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s and f > renal/acid-base > Flashcards

renal/acid-base Flashcards

1
Q

Uriniferous tubule: components

A

nephron w/ renal corpuscle, PCT, loop of Henle, DCT

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2
Q

Proximal convoluted tubule: structure

A
  • longest, most convoluted portion of uriniferous tubule
  • acidophilic cells w/ microvilli obscuring lumen
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3
Q

proximal convoluted tubule: function

A
  • reabsorbs 70% of water, most nutrients
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4
Q

loop of Henle: structure

A
  • 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
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5
Q

loop of Henle: function

A
  • maintains renal architecture
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6
Q

distal convoluted tubule: structure

A
  • last portion of renal tubule, shorter than PCT
  • simple cuboidal w/ sparse microvilli
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7
Q

distal convoluted tubule: function

A
  • reabsorbs remaining NaCl under aldosterone control
  • can reabsorb water in presence of ADH
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8
Q

glomerular filtration barrier: components

A
  • 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
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9
Q

principal cells: function

A
  • reabsorb Na+, H2O
  • secrete K+
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10
Q

intercalated cells: function

A
  • secrete H+, HCO3-
  • reabsorb K+
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11
Q

juxtaglomerular cells: functioin

A
  • low BP stimulates renin secretion
  • specialized smooth muscle cells
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12
Q

macula densa: location, function

A
  • part of DCT at juxtaglomerular apparatus
  • monitors NaCl level of ultrafiltration in DCT, stimulates juxtaglomerular secretion of renin when concentration or BP falls
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13
Q

juxtaglomerular cells: function

A

secrete renin when stimulated

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14
Q

ureter: mucosa

A

transitional epithelium w/ dense irregular CT, lamina propria

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15
Q

ureter: muscle

A

inner longitudinal, outer circular. third outer longitudinal layer present closer to bladder

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16
Q

bladder: mucosa

A
  • folded in relaxed state, straightens in distended state
  • transitional epithelium w/ dense irregular and loose CT, lamina propria
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17
Q

bladder: muscle

A

inner longitudinal, middle circular, outer longitudinal
- middle circular forms internal urethral sphincter

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18
Q

male urethra: portions

A

prostatic, membranous, spongy

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19
Q

prostatic urethra: epithelium

A

transitional

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20
Q

membranous urethra: epithelium

A

stratified columnar to pseudostratified

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20
Q

membranous urethra: muscle

A

located in deep perineal muscle, which forms external urethral sphincter

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21
Q

penile urethra: epithelium

A

in corpus spongiosum, stratified columnar to pseudostratified to non keratinized stratified squamous, glands of littre present

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22
Q

female urethra: epithelium

A
  • transitional near bladder, non keratinized strat squamous w/ pseudostratified patches
  • glands of littre present, skeletal muscle forms external urethral sphincter
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23
Q

equation: urinary excretion for substance “x”

A

excretion = [urine] x total volume

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24
Q

equation: clearance of substance “x”

A

clearance = ([plasmax] x GFR) + secreted - reabsorbed

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25
Q

podocytes function

A
  • specialized epithelial cells
  • contribute to filtration barrier
  • pedicles wrap around glomerular capillaries
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26
Q

ultrafiltration: pGC

A
  • favors filtration
27
Q

ultrafiltration: pBS

A

opposes filtration, generated by fluid in Bowman’s space

28
Q

ultrafiltration: πGC

A
  • opposes filtration
  • rises as plasma leaves, concentrating proteins
29
Q

ultrafiltration: πBS

A

favors filtration, normally negligible

30
Q

afferent constriction: effects

A
  • GFR decreases, RBF decreases
  • pGC decreases
  • resistance increases
31
Q

afferent dilation: effects

A
  • GFR increases, RBF increases
  • pGC increases
  • resistance decreases
32
Q

efferent constriction: effects

A
  • GFR increases, RBF decreases (blood backs up into glomerulus)
  • pGC increases
  • resistance increases
33
Q

efferent dilation: effects

A
  • GFR decreases, RBF increases
  • pGC decreases
  • resistance increases
34
Q

equation: filtration fraction

A

filtration fraction = GFR/RPF

(RPF = plasma entering kidney/time)

35
Q

equation: filtered load

A

load = [plasmax] x GFR

36
Q

autoregulation: myogenic mechanism

A
  • smooth muscle contracts when stretched
  • afferent arterioles stretch and contract
  • increases renal vascular resistance, decreases RBF
37
Q

autoregulation: tubuloglomerular feedback

A
  • NaCl dependent: NaCl in DCT determines GFR
38
Q

renal countercurrent mechanism: descending limb

A
  • permeable to water and small solutes
  • osmolarity of tubular fluid and interstitium can equilibrate
39
Q

early PCT: reabsorption

A
  • 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
40
Q

late PCT: reabsorption

A

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

41
Q

regulation of PCT: glomerulotubular balance

A
  • PCT adjusts Na+ reabsorption in parallel w/ GFR changes
  • GFR increases, reabsorption increases (πC increases, [plasma protein] increases)
42
Q

regulation of PCT: pressure diuresis

A
  • blood/ECF volume increase
  • pGC increases, πGC decreases
43
Q

thick ascending loop of Henle: reabsorption

A
  • 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
44
Q

Early DCT: reabsorption

A
  • Na+, Cl- into cell from tubular fluid via NCC
  • Na+ into blood, K+ into cell via Ka+/K+ ATPase
45
Q

Late DCT: reabsorption

A
  • aldosterone stimulates Na+ uptake
    (high aldosterone = high [protein] = high reabsorption)
46
Q

angiotensin II: stimulates

A
  • vasoconstriction
  • lower GFR, higher filtration fraction
  • promotes Na+ reabsorption in PCT
  • AVP secretion, aldosterone secretion
47
Q

diuresis: general effects

A

ECF volume expansion: hypoosmotic urine
- SNS, RAAS, AVP decrease
- ANP increases (inhibits Na+ reabsorption along tubules)
- GFR increases

48
Q

diuresis: effect on DCT, CD

A
  • low AVP = DCT and CD are impermeable to water
  • urea reabsorption decreases
  • low aldosterone = less Na+ reabsorption in DCT, CD
49
Q

antidiuresis: effects

A

ECF volume contraction: hyperosmotic urine
- RAAS, AVP increase
- GFR, ANP decrease
- aldosterone increases Na+ reabsorption, AVP increases urea reabsorption

50
Q

normal [HCO3-]

A

24 mM

51
Q

normal [HCO3-]/[CO2] ratio

A

20

52
Q

renal bicarb handling: reabsorption steps

A
  1. Bicarbonate combines w/ H+ to form carbonic acid in lumen
  2. Carbonic anhydrase converts carbonic acid to CO2, H2O on PCT membrane
  3. Diffuse across apical membrane, converted back to carbonic acid
  4. Carbonic acid dissociates into H+ and HCO3- in the cell
  5. H+ is transported back to the lumen for reuse, HCO3- is reabsorbed in the blood
53
Q

new bicarbonate formation: steps

A
  1. CO2 and water → carbonic acid in a-intercalated cell
  2. Carbonic acid dissociates into new bicarbonate and H+ ions
  3. Bicarbonate is reabsorbed into ECF, 4. H+ is transported to lumen
    In lumen: phosphate buffers H+, excreted into urine as titratable acid
54
Q

respiratory acidosis: acute

A
  • pH decreases
  • PaCO2 increases
  • [HCO3-] slightly increases
55
Q

respiratory acidosis: compensatory/ chronic

A
  • renal compensation: production of HCO3-, [HCO3-] increases drastically
  • over enough time, pH is brought back up to normal
  • PaCO2 remains high
56
Q

respiratory alkalosis: acute

A
  • pH increases
  • PaCO2 decreases
  • [HCO3-] decreases slightly
57
Q

respiratory alkalosis: compensatory/chronic

A
  • renal compensation: more HCO3- secreted
  • pH can eventually normalize
  • PaCO2 remains low
58
Q

metabolic acidosis: effects

A
  • pH, PaCO2, [HCO3-] decrease
59
Q

metabolic acidosis: from overproduction of acid

A
  • excess H+ is buffered by HCO3-, lowering [HCO3-]
  • wide anion gap
60
Q

metabolic acidosis: from excess bicarbonate loss

A
  • respiratory compensation increases ventilation, lowering PaCO2
  • norma anion gap, compensation by Cl-
61
Q

metabolic alkalosis: effects

A
  • pH, PaCO2, [HCO3-] increase
62
Q

metabolic alkalosis: causes

A
  • increased bicarbonate intake increased pH
  • severe acid loss
63
Q

metabolic alkalosis: compensation

A
  • respiratory compensation decreases ventilation
  • CO2 retained, pH lowered
64
Q

SNS affect on sodium reabsorption

A

catecholamines stimulate Na+ reabsorption in PCT, thick ascending loop of Henle, DCT, CD

65
Q

AVP: stimulated by

A
  • decreased plasma osmolarity, increased BV

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