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USMLE Renal > Physiology - Nephron > Flashcards

Physiology - Nephron Flashcards

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USMLE® Step 1 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
Q

What is cystinuria?

A
  • 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
Q

What other amino acids are poorly reabsorbed in cystinuria?

A

COLA

  • Cystine
  • Ornithine
  • Lysine
  • Arginine
27
Q

What is the thin descending loop of Henle impermeable to?

A

NaCl

28
Q

What is the osmolarity of the tubular fluid at each area of the nephron?

A
  • 300 mOsm (around glomerulus and when leaving PCT)
  • 600 mOsm in Outer Medulla
  • 1200 mOsm in Inner medulla
  • 120 at end of TAL
29
Q

Where is NaCl specifically reabsorbed?

A

Thick Ascending Loop of Henle

30
Q

What is the pump responsible for generating the low osmolarity in the TAL?

A

Na+/K+/2Cl-

31
Q

What causes the +ve charge in the lumen of the TAL?

A
  • 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
Q

What channels/pumps are present on the apical membrane of the distal tubule?

A
  • Na+/Cl- (same direction)

- Ca2+

33
Q

What channels are present on the basolateral membrane of the distal tubule?

A
  • NaKATPase
  • Cl- (out)
  • Na+(in)/Ca2+(out) cotransporter
34
Q

What are the 2 cell types present in the collecting duct?

A
  • Principal cell

- Intercalated cell (secrete H+)

35
Q

What channel is important on the apical surface of the intercalated cells of the CD?

A

H+/ATPase

36
Q

What is the channel by which sodium is reabsorbed by the principal cells in the CD?

A

ENaC (regulated by aldosterone)

37
Q

What channels are present on the apical surface of the principal cells?

A
  • ENaC
  • K+ (out)
  • H2O (in)
38
Q

What are the main substances secreted by the CDs?

A
  • Reabsorb Na+, H2O

- Secrete K+/H+

39
Q

Describe how loops and thiazides cause hypokalemia?

A

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
Q

What tranporters are increased by Aldosterone?

A

Principal cells

  • Na+/K+ATPase (basolateral)
  • ENaC (apical)

Intercalated cells
- H+ATPase

41
Q

What is the overall effect of Aldosterone (what substances are increased/decreased)?

A
  • Sodium/water resorption (increased effective circulating volume)
  • Increased K+ excretion
  • Increased H+ excretion
42
Q

What is the release of aldosterone stimulated by?

A
  • Angiotensin II
  • High K+
  • ACTH (minor effect)
43
Q

What are the 2 physiologic stimuli for ADH release?

A
  • Major: Hyperosmolarity

- Volume loss: non-osmotic release (does not depend on osmolarity, pituitary detects low ECV, emergency)

44
Q

What are the 2 receptors ADH acts on?

A
  • V1: Vasoconstriction

- V2: Antidiuretic response

45
Q

What cells contain the V2 receptors?

A

Principal cells (basolateral surface)

46
Q

What channels are activated by ADH?

A

AQP-2 channel

47
Q

What are the AQP channels which are always active?

A
  • AQP-3
  • AQP-4
    Both on Basolateral surface
48
Q

What would the urine osmolarity be in a high ADH state (parched)?

A

High - 1200mOsm

49
Q

What would the urine osmolarity be in a low ADH state (high water intake)?

A

Low - 60

50
Q

What is the effect of ADH on urea reabsorption?

A

Increases reabsorption of urea

- Maintains high osmotic gradients so ater ccn be reabsorbed in LOH

51
Q

Where are the transporters located that recycle the urea?

A

Thin descending limb

USMLE Renal (11 decks)

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