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Year 1 Urinary > Tubular function > Flashcards

Tubular function Flashcards

1
Q

What is the structure of a nephron?

A

Glomerulus, proximal convoluted tubule, Loop Of Henle (descending then ascending limbs), and comes up to the same glomerulus (produces the juxtaglomerular apparatus) to the distal convoluted tubule. Then passes off to bladder. NOTE, the afferent arteriole emerges from above, and the efferent leaves below. PERITUBULAR CAPILLARIES are capillaries supplied by the efferent arteriole.

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2
Q

What are the two parts of the collecting duct?

A

Cortical collecting duct and innerr-medullary collecting duct.

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3
Q

What is meant by ‘freely filtered’?

A

Meaning SOLUTE is found in the same concentration in the blood as the GF.

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4
Q

How is urine produced?

A
  1. Filtration of blood plasma. 2. Selective reabsorption of contents to be retained. 3. Tubular secretion of some components 4. Concentration of urine as necessary.
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5
Q

What is hyper-osmolarity and hypo-osmolarity?

A

HYPEROSMOLARITY: lots of solute. HYPOOSMOLARITY: low in solute, high in water.

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6
Q

What is tubular fluid?

A

Fluid contained within the tubules of the nephron network.

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7
Q

What is osmolarity?

A

Measure of the osmotic pressure exerted by a solution across a perfect semi-permeable membrane. it is a measure – therefore, of all the concentrations of the different solutes added together i.e. every ion. Measure das mosmol/L – 1 Osmole = 1 mole of dissolved solutes per litre. The greater the amount of dissolved particles, the greater the osmolarity.

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8
Q

What is the normal plasma osmolarity range?

A

285-295 mosmol/L.

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9
Q

What is the minimum and maximum urine osmolarity? Implication of range on plasma osmolarity?

A

50 – 1200 mosmol/L. 1200 denotes that the urine is concentrated during water suppression; 50 = the opposite. These large urine osmolarity fluctuations allow for plasma osmolarity to stay constant.

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10
Q

What must be the case about osmolarity in the body? What does this mean for plasma volume?

A

OSMOLARITY MUST BE KEPT CONSTANT: This explains why increased salt must be compensated with increased water and therefore LARGER VOLUME!

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11
Q

What is the most prevalent solute in the plasma and ECF?

A

Sodium.

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12
Q

What is the definition of paracellular and transcellular?

A

Para = across tight junctions and inter-cellular spaces. Intra = through cytosol of cell epithelium.

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13
Q

What are the two types of passive movement across cells?

A

PROTEIN-INDEPENDENT TRANSPORT: for lipophilic molecules, movement is dependent solely on concentration gradients. PROTEIN-DEPENDENT TRANSPORT: for hydrophilic molecules, movement is limited by number of protein channels available for movement.

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14
Q

What are the two types of active movement across cells?

A

DIRECTLY ATP-COUPLED: rate is dependent on availability of ATP. INDIRECTLY ATP-COUPLED: note that on baso-lateral surface, sodium movement is passive; the active process occurs at the Na+/K+ pump. Rate here depends on Na+ concentration gradient between the areas shown by green arrow.

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15
Q

What two ways can water move across tubular cells in the nephron?

A

Paracellularly through tight junctions OR intracellularly through protein channels called aquaporins.

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16
Q

What does transport maxima describe?

A

Solute concentration above which we cannot reabsorb anymore, so anything above these concentrations will appear in the urine e.g. glucose in diabetics.

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17
Q

How does transport maxima vary?

A

Applies to all substances but can vary depending on circumstances that stimulate transport and reabsorption.

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18
Q

What substances in the nephrons do not have specific protein transporters? How is this overcome?

A

Urea and water. This is overcome by water by utilising osmosis in response to build up of Na in intercellular spaces.

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19
Q

What is secretion?

A

Movement of substances from peritubular capillaries into tubular lumen. Can occur by diffusion or transcellular mediated transport.

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20
Q

What are the main things secreted into the urine?

A

H+ and K+ because of the antiporter mechanisms of reabsorption in the nephron tubules.

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21
Q

What is the process of reabsorption in the proximal convoluted tubule?

A

70% filtrate is reabsorbed – Na+ uptake by basolateral Na+ pump allows for cotransport where water and anions e.g. Cl- follow. Glucose is taken up by Na+/glucose co-transporter, and amino acids by Na+/amino acid co-transporter. Small proteins that enter the glomerular filtrate (this is normal for small proteins), are reabsorbed by endocytosis. All glucose and small proteins get reabsorbed.

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22
Q

What are the structural features of the proximal convoluted tubule? (x5)

A

□ Proximal convoluted has a dense brush border = high SA which is especially important because there’s large volumes of reabsorbed water – in APICAL MEMBRANE. □ Interdigitations in BASOLATERAL MEMBRANE. □ Cells are high in mitochondria for Na+ active transport. □ Cuboidal epithelium sealed with fairly water permeable tight junctions. □ Contains aquaporins which mediate transcellular water diffusion.

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23
Q

Small amounts of protein enter the filtrate: how are these reabsorbed?

A

There are receptor proteins on apical surface which has low specificity, but high affinity for protein. They bind to and endocytose the protein along with the receptor it is bound to. Inside the endosome containing the protein and receptor, pH drops, receptor dissociates, and returns to membrane.

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24
Q

How are low intracellular concentrations of reabsorbed substances maintained in PCT? Importance?

A

Blood flow. Important as a lot of reabsorption happens here.

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25
What is the role of Na+ in the early proximal tubule, and what mechanisms does Na+ use to do this? (x4)
* CO-TRANSPORT glucose and amino acids on apical surface. Glucose and amino acids move out passively from basolateral surface because of low concentration in blood. * COUNTER-TRANSPORT of H+ ions to regulate pH. * Exchange with potassium ions in direct ATP-dependent active-transport to maintain concentration gradients for passive diffusion of Na+ into cell at the apical surface. * Indirect movement of HCO3- out and into blood – explained in net flashcard.
26
How is Na+ indirectly responsible for reabsorption of HCO3- in PCT?
1. Na+/H+ exchange mechanism means that H2CO3 is formed in the tubular fluid, where HCO3- is present. 2. Presence of carbonic anhydrase means H2CO3 can be converted to H2O and CO2. 3. H2O and CO2 can cross the membrane and continue to associate (and dissociate) to form H2CO3 in the tubule cell. 4. H2CO3 in the tubule cell can dissociate to form H+ to replenish supply in cell, AND CRUCIALLY, form HCO3- again for movement out and into the blood.
27
What is the purpose of carbonic anhydrase activity in the PCT? (x2)
Na+ reabsorption and increased urinary acidity.
28
What happens in terms of secretion in the PCT?
There is net secretion.
29
Why is secretion in PCT important? (x2)
Route of excretion for some substances AND some drugs enter the tubular fluid here and act further down the nephron.
30
What is the major function of the loop of Henle? Name of mechanism?
Purpose is to concentrate the urine – creation of hyper-osmotic extracellular fluid. Done using the COUNTERCURRENT MECHANISM.
31
What happens in the countercurrent mechanism?
DESCENDING THIN TUBULE: passive osmotic equilibrium (aquaporins present). Ions and water move out down concentration gradient freely. ASCENDING THICK LIMB: Cl- actively pumped out of tubular fluid into ECF, and Na+ passively moves out because tubular fluid initially very watery. Impermeable to water. Results in hypo-osmotic (lots of water) tubular fluid and hyper-osmotic (lots of solute) extracellular fluid. This produces the environment for the large movement of water out and back into the blood in the descending limb – so lots of water can be retained in the body.
32
What happens to osmolarity at different depths of the medulla? What mechanism makes this happen?
Higher osmolarity (more salty) as you go further down the medulla. LOOK AT PHOTO AS THIS EXPLAINS WHY.
33
What is the nature of osmolarity of tubular fluid when it leaves ascending limb? Why?
Hypo-osmolar (more watery) than plasma because more sodium has been reabsorbed (90%) than water (85%) across the PCT and LOH by this point.
34
What is the mechanism of movement in ascending limb?
Na/K/CL co-transporter, where Cl-, Na+ and K+ are moved out of tubular fluid. Concentration gradients maintained by anti- and co-transporters in basolateral membrane. There is also SOME paracellular movement.
35
What do loop of Henle diuretics target?
Na/K/Cl co-transporter in ascending loop of Henle on apical surface.
36
What is the structure and physical characteristics of the descending and ascending limbs of the loop of Henle?
DESCENDING LIMB: thin, simple SQUAMOUS EPITHELIUM, quite passive so not many mitochondria, loose tight junctions because it concerns water reabsorption. ASCEDNDING LIMB: less thin, CUBOIDAL EPITHELIUM and many mitochondria because it concerns Na+ movement, few microvilli.
37
How is ascending limb impermeable to water? (x2)
Very tight, tight junctions. Unlike descending limb where there are loose tight junctions, so water can move paracellularly. ALSO lack aquaporins.
38
How are the vasa recta arranged?
Vasa recta are the capillaries. Vasa recta also arranged in a loop and blood in rapid equilibrium with the ECF. Loop structure stabilises hyper-osmotic sodium concentration.
39
The counter-current multiplier system is not enough to concentrate the urine: what other mechanism enhances the reabsorption of water in the loop of Henle and collecting duct?
MOVEMENT OF UREA! The circled areas are both permeable to urea. At these points, fluid inside the tubules are hyperosmolar (not much water), so concentration of urea is high! The process is: 1. At the distal end of collecting duct, urea moves out down concentration gradient into interstitium. Movement continues until equilibrium. 2. When this happens, concentration of urea in intersititum will be higher than concentration of urea in loop of Henle, so urea diffuses into descending limb of loop of Henle (and lower region of ascending limb). 3. Urea cycles back round to same region of the collecting duct where urea moves out again. This cycle continues and each time, urea concentration in interstitium continues to rise, so urine can be concentrated even more!
40
What family do urea transporters belong to?
SLC14A family.
41
What are the four types of urea transporter? Where are each found? Don’t emphasise these in revision!
UT-A2 (descending limb), UT-A1 and UT-A3 (inner medullary collecting duct – A1 in apical, and A3 in basolateral membrane) found in the nephron. UT-B1 found in the descending vasa recta.
42
What is the function f UT-A1/3 urea transporters?
Without these, there will be less urea in the medulla and less water reabsorption ability – so lesser ability to reduce urine output.
43
What is the function of UT-A2 urea transporters?
Not as important; but has same function as A1/3.
44
What is the function of UT-B1?
Concentrates the urine and reduces urine production.
45
How is the vasa recta another counter-current exchange system?
Vasa recta also supply tubule cells to keep them alive. They are completely permeable to solutes and water. This means that: • As blood comes down and follows descending limb, it loses water to interstitium, and solutes diffuse into the vasa recta from the interstitum. • Therefore, blood becomes more concentrated – same as interstitium. • As blood comes back up, it follows the ascending limb and picks up water. This is because of reabsorption, and decreased osmolarity of interstitium the further up the vasa recta moves (remember, blood osmolarity is the same as interstitium osmolarity, because vasa recta are freely permeable). At the same time, solutes move out into interstitum i.e. opposite to descending vasa recta. • Therefore, oxygen and nutrients are delivered without loss of gradient and interstitum osmolarity remains constant.
46
What is the major function of the distal convoluted tubule?
Adjustment of ion content of urine. Controls levels of sodium, potassium, H+ and NH4+.
47
How are the functions of the DCT controlled?
This occurs (mostly) at the distal part of the distal convoluted tubule. 1. ADH will change the amount of fluid in the tubule. 2. Aldosterone adjusts the ions in the tubules – sodium reabsorption dependent on aldosterone. There’s also adjustment of Na+/K+/H+/NH4+.
48
What is the structure of the distal convoluted tubule compared to the proximal tubule?
Distal has smaller diameter and no brush border with invaginations in surface. There are many more proximal than distal tubules. DCT contains invaginations – containing the ion pumps. DCT are more active so have more mitochondria. Cuboidal epithelium (same as proximal). Few microvilli unlike proximal.
49
Why are there many more PCTs than DCTs?
Because by the time the filtrate reaches the DCT, a lot of the filtrate has been reabsorbed, so no need to have to so many.
50
What is the mechanism of ion movement in the DCT?
Na+ and Cl- cotransporter is linked to Ca2+ reabsorption. 1. Na+/K+ pump on basolateral membrane pumping sodium out of cell. 2. This creates low concentration of sodium inside cell. 3. Therefore, sodium moves in passively by Cl- cotransport in apical surface AND Ca2+ COUNTER-transporter in basolateral surface. 4. Ca2+ moves in passively from tubular fluid to replace Ca2+ that has moved into blood.
51
What happens to DCT mechanism when Thiazides are used? Result and mechanism?
Blocks Na+/Cl- cotransporter. 1. Na+/K+ pump continues pumping as normal. 2. Low intracellular Na+ concentration must be compensated by Na+/Ca2+ counter-transporter. 3. So, more Na+ is pumped in and more Ca2+ out than normal from the counter-transporter. 4. This means that more Ca2+ must be moved in from the apical side from the tubular fluid. 5. RESULT: rise in plasma Ca2+!
52
What is the function of the juxtaglomerular apparatus? How does it exercise this function?
Endocrine specialisation – secretes renin to control blood pressure via angiotensin. Senses stretch in arteriole wall and [Cl-] in tubule. The components that take part in this mechanism are the (1) MACULA DENSA of distal convoluted tubule and (2) JUXTAGLOMERULAR CELLS of afferent arteriole. □ Renin released from apparatus. □ Renin converts Angiotensin I to II in the lungs. □ This produces more aldosterone. □ Vasoconstriction and increased blood pressure.
53
What is the macula densa?
Thickening where the distal tubule touches the glomerulus.
54
What is the function of the macula densa in the DCT?
Senses Na+ in the filtrate e.g. has Na+ been absorbed enough?
55
What affect does Na+ have on renin release in the juxtaglomerular apparatus?
A lot of Na+ in the DISTAL CONVOLUTED TUBULE inhibits renin release which means decreased angiotensin and decreased aldosterone = vasodilation AND increased urine production (= more Na+ removed). Increased salt intake means high blood pressure.
56
What happens to permeability of water in the DCT and collecting duct when there is NO ADH? Why?
Completely impermeable to water.
57
What is the purpose of the collecting duct?
Concentrates the urine.
58
What are the two types of cell in the collecting duct?
Principal and intercalated cell.
59
What is the function of the principal cell of the collecting duct?
Contains aldosterone-sensitive Na+ system, important in Na+, K+ and water balance. Mediated by Na/K ATP pump (linked to K+ channel).
60
What is the function of the intercalated cell in the collecting duct?
Important in acid-base balance using H+-ATP pump.
61
How does the collecting duct concentrate the urine? Aquaporins in luminal and basolateral membrane?
Remember, medulla has hyper-osmotic extracellular fluid, so water can move out of the collecting duct as urine passes down it. As it goes down the collecting duct, more and more water is removed, as the medulla gets more hyper-osmotic. Rate of water movement depends on aquaporin-2 in apical membrane, controlled by ADH. Basolateral membrane has aquaporin-3, not controlled by ADH. Allows for rapid movement of water into the blood once it has moved into the collecting duct walls.
62
What is the structure of ADH?
Peptide hormone of 9 amino acids.
63
What is another name for ADH?
Vasopressin.
64
How is ADH transcribed?
Derived from single transcript that also encodes neurophysin II and copeptin.
65
Where is ADH synthesised?
Hypothalamus and packaged into granules.
66
Where is ADH secreted?
Posterior pituitary.
67
Where does ADH bind?
Binds to specific receptors (V2) on basolateral membrane of principal cells in the collecting ducts.
68
What is the mode of action of ADH? (x2)
Causes insertion of aquaporins into apical cell membrane (mainly AQP-2) AND increases membrane localisation of UtA1 and UTA3 in the collecting duct which increases urea transport into loop of Henle and interstitial tissue. Both these increase water reabsorption.
69
What triggers ADH release? (x2)
1. When plasma osmolarity exceeds 300mosmol/L – by osmoreceptors in the hypothalamus. 2. Stimulated by marked fall in blood volume or pressure – monitored by baroreceptors or stretch receptors.
70
What chemical inhibits ADH release?
Ethanol i.e. alcohol – leads to dehydration as urine volume increases.
71
What is the negative feedback loop of ADH release and urine flow rate when plasma osmolarity falls? Limit?
Solute reabsorption without water reabsorption can lower urine osmolarity to a minimum of 50 mosmol/L = as dilute as the urine can get (already mentioned earlier, but this is contextual application).
72
What is the negative feedback loop of ADH release and urine flow rate when plasma osmolarity rises?
Plasma osmolarity increases in dehydration. There are two effects when this is recognised by osmoreceptors – thirst AND ADH release – aim is the increase water intake and decrease fluid loss respectively, to lower plasma osmolarity. ADH release means aquaporins inserted, so osmotic equilibration in cortex and medulla occurs = high urine osmolarity.
73
What are the possible disorders of water balance? (x2)
No/insufficient production of ADH; no detection of ADH (mutant ADH receptor); no response to ADH signal (mutant aquaporin).
74
What are the symptoms of diabetes insipidus? Why do these symptoms come about?
Excretion of large amounts of watery urine and unremitting thirst. Caused by disorder of water balance as previously described.
75
What proportion of sodium is reabsorbed at each region of the nephron? Note about sodium regulation? Overall in the nephron, what proportion of Na+ should be reabsorbed into the blood?
Remember, none happens in the descending limb, because it is impermeable - look at photo. \> 99%.
76
How does percentage of water remaining in filtrate change as filtrate moves through nephron?
Absorbed in PCT at the same rate as sodium, and reabsorbed in the descending limb. Ascending limb is impermeable to water, but DCT reabsorbs water further. The CD fine-tunes water reabsorption via ADH from central osmolarity receptors.
77
How does percentage of INULIN remaining in filtrate change as filtrate moves through nephron? What is inulin?
It is an exogenous (but small) substance and FREELY FILTERED and not reabsorbed and not secreted.
78
How does percentage of SODIUM remaining in filtrate change as filtrate moves through nephron?
Two thirds reabsorbed in PCT, the descending limb is impermeable to sodium, and the ascending limb absorbs another 20% or so. Last 20% reabsorbed equally across DCT and collecting duct.
79
How does percentage of GLUCOSE remaining in filtrate change as filtrate moves through nephron?
100% reabsorbed in PCT.
80
How does percentage of CREATININE remaining in filtrate change as filtrate moves through nephron?
Creatinine is freely filtered and actively secreted into the filtrate. It is also not absorbed. Therefore, as a percentage of the filtrate that is remaining, creatine would rise above 100%.
81
SUMMARY: How do epithelial cells of the nephron differ?
82
What syndromes are caused by single gene mutations that affect tubular function? (x3)
Renal tubule acidosis, Bartter syndrome, Fanconi syndrome (Dent’s disease).
83
What is renal tubule acidosis? Where does mutation effect?
It is a metabolic acidosis in the BLOOD from lowered HCO3- and increased CL-, or failure to excrete potassium – leads to impaired growth and hypokalaemia (low potassium). EFFECT PROXIMAL CONVOLUTED TUBULE.
84
What is the mechanism underlying renal tubule acidosis? (x2)
(1) Failure to excrete potassium, so urine does not remove acidity from blood. (2) Problem with carbonic anhydrase, so protons are not produced for excretion.
85
What is Bartter syndrome?
Excessive electrolyte SECRETION.
86
What happens in antenatal Bartter syndrome?
Premature birth and polyhydramios (lots of amniotic fluid). Severe salt loss, metabolic alkalosis, hypokalemia (reduced K+) and renin and aldosterone hypersecretion (because of fall in salt).
87
What is the mechanism of Bartter syndrome? Where does the mutation effect?
ASCENDING LOOP OF HENLE. Mutations in the following mechanism – photo.
88
What is Fanconi syndrome?
Increased excretion of uric acid, glucose, phosphate, low molecular weight proteins, and bicarbonate in the urine.
89
What does Fanconi syndrome affect?
Disease of the proximal tubules.
90
What is the mechanism of Dent’s disease?
Mutation affects acidification of endosome carrying protein into proximal convoluted tubule cell, so receptor that carries the protein cannot dissociate: * NORMALLY: H+ gets pumped into the endosome containing the protein-receptor complex, and pH goes down. At the same time, positive charge goes up, so electrochemical gradient means that it becomes harder to pump further H+ ions into the endosome. * More H+ ions need to be moved into the endosome to lower the pH enough for the protein-receptor complex to dissociate. SO, there is a counter-transporter that takes one H+ out (meaning some acidity is lost), and 2Cl- are pumped in – so more protons can be pumped in to lower pH further. * MUTATION: affects counter transport, so you cannot not get to low enough pH to dissociate the protein.
91
How is Na+ reabsorption increased in the nephron and Na+ levels preserved? (x5 components of the mechanism)
1. LOW BLOOD PRESSURE increases sodium reabsorption by REDUCING GFR; so more Na+ retained in blood rather than entering filtrate which increases water retention. Low BP also promoted by increase in SNS activity. 2. Another effect of increased SNS means PCT reabsorbs more sodium. 3. SNS activity activates juxtaglomerular apparatus --\> grannular cells secrete renin which increases Angiotensin II. Angiotensin II (increases blood pressure by vasoconstriction and) stimulates uptake of Na+ in PCT. 4. Angiotensin II also increases aldosterone levels which affects DCT and collecting duct by increasing Na+ uptake. 5. Low tubular sodium at juxtaglomerular apparatus also increases production of renin which increases angiotensin II and aldosterone – to mediate the same effects described above.
92
How does ANP increase GFR? (x4)
Atrial naturietic peptide increases GFR by by (i) increases diameter of afferent (and systemic blood vessels), and constricts efferent arteriole; (ii) reduces PCT activity; (iii) suppresses renin release at juxta apparatus; (iv) reduces Na+ reabsorption in collecting tubules esp. thick ascending limb. OVERALL = reduce blood pressure.
93
What triggers ANP release?
Repsonse to atrial stretch from increased blood pressure – remember, ANP reduces blood pressure.
94
Where is ANP produced? What else is produced with it?
Produced in atria with BNP.

Year 1 Urinary (8 decks)

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