Lecture 23: Kidney function III - The production of dilute urine by the kidney Flashcards Preview

1060 Human form and function > Lecture 23: Kidney function III - The production of dilute urine by the kidney > Flashcards

Flashcards in Lecture 23: Kidney function III - The production of dilute urine by the kidney Deck (32):
1

water is predominantly reabsorbed in the loop of Henle T/F?

False

 

It's pedominantlyreabsobed in the proximal tubule

2

Urine is always hypotonic to plasma T/F?

False

 

but it can be

3

Na+ reabsorption involves purely passive processes T/F??

False

4

ADH increases water reabsorption via aquaporins

True

5

Constant plasma osmolality is maintained by ??

1) Urine formation
2) Thirst 

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6

CONCENTRATED URINE (i.e. >300 mosmol/l)

Obliged to eliminate 600 mosmol of waste products each day. Maximum urinary concentration possible is 1,400 mosmol/l. Therefore obligatory water loss is 0.444 l of urine each day. 

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7

DILUTE URINE (i.e. <300mosmol/l) 

As low as 50 mosmol/l possible

Normally urine output is ~1-2 l/day

Excessive urine output is polyuria.

Maximum urine output ~23 l/day 

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8

effect of dehydration and over-hydration??

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9

What do osmoreceptors do??

Osmoreptors in the OVLT, MPO and SFO signal to magnocellular neurosecretory cells in paraventricular and supraoptic nuclei in hypothalamus.

These cells can produce and release ADH into blood through posterior pituitary. 

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10

control of ADH release in humans 

ADH very effective:

i)  Plasma half-life 10-20 min.

ii)  ADH release rapid 

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11

Other factors that affect ADH (vasopressin) secretion 

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12

Osmoreceptors are the main controllers of ADH levels but there are other factors

which are they?

Alcohol(inhibitsADH)

Nicotine(stimulatesADH)

 

Nausea (stimulates ADH)

Pain (stimulates ADH)

Stress(stimulatesADH) 

13

Action of anti-diuretic hormone (ADH) on Collecting Duct 

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14

what is diabetes insipidus ‘water diabetes’ ??

CHARACTERISTICS

(1) urination (polyuria ie. urine > 2l/day)

(2) thirst (polydipsia)
3) nocturia

 

TYPES

(1) Neurogenic (no ADH Secreted)

(i) congenital
(ii) head injury e.g. Trauma or brain tumour

(2) Nephrogenic

(i) inherited (mutated V2 receptor or aquaporin 2 channel)

(ii) acquired (infection or side effect of drug e.g. lithium) 

15

what is osmotic diuresis??

Increased urination due to small molecules (e.g glycerol, mannitol and excess glucose)
in renal tubule lumen 

 

CHARACTERISTICS:

(1) urination (polyuria)

(2) thirst (polydipsia)

MECHANISM:

i) Increased blood glucose.

ii) increased  Glomerular filtration of glucose.

ii) Increased osmolarity in filtrate.

iii) decreased water reabsorption from proximal tubule.

Later portions of nephron can not compensate. 

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16

what is the major intracellular cation in the body?

potassium

17

Potassium in the kidney??

5 mM extracellular fluid

150 mM intracellular fluid
affects membrane potential and excitability.
Maintains resting membrane potential

K+ intake is variable (40-120 mmoles/day).

Kidney filters ~800 mmoles/day.

Overall ~ 95% of this is REABSORBED. 

~65% reabsorbed passively at proximal tubule

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18

K+ transport pathways in thick ascending limb???

~ 30% of this is REABSORBED at thick ascending limb.

Na+:K+:2Cl ̄ cotransporter (NKCC2 transporter) 

 

5% is reabsorbed in the distal tubule. 

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19

K+ transport pathways in collecting duct ??

NB: intercalated and principal cells. 

K+ is reabsorbed by intercalated cells (in exchange for H+). 

But outweighed by

K+ secretion by principal cells. Exit Routes

i) K+ channels
(Renal Outer Medullary K+ channel; ROMK) (Ca2+activated big-conductance K+ channel; BK)

ii) K+:Cl- cotransporter. 

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20

FACTORS AFFECTING K+ SECRETION BY PRINCIPAL CELLS (COLLECTING DUCT) ??

1. Factors affecting Na+ entry through epithelial Na+ channels (ENaC).

2. Aldosterone stimulates K+ channels.

3. Tubular flow rate. High flow rates favour secretion.

4. Acid-base balance. Acidosis inhibits it and alkalosis enhances it.

Normal plasma K+ 3.5-5.0 mM 

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21

what is hypokalaemia ??

deficiency of potassium in the bloodstream.

plasma [K+]<3.5mM 

22

what causes hypokalaemmia??

A) Increased external losses 

GI tract e.g. Vomiting, diarrhoea 

Kidney e.g. diuretics, osmotic diuresis, hyperaldosteronism, transporter mutations (e.g. ENaC)

Skin e.g. burns, intense sweating 

 

B) Redistribution into cells

Metabolic Alkalosis

Insulin excess 

 

C) Inadequate K intake
Starvation and prolonged fasting 

-

Mild: K+ 3.0-3.5 mM

Moderate: K+ 2.5-3.0 mM

Severe: K+ < 2.5 mM 

23

cellular shifts in potassium 

(insulin)

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24

the types of hypokalemia?

Mild: K+ 3.0-3.5 mM

Moderate: K+ 2.5-3.0 mM

Severe: K+ < 2.5 mM 

25

Signs and Symptoms associated with hypokalemia ??

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26

Treatment of hypokalaemia??

TREATMENT (REPLACE K+)

Eat foods which are rich in potassium (e.g. bananas, spinach)

KCl administration (oral or i.v.)

Alkalosis correction

use of K sparing diuretics e.g.

spironolactone-inhibits aldosterone,

 

e.g. amiloride-inhibits principal cells sodium channels 

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27

hyperkalaemia??

plasma [K+]>5.5mM 

28

What causes hyperkalaemia??

A) Decreased external losses

Renal failure
Hypoaldosteronism

Action of drugs 

 

B) Redistribution out of cells

acidosis (exacerbated by lack of insulin in diabetic ketoacidosis)

tissue destruction/cell lysis e.g. rhabdomyolysis 

29

What are the signs and symptoms og hyperkalaemia??

all affect the cells ability to depolarize

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30

31

what are the types of hyperkalaemia ??

Mild: K+ 5.5-6.5 mM
Moderate: K+ >6.5-7.5 mM

Severe: K+ > 7.5 mM 

32

Treatment of hyperkalaemia??

TREATMENT

 

Short term (Stabilizing the cardiac membrane):

calcium iv to antagonise effect of K + on heart muscle

 

Intermediate term (Shifting-potassium into the cells):

insulin administered plus glucose to shift K + into cells.

 

Long term (Removing potassium from the body):

need to increase K + excretion with diuretics (e.g. loop diuretics and thiazide diuretics) or treat for renal failure.