renal/acid-base Flashcards
Uriniferous tubule: components
nephron w/ renal corpuscle, PCT, loop of Henle, DCT
Proximal convoluted tubule: structure
- longest, most convoluted portion of uriniferous tubule
- acidophilic cells w/ microvilli obscuring lumen
proximal convoluted tubule: function
- reabsorbs 70% of water, most nutrients
loop of Henle: structure
- descending thick limb is similar to PCT, ascending thick limb is similar to DCT
- longitudinal section: simple squamous epithelium w/ nuclei bulging into lumen, interstitial cells
loop of Henle: function
- maintains renal architecture
distal convoluted tubule: structure
- last portion of renal tubule, shorter than PCT
- simple cuboidal w/ sparse microvilli
distal convoluted tubule: function
- reabsorbs remaining NaCl under aldosterone control
- can reabsorb water in presence of ADH
glomerular filtration barrier: components
- anastomosing fenestrated capillaries coated w/ negatively-charged glycoproteins
- mesangial cells between capillaries provide support, control basement membrane turnover
- visceral layer w/ podocytes w/ pedicles forming filtration slits
– parietal layer w/ simple squamous
principal cells: function
- reabsorb Na+, H2O
- secrete K+
intercalated cells: function
- secrete H+, HCO3-
- reabsorb K+
juxtaglomerular cells: functioin
- low BP stimulates renin secretion
- specialized smooth muscle cells
macula densa: location, function
- part of DCT at juxtaglomerular apparatus
- monitors NaCl level of ultrafiltration in DCT, stimulates juxtaglomerular secretion of renin when concentration or BP falls
juxtaglomerular cells: function
secrete renin when stimulated
ureter: mucosa
transitional epithelium w/ dense irregular CT, lamina propria
ureter: muscle
inner longitudinal, outer circular. third outer longitudinal layer present closer to bladder
bladder: mucosa
- folded in relaxed state, straightens in distended state
- transitional epithelium w/ dense irregular and loose CT, lamina propria
bladder: muscle
inner longitudinal, middle circular, outer longitudinal
- middle circular forms internal urethral sphincter
male urethra: portions
prostatic, membranous, spongy
prostatic urethra: epithelium
transitional
membranous urethra: epithelium
stratified columnar to pseudostratified
membranous urethra: muscle
located in deep perineal muscle, which forms external urethral sphincter
penile urethra: epithelium
in corpus spongiosum, stratified columnar to pseudostratified to non keratinized stratified squamous, glands of littre present
female urethra: epithelium
- transitional near bladder, non keratinized strat squamous w/ pseudostratified patches
- glands of littre present, skeletal muscle forms external urethral sphincter
equation: urinary excretion for substance “x”
excretion = [urine] x total volume
equation: clearance of substance “x”
clearance = ([plasmax] x GFR) + secreted - reabsorbed
podocytes function
- specialized epithelial cells
- contribute to filtration barrier
- pedicles wrap around glomerular capillaries
ultrafiltration: pGC
- favors filtration
ultrafiltration: pBS
opposes filtration, generated by fluid in Bowman’s space
ultrafiltration: πGC
- opposes filtration
- rises as plasma leaves, concentrating proteins
ultrafiltration: πBS
favors filtration, normally negligible
afferent constriction: effects
- GFR decreases, RBF decreases
- pGC decreases
- resistance increases
afferent dilation: effects
- GFR increases, RBF increases
- pGC increases
- resistance decreases
efferent constriction: effects
- GFR increases, RBF decreases (blood backs up into glomerulus)
- pGC increases
- resistance increases
efferent dilation: effects
- GFR decreases, RBF increases
- pGC decreases
- resistance increases
equation: filtration fraction
filtration fraction = GFR/RPF
(RPF = plasma entering kidney/time)
equation: filtered load
load = [plasmax] x GFR
autoregulation: myogenic mechanism
- smooth muscle contracts when stretched
- afferent arterioles stretch and contract
- increases renal vascular resistance, decreases RBF
autoregulation: tubuloglomerular feedback
- NaCl dependent: NaCl in DCT determines GFR
renal countercurrent mechanism: descending limb
- permeable to water and small solutes
- osmolarity of tubular fluid and interstitium can equilibrate
early PCT: reabsorption
- Na+ and glucose into cell from tubular fluid via SGLT2
- Na+ into blood, K+ into cell via Na+/K+ ATPase
- Na+ in from tubular fluid, H+ into fluid by NHE3 (H+ obtained from carbonic anhydrase)
- Na+ and HCO3- cotransported into blood
late PCT: reabsorption
transcellular
- Na+ into blood, K+ into cell via Na+/K+ ATPase
- Cl- and K+ into blood by KCC, or Cl- through basolateral Cl- channels
paracellular
- Cl- leaves tubular lumen –> blood by tight junction
regulation of PCT: glomerulotubular balance
- PCT adjusts Na+ reabsorption in parallel w/ GFR changes
- GFR increases, reabsorption increases (πC increases, [plasma protein] increases)
regulation of PCT: pressure diuresis
- blood/ECF volume increase
- pGC increases, πGC decreases
thick ascending loop of Henle: reabsorption
- 2 Cl-, Na+, K+ into cell from tubular fluid via NKCC2
- Na+ into cell, H+ into tubular fluid via NHE3
- HCO3- into blood, Cl- into cell via AE2
- Na+ into blood, K+ into cell via Na+/K+ ATPase
Early DCT: reabsorption
- Na+, Cl- into cell from tubular fluid via NCC
- Na+ into blood, K+ into cell via Ka+/K+ ATPase
Late DCT: reabsorption
- aldosterone stimulates Na+ uptake
(high aldosterone = high [protein] = high reabsorption)
angiotensin II: stimulates
- vasoconstriction
- lower GFR, higher filtration fraction
- promotes Na+ reabsorption in PCT
- AVP secretion, aldosterone secretion
diuresis: general effects
ECF volume expansion: hypoosmotic urine
- SNS, RAAS, AVP decrease
- ANP increases (inhibits Na+ reabsorption along tubules)
- GFR increases
diuresis: effect on DCT, CD
- low AVP = DCT and CD are impermeable to water
- urea reabsorption decreases
- low aldosterone = less Na+ reabsorption in DCT, CD
antidiuresis: effects
ECF volume contraction: hyperosmotic urine
- RAAS, AVP increase
- GFR, ANP decrease
- aldosterone increases Na+ reabsorption, AVP increases urea reabsorption
normal [HCO3-]
24 mM
normal [HCO3-]/[CO2] ratio
20
renal bicarb handling: reabsorption steps
- Bicarbonate combines w/ H+ to form carbonic acid in lumen
- Carbonic anhydrase converts carbonic acid to CO2, H2O on PCT membrane
- Diffuse across apical membrane, converted back to carbonic acid
- Carbonic acid dissociates into H+ and HCO3- in the cell
- H+ is transported back to the lumen for reuse, HCO3- is reabsorbed in the blood
new bicarbonate formation: steps
- CO2 and water → carbonic acid in a-intercalated cell
- Carbonic acid dissociates into new bicarbonate and H+ ions
- Bicarbonate is reabsorbed into ECF, 4. H+ is transported to lumen
In lumen: phosphate buffers H+, excreted into urine as titratable acid
respiratory acidosis: acute
- pH decreases
- PaCO2 increases
- [HCO3-] slightly increases
respiratory acidosis: compensatory/ chronic
- renal compensation: production of HCO3-, [HCO3-] increases drastically
- over enough time, pH is brought back up to normal
- PaCO2 remains high
respiratory alkalosis: acute
- pH increases
- PaCO2 decreases
- [HCO3-] decreases slightly
respiratory alkalosis: compensatory/chronic
- renal compensation: more HCO3- secreted
- pH can eventually normalize
- PaCO2 remains low
metabolic acidosis: effects
- pH, PaCO2, [HCO3-] decrease
metabolic acidosis: from overproduction of acid
- excess H+ is buffered by HCO3-, lowering [HCO3-]
- wide anion gap
metabolic acidosis: from excess bicarbonate loss
- respiratory compensation increases ventilation, lowering PaCO2
- norma anion gap, compensation by Cl-
metabolic alkalosis: effects
- pH, PaCO2, [HCO3-] increase
metabolic alkalosis: causes
- increased bicarbonate intake increased pH
- severe acid loss
metabolic alkalosis: compensation
- respiratory compensation decreases ventilation
- CO2 retained, pH lowered
SNS affect on sodium reabsorption
catecholamines stimulate Na+ reabsorption in PCT, thick ascending loop of Henle, DCT, CD
AVP: stimulated by
- decreased plasma osmolarity, increased BV
