Kidney Function III Flashcards

1
Q

How is plasma osmolarity kept constant

A

Urine- dilute/ concentrated

thirst

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2
Q

Concentrated urine

A

greater than 300 mosmol/l

1) Have to remove 600 mosmol/day of waste products
2) Max urinary concentration = 1400 mOsmol/l
3) 600/1400= 0.428 L/day

This is the obligatory water loss- anything below this value is called oliguria

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3
Q

Dilute urine

A

Less than 300 mosmol/l

Min urinary concentration= 50 mOsmol/l
Urine output = 1-2 /day

Anything beyond this is called polyuria

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4
Q

Osmular Clearance

A

Cosm -ml/min

The volume of plasma cleared of osmotically active particles per unit time that could have resulted in urine isomolar to plasma

The calculation of all osmotically active particles
Cosm= Uosm x V / Posm

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5
Q

Free Water Clearance

A

(C h20) used to assess renal function

Ch20 = V - (Uosm x V)/Posm

Ch20 > 0 indicates hypo-osmotic urine- dilute urine
Ch20 = 0 indicates isometric urine wrt plasma
ch20 < 0 indicates hyper osmotic urine- concentrated urine

Possible range= -1.3 —> 14.5 ml/min

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6
Q

LOW WATER INTAKE

A

Plasma osmalality decreases

Osmoreceptors by hypothalamus detects this change

Posterior Pituatory

Increase in ADH

Kidneys

Increase in water reabsorption

Less water excreted in urine

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7
Q

HIGH WATER INTAKE

A

Plasma osmalality increases

Osmoreceptors by hypothalamus detects this change

Posterior Pituatory

Decrease in ADH

Kidneys

decrease in water reabsorption

More water excreted in urine

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8
Q

Where are osmoreceptors located in the hypothalamus

A

Organum vasculosum Lamina terminals

Median Preoptic nucleus

Subfomical organ

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9
Q

What do the osmoreceptors do?

A

Signal to the magnocellular neurosecratory cells in the paraventricular region and supraoptic nuclei in hypothalamus.
These cells contain the precursor for ADH which is released into the blood to the posterior pituitary via the axons. These are changed to ADH which is then released into blood

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10
Q

Why is ADH useful in the short term

A

Plasma half life is short

ADH release is rapid from the posterior pituatory

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11
Q

What else can osmoreceptors indicate-

A

Thirst- locates in the lateral preoptic, osmoreceptors aren’t activated until the plasma osmolality has reached 295mosm/kg

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12
Q

What else can affect ADH secretion

A

BP and BV

As the release is dictated by stretch mediated receptors found in the arteriole which sends neurally mediates signals to ADH containing neurons

1% change in plasma osmalility - plasma vasopressin change

5% change in volume results in plasma vasopresisin change

10% change in pressure results in plasma vasopressin change

Alcohol- decrease in ADH
Nicotine- increase in ADH
Nausea- increased in ADH
Pain- increase ADH
Stress- increase in ADH
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13
Q

ADH action in collecting duct

A

1) ADH binds to the V2 receptor on the basolateral membrane- 2nd messenger cAMP
2) This causes the fusion of AQP2 with the luminal membrane to allow movement of H20 to move by osmosis
3) water molecules then move through AQP3 and AQP4

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14
Q

Diabetes Insipidus

A

Effects the water reabsorption only

Characteristics- polyuria, thirst, nocturia

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15
Q

Type 1 Diabetes

A

Neurogenic- congenital
Head Injury

NO ADH

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16
Q

Type 2 Diabetes

A

Nephrogenic- inherited (mutated v2 receptor)

- acquired (infection/side effect of drug)

17
Q

Osmotic Diuresis

A

Characteristic- polyuria and polydipsia

Caused due to the fact that there are small molecules in the renal tube lumen. This means that there’s an increase in [glucose] blood which meant that there’s an increase in glomerular filtration of glucose. This increases the osmolarity in filtrate.

Ultimately this decreases water reabsorption from PT- past saturation

Bad because this will affect osmotic gradient- meaning that less water is being reabsorbed.

18
Q

Potassium

A

Major intracellular cation in the body

19
Q

Renal excretion of Potassium

A

Filtered, absorbed and secreted

20
Q

Filtration of K+

A

Small ion doesn’t bind to proteins so said to be freely filtered in the renal corpuscle

therefore filtration rate = 1.0

Filters 800 m moles/day

21
Q

Proximal Tubule- K+

A

65% is reabsorbed passively

due to K+ leak and K+/Cl- cotransporter

22
Q

Thick ascending limb- K+

A

30% is reabsorbed passively

Na+/K+/2Cl- con transporter using gradient of Na

23
Q

Distal Tubule-K+

A

5% si reabsorbed

K+/H+ exchanger

24
Q

Collecting Duct- K+

A

Intercalated cells

Principal cells

25
Q

Intercalated cells

A

K+ is being reabsorbed -

exchanged with H+
[K+] increases inside the cells
K+ diffuses out of the cell into the IF

26
Q

Principal cells-

A

secretes K+

K+ channels- ROMK and BK depending on the electrochemical gradients

K+/Cl- co transporter

ROMK-renal outer medullary K+ channel
BK- Ca2+ activated by conductance K+ channel

27
Q

What factors affect the K+ secretion by Principal cells

A

Acid Base Balance - acidosis inhibits and alkalosis enhances. High H+ in filtrate–> more positive charge —> inhibits movement

Tubular flow rate- high flow rate favours secretion- negative charges are washed away therefore K+ more likely to pass through down the electrochemical gradient

Aldosterone- stimulates the K+ channels
increasing the activity of Na+