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
calcium stones risk factors
decreased urine, hypercalcaemia, high oxalate consumption
renal stones symptoms
haematuria, pain colic
how test for uti
urine dipstick increase nitrates and leukocytes esterases
actiosns of loop, thiazide and K sparing diuretics and eg
loop - NaKCl. decresae Ca reabsorb. e.g. furosemide
thiazide - NaCl. increase ca reabsorb. e.g. bendroflumethiazide
K sparing:
1) ENaC blockers - e.g. amiloride
2) aldost antag - e.g. spironolactone
what diuretic for HF, liver failure, HT, conns?
conns - aldost antag
HF - loop e.g. furosemide
liver failure - aldost antag and loop
HT - thiazide e.g. bendroflumethiazide
pathology and causes of conns
increased aldosterone leads to increase Bp and hypokalaemia. Vision, headaches, strokes, MI, AKI
cause - adrenal adenoma, adrenal hyperplasia
thiazide ADRs
hypokalaemia, hypercalcaemia, hyperuricaemia, ED
aldost antag ADRs
hyperkalaemia, gyno
all diuretics ADRs
hyponatremia, hypovolemia, anaphylaxis
acidic and alkalemic symptoms
acidic - hyperkalaemia, arrhythmia, decrease hepatic function
alkalemia - tetany, parasthesia, death
how is hydrogen buffered in urine
phosphate and ammonia.
how hyper and hypokalemia affects ph?
hyper is acidosis
hypo is alkalosis
effects of aldosterone on K. How doe K stimulate aldosterone release
increases K excretion
high K in plasma stimulates aldosterone release
what is internal and external balance of K
internal - in and outof cells
external - kidneys
K shift into cells
alkalosis via KHX, exercise, insulin, aldosterone, increase K ecf
K shift out of cells
acidosis, decrease K ECF, trauma, plasma hyperosmolarity
causes of hypokalaemia
alkalosis, vomiting, diarrhoea, diuretics, conns
symptoms, ECG and treat hypokalaemia
symptoms - paralytic ileus, muscular weakness, CD dysfunction
ECG - shallow T wave to prominent U wave to ST depression
treat - oral/IV K, K sparing diuretic
hyper Kalaemia causes, ECG and treat
causes - CKD, NSAIDs, acidemia
ECG - tall tented T waves, prolonged PR, widened QRS, VFib
treat - IV calcium gluconate, insulin, oral K binding resin, decrease intake
Bladder PS, somatic and symp innervations
PS - S2-4
somatic - S2-4 pudendal
symp - T10-L2 hypogastric
what controls micturition
pontine micturition centre
what is stress urge and overflow UI
stress - excess pressure on bladder leads to leaking
urge - urgent desire + leaking
overflow - no urge to pee, overfull bladder + leaking
how manage UI
less caffeine, weight loss, stop smoking, bladder training, botulism, B3 agonist, anticholinergic, sling, artifical urinary sphincter
AKI pre renal causes
hypovolemia, NSAIDs, ACEi
AKI renal causes
renal artery occlusion, glomerulonephritis, toxins (gentamicin), pre-eclampsia
AKI post renal causes
tumour, BPH, ureteric stricture, megaureter
AKI investigation
FENa, BP, urinalysis, imaging
AKI management
IV fluids
if high K - calcium gluconate
if acidosis - protein restrict and bicarb
causes of macroscopic haematuria
myoglobin, IgA nephropathy
symptoms of nephrotic and nephritic
nephrotic - oedema, hypoalbuminaemia, proteinuria, hyperlipidaemia
nephritic - haematuria, increase BP, small proteinuria, oligouria
causes of nephritic
PIG ARM - IgA nephropathy, good pastures, alport, rapidly progressive Gn, membrane proliferative GN
causes nephrotic
Mum Fight Me im SAD
Membranous GN, FSGS, Minimal change GN, SLE, Amyloidosis, diabetic nephropathy
pathology and type of hypersensitivity of membranous GN, diabetic neph, IgA neph, alport, goodpasture, vasculitis
membranous GN - IgG depostion. T3HS
diabetic neph - thick BM, microvascular disease, mesangial sclerosis
IgA neph - IgA in mesangium. T3HS
alport - abnormal collagen IV and therefore abnormal BM. deafness, X linked
good pasture - IgG targets collagen IV. T2HS
vasculitis - ANCA leads to BV damage. T2HS
gene affecting prostate cancer. symptoms. diagnosis
BRCA2 gene
symptoms - asymptomatic till late. haematuria, bone pone of mets.
diagnosis - DRE, serum PSA, USS
TNM staging
size/4, nearby lymph/3, mets/1
caues of CKD and symptoms
causes - infection, hypertension, diabetes, polycystic kidney disease, alport
symptoms - acidosis, pericarditis, anemia, osteomalacia, hypervolemia, osteitis fibrosa cystic (increase phosphate reduces calcium reabsorb increases PTH). Fatigue, breathlessness, pain, N&V, coma
CKD investigate and manage
investigate with 24 hour creatinine clearance
manage - lifestyle, ACEi, statin, treat BP
sensory inervation of kidneys and ureter
kidneys - T10-11
ureter - T12-L2
blood supply of ureter
1/3 - renal arteries
2/3 - common iliac, AA, gonadal
3/3 - internal iliac
