Physiology - Nephron Flashcards

1
Q

What substances are reabsorbed in the Proximal Tubule?

A

100%

  • Glucose
  • Amino acids

67%

  • Water
  • Bicarb
  • NaCl
  • K+
  • Phosphate
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2
Q

What side does the Na+/K+ATPase pump lie on and what does it create?

A
  • Lies on basolateral side

- Decreases Na+ intracellularly - generating a conc. gradient between tubule cells and tubular fluid

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3
Q

Via what channel does glucose get reabsorbed?

A

SGLT2 (in proximal tubule)

- Sodium co-transporter

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4
Q

What molecules are secreted by the proximal tubule?

A

Anions:

  • Hydroxide (-OH)
  • Formate
  • Oxalate
  • Sulfate
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5
Q

What ion is taken up by the transporter which excretes anions?

A

Cl-

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6
Q

What transporters channels are present on the basolateral surface of the PCT cells?

A
  • Na/KATPase
  • K+ Cl cotransporter
  • Glucose
  • Na+ HCO3- cotransporter
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7
Q

What substances are taken into the blood via the paracellular route in the PCT?

A
  • H2O

- NaCl

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8
Q

At what level does glucose appear in the urine?

A

160mg/dL

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9
Q

At what level do all glucose levels become saturated?

A

350mg/dL

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10
Q

Why is a diabetes diagnosis from urine unreleable in pregnancy?

A
  • Some glycosuria is normal in pregnancy
  • Serum testing needed for diagnosis
  • Increased GFR in pregnancy
  • Decreased glucose reabsorption in pregnancy
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11
Q

What ion are amino acids reabsorbed with in the PCT?

A

Na+

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12
Q

What is Hartnup disease?

A
  • No typtophan transporter in PT
  • Tryptophan deficiency
  • Skin rash resembling pellagra (plaques, desquamation)
  • Amino acids in urine
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13
Q

What transporter excretes H+ in the PCT?

A

Na+/H+ cotransporter

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14
Q

What reactions does Carbonic Anhydrase catalyse?

Describe the pathway of H2CO3 and how the urine is acidified and how HCO3- is taken up in blood

A

H2CO3 to Co2 + H2O

  • In Tubular fluid
  • Co2 and H2O can then be taken up

Can also convert CO2 + H2O to H2CO3 in the tubular cells

H2CO3 can then be converted to H+ and HCO3-

H+ enters urine via H+/Na+ antiporter

HCO3- enters blood via HCO3-/Na+ cotransporter

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15
Q

Via what transporter does HCO3- enter the blood?

A

HCO3-/Na+ cotransporter on basolateral membrane

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16
Q

What do carbonic anhydrase inhibitors do?

A
  • Alkalises urine - bicarb loss in urine, acidifies body (used in alkalosis)
  • Weak diuretic (block Na+ reabsorption)
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17
Q

What is Type II Renal Tubular Acidosis?

A
  • Ion defect
  • Inability to absorb bicarb
  • Metabolic acidosis
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18
Q

What is Fanconi syndrome?

A
  • Loss of proximal tubule functions
  • Impaired resorption of solutes
  • HCO3-, glucose, amino acids, phosphate lost
  • Polyuria and polydipsia (diuresis from glucose), normal serum glucose
  • Non anion gap acidosis (loss of HCO3-)
  • Hypokalemia (increased nephron flow)
  • Hypophosphatemia (loss of phosphate)
  • Amino acids in urine
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19
Q

What are the 2 forms of Fanconi syndrome?

A
  • Inherited or acquired
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20
Q

When and what does inherited Fanconi syndrome present with?

A

Infancy

  • Cystinosis - accumulation of cysteine (
  • Lysosomal storage disease
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21
Q

What are acquired causes of Fanconi Syndrome?

A
Lead poisoning 
Multiple Myeloma 
Drugs 
- Cisplatin 
- Ifosfamide (alkylating agent)
- Valproate 
- Aminoglycoside antibiotics 
- Deferasirox (iron chelator)
22
Q

Where is urea generated?

A

The liver and protein metabolism

23
Q

Where in the nephron is urea reabsorbed?

A

Medullary Collecting duct

- Enters medullary interstitium

24
Q

What are the 3 solutes responsible for the high osmolarity in the medulla?

A
  • Na
  • Cl
  • Urea
25
What is cystinuria?
- Different from cystinosis - Proximal tubule defect - Impaired reabsorption of cystine - Cystine kidney stones - +ve Sodium cyanide nitroprusside test - Stones may form staghorn calculi - Urine crystal is hexagonal
26
What other amino acids are poorly reabsorbed in cystinuria?
COLA - Cystine - Ornithine - Lysine - Arginine
27
What is the thin descending loop of Henle impermeable to?
NaCl
28
What is the osmolarity of the tubular fluid at each area of the nephron?
- 300 mOsm (around glomerulus and when leaving PCT) - 600 mOsm in Outer Medulla - 1200 mOsm in Inner medulla - 120 at end of TAL
29
Where is NaCl specifically reabsorbed?
Thick Ascending Loop of Henle
30
What is the pump responsible for generating the low osmolarity in the TAL?
Na+/K+/2Cl-
31
What causes the +ve charge in the lumen of the TAL?
- Na/KATPase brings K+ into the cell - K+ channel on apical membrane brings +ve charge into lumen - This postive charge in the lumen then drives the Na+/K+2Cl- pump (all travel into cell) - Allows Mg2+ and Ca2+ to enter the blood via the paracellular route
32
What channels/pumps are present on the apical membrane of the distal tubule?
- Na+/Cl- (same direction) | - Ca2+
33
What channels are present on the basolateral membrane of the distal tubule?
- NaKATPase - Cl- (out) - Na+(in)/Ca2+(out) cotransporter
34
What are the 2 cell types present in the collecting duct?
- Principal cell | - Intercalated cell (secrete H+)
35
What channel is important on the apical surface of the intercalated cells of the CD?
H+/ATPase
36
What is the channel by which sodium is reabsorbed by the principal cells in the CD?
ENaC (regulated by aldosterone)
37
What channels are present on the apical surface of the principal cells?
- ENaC - K+ (out) - H2O (in)
38
What are the main substances secreted by the CDs?
- Reabsorb Na+, H2O | - Secrete K+/H+
39
Describe how loops and thiazides cause hypokalemia?
Increased Na delivery to CD -> More into cell via ENaC - > Na+ can then be exchanged for K+ which is brought into the cell - > increased K+ excretion - > Contributes to hypokalemia with loops thiazides
40
What tranporters are increased by Aldosterone?
Principal cells - Na+/K+ATPase (basolateral) - ENaC (apical) Intercalated cells - H+ATPase
41
What is the overall effect of Aldosterone (what substances are increased/decreased)?
- Sodium/water resorption (increased effective circulating volume) - Increased K+ excretion - Increased H+ excretion
42
What is the release of aldosterone stimulated by?
- Angiotensin II - High K+ - ACTH (minor effect)
43
What are the 2 physiologic stimuli for ADH release?
- Major: Hyperosmolarity | - Volume loss: non-osmotic release (does not depend on osmolarity, pituitary detects low ECV, emergency)
44
What are the 2 receptors ADH acts on?
- V1: Vasoconstriction | - V2: Antidiuretic response
45
What cells contain the V2 receptors?
Principal cells (basolateral surface)
46
What channels are activated by ADH?
AQP-2 channel
47
What are the AQP channels which are always active?
- AQP-3 - AQP-4 Both on Basolateral surface
48
What would the urine osmolarity be in a high ADH state (parched)?
High - 1200mOsm
49
What would the urine osmolarity be in a low ADH state (high water intake)?
Low - 60
50
What is the effect of ADH on urea reabsorption?
Increases reabsorption of urea | - Maintains high osmotic gradients so ater ccn be reabsorbed in LOH
51
Where are the transporters located that recycle the urea?
Thin descending limb