Theme 3 - Part II Flashcards

1
Q

LOH

  • Use
  • Thin descending
  • Thick ascending
A

Recover fluid and solute form glomerular filtrate

Thin descending: Flat, no active transport and freely permeable. TJ

Thick ascending: Tubular wall impermeable. Specialised Na+/K+/2Cl- cotransporter

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2
Q

Fluid in LOH [3]

A

Entering fluid = isotonic

Water reabsorbed OUT & filtrate is hypertonic (1,200 mOsm)

Solute pumped OUT ascending LOH -> hypotonic (150mOsm)

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3
Q

Countercurrent Multiplication [3]

A

Create large osmotic gradient within medulla

Facilitated by Na+/K+/2Cl-
transport in ascending limb of LOH

Permits passive reabsorption of
water from tubular fluid in
descending LOH

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4
Q

Urea [5]

A

Freely filtered at glomerulus

Some reabsorption in PT

LOH & distal tubule relatively impermeable

Urea can diffuse out of
collecting duct into medulla
down its concentration
gradient

This adds to the osmolality
of medullary interstitium

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5
Q

LOH reabsorption

A

Water (DL), Sodium (AL), Potassium (AL), Chloride (AL)

HCO3-, Calcium and Magnesium

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6
Q

LOH secretion

A

Urea (variable from collecting duct)

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7
Q

Distal tubule [2]

A

Active transport - absorb/secrete solute

Sodium and chloride ions ACTIVELY reabsorbed from tubular fluid

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8
Q

Na+ and Cl- for K+ exchange

A

Throughout DT

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9
Q

Exchange throughout DT

A

Na+ and Cl- for K+ exchange

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10
Q

Na+ and K+ exchange in

A

Late DT and early collecting duct

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11
Q

Principal cells

A

Increase aldosterone = Increase DT sodium reabsorption and inhibit juxtaglomerular cells -> renin -> Ang I -> Ang II

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12
Q

Intercalated cells

  • alpha [2]
  • beta [2]
A

Alpha:

  • Secrete acid via H+/Na+ or H+/K+ by H+/ATPase
  • Reabsorb bicarbonate

Beta

  • Secrete bicarbonate via Pendrin
  • Reabsorb acid
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13
Q

Na+ and H+ exchanged in

A

DT and early collecting duct

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14
Q

DT and early collecting duct

A

Na+ and H+ exchanged in

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15
Q

Late DT and early collecting duct

A

Na+ and K+ exchange

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16
Q

Collecting Duct

A

Relatively impermeable to movement of water & solutes (increase by ADH)

Nonapeptide Vasopressin

17
Q

Vasopressin [5]

A
  • Nonapeptide
  • Hypothalamic input to posterior pituitary
  • 10-15min plasma half life
  • V2 receptor - basal membrane of principal cells in DT and collecting duct
  • Activate intracellular AQP2 expression
18
Q

Max Circulating ADH [3]

A

Collecting duct becomes permeable to water because max AQP2 insertion

Low delivery to CD - 8L/day

Urine volume = 300mL/day

19
Q

No Circulating ADH

A

Reabsorption at various sites

Collecting duct impermeable to water - no AQP2

Large volume of water excreted = 30L/day

20
Q

Nephrogenic [3]

A

Due to inability of kidney
to respond normally to ADH

Treatment:
Chlortalidone (diuretic)

Indometacin (anti-inflammatory)

21
Q

Neurogenic [4]

A

Due to lack of ADH production
by the brain

Treatment:
Desmopressin (ADH analogue)
Vasopressin
Carbamezapine (anti-convulsive)

22
Q

Chlortalidone

A

Diuretic

Nephrogenic Diabetets Insipidus

23
Q

Indometacin

A

Anti-inflammatory

Nephrogenic Diabetets Insipidus

24
Q

Desmopressin

A

ADH analogue

Neurogenic Diabetets Insipidus

25
Q

Carbamezapine

A

Anti-convulsive

Neurogenic Diabetets Insipidus

26
Q

SIADH

A

Excessive ADH release
Hyponatraemia & possible fluid overload
V2 receptor blockers - Demeclocycline and Tolvapton

27
Q

V2 receptor blockers

A

Demeclocycline and Tolvapton

28
Q

ADH

  • Stimulate
  • Inhibit
A

Stimulated by: Nicotine, Ether, Morphine and Barbiturates

Inhibited by: ADH release