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Urinary physiology Flashcards

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1
Q

What are the functions of the kidneys?

A

Removes metabolic waste from blood by filtration and excretion
Regulates plasma electrolytes and blood pressure (by renin-angiotensin mechanism)
Help to stabilize the PH
Reabsorption of small molecules (amino acids. Glucose, and peptides)
Produces erythropoietin (a stimulant of RBC production by bone marrow)

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2
Q

What is the vertebral levels of the kidneys?

A

Retroperitoneal position at T12-L3

Partly peritonised

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3
Q

What does the urinary system develop from?

A

Intermediate mesoderm + cloaca
Intermediate Mesoderm (nephrogenic cord/urogenital ridge) gives rise to kidney & ureter
Cloaca gives rise to urinary bladder & urethra

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4
Q

What do the kidneys develop from?

A

Arises from intermediate mesoderm forming the urogenital ridge either side of the aorta
Develops into three sets of tubular nephric structures
Phronephros
>Mostly progresses, cranial most tube
Mesonephros
Meranephros

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5
Q

What happens to the mesonephros?

A

Located along the midsection of the embryo and develops into mesonephric tubules + duct
Tubules regress, however the duct persists opening into the cloaca

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6
Q

What happens to the metanephros?

A

Gives rise to the definitive adult kidney.
Develops from an outgrowth of the caudal mesonephric duct, theureteric bud, and from a condensation of nearby intermediate mesoderm, themetanephric blastema.

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7
Q

What does the metanephric blastema go on to create?

A 
excretory portion of kidney (nephron):
Excretory tubules (Nephrons)
-Bowman’s Capsule
-PCT
-Loop of Henle
-DCT
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8
Q

What does the uteric bud go on to form?

A

collecting portion of kidney:
Collecting ducts
Calyces
Ureters

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9
Q

How does the nephron develop?

A

Metanephric vesicle turns into the metanephric tubule
This merges with the collecting duct
The glomerulus then invaginates the nephron
The uriniferous tubule lengthens

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10
Q

Why and how do the kidneys ascend?

A

Mainly due to differential growth of lower body inferiorly away from kidneys (appear to “ascend”)
Kidneys come to lie retroperitoneally in upper abdomen (T12-L3)
Hilum rotates from ventral to medial (~90degrees)
Ascent stops when contact with adrenal (suprarenal) glands
Segmental breakdown and reform of vascular supply during ascent
Accessory renal arteries (always at inferior pole)

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11
Q

How does the cloaca divide?

A 
Cloaca divided by urorectal septum into urogenital sinus and rectum.
Parts of UG sinus:
Cranial
Pelvic
Caudal
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12
Q

How does the trigone develop?

A

Trigone derived from absorption of mesonephric ducts

Mesodermal lining replaced with endodermal epithelium

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13
Q

What does the urogenital sinus become?

A 
Urogenital sinus gives rise to:
Cranial part 
 - forms bladder
Middle part 
- forms prostatic and membranous urethra in males, and entire urethra in females
Caudal part 
- forms penile urethra in males
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14
Q

What is the process of filtration?

A

Receives ~20-25% of CO
No red blood cells and only a fraction of the plasma is filtered through bowman’s capsule
Remainder passes via efferent arterioles into peritubular capillaires and then renal veins

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15
Q

What is filtration dependant on?

A

Filtration dependent on hydrostatic forces + oncotic pressure

Glomerular capillary pressure higher than other capillaries because afferent arterioles short + wide so high hydrostatic pressure
Combined with efferent being thin builds up pressure to be able to filter

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16
Q

What affects GFR?

A

Dependent on afferent/efferent diameter controlled by
Sympathetic VC nerves –> afferent and efferent constriction, greater sensitivity of afferent arteriole.
b) Circulating catecholamines –> constriction 1°ily afferent
c) Angiotensin II –> constriction, of efferent at [low], both afferent and efferent at [high].

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17
Q

What is autoregulation?

A

Renal vasculature has intrinsic ability to adjust resistance in response to arterial BP changes
BF/GFR kept almost constant (autoregulation)
When MBP is 50 or less filtration would stop
Independent of nerves or hormones
Dilation of afferent arterioles if mean arterial pressure decreases, constriction if increases

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18
Q

What happens in the kidneys when bloodpressure is compirmised?

A

I.e in haemorrhage
Activation of sympathetic VC nerves and AII can override autoregulation liberating blood to immediately more important organs
However, prolonged exposure to a reduction on renal BP can lead to irreparable damage and potential death

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19
Q

What is responsible for reabsorption?

A

Peritubular vessels

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20
Q

How does reabsorption happen in the kidneys?

A

Offers resistance along whole length of peritubuluar vessels, so large pressure drop allowing hydrostatic pressure to fall as well
PPC very low because hydrostatic P overcoming frictional resistancein efferent arteriols
PP high compared to normal, loss of 20% plasma concentrates plasma protein
PP&raquo_space; PPC only reabsorption

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21
Q

What are the mechanisms of reabsorption?

A

Many substances reabsorbed by carrier proteins
Have maximum transport capacity due to saturation of carriers
If maximum exceeded, rest is excreted
Glucose is one such molecule, freely filtered. Up to 10mmoles will be reabsorbed

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22
Q

How does the kidney regulate substances?

A

Sulphate and phosphate ions for example
Their Tm set at a level where normal plasma causes saturation
Causes excretion of anything above normal

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23
Q

How is sodium reabsorbed?

A

Reabsorbed via active transport in proximal tubule
Chlorine follows the electrical chemical gradient
Causes osmotic force that brings water with it

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24
Q

What is the process of reabsorption for the main ions?

A

Sodium by active transport
Electrochemical gradient drives anion reabsorption
Water moves by osmoles
Concenterations of other solutes increases as other fluid in lumen decreases
>Non actively reabsorbed solutes depends on the amount of water removed, and permeability of membrane to any solute

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25
Why is sodium reabsorption so important for the kidneys?
Concentrates the tubule creating greater concentration gradient for passive molecules High sodium in tubule facilitates glucose transport, low sodium inhibits as they share the same molecule from the lumen side
26
What is tubular secretion>
Transport substances from peritubular capillaries into the lumen Important for protein bound molecules due to restricted filtration Carrier proteins not very specific so that organic acids can be used for other molecules like drugs
27
How do the kidneys handle potassium?
Balance essential for life (based on Tm) Reabsorbed at proximal tubule Any increase in renal tubule cell potassium will lead to postassium secretion. And reduction in intracellular potassium leads to decreased secretion.
28
How does aldosterone affect potassium secretion?
Secretion also regulated by aldosterone Increase in potassium in ECF stimulates aldosterone release Aldosterone stimulates kidneys to increase tubule cell potassium secretion Also stimulates sodium reabsorption at distal tubule Hydrogen ions actively secreted from tubule cells to maintain acid/base balance
29
What is the maximum concentration of urine?
4x concentration of plasma
30
What is obligatory water loss?
Waste products + excess ions that must be excreted every day ~ 600mosmoles Requires at least 500mls of water to be excreted Must ingest water otherwise will urinate to death If excess water intake can have 10x dilution
31
What mechanism is behind water being extracted form urine?
In loop of henle, the ascending limb actively co-transports sodium/chlorine out of tubule lumen into intersitium. Impermeable to water Descending limb is freely permeable to water, buy relativelt impermeable to sodium chloride
32
What is the process of the loop of henle?
Descending limb exposed to greater osmolarity in interstitium, water moves out to equate it Water reabsorbed into the vasa recta (no longer in interstitium) Concentrated fluid in descending limb delivers high concentration to ascending limb Here sodium chloride Is actively transported out, further concentrating interstitium Net effect, progressively concentrated as it moves down descending limb Progressively diluted as it moves up ascending limb Never more than 200osmole gradient at any horizontal level
33
What effect does furosemide have on the loop of henle?
Stops use of active transporter of NaCl from ascending limb so all concentration differences lost - isotonic urine
34
What does the counter current in the loop of henle accomplish?
Significance - increasingly concentrated gradient in interstitium Functions of vasa recta 1. Provide O2 for medulla. 2. In providing O2 must not disturb gradient. 3. Removes volume from the interstitium
35
What are the vasa recta?
Specialised arrancement of peritubular capillaries Arranged in hair-pin loops so they do not interfere with the gradient Freely permeable to water and solutes flow rate through the vasa recta is very low so that there is plenty of time for equilibration to occur with the interstitium, further ensuring that the medullary gradient is not disturbed
36
What controls the permability of the collecting duct?
ADH
37
What is ADH?
A polypeptide synthesises in hypothalamus Posterior pituirary hormone Half life ~10 minutes so can be rapidly adjusted to body's need
38
What is the primary function of ADH?
Plasma osmolarity control When plasma osmolarity pressure increases, ADH secretion increases Changes in neuronal discharge mediated by osmoreceptors in anterior hypothalamus Other receptors mediate thirst
39
What is the mechanism of osmoreceptors?
When high osmolarity, water leaves cell shrinking it Stretch sensitive ion channels activated leading to more ADH secretion When low osmolarity water enters cell swelling it >Decrease in ADH Small changes in either direction lead to rapid secretion/ inhibition of ADH Osmolarity and not tonicity
40
How does ADH achieve its effect?
Concentrates urine in the collecting duct via controlling its permeability Due to water channels in luminal membrane
41
What happens in maximal ADH levels?
Small volume of highly concentrated urine Water absorbed by vasa recta 1200 mOsM
42
What happens in the absence of ADH?
Colloecting duct impermeable to water, so no water moves out Therefore no change in water content Some ions can be further absorbed, so osmolarity can decrease further
43
What happens to urea in the presence of ADH?
In presence of ADH, water moving from collection ducts concentrates the urea in the ducts Permeability of membrane to urea increased by ADH So in antidiurectics with high ADH levels, more urea is reabsorbed in order to save water Water conservation more important than urea effects
44
What happens to the ECF volumes with varying levels of ADH?
Increase­ ECF volume with decrease [ADH] Decrease ECF volume with increase ­ [ADH] Inverse relationship Low pressure receptors in L/R atria + great veins - monito return of blood to heart High P receptors carotic/aortic arch baroreceptors If fluid levels drop, like in haemmorhage, ADH increases
45
What stimuli increase ADH release?
Pain, emotion, stress, exercise, nicotine, morphine. Following traumatic surgery, inappropriate ADH secretion occurs, need to be careful about monitoring H2O intake.
46
What stimuli decrease ADH?
Alochol | Caffiene
47
What is diabetes insipidus?
Hypothalmic areas become diseased or otherwise damaged Or collecting duct insensitive to ADH Patients characterised by polyuria and polydipsia Treated by giving ADH
48
What is peripheral diabetes insipidus?
Peripheral DI when collecting duct unresponsive to ADH can't give ADH, >normally secondary to hypokalaemia/calcaemia >returns to normal after ion disorders corrected
49
What is sodium regulation dependant on?
Dependent on high/low pressure baroreceptors
50
How does a decrease in ECF volume affect sodium regulation?
Decrease in blood pressure. Detected by carotid sinus Sympathetic discharge + ADH release Causes renal arterial constriction + renin and increase in angiotensin II End result increase in proximal tubule NaCl + water reabsorption Increase in aldosterone, leading to distal tubule reabsorption
51
What does sympathetic innervation of the kidneys lead to?
Increased arteriolar constriction and renin The increased renin leads to more angiotensin II being produced ATII leads to sodium reabsorption from proximal tubule due to decrease in peritubular hydrostatic pressure Also leads to more aldosterone thus increase in sodium reabsorption in distal tubule
52
What is angiotensin important for?
Important in regulation of distal tubule sodium reabsorption >Increases potassium secretion at distal tubule Increase in weight due to water retention >Volume expansion
53
What does prolonged aldosterone lead to?
Stimulates ANP from atrial cells >Loss of sodium/water (Although continued loss of potassium)
54
What is the juxtaglomerular apparatus?
Smooth muscle of the media of the afferent arteriole, just before it enters the glomerulus has become specialized, containing large epithelial cells with plentiful granules = Juxtaglomerular cells (JG). They are closely associated with a histologically specialized loop of the distal tubule = the macula densa. The two together form the Juxtaglomerular apparatus. Produce renin
55
What is renin?
Proteolytic enzyme acting on angiotensin Produced by JG cells Splits angiotensin I allowing it to be converted into angiotensin II by ACE
56
What is the function of angiotensin?
Angiotensin stimulates aldosterne secreting cells in zona glomerulosa of adrenal cortex Aldosterone passes in the blood to the kidney where it stimulate sodium reabsorption in distal tubule Potent vaso constrictor - contributes to TPR increase Stimulates ADH secretion Stimulates thirst mechanism
57
Whatt influences renin release?
Increase when pressure in afferent arteriole decreases Increased by Sympathetic nerve activity (release by b1 cells) Inversely proptional to rate of delievery of NaCl at macula densa Angiotensin feedback control ADH inhibits renin release
58
How is GFR regulated?
When GFR increases (and hence flow past macula densa) >Macula densa sends signals to afferent arterioles to constrict Resistance in afferent article increases Hydrostatic pressure in glomerulus decreases And thus GFR decreases Opposite to increase GFR
59
What effect does loss of brain perfusion + loss of sufficient volume have on ADH + fluid balance?
Normally, osmolarity is main determinant of ADH >But if sufficient volume change to compromise brain perfusion, volume becomes primary drive Once volume is restored, then osmolarity will be normalised
60
What is ANP?
Atrial natriutetic peptide Promotes sodium excretion Counteracts aldosterone sodium reabsorption Lowers blood volume
61
What is osmotic diuresis?
In uncontrolled DM where BG exceeds maximum reabsorptive capacity Net result less water and sodium reabsorbed + glucose Results in large volume of isotonic urine and venous pressure decreases >Releases ADH but lack of intersitial gradient means inneffective Severe salt/water depletion Potential hyperglycaemic coma
62
What is the process of osmotic diuresis in the proximal tubule?
Glucose remains in tubule and exerts osmotic effect to retain water Sodium concentration decreased as more water >Therefore sodium gradient decreased and thus reabsorption Furthermore decreased ability to absorb glucose due to shared synport with sodium
63
What is the process of osmotic diuresis in the loop of henle + distal tubule?
In descending limb of loop of henle movement of water out of the tubule is reduced Due to osmotic gradient reduced, thus lower concentration of fluid Fluid in ascending limb is thus less concentrated, and considerable reduction in volume of NaCl/water reabsorbed Interstitial gradient gradually abolished Large volume in distal tubule inhibits renin release, thus less sodium reabsorbed
64
What are the sources of pH changes?
Respiratory acid | Metabolic acid
65
How is respiratory acid formed?
Formation of carbonic acid Usually not a net contributor because increase in acid causes increase in ventilation to get rid of it Problems occur if lung function impaired
66
How is metabolic acid formed?
Via metabolism Inorganic acids - Containing amino acids (Sulphuric and phosphoric acids) from phospholipids Organic acids - fatty/lactic acids In normal diet net gain to body of hydrogen
67
What are buffers?
Minimise changes in pH when hydrogen's added/removed pH definied in terms of ratio of base to acid Exracelular bufers >Need 20 units of bicarbonate to carbonic acid
68
What are the normal ranges for biochem?
pH - 7.4: 7.37-7.43 pCO2 5.3kpa: 4.8-5.9 (4ommHg: 36-44) HCO3 24mmoles/l: 22-26
69
How is the buffer system maintained?
To bring pH down, H+ + HCO3- forms carbonic acid Carbonic acid dissolves in water to form water + carbon dioxide To stop the equilibrium, ventilation is increased to decrease CO2 Allows for more carbonic acid to dissolve and keeps pH constant H+ has not been elimited from the body, only buffered Ventilation decreases to free up the hydrogen ions if an increase in pH
70
How can pH be eliminated from the body?
Via kidneys | \excretion coupled to regulation of plasma bicarbonate
71
What are the other buffers in the ECF?
Plasma proteins | Dibasic phosphate
72
What are intracellular buffers?
Proteins, organic/inorganic phosphates, >in erythrocytes haemoglobin Buffering causes changes in plasma electrolytes to maintain chemical neutrality. >Movement of hydrogen must be accompanied by Cl-, or exchanged for a cation like K+ In acidosis, K+ out of cells into plasma can cause hyperkalaemia and potential death Bone carbonate provides additional store of buffer, but in chronic renal failure can lead to wasting of bones
73
How do the kidneys regulate bicarbonate?
Reabsorbs filtered bicarbonate Generated new bicarbonate Both depend on active hydrogen ion secretion from tubule cells into lumen
74
Hos is bicarbonate reabsorbed by the kidneys?
Active H+ secretion from tubule cells coupled to passive Na+ reabsorption Filtered bicarbonate reacts with secreted hydrogen to form carbonic acid. >IN presence of carbonic anhydrase in luminal membrane it dissolves in to carbon dioxide/water CO2 freely permable and enters cell Within cell, CO2 forms carbonic acid again, and dissociates into H+ and bicarbonate Hydrogen ions secreted Bicarbonate pass into peritubular capillaries with sodium
75
What is the normal pH range of urine?
4.5-5 - 8 | Buffered in urine as well
76
What is titratable acidity?
1. Na2HPO4 in the lumen. One Na+ is reabsorbed in exchange for secreted H+. >This monobasic phosphate removes H+ from the body. 2. Source of new bicarbonate indirectly from CO2 from blood. Enters tubule cells, forms carbonic acid + dissociates. >New CO3- passes into peritubular capillaries with Na+ 3. Occurs in distal tubule via K+ ions not reabsorbed 4. Dependent on carbon dioxide in blood
77
How is ammonium excreted?
Generates new bicarbonate and excretes hydrogen >Only used for acid loads NH3 is lipid soluble, NH4+ is not Produced via desegregation of amino acids. Moves into tubule lumen and combines with excreted H+ NH4+ then combines with Cl- to form NH4Cl which is excreted New bicarbonate absorbed with sodium In proximal tubule, NH4+/Na+ cotransporter, but net result same When pH falls, increase in renal glutaminase activity to produce more ammonium ions Takes 4-5 days to reach maximal effect Takes time to switch off as well
78
What is respiratory acidosis?
pH fallen due to respiratory change Reduced ventilation and therefore retention of CO2 Causes increase secretion of hydrogen ions and increase in bicarbonate but takes time High PCO2
79
What are the acute causes of respiratory acidosis?
Drugs depressing medullary respiratory centre >Barbituates/opiates Obstructions of major airways
80
What are the chronic causes of respiratory acidosis?
Lung disease >Bronchitis, emphysema, asthma Blood gases never normalised due to primary disturbance remaining unresolved Problems develop if patients with lung disease develops renal dysfunction
81
What is respiratory alkalosis?
Fall in PCO2 through increased ventilation Alkaline conditions dealt with via bicarbonate reabsorptive mechanism Less hydrogen secreted, thus less bicarbonate reabsorbed Ventilation must be normalised to correct disturbance
82
What are the acute causes of respiratory acidosis?
Voluntary hyperventilation Aspirin First ascent to altitude
83
What are the chronic causes of respiratory alkalosis?
Long term residence at altitude | Stimulates peripheral chemoreceptors to increase ventilation
84
What is metabolic acidosis?
Decrease in bicarbonate concentration Either loss of ions or increased buffering PCO2 must be decreased to protect pH Stimulates ventilation
85
What are the causes of metabolic acidosis?
Increase in hydrogen production (ketoacidosis in diabetics, lactic acidosis) Failure to excrete normal dietary load (ie renal failure) Loss of bicarbonate in diarrhoea
86
What is kussmaul sign?
Established clinical sign of renal failure o diabetic ketoacidosis Increased depth of ventilation
87
What does an increase in metabolic hydorgen ions lead to?
Immediate buffering in ECF and then ICF Respiratory compensation within minutes Renal correction of distrubance takes longer to develop the full response to increase hydrogen excretion and generate new bicarbonate Respiratory compensation delays renal correction, but protects pH
88
What is metabolic alkalosis?
Increase in bicarbonate, needs increase in PCO2 to protect pH
89
What are the causes of metabolic alkalosis?
Increase ion loss with vomiting Aldosterone excess, excess liquorice ingestion - increased renal hydrogen loss Excess administration of bicarbonate - only likely if renal function impaired Massive blood transfusions due to citrate in blood bank - 8 units before effect
90
What is the summary of respiratory acidosis?
Hydrogen ions: Increase pH: Decrease Primary disturbance: increase if PCO2 Compensation: Increase of HCO3
91
What is the summary of respiratory alkalosis?
Hydrogen ions: Decrease pH: Increase Primary disturbance: Decrease if PCO2 Compensation: Decrease of HCO3
92
What is the summary for metabolic acidosis?
Hydrogen ions: Increase pH: Decrease Primary disturbance: Decrease of HCO3 Compensation: Decrease if PCO2
93
What is the summary for metabolic alkalosis?
Hydrogen ions: Decrease pH: Increase Primary disturbance: Increase of HCO3 Compensation: Increase if PCO2
94
What factors affect creatinine?
Muscle mass Dietary intake Drugs
95
What is PAH?
Organic anion - para-amino-hippuric acid Used to measure renal plasma flow 90% normally cleared from plasma
96
How are the sphincters of the bladder controlled?
nternal sphincter - passively controlled | External - skeletal muscle - higher CNS
97
Where does micturition get its motor innervation from?
Pelvic nerves - parasympathetic >Increase in activity leads to increase in contraction of detrusor muscle Sparse sympathetic supply (hypogastric nerves) inhibit bladder >Close internal urethral sphincter >Prevent reflux of semen into bladder during ejaculation L1-L3 Somatic mononeurones (pudenal nerves) innervate external sphincter >Keeps sphincter closed, even against strong S2-S4 bladder contractions
98
Where does micturition gets its sensory innervation from?
Stretch receptor afferents from bladder wall As it filled increase innervation of nerves to spinal cord via interneurones Leads to Excitation of parasympathetic outflow Inhibition of sympathetic outflow Inhibition of somatic motoneurones to external sphincter Pathways to sensory cortex convey sensation of fullness
99
How is voluntary delay of micturition acheived?
Descending pathways Inhibit somatic motor neurones Relaxation of muscles of pelvic floor Perineal muscles and external sphincter can be contracted voluntarily, preventing urine flow flowing down the urethra or interrupting the flow once urination begins. After urination, female urethra empties by gravity. Urine remaining in the male urethra is expelled by contractions of the bulbocavernosus muscle
100
How is involuntary delay of micturition achieved?
Inhibit parasympathetic | Stimulate somatic nerves to external spincter
101
What can lead to abnormalities in micturition?
Interruption of afferent nerves interruption of both afferent and efferent nerves interruption of facilitatory and inhibitory descending pathways from the brain. In all 3 types the bladder contracts but the contractions are generally insufficient to empty the bladder completely and urine is left in the bladder.

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