kidney
see book
capsule, renal column and pyramid, minor calyx, cortex, renal pelvis
histo of PCT, thin AL, thick AL, DCT
PCT - cuboidal with brush border
thin AL - simple squamous
thick AL - cuboidal
DCT - cuboidal, larger lumen than PCT
bladder histology
urothelium, LP, 3x SM, adventitia
transporters in PCT
apical - NaH antiporter, SGLT1, AA vit symporters, Anion/cation exchangers
basolateral - NaKATPase
Ascending loop transports
apical - NaKCl, ROMK (to lumen)
basolateral - NaKATPase
DCT transporters
apical - NaCl symporter. Ca diffusion (PTH activated)
basolateral - NaKATPase
principal CD and intercalated CD
principal - ENaC, AQP2
intercalaed - reabsorb Cl, secrete H+
function of macula densa and location
lines thick AL. increase NaCl = constriction of afferent by adenosine. Decrease NaCl = dilate afferent by prostaglandin. NaCl detected by NaKCl
how measure GFR and RPF
GFR - inulin
PFR - PAH
what 4 mechanisms can be used to influence NaCl reabsorption
RAAS, sympathetic stimulation, ADH, Atrial natriuretic peptide (increase GFR and therefore increase excretion of Na)
how RAAS works and effects
juxtaglomerular cells reelase renin in response to - decrease Na reaching macula densa, or sympathetic, or decrease perfusion pressure by baroreceptors
Renin converts AG1 to AG2 which increase aldosterone which; increases ENaC, constricts afferent and efferent arterioles, increase NHX, increase thirst via ADH, decrease bradykinin
When and whereis ADH release
decreased pressure (by baroreceptors) or increased osmolarity. detected by osmoreceptors in OVLT of hypothalamus but released by post pit
effects of ADH
increase AQP2 in CD and increase NaKCl
what is mild, moderate and severe HT
mild - 140-160 / 90-99
+20/10
causes of secondary hypertension
NSAIDs, CKD, cushings
what is symptoms and pathology of syndrome of inappropriate ADH. treaat?
increase ADH leads to increase BP. Retention of water but not solute results in hyponatremia which leads to N&V, lethargy, seizures
treat with ADH receptor anatgonists
how is corticopapillary osmotic gradient made?
inner medulla has higher osmolarity than cortex or outer medulla
1) ascending limb impermeable to water and therefore solutes enter medulla. filtrate hypotonic
2) descending limb impermeable to salts and therefore water enters medulle. filtrate hypertonic.
3) vasa recta absorbs salt and water.
where is calcium reabsorbed
10% in DCT under PTh. rest in PCT and LoH
causes, symptoms and treat of hypercalcaemia
causes - PT tumour, malignancy making PTrH
symptoms - stones, bones (bone pain), groans (lethargy), moans (abdo pain), thrones (polyuria polydipsia), psychiactric overtones (depression)
treat - loop diuretics (increase ca excretion). treat underlying