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Kofi: Pure Clinical Sem 3 > Urinary: Physiology > Flashcards

Urinary: Physiology Flashcards

1
Q

What are the sodium channels in the proximal tubule?

A

Na-H antiporter
Na-Glucose symporter
Na-AA co-transporter
Na-Pi

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2
Q

What are the sodium channels in the loop of henle?

A

NaKCC symporter

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3
Q

What are the sodium channels found in the early distal tubule?

A

NaCl symporter

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4
Q

What are the sodium channels found in the late distal tubule and collecting tubule?

A

ENaC (epithelial Na channels)

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5
Q

What are the histological features of the proximal tubule?

A
  • Brush border
  • Large outside diameter
  • Lots of mitochondria (incredibly active)
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6
Q

What are the solutes transported in the 1st segment of the proximal tubule?

A 
-Apical
Na-H exchange 
Co-transport with glucose
Co-transport with amino acid or carboxylic acids
Co-transprt with phosphate

-Basolateral
3 Na-2K ATPase
NaHCO3- co transporter for acids and bases

  • Aquaporin channels
  • Chloride concentration increases
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7
Q

What are the solutes transported in the 2nd segment of the proximal tubule?

A

Basolateral
3Na-2K ATPase

Apical
Na+ is reabsorbed via Na-H exchanger

Paracellular and transcellular transport of Cl-

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8
Q

What is the overview of the function of the proximal collecting tube?

A
  • Highly water permeable so bulk transport of water reabsorption
  • Reabsorption is isosmotic with plasma
  • Reabsorbs 65% water, 100% glucose and amino acids, 67% of sodium
  • Driving force for reabsorption is osmotic gradient established by solute absorption, hydrostatic force in the interstitum, oncotic force in peritubular capillary due to loss of 20% filtrate at glomerulus but cells and proteins left in blood
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9
Q

What are the features of the thin descending limb?

A
  • Lots of aqua porin channels
  • No mitochondria
  • Loose junctions
  • No brush border
  • Thin
  • Flattened
  • Passive in nature
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10
Q

What are the features of the thick segment of the ascending limb?

A
  • Impermeable to water
  • Many mitochondria
  • No aqua porin
  • Lots of active transport for sodium reabsorption
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11
Q

What is the function of the thick and thin descending limb?

A
  • Paracellular reuptake of water due to increased intercellular concentrations of sodium
  • Concentrates sodium and chloride ions in the lumen of the descending limb ready for active transport in the ascending
  • Highly permeable to water due to AQP (1 channels always open)
  • Impermebale to Na
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12
Q

What is the function of the thin ascending limb?

A
  • Passive sodium reabsorption due the actions of the descending limb.
  • Epethelium permits passive reabsorption by paracellular route
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13
Q

What is the function of the thick ascending limb?

A
  • NKCC2 transrptoer that transports sodium, (2)chloride and potassium from lumen to cells
  • Na+ ions move into the interstitum due to the action of 3Na-2K-ATPase
  • ROMK channels move potassium from the cell into the lumen to allow the NKCC2 channels to work
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14
Q

What is the clinical significance of the thick ascending limb?

A

Sensitive to hypoxia due to the amount of energy use

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15
Q

Give an overview of the loop of henle reabsorption.

A
  • Descending limb reabsorbs water and not NaCl
  • Ascending limb reabsorbs NaCl but not water
  • The tubule fluid leaving the loop is hypo-osmotic compared to plasma
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16
Q

Outline features of reabsorption in the distal convoluted tubule

A
  • Hypo-osmotic fluid enters (100 mOsm/Kg)
  • Active transport of 5-8% of Na+
  • Water permeability is low
  • Has 2 regions DCT1 and DCT1
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17
Q

What are the channels present in DCT1?

A

Apical

  • NaCl enters across apical membrane via electro-neutral NCC transporter
  • NCC transporter is sensitive to thiazides diuretics

Basolateral

-3Na-2K-ATPase

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18
Q

What are the channels present in the distal convoluted tubule 2?

A

Apical

  • Na+ enter via ENaC
  • NaCL enters by the NCC

Basolateral

  • 3Na-2K-ATPase
  • KCC4
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19
Q

Which channels are affected by amiloride diuretics?

A

ENaC channels

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20
Q

What detects changes in plasma osmolarity?

A

Hypothalmic osmoreceptors

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21
Q

What are the 2 efferent pathways to regulate plasma osmolarity and their effect?

A
  • ADH: Acts on the kidney to control renal water excretion

- Thirst: Trigger brain for drinking behaviour to cause an effect on the water intake

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22
Q

Where are osmoeceptors found?

A
  • Located in the OVLT of the hypothalamus.

- Leaky endothelium is exposed directly to the systemic circulation to sense the changes in plasma osmolarity

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23
Q

What physiologically inhibits ADH?

A

-Decreased osmolarity inhibits ADH

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24
Q

What happens to the osmotic and haemodynamic relationship in circulatory collapse?

A
  • Kidney continues to conserve H2O even though this will reduce osmolarity of body fluids
  • Volume is more important than osmolarity if volume crashes
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25
Q

Describe the efferent pathway of thirst?

A
  • Stimulated by an increase in fluid osmolarity
  • Salt ingestion is the analogue of thirst
  • Large deficits in water only partially compensated for in the kidney and ingestion is the ultimate compensation.
  • Stop when sufficient fluid has been consumed
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26
Q

What is central diabetes insipidus?

A
  • Plasma ADH levels are too low
  • Damage done to the hypothalamus or pituitary gland
  • Brain injury
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27
Q

What is nephrogenic diabetes insipidus?

A

-Acquired insensitivity of the kidney to ADH

28
Q

How are problems with ADH secretion managed?

A
  • In both water is inadequately reabsorbed so a large quantity of urine is produced
  • Managed clinically by ADH injections or by ADH nasal spray
29
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion

  • Characterised by excessive release of ADH from posterior pituitary gland or another source
  • Dilutional hyponatraemia in which the plasma sodium levels are lowered and total body fluid is increased
30
Q

What happens to the aqua porin channels when plasma osmolarity decreases?

A
  • No ADH stimulation
  • No stimulation of Aqua porin 2 in apical membrane
  • AQP3 and 4 on basolateral membrane only of the latter DCT and collecting ducts and act as an exit for water entering AQP2
  • Limited water reuptake in latter DCT and collecting duct
  • Loss of large amount of hypo osmotic urine
  • Diuresis
31
Q

What happens to the aqua porin channels when plasma osmolarity increases?

A
  • Release of ADH causes the insertion of AQP2 channels into the apical membrane
  • Water moves out of the collection duct into hyper osmotic environment if there are AQP in both the apical and the basolateral epithelium of the tubule cells
32
Q

What is the range for the vertical osmotic gradient in the kidney?

A
  • 300 mOsm/kg at corticomedullary border

- 1200 mOsm/kg in medullary interstitum at papilla

33
Q

What are the essential mechanisms to maintain the vertical osmotic gradient?

A
  • Active NaCl transport in thick ascending limb
  • Recycling of urea (effective osmole)
  • Unusual arrangement o blood vessels in medulla descending components in close opposition to ascending components
34
Q

Why is urea an effective osmole?

A
  • Doesnt cross the membrane easily
  • Urea reabsorption from medullary collecting duct
  • Cortical collecting duct cells are impermeable to urea
  • Movement into interstitum and diffusion back in Loop
  • Under the influence of ADH fraction excretion of urea decreasing and urea re-cylcing increases
35
Q

How does the vasa recta maintain the concentration gradient?

A

Flow in vasa recta is in the opposite redirection to fluid flow in the tube, the osmotic gradient is maintained. Vasa recta acts as a counter current exchanger.

36
Q

Vasa recta can actively transport. True/False

A

False

37
Q

What happens in the descending limb of the vasa recta?

A
  • Isoosmotic blood in vasa recta enter hyper osmotic medullary region
  • Na+,Cl- and urea diffuse into the lumen of vasa recta
  • Osmolarity of the blood in vasa recta increases as it reaches tip of hairpin loop
38
Q

Why is blood flow in the vasa recta slow?

A

Blood flow is compromised to :

  • Deliver nutrients
  • Maintain medulaary hyper tonicity
39
Q

How does the shape of the vasa recta and loop of henle allow for the courter current exchange?

A

-Both hairpin configurations

40
Q

What happens in the ascending limb of vasa recta?

A
  • Blood ascending towards cortex will have higher solute content than surround interstitum
  • Water moves in from the descending limb of the loop of henle
41
Q

What is a diuretic?

A

A substance that promotes a diuresis by increase in renal excretion of water and sodium to reduce ECF volume

42
Q

When are diuretic used clinically?

A

Conditions where sodium and water retention cause expansion of ECF volume

43
Q

What is the effect of diuretics reducing ENaC activity on K+ secretion?

A

Reduction of K+ secretion

44
Q

How do Diuretic work? (4 ways)

A
  • Direction action on cell to block Na+ transporters in luminal membrane (Loop diuretic, Thiazide Diuretics, K+ sparing diuretics)
  • By antagonising the action of aldosterone
  • By modification of filtrate content
  • By inhibiting activity of enzyme carbonic anhydrase
45
Q

How do loop diuretics work?

A
  • Block apical NKCC transporter
  • Na and Cl not absorbed so medullary tonicity is less
  • This reduces water reabsorption further down the tubule
  • Leads to Na+ and water loss

Very potent diuretics

46
Q

What are the effect of loop diuretics in heart failure?

A

Used in heart failure for treatment of symptoms

  • Diuretic effect
  • Vaso and veno dilation to decreased after load/preload
  • Reduces symptoms but no effect on reducing mortality
47
Q

What is given in acute pulmonary oedema?

A

-IV Furosemide

48
Q

When are loop diuretics used?

A
  • Heart failure
  • Nephrotic syndrome
  • Renal failure
  • Cirrhosis of liver
  • Hyper calcaemia
49
Q

What are the effect of loop diuretics on calcium absorption?

A

Blockage of the NKCC channels:

  • Impairs calcium reabsorption as lumen positive potential isn’t created by K+ drifting into the lumen
  • More calcium is exerted in urine
  • Furosemide given together with IV fluids
50
Q

What are the effects of Thiazide diuretics?

A
  • Secreted into lumen in PCT
  • Block Na-Cl transporter in DCT
  • Travel downstream to act at DCT
  • Increase Na+ loss in urine
  • Reduces Ca2+ loss in urine
51
Q

When are thiazide diuretics used?

A

-Widely used in hypertension

ineffective in renal failure as less potent compared to loop diuretics

52
Q

What are the side effects of thiazide diuretics?

A
  • Higher incidence of hypokalaemia
  • Impotence
  • Gout
53
Q

What are the type of K+ sparing diuretics?

A

Act on late distal tubule and collecting duct

  • Inhibitors of ENaC (amiloride)
  • Aldosterone antagonists (spironolactone)
54
Q

What are the mechanism of action for potassium sparing diuretics?

A
  • Reduces ENaC activity directly or indirectly
  • Reduce loss of K+
  • Both can produce life threatening hyperkalaemia especially if used with ACE inhibitors, K+ supplement or in patients with renal impairment
  • Both are mild diuretics affecting only 2% of Na+ reabsorption
55
Q

What are the non diuretic situations that feature the use of aldosterone antagonists?

A
  • Reduction of mortality in heart failure (used in the long term treatment of heart failure)
  • Preferred duct for ascites and oedema in cirrhosis
  • Used as additional therapy in hypertension if other treatment aren’t effective
  • Treatment of hypertension in Conn’s syndrome
56
Q

What are ENaC blockers like amiloride used in combination with?

A

K+ losing diuretics

57
Q

How can diuretics contribute to hypokalaemia?

A
  • Diuretics may lead to reduced circulatory volume
  • Activtion of RAAS
  • Increase in Aldosterone secretion
  • Increase in Na+ absorption and K+ secretion
  • Hypokalaemia
58
Q

How can K+ sparing diuretic cause hyperkalemia?

A
  • Reduction in Na+ reabsorption
  • Reduces potassium loss in urine as negative potential for movement of potassium isn’t created
  • Hyperkalaemia
59
Q

What is the reason for use of loop/thiazide diuretics and a K+ sparing diuretic in combination?

A

-Used to minimise changes in potassium

Thiazide/Loop diuretics can be used with only potassium supplements if necessary

60
Q

What should be avoided with use of K+ sparing diuretics?

A
  • Potassium supplement
  • Impaired renal function
  • Increase in risk of hyperkalaemia

Concomitant use with ACEI/ARB - regular K+ monitoring required

61
Q

What is activated in nephrotic syndrome?

A
  • Reduced circulatory volume
  • RAAS activated
  • Na+ and water retention
  • Expansion of ECF
  • More oedema
62
Q

What are the adverse effects of diuretics?

A
  • Potassium abnormalities
  • Hypovolaemia especially in loop diuretic
  • Hyponatraemia
  • Increase in uric acid levels in blood (with Thiazides, Loop Diuretics) can precipitate attack of gout
  • Metabolic effects (glucose intolerance, LDL levels)
  • Thiazides (erectile dysfunction)
  • Spironolactone causes gynaecomastia
63
Q

How do carbonic anhydrase inhibitors work?

A
  • Inhibits action of carbonic anhydrase in brush border and PCT cells
  • Loss of HCO3- so osmolarity of lumen increases
  • Can cause metabolic acidosis due to loss of HCO3- in urine
64
Q

Which condition in the eye are carbonic anhydrase inhibitors useful to treat?

A
  • Useful in the treatment of Glaucoma

- Reduces formation of aqueous humour in the eye by about 50%

65
Q

What is the mechanism for osmotic diuretics?

A
  • Acts by altering the osmolarity to affect renal water absorption
  • Small inert molecule increase the plasma osmolarity thus drawing out fluid from tissues and cells
  • Osmolarity of the filtrate in increased in the kidney
  • Loss of water, Na+ and K+ in the urine
  • Doesn’t inhibit enzymes or transport proteins
66
Q

What are other substances with diuretic action?

A
  • Alcohol (inhibits ADH release)
  • Coffee (increase GFr and decreases Na+ reabsorption)
  • Drugs that inhibit action of ADH on collecting ducts
67
Q

What are some diseases causing diuresis?

A
  • Diabetes Mellitus
  • Cranial Diabetes Insipidus
  • Nephrogenic Diabetes insipidus
  • Psychogenic polydipsia

Kofi: Pure Clinical Sem 3 (44 decks)

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