Quiz 1 Flashcards
(45 cards)
urine flow
1ml/min
Glomerularfiltration rate:
125ml/min 180L/day
Filtration fraction
FF= GFR/RPF
125/660 ~~20%
filtration barriers
capillary
endothelium (cells)
basement
membrane
(charge)
podocyteslit
(protein)
pressure differences in glomeruli
Inglomerulus Starling forces favorfiltration:
Δ hydrostatic pressure ~ 40 mm Hg
Δ oncotic pressure ~22 mm Hg
net filtration pressure ~ 18 mm Hg
Control of Bladder
low volume: sympathetic signals dominate • bladder relaxed • internal sphincter contracted
Filling : Sensory signals trigger parasympathetic response • bladder contracts • internal sphincter relaxes • external sphincter contracted (somatic override)
Emptying (micturition): external sphincter relaxes parasympathetic responses dominate • contract detrusor • relax internal sphincter
Detrusor muscle:
- during filling - relaxed via sympathetic B2
- during emptying, contracted via parasym M
INternal schincter:
- during filling: contracted via sympath A1
- during emptying, relaxed via parasym M
External schinter:
- during filling - contracted - volun
- during emptying - relaxed also voluntary
measuring GFR
Inulin is • filteredand excreted • not reabsorbed by tubules • not secreted by tubule rate of excretion =rate of filtration
GFR = Uinulin•V’/Pinulin
urine inulin levels times urine flow rate divided by plasam inulin levels
same with creatine (a little secreted)
GFR ≈ C/Pcr = eGFR
regulation of GFR
Constrict afferentarteriole: DECREASE capillary pressure DECREASE GFR Constrict efferentarteriole: INCREASE capillary pressure INCREASE GFR
decreased during exercise, heart failure and shock
increased sympathetic tone, consstriction of afferent arteriole, decrease in GFR
increased during volume expansion - increased atrial pressure signals the release of ANP - dilates afferent arteriole
decreased in chronic kidney disease
decreases with normal aging
glucose
normally no excretion in urine
SGLT2: early proximal tubule (PCT = S1, S2)
1 Na/glucose
reabsorbs most of filtered glucose
(drugs inhibit this to treat T2D - excrete excess sugar)
SGLT1: late proximal tubule (PST = S3)
2Na/glucose
reabsorbsremaining glucose
Urea
liver converts NH3 to urea - kidneys excrete it
Urea is partially absorbed in prox tubule by passibe diffusion (through tight junctions)
PAH
PAH: amount entering kidney via renal artery
=amount excreted in urine
RPF • RA(PAH)= U(PAH) * V
RPF = U(PAH) * V/ RA(PAH)
Renal plasma flow equals the urine PAH con times the urine flow divided by the plasma PAH con
clearance
“Clearance” of any substance S is its rate of excretion normalized to its plasmaconcentration:
Cs = excretion/PS=US•V’/PS
clearance of glucose = 0
clearance of CR = GFR
clearance of PAH = RPF
development
kidneys come from intermediate mesoderm
ureteric bud and mesenteric blastema are important
** Kidney development is dependent on reciprocal induc.ve interac.ons between the met mess and ub***
The ureteric bud gives rise to the ureter, renal pelvis, calyces and collec.ng ducts
the metanephric mesenchyme: nephron epithelia (from the renal corpuscle to distal convoluted tubule)
kidneys normally ascend during development
bladder comes from endoderm
renal development problems
Congenital anomalies of the kidney and urinary tract (CAKUT)
- -renal agenesis- absence of kidney
- -renal hypodysplasia- small and/or abnormal tubules (cystic)
- -urinary tract obstruction – hydronephrosis
- -reflux–infection and parenchymal damage
if no ureteric bud - renal agenesis - not enough ammniotic fluid - oligohydramnios (- potter syndrome - usually fatal
if too many UBs - multiple ureters, not hte end of the world - only a problem if they insert at a weird place - cause an obstruction
- RET and ROBO are important signaling factors
obstructions - hydropnephrosis - renal pelvis is enlarged
- could have pelvic kidney if one or both dont ascend normally
Polycystic kidney disease : Abnormal control of tubule diameter PKD1 PKD2
Renal hypoplasia : Premature cessation of nephrogenesis
normal levels
Na: 140 Cl: 100 K: 4.5 HCO3: 24 pH: 7.35-7.45 osmolarity (290 mOsM) creatinine: 1.2 pCO2 = 40
Sodium
consume 100meq daily
filter 1.5 kg/day
excrete .1 moles/ day
reaborbed in cells via: exchangers (H+), channels, and cotransport (K)
– these driven by low cell Na conce (pumped out other side using ATP) and also neg cell voltage
Na transport in proximal tublule
Na+ transport by the proximal tubule •cotransportwith nutrients •exchange for H+ (HCO3- reabsorption) •Cl- reabsorption coupled to Na+ coupled anion exchange paracellular transport •water follows (isotonic reabsorption)
•diuretics –> • acetazolamide • mannitol
NaClreabsorption in TALH
co transporter: Na/K/Cl
k is receycled
– furosemide blocks this transporter
Na reabsprot in DCT
Na/ Cl cotransporter blocked by thiazides
• cotransportwith Cl• Cl- reabsorption coupled directly • water does not follow NaCl: urine diluted • diuretics - thiazides
Na transport through CD
•transport through channels •coupled to K+ secretion •Cl- reabsorption •electrical coupling(paracellular) •exchange with HCO3- (ICs) •water reabsorption depends on ADH •highly regulated (aldosterone) •diuretics -K-sparing diuretics - •amiloride - •angiotensin receptor antagonists/ACE inhibitors - •mineralocorticoid receptor blockers
summary of diuretics
proximal tubule: carbonic anhydrase inhibitors acetazolamide/altitude sickness, glaucoma
thick ascending limb: NaKCl2 inhibitor furosemide/acute CHF, hypertension
distal convoluted tubule: NaCl inhibitor thiazides/hypertension
connecting tubule/collecting duct: Na channel blockers amiloride/hypokalemia, with thiazides for hypertension connecting tubule/collecting duct: RAA antagonists captopril, losartan/hypertension, heart failure spironolactone/edema with CHF, nephrotic syndrome
Potasium
hyperkalemia: muscle weakness cardiac arrhythmias •widened QRS •shortened QT •fibrillation metabolic acidosis
hypokalemia: •muscle weakness •cardiac arrhythmias •reduced renal blood flow, GFR •metabolic alkalosis
- compensate for loss of K during exercise with increase in sympathetic tone
K transport in PCT
•Na reabsorption drives Cl, water reabsorption. •K in lumen is concentrated, reabsorbed through tight junctions. •In late proximal tubule, + voltage in lumen is added driving force.
K transport in TALH
•cotransport through Na/K/2Cl (furosemide). •Partial recycling across luminal membrane (K channels). •Reabsorption through tight junctions (+ lumen p.d.)
K transport in DCT - principal :
•K uptake through Na/K pump. •K efflux through apical channels •Coupled to Na reabsorption •K can be concentrated in urine (tight junctions, large voltage)
transport in intercalated cells:
•connecting tubule, cortical and outer medullary collecting ducts •K reabsorption through H/K pump (similar to stomach). •Stimulated by low dietary K.
aldostrerone helps balance K levels - high K intake, increased aldosterone, increased Na retention which is exhcanged and gets rid of excess K
summary of K
K excretion increased by: • high dietary K • mineralocorticoids • Na delivery to distal nephron • loop and thiazide diuretics
K excretion decreased by:
•low dietary K
•acidosis
•K-sparing diuretics (amiloride)
calcium and magnesium regualtion
—•Paracellular reabsorption in proximal tubule
•Na reabsorption drives Cl, water reabsorption. •Ca2+ and Mg2+ in lumen are concentrated, reabsorbed through tight junctions. •In late proximal tubule, + voltage in lumen is added driving force.
—•Paracellular reabsorption in TALH
Reabsorption through tight junctions driven by + lumen voltage
- Regulated reabsorption in distal nephron
- uptake across luminal membrane through specific channels. •efflux across basolateral membrane through pumps, exchange with Na •regulated (PTH for Ca2+)
