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*LSS Urinary Y1* > Tubular Function > Flashcards

Tubular Function Flashcards

1
Q

What is Reabsorption?

A

Molecules that enter the filtrate produced by ultrafiltration but that are subsequently absorbed from the tubule to be returned to the blood

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2
Q

What is Secretion?

A

Active or passive movement of molecules from the blood into the tubular filtrate (mainly H+/K+ but also choline, creatinine and penicillin/drugs)

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3
Q

What is the difference between transcellular and paracellular transport?

A

Transcellular transport: through the renal tubular cell walls

Paracellular transport: via the tight junctions between cells

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4
Q

What are the two types of Passive movement?

A

Protein independent transport: for lipophilic molecules (rate increases linearly with concentration)

Protein-dependent transport: for hydrophilic molecules (rate limited by the number of protein transporters)

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5
Q

What are the two types of Active movement?

A

Primary: directly coupled to hydrolysis

Secondary: indirectly coupled to ATP hydrolysis (ATP used to establish a concentration gradient for symport/antiport)

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6
Q

How can water move in the kidneys?

A

Water can move through tight junctions and via aquaporins on cell surface membranes (low to high osmolarity)

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7
Q

How is protein reabsorbed from the primary urine?

A

As some protein does enter primary urine, receptors on the tubular wall have low specificity and high affinity, leading to endocytosis to vesicle; endosome pH decreases, leading to detachment and recirculation of receptors to the membrane

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8
Q

How is glucose reabsorbed?

A

Up to 10-15mmol/L can be reabsorbed by co-transport with sodium

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9
Q

Why does glycosuria occur?

A

If there is more than 10-15 mmol/L, all channels are saturated

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10
Q

How is Bicarbonate reabsorbed?

It’s way more complicated than it needs to be…

A

Apical membrane pumps in the early PCT exchange sodium in the lumen for protons, increasing [H+]; these protons react with bicarb to form H2CO3 which splits to H2O and CO2 when catalysed by carbonic anhydrase; these soluble components enter the epithelial cells where carbonic anhydrase catalyses the breakdown to release HCO3- which can enter the blood

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11
Q

What does the PCT reabsorb?

A

Glucose, amino acids, chloride ions, sodium and vitamins; continually pumps sodium out of the cell to the peritubular capillaries using an Na+/K+-ATPase pump to maintain concentration gradients

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12
Q

What are the substances that the PCT absorbs passively and actively?

A 
Passive = urea and water
Active = glucose, amino acids, sodium, potassium, calcium, VitC, uric acid - sensitive to metabolic poisons
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13
Q

What is the structure of the PCT?

A

Cuboidal epithelium, sealed with tight junctions with a brush border to maximise area and rate

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14
Q

What is tubular fluid, and what does it contain?

A

Present within the tubules, produced from ultrafiltration of blood; contains glucose, small proteins, urea, electrolytes, water and other molecules filtered from the blood

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15
Q

What is the luminal membrane?

A

Faces the lumen and contains many co-transporters that use sodium to facilitate reabsorption of key substances such as glucose (and antiporters for protons) as well as aquaporins for water

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16
Q

What is the Basolateral membrane?

A

Contains protein channels to allow specific molecules to cross the membrane and enter the peritubular capillaries, as well as Na+/K+-ATPase pumps and a Cl-/HCO3- exchanger

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17
Q

What are Peritubular capillaries?

A

They run alongside the epithelial cells

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18
Q

What are the functions of tight junctions in epithelial cells?

A

They join the epithelial cells; allow passage of K+/Mg2+/Cl-/H2O/urea via transcellular route

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19
Q

What is the role of Na+/K+-ATPase?

A

Actively exchanges 3 Na+ in the lining for 2 K+ in the blood to establish a concentration gradient for co-transport of molecules

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20
Q

What are the three ways an ion can be transported?

A

Ion-selective channel
Co-transport of two solutes
Counter-transport of two solutes

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21
Q

What is an Ion-selective channel, and what is the most common one?

A

Potassium can diffuse from the lining to the lumen of the tubule of the ascending Loop of Henle via a selective channel

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22
Q

When does Co-transport of two solutes occur?

A

Na+/Cl- co-transporter moves sodium into cells lining the DCT passively down its concentration gradient, carrying chloride ions simultaneously

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23
Q

When does Counter-transport of two solutes occur?

A

Na+/K+-ATPase e.g. on DCT cells exchanges 3 Na+ in the lining for 2 K+ in the blood

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24
Q

What is the renal tube acidosis mutation?

A

Monogenic mutation leading to failure to secrete protons or faulty carbonic anhydrase leads to accumulation in blood, leading to hyperchloremic metabolic acidosis, impaired growth and hypokalaemia

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25
Q

What is Bartter syndrome?

A

Mutation in the Na+/Cl-/K+ cotransporter means it is no longer functional, leading to excessive electrolyte secretion, salt loss, hypokalaemia and a metabolic alkalosis

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26
Q

What is Fanconi syndrome?

A

PCT disease associated with renal tubular acidosis, leads to secretion of uric acid, glucose, phosphate, bicarbonate and low MW proteins

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27
Q

How much of glucose and Na are reabsorved in the PCT?

A

100% Glucose

65% Na

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28
Q

What proportion of solutes filtered does the PCT reabsorb?

A

60-70%

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29
Q

How much sodium is reabsorbed in each section of the nephron?

A

PCT: 65%
LoH: 25%
DCT: 8%

30
Q

How does the PCT create a concentration gradient for water reuptake?

A

Na+/K+-ATPase pumps sodium out of the cells lining the tubule to peritubular capillaries to establish a concentration gradient; glucose, amino acids, sodium, potassium, calcium and vitamins are then co-transported to the lining along sodium’s concentration gradient (secondary active transport)

31
Q

How does the Ascending LoH create a concentration gradient for water reuptake?

A

Na+/K+-ATPase pumps sodium ions out of the cells lining the loop to the blood, establishing a concentration gradient so that the Na+/K+/Cl- transporter can move Na+, 2 Cl- and K+ out the lumen into the lining - (many mitochondria to allow for active transport)

32
Q

How does the DCT create a concentration gradient for water reuptake?

A

Na+/K+-ATPase pumps sodium ions out of the cells lining the tubule to the blood, establishing a concentration gradient so that chloride ions can be co-transported into the cell at the apical surface, then entering the blood passively basolaterally; calcium is also reabsorbed because sodium pumped to the blood is exchanged for Ca2+ ions at the basolateral surface, establishing a concentration gradient so that more enter the lining via facilitated diffusion

33
Q

What are the aldosterone-sensitive cells of the kidney?

A

Principle cells - Have tight junctions limit paracellular transport

34
Q

What are intercalated cells?

A

ATP dependent proton pump to regulate acid base balance

35
Q

What is the effect of increased dietary sodium?

A

Increases blood osmolarity, increasing ECF volume and hence BP; if need to remove sodium then atrial natriuretic peptide can act on nephron to decrease reabsorption

36
Q

What is the effect of decreased dietary sodium?

A

Decreases blood osmolarity, decreasing ECF and volume and hence BP; if need to reabsorb/retain more sodium then SNS discharge, AGTII and aldosterone can stimulate nephron to retain more

37
Q

Define Osmolarity:

A

Measure of the osmotic pressure exerted by a solution across a perfect semi-permeable membrane - dependent on the number of particles in a solution (not nature of the particles) - 1mmol/L of Na2HPO4 = 3 mosmoles/L as each ion counted separately

38
Q

What is normal plasma osmolarity?

A

285-295 mosmol/L; largely sodium (140mmol/L) and chloride (105 mmol/L)

39
Q

What is normal urine osmolarity?

A

50-1200 mosmol/L; largely sodium (50-200 mmol/24hrs) and potassium (40-100 mmol/24hrs)

40
Q

What is interstitial osmolarity?

A

Exists in gradient, with highest osmolarity at the base, and lowest at the top (300-1200 mosmol/l)

41
Q

What happens if plasma osmolarity is high?

A

An increase in thirst - increasing drinking and leading to polyuria

42
Q

Explain basically what happens in the descending and ascending loop of Henle:

A

dLoH: water leaves
aLoH: salt comes out

43
Q

How is a conc gradient established in the LoH?

A
  1. Salt actively pumped out of the aLoH, generating an osmotic gradient to the interstitium
  2. Water leaves the dLoH via osmosis into the interstitium, concentrating the filtrate
  3. Filtrate from the dLoH enters the aLoH and salt is actively removed, decreasing the concentration as it rises, so less salt is removed at the top
44
Q

Which areas are permeable to Urea?

A

Base of LoH/CD: both permeable to urea; urea concentration increases down the CD, so diffuses out of the CD to the interstitium, and then into the LoH base

45
Q

What are the Urea transporters, and where are they found?

A

UT-A1 and UT-A3 in CD, UT-A2 in the dLoH (and UT-B1 in the vasa recta)

46
Q

What are the Vasa Recta?

A

Straight arterioles in the medulla:
Permeable to water and solutes; water diffuses out of the descending limb and solutes dissolve in; in ascending limb, water gained and solutes left - allows oxygen and nutrients to be delivered without the loss of a gradient

47
Q

What is a Hypoosmolar environment and how is it created?

A

Created by countercurrent, dLoH permeable to water not salt, aLoH to salt not water and urea permeability at the bottom of the loop and CD; required to reabsorb water as removal of water would increase osmolarity

48
Q

What is Vasopressin in the context of the kidney?

A

9aa peptide hormone secreted from PPG in response to increased osmolarity/reduced volume; binds to V2 receptors of principal cells

49
Q

What is the mechanism of Vasopressin?

A

Causes insertion of AQP2 molecules to the luminal membrane (increasing permeability to water); also stimulates urea transport from CD to the aLoH/interstitium by increasing UT-A1 and UT-A3

50
Q

What is the stimulus to release Vasopressin?

A

Osmoreceptors in the hypothalamus stimulate release if osmolarity above 300mOs; also triggered by a marked fall in blood volume/pressure monitored by baroreceptors

51
Q

How does ethanol cause dehydration?

A

Inhibits release of Vasopressin

52
Q

What is the effect of decreased plasma osmolarity on ADH?

A

Decreases ADH, decreases CD permeability, increases flow rate

53
Q

What is the effect of increased plasma osmolarity on ADH?

A

Increased ADH, increased CD permeability, decreased flow rate (and triggers a thirst response, increasing water intake and decreasing osmolarity)

54
Q

What is Diabetes Insipidus?

A

Either no production of ADH in the brain or no detection of (mutant receptor)/response (mutant aquaporin) to ADH in the kidneys - unrelenting thirst

55
Q

What is the Macula Densa mechanism?

A

Shrink due to hyperosmolar environment leading to PGE2 and NO production/release that then leads to the release of renin

56
Q

What stimulates renal production of Renin?

A

Decreased renal BP, decreased fluid volume or increased SNS discharge

57
Q

What inhibits renin production?

A

Increased renal BP, increased fluid volume or decreased SNS discharge/ANP leads to reduced renin secretion and hence downstream less aldosterone and sodium/water reabsorption

58
Q

What are the effects of AGTII?

A

Adrenal gland: aldosterone synthesis

PCT: increased sodium uptake, increased water reabsorption and hence increased ECF and blood pressure

Vascular system: increased vasoconstriction and hence blood pressure

59
Q

What is aldosterone?

A

Steroid hormone released from adrenal cortex in response to AGTII/fall in blood pressure detected by baroreceptors/decreased osmolarity of ultrafiltrate

60
Q

What are the effects of Aldosterone?

A

Increased sodium reabsorption (induces expression of apical Na channel of CD and promotes activity by binding to intracellular steroid hormone receptor (with HSP), causing release of the HSP, dimerisation and entrance to the nucleus to increase transcription)

Increased potassium secretion (induces Na+/K+-ATPase pump formation by using the same intracellular receptor mechanism)

Increased hydrogen ion secretion

61
Q

What is hypoaldosteronism?

A

Reduced DCT sodium reabsorption leads to urinary loss and ECF/BP volume decrease - increasing renin, AGTII and ADH (causes dizziness, salt craving and palpitations)

62
Q

What is hyperaldosteronism?

A

Increased DCT sodium reabsorption leads to reduced urinary loss, increased ECF volume and reduced renin/AGTII/ADH (and increased A/BNP) - (causes muscle weakness, polyuria and thirst)

63
Q

What is Liddle’s Syndrome?

A

Inherited hypertension due to mutation in the aldosterone activated sodium channel to become permanently activated causing sodium retention

64
Q

What are the effects of Hyper/hypovolemia on Renin and renal vasculature?

A

Hypervolaemia: decreased SNS activity decreases renin release and decreases arteriolar vasoconstriction, increasing GFR

Hypovolaemia: increased SNS activity increases renin release and increases arteriolar vasoconstriction, decreasing GFR

65
Q

What can Hyperkalaemia cause?

A

Depolarises membranes leading to action potentials and heart arrhythmias

66
Q

What can hypokalaemia cause?

A

Leads to arrhythmias including asystole

67
Q

What is the response to K+ intake?

A

Increased plasma potassium enters tissue immediately due to insulin, aldosterone and adrenaline (via Na+/K+-ATPase)

Immediate kidney response: potassium does not rise as enters cells due to pump

68
Q

Describe the interaction of K+ with Principle cells:

A

Use a Na+/K+-ATPase pump to move potassium into the principal cells, before it then leaks out to tubule via apical channels; regulated by membrane potential (if inside more positive, more potassium will leak)

69
Q

What is the effect of Aldosterone on K+?

A

Can stimulate uptake to principal cells, leading to more entering the tubule (also stimulates apical potassium channel)

70
Q

How is Potassium release from CD caused?

A

Cilia stimulate PDK1 that causes a cascade to increase intracellular calcium to activate potassium channels, releasing more potassium

71
Q

Describe the epidemiologies of Hypo/Hyperkalaemia:

A

Hypokalaemia: very common in 20% patients; caused by diuretics, vomiting, diarrhoea or genetic disruptance
Hyperkalaemia: common in 1-10% patients; seen in response to K+ sparing diuretics, ACE inhibitors and the elderly

*LSS Urinary Y1* (4 decks)

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