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104-theme 3-the excretory system and renal function > formation of urine > Flashcards

formation of urine Flashcards

1
Q

what are the 5 stages of urine formation?

A
  • glomerulus- filtration of blood
  • proximal tubule- reabsorption of filtrate, secretion into tubule
  • loop of Henle- concentration of urine
  • Distal tubule- modification of urine
  • collecting duct- final modification of urine
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2
Q

what is the force of filtration?

A
  • blood pressure

- differing diameter of afferent and efferent arterioles

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3
Q

what is glomerular filtration rate? 5

A
  • 125ml/min
  • rate at which glomerular filtrate is produced
  • can be measured clinically as an indicator of renal function
  • generally remains the same even when systemic BP changes
  • this is due to a regulatory mechanisms known as auto-regulation of renal blood flow
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4
Q

what is glomerular filtration? 4

A
  • the first stage of urine formation
  • ultrafiltration= filtration on a molecular scale
  • all small molecules are filtered
  • cell and large molecules remain in the blood
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5
Q

what is glomerular filtration dependent on? 2

A
  • blood pressure

- renal blood flow

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6
Q

what does glomerular filtrate have to pass through? 3

A
  • pores in the glomerular capillary
  • the basement membrane of Bowman’s capsule (includes contractile mesangial cells)
  • epithelial cells of Bowman’s capsule (podocytes) via filtration slits into capsular space
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7
Q

describe auto-regulation of renal blood flow? 2

A
  • renal blood flow is subject to auto regulation over a broad range of systemic BPs
  • persists in denervated kidneys and isolated kidneys, so its not a neuronal or hormonal response but a local effect
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8
Q

what are the two hypotheses for auto regulation of renal blood flow?

A

Myogenic- autoregulation is due to response of renal arterioles to stretch (starlings’ law)
Is BP decreases, renal artery and efferent arterioles automatically constrict to maintain a constant renal blood flow

Metabolic- renal metabolites modulate afferent and efferent arteriolar contraction and dilation

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9
Q

describe reabsorption from the proximal tubule? 4

A
  • glomerular filtrate enters the proximal tubule
  • 60-70% of filtered water, Na+, HCO3-, Cl-, K+ and urea are reabsorbed
  • almost all of glucose, amino acids and filtered proteins are reabsorbed
  • the driving force for this reabsorption is Na+/K+ ATPase
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10
Q

describe hoe NA+/K+ ATPase can drive reabsorption? 4

A
  • Na+/K+ ATPase pumps out Na+ from cells into the blood against the chemical and electrical gradients
  • this requires ATP
  • this is accompanied bu the entry of K+ ions which rapidly diffuse out of the cell
  • 3Na+ in and 2K+ out
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11
Q

describe sodium reabsorption from the PT? 4

A
  • against chemical gradients
  • PT cells have a low intracellular Na+ concentration due to the action of the NA+/K+ ATPase
  • PT cells have an overall negative charge due to the presence of intracellular proteins
  • Cl- follows Na+ by facilitated diffusion, phosphate and sulphate are cotransported with Na+
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12
Q

describe water reabsorption from the PT? 6

A
  • 60-70% of filtered water is reabsorbed in the PT, active transport of Na+ out of PT cells is the driving force
  • movement of solutes reduces the osmolality of tubular fluid and increases osmolality or interstitial fluid
  • a net flow of water from tubule lumen to lateral spaces occurs by transcellular and paracellular routes
  • transcellular routs involve aquaporins channels located on apical and basolateral surfaces
  • there is no active water reabsorption along the nephron- it occurs by osmosis and it follow sodium
  • the PT is highly permeable to water. water flow from the tubule to lateral spaces occurs by paracellular and transcellular routes
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13
Q

describe how transcellular routes involve aquaporins? 5

A
  • aquaporins are specific water channels located in the cell membranes
  • there are 13 different types, 6 in the kidney
  • Aquaporin-1 (AQP-1)
  • Abundant distribution in proximal tubule. Also, other parts of the tubule where water is reabsorbed- descending limb of LOH
  • Aquaporin-2 (AQP2)
  • Present in collecting duct on apical surface. AQP-2 channel expression is controlled by antidiuretic hormone (ADH)
  • Aquaporins-3 & 4 (AQP3 and AQP4)
  • Present on basolateral surface of tubular cells involved in water reabsorption
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14
Q

describe glucose reabsorption from the PT? 2

A
  • glucose is co-transported into the PT with Na+ very efficiently so very little is excreted
  • urinary excretion of glucose indicates diabetes
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15
Q

describe SGLT2 inhibitors?

A
  • possible new drug for controlling type 2 diabetes
  • the idea is to make diabetic patients excrete more glucose leading to an overall hypoglycaemia effect
  • dapagluflozin
  • canagluflozin
  • empagliflozin
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16
Q

describe further reabsorption in the PT? 4

A
  • POTASSIUM- 70% of filtered K+ is reabsorbed in the PT, mostly passively via tight junctions
  • UREA- 40-50% filtered urea is reabsorbed passively in the PT down its concentration gradient
  • AMINO ACIDS- 7 independent transport processes for reabsorption of AAs from the PT- depends on the type of AA, type of AA, high Tm for transport so that as much as possible is reabsorbed from PT
  • proteins- reabsorbed from PT via receptor- mediated endocytosis
17
Q

describe protein reabsorption form the PT? 3

A
  • small amounts of the protein pass into filtrate via the glomerulus
  • these are reabsorbed by pinocytosis- vesicles are transported into the cell, degraded by lysosomes and amino acids returned to the blood
  • only cited transport capacity (low Tm) proteinuria is a sign of glomerular damage and impending renal failure
18
Q

describe secretion into the PT? 2

A
  • some endogenous substances and drugs cannot be filtered at the glomerulus- this may be due to their size or protein binding
  • specialised pumps in the PT can transport compounds fro the plasma into the nephron
19
Q

describe secretion of PAH (para- hippurate) into the PT? 4

A
  • PAH is secreted into the PH from the blood
  • not an endogenous compound so PAH can be used as a tool to measure tubular secretion
  • transported into PT cells from blood with alpha-ketoglutarate or other di/tri carboxylates
  • transported out of the PT ells in exchange for another anion present in the PT lumen
20
Q

describe the loop of Henle? 6

A
  • Tubular fluid is further modified in this part of the nephron
  • The aim here is to recover fluid and solutes from the glomerular filtrate
  • The process can be divided into two stages:
  • Extraction of water in the descending limb
  • Extraction of Na+ and Cl- in the ascending limb
  • This process is of more importance for juxtamedullary nephrons which have longer loops of Henle
21
Q

describe the thin descending limb? 3

A
  • Cells are flat, no active transport of salts
  • But freely permeable to water via Aquaporin-1 channels
  • Also, some movement of water via tight junctions
22
Q

describe the thick ascending limb? 3

A
  • Tubular wall is impermeable to water
  • But has specialised Na+/K+/2Cl- co-transporters
  • Transport Na+, K+, Cl- reabsorbed- but no water
23
Q

describe the concentration of the fluid in the LOH at different points? 5

A
  • Fluid entering LOH from proximal tubule is isotonic
  • Water reabsorbed out of descending LOH
  • By the tip of the LOH, the filtrate is hypertonic (very concentrated)
  • Solutes are then pumped out of the ascending LOH
  • By the end of the LOH, the filtrate entering the distal tubule is hypotonic
24
Q

describe countercurrent multiplication? 9

A
  • Creates large osmotic gradient within the medulla
  • Facilitated by Na+/K+/2Cl- transport in ascending limb of the LOH
  • Permits passive reabsorption of water from tubular fluid in descending LOH
  • .
  • Urea also plays a part
  • Active transport of NaCl contributes- the remainder is due to urea
  • Urea freely filtered at the glomerulus
  • Some reabsorption in proximal tubule, but LOH and distal tubule relatively impermeable to urea
  • Urea can diffuse out of the collecting duct into the medulla down its concentration gradient
  • This adds to the osmolality of medullary interstitial
25
Q

describe the distal tubule? 11

A
  • The distal tubule performs further adjustment of urine
  • Active absorption and secretion of solutes takes place here
  • Sodium and chloride ions are actively reabsorbed from the tubular fluid
  • This is an exchange for potassium or hydrogen ions which are secreted into the tubular fluid
  • Na+ and Cl- exchanged for K+ throughout DT
  • Na+ exchanged for K+ in late DT and early collecting duct
  • This involves specialised cells called principal cells
  • These cells are sensitive to aldosterone
  • Na+ exchanged for H+ in DT and early collecting duct
  • This involves specialised cells called intercalated cells
  • Subtypes exist called alpha and beta intercalated cells
26
Q

describe principal cells? 3

A
  • Exchange Na+ for K+ in the late DT and early collecting duct
  • This involves specialised cells called principal cells which are sensitive to aldosterone
  • This exchange forms parts of the RAAS
27
Q

what do alpha-intercalated cells do? 2

A
  • Secretes acid via H+/Na+ or H+/K+ exchange involving ATPase or H+ATPase
  • Reabsorbs bicarbonate
28
Q

what do beta- intercalated cells do? 2

A
  • Secrete bicarbonate via pendrin

- Reabsorbs acid

29
Q

describe the collecting duct? 7

A
  • The collecting duct is relatively impermeable to movement of water and solutes
  • However, the permeability of the collecting duct can be considerably increased the action of ADH
  • The most important hormone that regulates water balance, it is a nonapeptide
  • Also known vasopressin or 8-arginine-vasopressin
  • Release from the posterior pituitary subsequent to hypothalamic inputs
  • Plasma half-life is 10-15 minutes
  • ADH acts vasopressin receptors on basal membrane of principal cells in DT and collecting duct cells leading to activation of intracellular water channels
30
Q

describe the modification of urine volume by maximal circulating ADH? 4

A
  • Collecting duct becomes permeable to water due to maximal AQP2 insertion so water reabsorption occurs
  • Reabsorbs up to 66% of the water entering the collecting duct
  • Delivery of fluid to the collecting duct is low
  • Urine volume can be reduced to 300ml/day
31
Q

describe the modification of urine volume when there is no circulating ADH? 3

A
  • Reabsorption of water occurs at various sites in the nephron
  • However, the collecting duct wall becomes impermeable to water due to no AQP2 so a large volume of water is excreted
  • Lack of ADH: diabetes insipidus- treated using synthetic ADH
32
Q

describe diabetes insipidus? 10

A
  • Nephrogenic:
  • Due to the inability of kidney to respond normally to ADH
  • Treatment:
  • Chlortalidone (diuretic)
  • Indomethacin (anti-inflammatory)
  • .
  • Neurogenic:
  • Due to the lack of ADH production by the brain
  • Treatment:
  • Desmopressin (ADH analogue)
  • Vasopressin
  • Carbamazepine (anti-convulsive)
  • .
  • Dipsogenic
  • Gestational
33
Q

what is SIADH? 4

A
  • syndrome of inappropriate ADH
  • Excessive release of ADH due to head injury, unwanted effects of drugs
  • SIADH can cause hyponatraemia and possibly fluid overload
  • Treatment:
  • V2 receptor blockers (ADH inhibitors)
34
Q

where is ADH synthesised and released?
what increases release? 4
what inhibits release?

A
  • ADH synthesised in the hypothalamus and then stored and released from the posterior pituitary
  • Agents which increase ADH release:
  • Nicotine
  • Ether
  • Morphine
  • Barbiturates
  • .
  • .
  • Agents which inhibit ADH release:
  • Alcohol
35
Q

what happens to the water and solutes that are reabsorbed from the tubule?

A
  • It is all taken back into the peritubular vessels and vasa recta surrounding the tubule

104-theme 3-the excretory system and renal function (14 decks)

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