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Homeostasis > Renal physiology and body fluid homeostasis (part 1) > Flashcards

Renal physiology and body fluid homeostasis (part 1) Flashcards

1
Q

What is osmolarity?

A

Number of particles of osmotic substance per litre solvent

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2
Q

What is osmolality?

A

Number of particles of osmotic substance per kg solvent

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3
Q

What types of measurement is osmolality?

A

Colligative, meaning that it is only dependent on number of particles present, not properties of the particles.

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4
Q

What factors is movement of water between plasma and IF dependent on?

A
  • Hydrostatic pressure
  • Colloid osmotic pressure

(Starling forces)

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5
Q

What factors is movement of water between IF and ICF dependent on?

A

Osmotic pressure

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6
Q

What are the criteria that determine good indicator for determining volume of cellular compartment?

A
  1. Restricted to 1 compartment
  2. Evenly distributed
  3. Little influence on total volume
  4. Does not get metabolised/excreted
  5. Non-toxic
  6. Easily measured
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7
Q

What is the gold-standard indicator for plasma volume?

A

Evans blue (binds to albumin)

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8
Q

What indicators are used to meaure total body water volume?

A
  • D2O
  • HTO
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9
Q

What percentage of CO do the kidneys take?

A

25%

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10
Q

What is the structure of the renal vascular system?

A

Renal arteries → Interlobar arteries → Arcuate arteries → Interlobular arteries → Afferent arterioles → Glomerulus → Efferent arterioles → Peritubular capillaries/vasa recta → VENOUS SYSTEM

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11
Q

What is the name given to nephrons with LoH extending into inner medulla?

A

Juxtamedullary nephron

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12
Q

What is the purpose of excretion/reabsorption in the kidneys?

A
  • Regulation
  • This system ensures that all toxic substances (known and unknown) are excreted from the body.
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13
Q

What is the difference between ionic concentration in glomerular filtrate compared to plasma?

A
  • Concentration of -ve ions slightly higher and +ve ions slightly lower.
  • This is because -ve plasma proteins repel -ve ions and attract +ve ions.
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14
Q

What is the function of the filtration barriers?

A
  • Filtration barriers prevent the passage of particles >4 nm in diameter.
  • Molecules between 2-4 nm are selectively filtered (by charge).
  • All molecules <1 nm in diameter freely pass through the barrier.
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15
Q

What are the effects of afferent arteriole vasoconstriction?

A
  • ↓ Glomerular pressure
  • ↓ Glomerular flow
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16
Q

What are the effects of efferent arteriole vasoconstriction?

A
  • ↓ Glomerular flow
  • ↑ Glomerular pressure
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17
Q

How is autoregulation achieved?

A

​1. Myogenic

  1. Tubulo-glomerular feedback
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18
Q

What are the control mechanisms for GFR?

A
  1. Sympathetic nervous system: Stimulates arteriolar vasoconstriction via NAd.
  2. Endocrine: Angiotensin II constricts the efferent arterioles. ADH acts as vasoconstrictor. ANP acts as vasodilators of both afferent and efferent arterioles
  3. Paracrine: Endothelins vasoconstrict. NO vasodilates in response to excess vasoconstriction due to AII and NAd for example.
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19
Q

What are the factors affecting GFR?

A
  1. Kf: Influenced by capillary membrane area and filtration barrier permeability. This may be caused by contraction of mesangial cells (under AII stimulation) or blockage of the filtration slits by proteins (e.g. myoglobin).
  2. PB: Urinary tract obstruction (e.g. kidney stones) can cause back-up of filtrate into the nephrons, which increases PB and thus decreases GFR.
  3. σ: Increased plasma protein permeability can be caused by pathologies (e.g. nephrotic syndrome). This may lead to increased GFR, which ultimately results in oedema.
  4. πC: Increased flow decreases the rate at which πC decreases along the glomerular capillary, which increases the filtration that takes place.
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20
Q

Why do starling forces in the glomerular capillaries favour reabsorption?

A
  1. Colloid osmotic pressure always high because of ultrafiltration in the glomeruli.
  2. Hydrostatic pressure is always low because of the high resistance afferent and efferent arterioles.
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21
Q

What is clearance?

A

Hypothetical volume of blood that would need to be completely cleared of a substance each minute to produced observed excretion rate.

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22
Q

What are the properties of a substance for which clearance = GFR?

A
  1. Freely filtered
  2. Not reabsorbed
  3. Not secreted
  4. Not metabolised/synthesised in body
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23
Q

What is a clearance ratio?

A

CR = Cx/CInulin

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24
Q

What is the significance of the clearance ratio?

A

CR > 1 = Net secretion (+ free filtration)

CR <1 = Net reabsorption

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25
Q

What is the significance of PAH?

A

CPAH ≈ Renal blood flow

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26
Q

How is Na+ reabsorbed in the early PCT?

A
  1. Na+/K+ ATPase activity in on the basolateral membrane of the PCT epithelial cells maintains a constant low [Na+] in the cytosol of the cells. This promotes the diffusion of Na+ ions from the filtrate into the cell.
  2. High ECF [Na+] created by the pump, which promotes diffusion of [Na+] back into the plasma.
27
Q

Why is transcellular reabsorption of Cl- a problem?

A

Transcellular reabsorption challenging due to cell being –ve as result of proteins.

28
Q

How is Cl- reabsorbed in the late PCT?

A
  • Cl- reabsorption depends on exchange of other anions.
  • The anions are recycled (in similar way as HCO3- reabsorption, associated with protons) in order to allow continuous Cl- reabsorption.
29
Q

What are the organic anions secreted into PCT lumen?

A
  • Prostaglandins
  • Cyclic AMP & GMP
  • Bile salts
  • Drugs (e.g. penicillin)
30
Q

What are the organic cations secreted into the PCT lumen?

A
  • Creatinine
  • Adrenaline & noradrenaline
  • Dopamine
  • Drugs (e.g. dopamine, morphine…)
31
Q

What is extracellular K+ used for?

A
  • Resting potential
  • Repolarisation phase of action potential
  • Vascular tone (low [K+] → Vasoconstriction, high [K+] → Vasodilation)
32
Q

What is intracellular K+ used for?

A
  1. Maintenance of cell volume
  2. Cellular pH regulation
  3. Cell enzyme function (some enzymes dependent on K+)
  4. DNA/protein synthesis (lack of K+ → decreased DNA/protein synthesis)
33
Q

What are the extrinsic stresses of [K+]?

A

Diet

34
Q

What are the stresses that cause ICF to ECF shift of K+?

A
  1. Exercise: Continued muscle stimulation causes K+ to be released into ECF.
  2. Acidosis: Movement of H+ into the cell as a result of acidosis displaces K+ and increases ECF [K+] (as well as reducing Na+/K+-ATPase and NKCC2 activity).
  3. Dehydration: Causes cells to shrink, which causes loss of K+.
  4. Cell lysis: Cells contain high [K+]. Cell lysis causes that K+ to be released into ECF (e.g. chemotherapy).
35
Q

What are the stresses that cause an ECF to ICF shift of K+?

A
  1. Hyperhydration: Causes cells to swell, which causes uptake of K+.
  2. Insulin.
  3. Adrenaline.
36
Q

What are the effects of hyperkalaemia?

A
  • If [K+]E too high, then hyperkalaemia occurs and cells depolarise, increasing excitability. This can lead to cardiac arrhythmias.
  • Hyperkalaemia causes T waves to become larger and QRS complex to become smaller. T waves become larger due to greater repolarisation as a result of inward rectifying K+ channels. QRS becomes smaller due to smaller depolarisation as result of inactivating Na+ channels.
37
Q

What are the effects of hypokalaemia?

A
  • If [K+]E too low, then hypokalaemia occurs and cells hyperpolarise, deceasing excitability. This can lead to cardiac arrhythmias, muscle weakness/paralysis.
  • Hypokalaemia causes T waves to decrease and the appearance of U wave. T wave is small as repolarisation is slow. U waves are delayed repolarisation of the ventricles.
38
Q

What are the factors that promote ECF → ICF shift of K+ during hyperkalaemia?

A
  • High [K+]e (passive)
  • Aldosterone (feedback)
  • Adrenaline (feedforward)
  • Insulin (feedforward)
39
Q

What is the sequence of events in aldosterone release?

A
  1. Raised [K+]E detected by aldosterone-secreting cells in the adrenal cortex.
  2. Raise [K+]E causes depolarisation which causes voltage-gated Ca2+ to open, resulting in Ca2+ influx into the cell.
  3. Raised [Ca2+] causes more aldosterone to be secreted into the blood, which acts on the kidneys to increase K+ excretion and increases activity of Na+/K+ ATPase, possibly by increasing PNa and influx of [Na+] into the cell through Na+/H+ exchanger or NKCC.
40
Q

How is K+ handled in the nephron?

A
  • PCT: Unregulated reabsorption (67%)
  • AL of LoH: Unregulated reabsorption (12%)
  • DCT: Secretion (principle cells)
41
Q

What are the K+ channels in the principle cell relating to secreted?

A
  1. Basolateral membrane K+ channels: Pumps K+ ions out of epithelial cells in process of ‘K+ cycling’. This allows for Na+ to diffuse into cells from the filtrate even when K+ is not being secreted.
  2. SK (Ca2+-activated K+) channels: Allows K+ to be secreted into the filtrate.
  3. Na+/K+-ATPase: Pumps K+ out of ECF into the cell.
42
Q

What are the factors influencing K+ reabsorption in the kidneys?

A
  1. High plasma [K+]: Enhances activity of Na+/K+ ATPase, which increases [K+] in principle cells, increasing diffusion gradient and thus excretion into filtrate.
  2. Aldosterone: Aldosterone increases gene expression of certain proteins that promote the activity of SK channels, ENaC channels and Na+/K+ ATPase, which subsequently promotes K+ secretion.
  3. Tubular flow rate: High tubular flow rate maintains low filtrate [K+]. This ensures that there is a steep concentration gradient between inside of principle cells and filtrate, which increases rate of secretion. Increased flow also increases [Na+] delivery, which increases activity of Na+/K+-ATPase.
  4. Depolarising the cell by enhancing entry of Na+ through ENaC channels promotes secretion of K+ as it makes the electrochemical gradient steeper.
43
Q

What are the effects of aldosterone on K+ reabsorption during hypovolaemia?

A
  • Aldosterone release during hypovolaemia increases Na+ reabsorption, but has no effect on K+ secretion
  • Other Na+ retention mechanism decrease tubular flow, decreasing K+ secretion, thus balancing the effects of aldosterone on increasing K+.
  • However, aldosterone without other Na+ retaining mechanisms does increase K+ excretion.
44
Q

How is K+ reabsorbed in the PCT?

A

In the PCT, Na+/K+ ATPase in the membrane lining the paracellular space results in K+ being pumped out of the paracellular space and into the cell. This produces a low [K+] in the paracellular space. This in addition to reabsorption of water paracellularly (due to high intercellular [Na+] also reabsorbs K+ by the process of solvent drag.

45
Q

How is K+ reabsorbed in the tAL of LoH?

A

In the tAL of LoH, K+ is reabsorbed passively by solvent drag paracellularly and transcellularly by secondary active transport through Na+/K+/Cl- exchangers (NKCC2) in a ratio of 1:1:2.

46
Q

How is K+ reabsorbed in the DCT?

A

In the DCT and collecting ducts, K+/H+-ATPase reabsorbs K+ in exchange for secreting H+ (in type A intercalated cells). This response is promoted by low [K+]E. It then passively diffuses across basolateral membrane through K+ channels. A considerable amount of paracellular reabsorption also occurs as a result of high luminal [K+].

47
Q

What is the significance of loop diuretics?

A

Frusmide inhibits NKCC2, decreasing K+ reabsorption.

48
Q

What are the effects of ADH on K+ secretion?

A
  • Decreased tubular flow rate decreases secretion.
  • Increased SK activity increases secretion.
  • No net effect.
49
Q

What are the causes of clinical hypokalaemia?

A
  1. Diuretics
  2. Diarrhoea/vomiting
  3. Reduced intake
50
Q

What are the clinical causes of hyperkalaemia?

A
  1. Renal failure
  2. Iatrogenic (caused by doctors)
  3. Cell lysis (e.g. due to chemotherapy)
  4. Pseudohyperkalaemia (hyperkalaemia detected by blood test, but due to lysis of RBCs in blood taking process)
  5. Dehydration
51
Q

What are the physiological stresses on pH?

A
  1. Respiration (produces CO2)
  2. Metabolism (e.g. Cys/Met → H2SO4, Asp/Glu → HCO3-)
  3. Diet
52
Q

What are the buffer systems present in plasma?

A
  1. HCO3-
  2. HPO42-
  3. Plasma proteins (especially His groups)
  4. Bone (H+ displaced Ca2+ in bone)
53
Q

What are the apical H+ channels in the PCT?

A
  • H+-ATPase
  • NHE3
54
Q

What are the basolateral H+ channels in the PCT?

A
  • NBCe1
  • Cl-HCO3 exchanger
55
Q

What are the apical H+ channels in the TAL?

A
  • H+-ATPase
  • NHE3
56
Q

What are the basolateral H+ channels in the TAL?

A
  • NBCe1
57
Q

What are the apical H+ channels in the DCT?

A
  • K+/H+ exchanger
  • H+-ATPase
58
Q

What are the basolateral H+ channels in the DCT?

A
  • Cl-HCO3 exchanger
59
Q

What are the fates of NH3 in the kidneys?

A
  1. NH4+ dissociates to NH3 and H+. NH3 then diffuses into PCT and is re-secreted. NH3 is thus recycled.
  2. Diffuses into collecting duct where low pH converts NH3 into NH4+. It is charged and so becomes trapped, getting excreted (ammonium trapping).
  3. Excess ammonia is carried back to the liver in blood to be converted to urea.
60
Q

What are the intrinsic responses to respiratory acidosis?

A

The higher PCO2, the higher the rate of H+ secretion and HCO3- production from PCT cells (probably by upregulation of NHE3 and NBCe1).

61
Q

What are the intrinsic responses to metabolic acidosis?

A

The lower the blood [HCO3-], the higher the rate of HCO3- production and H+ secretion from PCT cells (due to increased activity of NBCe1). In chronic acidosis, NHE3 and NBCe1 are further upregulated. Metabolic acidosis also stimulates ammoniagenesis.

62
Q

What are the intrinsic responses to metabolic alkalosis?

A

Inhibits H+ secretion and HCO3- production in the PCT by inhibiting the activity of NBCe1. Increases number of Type B intercalated cells in DCT/CD, thus increasing HCO3- secretion.

63
Q

What are the extrinsic factors influencing H+ secretion in the kidneys?

A
  1. Angiotensin II: Stimulates NHE in PCT cells.
  2. Aldosterone: Stimulates K+/H+-ATPase in type A cells of the collecting ducts increasing H+ secretion and K+ reabsorption.
  3. Cortisol: Released in response to low pH. Increases transcription of NHE and NBC.
  4. PTH: Release stimulated in prolonged acidosis. Promotes H+ secretion from TAL and DCT, as well as decreasing HPO42- reabsorption in PCT (increasing buffering capacity of urine).

Homeostasis (15 decks)

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