Renal Physiology ( 15% ) Flashcards

1
Q

Which of the following regarding the nephron is true

  • The capillary endothelium has 4nm pores.
  • Filtration slits are approximately 8nm wide
  • Filtration slits formed by podocytes are closed by a thin membrane
  • Mesangial cells are located between the basal lamina and the podocytes.
  • Mesangial cells function only as flow regulation.
A

Filtration slits formed by podocytes are closed by a thin membrane

  • The capillary endothelium has 70-90nm pores
  • Filtration slits are approximately 25nm wide.
    • 8nm is the maximum size of filtered particles
  • Mesangial cells are located between the basal lamina and the endothelium
  • Mesangial cells function as flow regulation, Secrete BL/ECM, and take up immune complexes
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2
Q

regarding the tubules of the nephron which is false

  • the DCT has a thick brush border
  • the PCT is approximately 15mm long
  • the collecting duct epithelium contains intercalated cells
  • the longest loops of henle are in juxtamedullary nephrons
  • the juxtaglomerular apparatus contains 3 types of cells
A

the DCT has no brush border

3 cells in the JGA are Juxtaglomerular cells, lacis cells, and macula densa

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3
Q

Which of the following is false regarding the renal circulation

  • The lymph drainage is into the superior mesenteric vein
  • The descending vasa recta is non-fenestrated
  • The pressure drop across the glomerulus is in the order of 1-3mmHg
  • The kidneys receive approximately 25% of CO
  • Renal blood flow exhibit autoregulation across a perfusion pressure range of approximately 90-220mmHg
A

The lymph drainage is into the thoracic duct

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4
Q

Which of the following effects on the renal blood flow is true

  • Increased by NA
  • Increased by high protein diet
  • Increased by angiotensin II
  • Decreased by ACh
  • Decreased by DA
A

Increased by high protein diet

increases blood flow

  • decreased by NA (constricts vessels)
  • reduced by angiotensin II (arteriolar constrictor)
  • increased by ACh (venodilation)
  • increased by DA (renal venodilation)
  • Prostaglandins increase cortical flow, reduce medullary.
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5
Q

In the normal structure of the kidney

  • Mesangial cells can assist in the regulation of glomerular function
  • Basal lamina has filtration slits of 25nm
  • DCT has a less obvious brush border than the PCT.
  • The macula densa is located in walls of the afferent arteriole near the termination of the thick ascending loop of Henle.
  • The collecting ducts commence at the corticomedullary junction.
A

Mesangial cells can assist in the regulation of glomerular function

  • podocytes have filtration slits of 25nm.
    • endothelial cells have slits of 70-90nm
    • functionally 8nm is the size that can pass due to negative charge inside cells
  • DCT has no brush border (only in the PCT)
  • The macula densa is located in walls of the juxtaglomerular appartus, closely related to the a**fferent arteriole, near the termination of the thick ascending loop of Henle.
  • The collecting ducts commence in the cortex
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6
Q

Renal blood flow

  • Glomerular capillaries drain into peritubular veins.
  • Renal autoregulation is prevented by denervation.
  • Oxygen extraction is higher in the cortex than the medulla.
  • Kidney’s receive approximately 15% CO.
  • Angiotensin II causes greater constriction of the efferent than the afferent arteriole
A

Angiotensin II causes greater constriction of the efferent than the afferent arteriole

  • efferent arterioles drain into peritubular veins. Glom caps drain into efferent arterioles.
  • Renal autoregulation is maintained in denervation.
  • Oxygen extraction is higher in the medulla than the cortex.
    • Due to all the glomeruli, cortical blood flow is high, but as filtration is a passive process, oxygen extraction is low. The opposite applies to the medulla, which needs low blood flow to maintain its osmotic gradient, but has a high oxygen extraction
  • Kidney’s receive approximately 20-25% of CO
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7
Q

What is the GFR (ml/min) if the urinary concentration of inulin is 40mg/mL, the urinary flow rate is 60mL/h and the plasma concentration is 0.4mg/ml

  • 0.6
  • 2.6
  • 100
  • 160
  • 1000
A

100

GFR = ([urinary] / [serum]) x flow rate

= (40 / 0.4) x 1

=100

60ml/h = 1 ml/mon

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8
Q

The filtration fraction of the kidney is

  • 0.1
  • 0.2
  • 0.3
  • 0.4
  • 0.5
A

0.2

GFR/RPF

Total blood flow to kidneys 1.2-1.3L/min

RPF usually 700ml/min

GFR ~125ml/min

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9
Q

Which of the following would be best used for measuring GFR

  • Radiolabelled albumin
  • Inulin.
  • Deuterium oxide
  • Tritium oxide
  • Mannitol
A

Inulin.

Gold standard

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10
Q

given the following values, calculate the GFR: urine PAH 90, plasma PAH 0.3, urine inulin 35, plasma inulin 0.25, urine flow 1mL/min, Hct 40%

  • 120
  • 150
  • 180
  • 240
  • 400
A

150

RPF = 90 / 0.3 = ~300ml/min

GFR = 35/0.25 = 140ml/min

(do not need the haematocrit as this is just used to work out the total renal blood flow - TRBF = RPF x 1 / 1-hct)

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11
Q

What is the clearance of a substance when its concentration in plasma is 1mg/mL, its concentration in urine is 10mg/mL and urine flow is 2mL/min

  • 2mL/min
  • 10mL/min
  • 20mL/min
  • 200mL/min
  • clearance cannot be determined from the information given
A

= (10 / 1) x 2

=20ml/min

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12
Q

Regarding filtration in the nephron which is false

  • Contraction of mesangial cells decreases GFR
  • Particles less than approx 4nm are freely filtered
  • Angiotensin II and vasopressin causes mesangial cell contraction
  • Exchange across the glomerular capillaries is diffusion not flow limited.
  • Albuminuria in nephritis occurs without an increase in filtration size
A

Exchange across the glomerular capillaries is flow limited.

  • There is little in the way to stop small particles crossing.*
  • Ang II and vasopressin do cause contraction - if hypotensive, want to reduce GFR to preserve BP*
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13
Q

regarding tubuloglomerular feedback, which is true

  • tends to maintain renal blood flow.
  • the sensor is JG cell.
  • operates via contraction of the mesangial cells.
  • acts to reduce GFR if the flow rate in the ascending loop of Henle falls
  • GFR is modulated via contraction or dilation of the afferent arteriole
A

GFR is modulated via contraction or dilation of the afferent arteriole

  • tends to maintain the salt load to the distal tubule
  • the sensor is Macula densa
  • operates via relaxation of the mesangial cells.
  • acts to increase GFR if the flow rate in the ascending loop of Henle falls
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14
Q

The juxtaglomacular apparatus

  • Contains macular densa cells in afferent and efferent arterioles.
  • Contains juxtaglomerular cells in the afferent arterioles only.
  • Responds to a fall in arterial pressure by increasing renin secretion
  • Responds to an increase in Na concentration by increasing GFR.
  • Releases renin which is activated by angiotensin I.
A

Responds to a fall in arterial pressure by increasing renin secretion

  • Contains macular densa cells in the DCT.
  • Contains juxtaglomerular cells in the afferent, and to a lesser extent efferant arterioles
  • Responds to an increase in Na concentration by d**ecreasing GFR
  • Releases renin which activates angiotensin
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15
Q

renal autoregulation

  • the macula densa cells sense change in afferent arteriolar pressure.
  • falling GFR results in feedback to decrease efferent arteriolar pressure.
  • falling GFR results in an increase in renin secretion from the macula densa cells.
  • decreased macula densa concentration of NaCl results in dilation of the afferent arteriole
  • decreased GFR decreases NaCl reabsorption in the ascending loop of Henle.
A

decreased macula densa concentration of NaCl results in dilation of the afferent arteriole

Hypotonic fluid -> increase filtration as likely volume overloaded

  • Juxtaglomerula cells sense change in afferent arteriolar pressure.
  • falling GFR results in feedback to increase efferent arteriolar pressure/resistence (via Ang II)
  • falling GFR results in an increase in renin secretion from the JG cells
  • decreased GFR decreases NaCl reabsorption in the PCT
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16
Q

With regard to tubuloglomerular feedback

  • The GFR increases when flow through the distal tubule increases.
  • The macula densa on the afferent arteriole is the sensor.
  • The afferent arteriole is constricted by TXA2.
  • It is designed to maintain Na re-absorption.
  • It does not operate in individual nephrons.
A

It is designed to maintain Na re-absorption.

  • The GFR decreases when flow through the distal tubule increases.
  • The macula densa in the DCT is the sensor.
  • The afferent arteriole is constricted by adenosine
    • ​Increasing Na/Cl flow-> increased Na-K-ATPase activity in macula densa -> increased adenosine (due to increased ATP hydrolysis) -> Ca release from macula densa to smooth muscle -> vasoconstriction (and also reduced renin release by JG cells)
  • It does operate in individual nephrons - alters flow nephon to nephron (much like alveoli vary their flow depending on individual O2 concentration)
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17
Q

All of the following effect GFR except

  • Changes in renal blood flow
  • Urethral obstruction
  • Dehydration.
  • Oedema outside of the renal capsule
  • Glomerular capillary pressure
A

Oedema inside of the renal capsule

  • Dehydration increases plasma oncotic pressure*
  • Urethral obstruction increases hydrostatic pressure in bowmans capsule*
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18
Q

With regard to the kidney

  • Has optimum autoregulation over a range of 60-100mmHg.
  • Medullary blood flow is greater than cortical blood flow.
  • PGs decrease medullary blood flow
  • PGs increase cortical blood flow
A

PGs decrease medullary blood flow

PGs increase cortical blood flow

As per Ganongs both of these are correct

  • Has optimum autoregulation over a range of 90-220mmHg
  • Medullary blood flow is less than cortical blood flow.
    • Cortical blood flow needs to be high to have enough to filter the glomeruli
    • Medullary flow can be low as its actions are active (with the vasa recta etc)
    • Medullary O2 consumption is higher than cortical for these reasons too.
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19
Q
  1. concerning the glomerular filtration rate (GFR), it:
  • a. is approximately 250ml/min in an average sized normal man.
  • b. exceeds the clearance of a substance if there is net tubular reabsorption
  • c. is independent of the size of the renal capillary bed.
  • d. is greater for anionic than for cationic molecules of equal size.
  • e. is maintained despite a fall in systemic pressure below 90mmHg.
A

b. exceeds the clearance of a substance if there is net tubular reabsorption

  • a. is approximately 125**ml/min in an average sized normal man.
  • c. is dependent on the size of the renal capillary bed.
  • d. is less for anionic than for cationic molecules of equal size. due to the negative charge of podocytes
  • e. is maintained until a fall in systemic pressure below 90mmHg.
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20
Q
  1. GFR:
  • a. Is higher per body surface area in women
  • b. Increases with a decrease in MAP
  • c. Normally 80% of filtrate is reabsorbed
  • d. Is accurately estimated by serum creatinine
  • e. Decreases with ureteral obstruction
A

e. Decreases with ureteral obstruction

  • a. Is higher per body surface area in men
  • b. decreases with a decrease in MAP
  • c. Normally >**99% of filtrate is reabsorbed
  • d. Is roughly estimated by serum creatinine as this varies based on muscle mass, age, gender etc
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21
Q

In the loop of Henle

  • Descending limb is impermeable to water
  • Thin ascending limb is permeable to water
  • Thick ascending limb is permeable to water
  • Fluid in the descending limb becomes hypotonic
  • Fluid at the top of the ascending limb is hypotonic cf plasma
A

Fluid at the top of the ascending limb is hypotonic cf plasma

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22
Q

With respect to tubular function

  • Creatinine resorption is dependent on tubular flow rates
  • Creatinine is secreted by the tubules
  • Sodium is actively transported out of the thin portion of the loop of Henle.
  • glucose resorption occurs by passive diffusion mainly in proximal tubules.
  • urine acidification does not occur in the collecting tubules
A

Creatinine is secreted by the tubules

  • Creatinine resorption is independent of tubular flow rates
  • Sodium is actively transported out of the thick portion of the loop of Henle.
  • glucose resorption occurs by secondary active transport mainly in proximal tubules.
  • urine acidification ???? occur in the collecting tubules
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23
Q

Regarding renal tubular function

  • The clearance is less than the GFR if there is tubular secretion.
  • The active transport of Na occurs in all portion of the tubule.
  • Proximal tubular reabsorptate is slightly hypotonic.
  • Water can leak across tight junctions back into the tubule lumen
  • 30% of the filtered water enters the DCT.
A

Water can leak across tight junctions back into the tubule lumen

  • The clearance is more than the GFR if there is tubular secretion.
  • The active transport of Na occurs in most portions of the tubule, except the thin LoH
  • distal tubular reabsorptate is slightly hypotonic. Proximal tubule is isotonic
  • 15% of the filtered water enters the DCT - the reabsorption of this remainder determines urine conc/volume
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24
Q

Which is false about the loop of Henle

  • Descending loop is permeable to water
  • Ascending loop is impermeable to water
  • Chloride is transported out of the thick part of the ascending limb
  • At the top of the ascending loop the tubular fluid is hypotonic
  • Tubular fluid is hypertonic as it enters the descending limb
A

Tubular fluid is isotonic as it enters the descending limb

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25
Q

With respect to the counter current system

  • The loops of Henle act as counter current exchangers.
  • Solutes diffuse out of vessels conducting blood towards the cortex
  • Water diffuses out of the ascending vessels.
  • Water diffuses into the collecting ducts.
  • Counter current exchange is passive and can operate even if counter current multiplication ceases.
A

Solutes diffuse out of vessels conducting blood towards the cortex

ie the ascending LoH

  • The loops of Henle act as counter current multipliers.
    • LOH = CC multipliers. Vasa recta = CC exchangers
  • Water does not diffuses out of the ascending vessels, as they are Impermeable to water
  • Water diffuses out of the collecting ducts, assuming ADH is present
  • Counter current exchange is passive, but relies on CCM to set up its gradients or it ceases to function.
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26
Q

regarding the osmolality of renal tubular fluid it is

  • hypotonic in the loop of Henle.
  • isotonic in the PCT
  • hypertonic in the DCT.
  • hypotonic in the collecting duct. Hypotonic when it enters but then can vary
  • hypotonic in the PCT
A

isotonic in the PCT

  • hypertonic in the descending loop of Henle.
  • hypotonic in the DCT.
  • hypotonic early in the collecting duct, but if ADH is present can be very hypertonic by the end
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27
Q

regarding the PCT which is false

  • Na is co-transported out with glucose
  • Na is actively transported into the intracellular spaces by Na/K ATPase
  • The cells are characterized by a brush border and tight junctions
  • ADH increases the permeability of water by causing the rapid insertion of water channels into the luminal membrane.
  • Water moves out passively along osmotic gradients
A

ADH increases the permeability of water by causing the rapid insertion of water channels into the luminal membrane.

This occurs in the CD. PCT has aquaporin 1 in basolateral and apical membrane, and is not triggered by ADH

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28
Q

the thin ascending loop of Henle is

  • relatively permeable to water
  • relatively impermeable to Na
  • permeable to both Na and water
  • relatively impermeable to water
  • relatively impermeable to both Na and water
A

relatively impermeable to water

Reabsorbs solutes but less than thick asceding LoH i think

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29
Q

The thick ascending loop of Henle

  • Is impermeable to water
  • Has maximal permeability to NaCl.
  • Is relatively permeable to water.
  • Is impermeable to NaCl.
  • Is a site where there is no active transport of Na
A

Is impermeable to water​

  • Thin ascending LoH has maximal permeability to NaCl
  • Is relatively impermeable to water.
  • Is somewhat permeable to NaCl.
  • Is a site where there is active transport of Na.
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30
Q

What is the osmolality of the interstitium of the tip of the papilla

  • 200
  • 800
  • 1200
  • 2000
  • 3000
A

1200

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31
Q

with regard to osmotic diuresis

  • urine flows are much less than in water diuresis.
  • ADH secretion is almost zero
  • The concentration of the urine is less than plasma.
  • Increased urine flow is due to decreased water resorption in the proximal tubule and loop of Henle
  • Osmotic diuresis can only be produced by sugars such as mannitol.
A

Increased urine flow is due to decreased water resorption in the proximal tubule and loop of Henle

  • urine flows are much more than in water diuresis.
  • ADH secretion Can approach maximal
  • The concentration of the urine is more than plasma
  • Osmotic diuresis can be produced by sugars such as mannitol, and a**ny solute that is filtered but not absorbed
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32
Q

During an osmotic diuresis, which is true

  • The concentration of sodium delivered to the loop of Henle falls
  • The sodium concentration in the interstitium of the PCT falls.
  • Increased fluid load but decreased sodium load to the DCT.
  • The concentration gradient in the medullary pyramid rises.
  • Volumes of urine are less than a pure water diuresis.
A

The concentration of sodium delivered to the loop of Henle falls

  • The sodium concentration in the interstitium of the PCT rises as less water is absorbed
    • ​cf LoH and CD where the interstitial osmo falls as less Na is reabsorbed -> less osmotic gradients -> lower interstitial Na load
  • Increased fluid load but increased sodium load to the DCT (but reduced sodium concentration)
  • The concentration gradient in the medullary pyramid f**alls
  • Volumes of urine are more than a pure water diuresis.
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33
Q

Osmotic diuresis

  • Increased urine flow is due to decreased water reabsorption in the PCT and loops
  • In osmotic diuresis the amount of water reabsorbed in PCT is normal.
  • Na reabsorption from the proximal tubules is unaffected by osmotic load.
  • Medullary hypertonicity is increased.
  • ADH prevents the concentration of urine approaching that of plasma.
A

Increased urine flow is due to decreased water reabsorption in the PCT and loops

  • In osmotic diuresis the amount of water reabsorbed in PCT is reduced
  • Na reabsorption from the proximal tubules is impaired by high osmotic load
  • Medullary hypertonicity is decreased
  • ADH allows the concentration of urine to approach that of plasma.
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34
Q

regarding the bladder, which is false

  • there is no somatic innervation to the detrusor muscle
  • the reflex contraction of the detrusor usually begins at approximately 300-400mL
  • long term lesions of the cauda equine produce a dilated thin walled bladder
  • micturition is fundamentally spinal cord reflex
A

long term lesions of the cauda equine produce a dilated thin walled bladder

  • Initially thin walled and overfilled, but with time reflex contactions return resulting in a small hypertrophied bladder that causes dribbling of urine.*
  • Afferent nerve damage causes a dilated thin-walled bladder*
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35
Q

In micturition

  • Contraction of the trigone is mainly responsible for emptying of the bladder.
  • The relationship between bladder volume and intravesical pressure has a linear relationship.
  • The first urge to urinate is produced at 250mL.
  • Urine in the female urethra empties by contraction of the periurethral smooth muscle.
  • Sympathetic nerves play no role in micturition
A

Sympathetic nerves play no role in micturition

  • Contraction of the detrusor (circular muscle) is mainly responsible for emptying of the bladder.
  • The relationship between bladder volume and intravesical pressure has a linear relationship only at part Ib, which is a partially filled bladder
  • The first urge to urinate is produced at 350mL
  • Urine in the female urethra empties by gravity. In males a few contractions of bulbocavernosus is needed to empty the urethra.
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36
Q

In the normal bladder, micturition is

  • Initiated by the pelvic nerves
  • Co-ordinated in the lumbar portion of the spinal cord.
  • Initiated at a volume of 600mL.
  • Significantly affected by sympathetic nerves.
  • not facilitated at the level of the brain stem.
A

Initiated by the pelvic nerves

  • Co-ordinated in the sacral portion of the spinal cord.
  • Initiated at a volume of 350mL
  • Not at all affected by sympathetic nerves
  • Inherently a spinal reflex, but can be facilitated or inhibited at the level of the brain stem
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37
Q

The reabsorption of Na in the proximal tubules

  • Reabsorbs 80% of the filtered sodium load.
  • Causes increased hypertonicity.
  • Is powered by N/H ATPase.
  • Shares a common carrier with glucose.
  • All of the above
A

Shares a common carrier with glucose.

SGLT - secondary active reabsorption of glucose

  • Reabsorbs 60% of the filtered sodium load
  • Na reabsorption in the PCT carries water with it, so fluid remains isotonic
  • Na/H is a passive exchanger, utilising the conc gradient set up by Na-K-ATPase in the basolateral membranes
38
Q

Which of the following is most permeable to water

  • Thin ascending limb of the loop of Henle
  • Distal convoluted tubule
  • Thin descending limb of the loop of Henle
  • Cortical portion of the collecting tubule
  • Thick ascending loop of Henle
A

Thin descending limb of the loop of Henle

39
Q

with regard to urea

  • it moves actively out of the proximal tubule
  • it plays no part in the establishment of an osmotic gradient in the medullary pyramids.
  • all of the tubular epithelium is impermeable to urea except for the inner medullary portion of the collecting duct.
  • a high protein diet reduces the ability of the kidneys to concentrate urine.
  • ADH has no effect on the movement of urea across tubular epithelium.
A

Does not appear to be a correct answer

  • it moves passively out of the proximal tubule, by facilitated diffusion through channels
    • ​An amount equal to that reabsorbed is secreted back into the LoH (~50% total)
  • it plays a large part (50%) in the establishment of an osmotic gradient in the medullary pyramids.
  • Urea is reabsorbed in the PCT, DCT, and primarily the CD
  • a high protein diet increases the ability of the kidneys to concentrate urine, as there is more urea
  • ADH causes increased urea reabsoprtion (increasing the concentrating ability of the kidney) by increasing the number of transporters in the CD
40
Q

regarding water excretion in the kidney, which one is false

  • a minimum of 87% of filtered water is reabsorbed
  • aquaporin 2 is inserted into the luminal membrane of the collecting duct under the control of vasopressin
  • the DCT removes approximately 5% total filtered fluid
  • the thin part of the ascending loop of Henle is permeable to water
  • the PCT removes 60 – 70% of the filtered load
A

the thin part of the ascending loop of Henle is impermeable to water

41
Q

calculate the free water clearance based on the following values. Urine flow 200mL/h, plasma osmolality 300mOsm/kg and urine osmolality 450 mOsm/kg

  • 100 mL/h
  • 77 mL/h
  • 300mL/h
  • -77 mL/h
  • -100mL/h
A

Free water clearance = flow - ((urine osm x flow) / Plasma osm)

=200 - (450 x 200)/300

= 200 - (90000 / 300)

= -100ml/hr

42
Q

regarding Na handling by the kidney, which is false

  • aldosterone acts via synthesis of new sodium channels
  • ANP produces a diuresis through the inhibition of Na/K ATPase
  • Angiotensin II acts to increase Na absorption in the PCT
  • PGE2 causes a natriuresis
  • Daily output can range from 1 – 400mEq/d
A

ANP produces a diuresis through downregulation of ENaC in the CD

  • Ang II increases Na-H exchanger in PCT*
  • Aldosterone upregulates ENaC in CD (counteracts ANP)*
43
Q

Regarding the regulation of K excretion, which of the following is true

  • The rate of K excretion is inversely proportional to the rate of flow of tubular fluid.
  • K secretion is increased in conditions of alkalosis.
  • Hypoaldosteronism produces elevated urinary K levels.
  • Carbonic anhydrase inhibitors decrease the excretion of K.
  • Increased Na delivery to the collecting ducts leads to increased K reabsorption.
A

K secretion is increased in conditions of alkalosis.

As K is reabsorbed in the CD in exchange for H (H-K-ATPase), so in alkalosis, H+ will be reabsorbed, increasing K excretion.

  • The rate of K excretion is proportional to the rate of flow of tubular fluid, as rapid flow does not allow [K] to reach a value that stops secretion
  • Hypoaldosteronism produces decreased urinary K levels, as there is less Na-K-ATPase activty, hence less K excretion
  • Carbonic anhydrase inhibitors increase the excretion of K.
    • CA inhibitors result in reduced H+ secretion (create an alkalotic urine/serum acidosis), with resultant increase in Na+ and K+ secretion
  • Increased Na delivery to the collecting ducts leads to increased K secretion.
    • Potassium is secreted in CD, and increased Na delivery will likely enhance secretion as urine tubular flow will be increased
44
Q

In the kidney

  • K is actively reabsorbed in the DCT.
  • K excretion is decreased when H secretion is decreased.
  • K does not compete with H in tubular fluid
  • The rate of K secretion is proportionate to the rate of flow of tubular fluid in the distal nephron
  • K is reabsorbed and Na secreted in DCT
A

The rate of K secretion is proportionate to the rate of flow of tubular fluid in the distal nephron

  • K is actively secreted in the DCT.
  • K excretion is increased when H secretion is decreased.
    • K-H-ATPase exchanges K for H, so if the excretion of one is increased, the other will decrease
  • K does compete with H in tubular fluid
  • K is secreted and Na reabsorbed in DCT.
    • Na is never excreted in the kidneys. Potassium is first absorbed along with Na, then excreted in DCT
45
Q

In regards to the renal handling of Na

  • Na is actively transported out of all parts of the renal tubule.
  • Na is pumped out of the thin portion of the loop of Henle by Na/K ATPase.
  • The N/K ATPase extrudes 1 Na in for 1 K out of the tubular cell.
  • Most of the Na is actively transported out of the tubular cell into the lateral intercellular spaces
  • Around 60% of Na is reabsorbed back into the circulation.
A

Most of the Na is actively transported out of the tubular cell into the lateral intercellular spaces

  • Na is actively transported out of most parts of the renal tubule, except the thin loops
  • Na is not pumped out of the thin portion of the loop of Henle by Na/K ATPase, as it is not transported out of the thin loop, but also is not ‘pumped’ out, it follows a concentration gradient set up by basal Na-K-ATPase.
  • The N/K ATPase extrudes 3 Na out for 2K in of the tubular cell.
  • Around 99% (97-100% depending on aldosterone) of Na is reabsorbed back into the circulation
46
Q

In the kidney

  • K secretion in DCT and collecting ducts mainly occur through Na dependent transport mechanism.
  • pH of 4.5 in the urine is the limiting pH for H secretion
  • for each H secreted, 2 Na ions are reabsorbed.
  • the H secretion in the PCT is mainly dependent on ATP driven proton pump.
  • the carbonic anhydrase inhibitors increase H secretion.
A

pH of 4.5 in the urine is the limiting pH for H secretion

  • K secretion in DCT and collecting ducts mainly occur through H+ dependent transport mechanism.
  • for each H secreted, 1 Na ions is reabsorbed
  • the H secretion in the PCT is mainly dependent on 2’ active transport (Na-H exchanger)
  • the carbonic anhydrase inhibitors decresases H secretion (alkaline urine, acid plasma)
47
Q

In the kidney

  • Glucose is secreted by the collecting duct.
  • The renal threshold refers to glucose resorption from the urine.
  • Glucose is reabsorbed by 2ndary active transport
  • Glucose is reabsorbed in the loop of Henle
  • There is no glucose carrier in the kidney
A

Glucose is reabsorbed by 2ndary active transport

  • Glucose is absorbed by 2’ active transport in PCT (Na-glucose co-transporter)
  • The renal threshold refers to glucose loss from the urine
    • Nick questions why this was wrong - techinically it is the threshold at which glucose cannot by reabsorped any longer. Unclear why it is wrong but I have taken a guess above.
    • “RT for glucose is the plasma level at which glucose first appears in the urine in more than normal minute amounts”
  • Glucose is reabsorbed in the PCT
  • The glucose carrier in the kidney is SGLT from tubule to cell, and GLUT from cell to interstitium
48
Q

With respect to filtered water by the nephron

  • At the end of the PCT 15% of filtered water is resorbed.
  • 5% of filtered water is removed by the DCT
  • <87% of filtered water is reabsorbed when the urine volume is 23L in 24hours.
  • 30% of filtered water is removed by the loop of Henle.
  • total solute excretion over 24 hours depends on the urine volume
A

5% of filtered water is removed by the DCT

  • At the end of the PCT 60% of filtered water is resorbed.
  • At least 87% of filtered water is reabsorbed when the urine volume is 23L in 24hours
  • 15% of filtered water is removed by the loop of Henle.
  • total solute excretion over 24 hours is generally fairly stable, and dependent on solute load.
49
Q

In the kidney

  • Glucose is removed from the urine by secondary active transport
  • 100% glucose is absorbed in the DCT.
  • the calculated renal threshold for glucose is lower than its actual value.
  • phlorizin enhances glucose binding to the sodium – glucose symport
  • levo isoform of glucose is more efficiently transported by the sodium – glucose symport
A

Glucose is removed from the urine by secondary active transport

  • 100% glucose is absorbed in the PCT
  • the calculated renal threshold for glucose is higher than its actual value.
50
Q

Regarding the renal handling of sodium

  • 80% of the total filtered sodium load is reabsorbed.
  • Na is actively transported out of all parts of the renal tubule except for the thin portion of the loop of Henle.
  • Only a minority of Na is actively transported via the lateral intercellular spaces.
  • Na transport is coupled to the movement of H and glucose but not to amino acids and phosphates.
  • The Na/H exchanges in the proximal tubule extrudes one Na for every H reabsorbed
A

Na is actively transported out of all parts of the renal tubule except for the thin descending limb of LoH

In all other places it is actively absorbed by basolateral Na-K-ATPase setting up concentration gradients that allows it to use channels (ENaCs), cotransporters (Na-K-2CL, SGLT etc), or exchangers (Na-H)

  • 96-99% of the total filtered sodium load is reabsorbed.
  • a majority of Na is actively transported via the lateral intercellular spaces.
  • Na transport is coupled to the movement of H, glucose, amino acids, and phosphates.
  • The Na/H exchanges in the proximal tubule absorbs one Na for every H extruded
51
Q

with respect to how sodium is handled by the kidney

  • is actively transported out of all parts of the renal tubule except the thick portion of the LOH.
  • changes in aldosterone concentration takes ~ 6 hours before an appreciable change to sodium reabsorption is noted.
  • increasing intracellular Ca concentration inhibits sodium reabsorption
  • most of the Na/H exchange by active transport is performed in the DCT.
  • tubuloglomerular feedback ensures a constant proportion of Na is reabsorbed for any change in the GFR
A

tubuloglomerular feedback ensures a constant proportion of Na is reabsorbed for any change in the GFR

  • is actively transported out of all parts of the renal tubule except the descending LoH and CD
  • changes in aldosterone concentration takes 30min before an appreciable change to sodium reabsorption is noted, due to non-genomic action (stimulation of Na-K-ATPase)
  • increasing intracellular Ca concentration inhibits sodium reabsorption
  • most of the Na/H exchange by active transport is performed in the PCT
52
Q

Water excretion

  • At least 95% is reabsorbed.
  • 50% of the filtered water is reabsorbed by the end of the PCT.
  • the first part of the DCT is impermeable to water
  • water tends to recirculate in the medullary pyramids.
  • decreasing the tonicity in the medulla has no effect on water excretion.
A

the first part of the DCT is impermeable to water

  • At least 87% is reabsorbed
  • 65% of the filtered water is reabsorbed by the end of the PCT.
  • solutes tends to recirculate in the medullary pyramids, water is absorbed back into the systemic circulation
  • decreasing the tonicity in the medulla impairs the ability to produce concentrated urine, as concentration gradients arent as large
53
Q

In the kidney Na is mostly absorbed with

  • HCO3
  • Glucose
  • K
  • Ca
  • Cl
A

Cl

  • HCO3 was given as correct but I think is wrong*
  • 60% of Na reabsorption occurs in the PCT, as a result of Na-H exchange*
  • Chloride almost always follows Na shifts in order to preserve electroneutrality - this is the answer on another question which does not include HCO3 as an option*
  • Indirecly HCO3 is taken up, as H2O and CO2 (products of carbonic anhydrase)*
54
Q

With regards to the regulation of K excretion, K is

  • Passively reabsorbed in the DCT.
  • secretion does not undergo adaptation
  • excretion is increased when H ion secretion is increased.
  • is actively reabsorbed in the PCT
  • excretion is independent of Na concentration in the distal tubular fluid
A

is actively reabsorbed in the PCT

  • Passively secreted in the DCT.
  • secretion does undergo adaptation, and generally matches K intake
  • excretion is decreased when H ion secretion is increased.
  • excretion is dependent on Na concentration in the distal tubular fluid - low Na reaching the distal tubule causes a reduction in K excretion.
55
Q

The greatest permeability to urea is found in

  • Inner medullary portion of the collecting tubule
  • DCT
  • Thin descending limb of loop of Henle
  • Thick ascending limb of loop of Henle
  • Thin ascending limb of loop of Henle
A

Inner medullary portion of the collecting tubule

  • Absorbed by urea-channels by facilitated diffusion.*
  • When ADH is high, more urea is reabsorbed, creating a larger diffusion gradient to allow more absorption of water*
56
Q
  1. Regulation of potassium excretion in the kidney involves:
  • a. Secretion by proximal tubule cells
  • b. Exchange with Na+ on the tubular side via an active pump
  • c. Passive reabsorption in the ascending limb of the loop of Henle
  • d. Active reabsorption in the proximal tubules
  • e. Active exchange with Ca2+ via a K+/Ca2+ exchange
A

d. Active reabsorption in the proximal tubules

  • a. Secretion by distal tubule cells
  • b. Exchange with Na+ on the interstitial side via an active pump
  • c. active reabsorption in the proximal tubules
  • e. ???Active exchange with Ca2+ via a K+/Ca2+ exchange
57
Q
  1. Sodium reabsorption in the kidney is:
  • a. Actively transported in the thin portions of the loop of Henle
  • b. Coupled to the movement of glucose and amino acids in the distal tubule
  • c. Decreased by atrial natriuretic peptide
  • d. Reabsorbed against its concentration gradient
  • e. Independent of chloride absorption
A

c. Decreased by atrial natriuretic peptide

  • a. Actively transported in the thin portions of the loop of Henle
  • b. Coupled to the movement of glucose and amino acids in the proximal tubule
  • d. Reabsorbed down its concentration gradient
  • e. Dependent on chloride absorption - Na-2Cl-K cotransporter in Thick ascending limb, and Na-Cl CT in the DCT
58
Q
  1. In the distal tubular cells:
  • a. K+ secretion is mainly by active transport mechanisms
  • b. K+ secretion is decreased in acidosis
  • c. K+ secretion is increased when Na+ delivery to the tubule is decreased
  • d. Loop diuretics will cause decreased K+ secretion
  • e. K+ is reabsorbed by the Na+/K+/2Cl- transporter
A

b. K+ secretion is decreased in acidosis

As K is reabsorbed in the CD in exchange for H via the K-H-ATPase

  • a. K+ secretion is mainly by passive transport mechanisms (though this seems to happen more in the CD than DCT)
  • c. K+ secretion is reduced when Na+ delivery to the tubule is decreased
  • ????d. Loop diuretics will cause ??? K+ secretion as they inhibit the Na-K-2Cl cotransporter, leading to more K+ in the urine, and this can lead to a hypokalaemia (and H+ retention)
  • e. K+ is reabsorbed by the Na+/K+/2Cl- transporter - this occurs in the Thick ascending LoH
59
Q
  1. With regard to osmotic diuresis
  • a. Urine flows are much less than in a water diuresis.
  • b. Vasopressin secretion is almost zero.
  • c. The concentration of the urine is less than plasma.
  • d. Increased urine flow is due to decreased water reabsorption in the proximal tubule and loop of Henle
  • e. Osmotic diuresis can only be produced by sugars such as mannitol.
A

d. Increased urine flow is due to decreased water reabsorption in the proximal tubule and loop of Henle

  • a. Urine flows are much more than in a water diuresis.
  • b. Vasopressin secretion is Normal / elevated (cf water diuresis, where it is almost zero)
    • ​Body is trying to retain water but unable to overcome the osmotic gradient produced by the osmotic agent
  • c. The concentration of the urine is the same as plasma.
    • Water diuresis the urine concentration is lower (osmotic diuresis is due to osmotically active agent in the urine)
  • e. Osmotic diuresis can be produced by sugars such as mannitol, as well as by NaCl, glucose
60
Q

With regard to the effects of hormones on the renal tubules, which is correct

  • Aldosterone increases K reabsorption from the distal tubule.
  • Angiotensin II increases H secretion from the proximal tubule
  • ADH increases water reabsorption in the PCT.
  • ANP decreases Na reabsorption from the PCT.
  • PTH increases PO4 reabsorption.
A

Angiotensin II increases H secretion from the proximal tubule

By upregulating Na-H exchanger

  • Aldosterone increases K secretion from the distal tubule.
    • Stimulates Na-K-ATPase
  • ADH increases water reabsorption in the CD
  • ANP decreases Na reabsorption from the CD
    • ​ANP / ADH have opposing actions in the CD
  • PTH increases PO4 Excretion
61
Q

What factor decreases renin secretion

  • Hypovolaemia
  • Supine position
  • Cardiac failure
  • Na depletion
A

Supine position

The others all create a low BP or low Na state, where not enough Na is getting to the macula densa

62
Q

With regard to the renin-angiotensin system

  • Prorenin has 50% the activity of renin
  • Renin secretion will be increased by propranolol.
  • Angiotensinogen is synthesised by the liver
  • Angiotensin I in a potent vasodilator
  • Angiotensin II acts at receptors in the nucleus
A

Angiotensinogen is synthesised by the liver

  • Prorenin has essentially no biologic activity
  • Renin secretion will be decreased by propranolol, as it blocks symp nerves
  • Angiotensin I is essentially inert
  • Angiotensin II acts at GPCR receptors
63
Q

ANP

  • Stimulates the secretion of vasopressin.
  • Secretion will be decreased by scuba diving
  • Is a typical dual chain helix structure
  • Stimulates EPO production
  • Has generally the opposite action to angiotensin II
A

Has generally the opposite action to angiotensin II

  • Inhibits the secretion of vasopressin.
    • Vasopressin wants to conserve fluid, ANP lose it
  • Secretion will be increased by scuba diving, as increased pressure outside the body causes an increase in venous pressure -> increased atrial stretch -> ANP
  • Pretty sure its mainly hypoxia that Stimulates EPO production
64
Q

Renin secretion is increased by

  • High Na and Cl reabsorption across the macula densa
  • Increased afferent arteriole pressure
  • Prostaglandins
  • ADH
  • Angiotensin II
A

Prostaglandins

(as well as sympathetic nerve activity and catecholamines)

Others all reduce it

65
Q

ADH secretion is increased by

  • Alcohol
  • Carbamazepine
  • Increased ECF volume
  • Angiotensin I
  • Lying supine
A

Carbamazepine

  • ADH promote water retention.*
  • Increase: Standing, Angiotensin II, exercise/stress/pain, decreased ECF volume, N+V, increased plasma oncotic pressure*
  • Decrease: Alcohol, increased ECF volume, decreased plasma osmo*
66
Q

EPO

  • Acts to increase RBC by cell division
  • Is principally inactivated by the spleen
  • Causes increase in RBC in 24 hours
  • Is produce by the adrenal gland
  • Production is inhibited by Theophylline
A

Production is inhibited by Theophylline

  • Produced in the kidney*
  • Increases RBC by increasing the number of stem cells*
  • Causes RBC increase in 2-3 days*
  • Inactivated in the liver.*
67
Q

ANP

  • Increases systolic BP
  • Increases the responsiveness of vascular smooth muscle to dopamine
  • Inhibits the secretion of ADH
  • Has the highest affinity for ANPR-C receptors
  • The effects in the brain are the same as seen with angiotensin II
A

Inhibits the secretion of ADH

  • Aims to reduce systolic BP
  • Increases the responsiveness of vascular smooth muscle to dopamine??
68
Q

Which of the following is true of the renin angiotensin system

  • Renin causes the release of aldosterone.
  • Angiotensinogen is converted to angiotensin I in the lungs.
  • Increased Na reabsorption at the macula densa causes increased renin
  • Prostaglandins increase the secretion of renin
  • Oestrogens decrease production of angiotensinogen
A

Prostaglandins increase the secretion of renin

As do sym nerve activity and catecholamines

  • Renin causes (via Ang I) Ang II to releases aldo
  • Angiotensinogen is converted to angiotensin I by renin in the circulation.
    • Ang I -> Ang II via ACE in the lungs
  • Increased Na reabsorption at the macula densa causes decreased renin
  • Oestrogens ?increase production of angiotensinogen
69
Q

All are true of ANP except

  • It causes natriuresis
  • It lowers BP
  • Circulating ANP has a short half life
  • ANP has the greatest affinity for the ANPR-B receptor on the glomerulus
  • It is released when atrial muscle is stretched
A

ANP has the greatest affinity for the ANPR-_A_ receptor on the glomerulus

70
Q

In chronic acidosis the major adaptive buffering system in the urine is

  • Carbamino compounds
  • HCO3
  • Ammonia
  • Histidine residues
  • Phosphate
A

Ammonia

“In chronic acidosis, glutamine synthesis in the liver is increased, using some NH4 which is usually converted into urea, and the glutamine provides the kidneys with another source of NH4”

Acutely, the major buffer systems in the urine (and CSF) are bicarbonate and phosphate.

In respiratory acidosis, the renal compensation is through HCO3 (increasing intracellular PCO2 -> increased H+ secretion due to increased intracellular CA activity, which then combines with HCO3 in the tubule to H2CO3 -> H20 + CO2 via tubular CA)

In metabolic acidosis the buffer systems of HCO3-, NH3-, and HPO4- are used for compensation (otherwise the urine pH would quickly reach 4.5 and no further H+ could be secreted)

71
Q

These gases – pH 7.32, pCO2 31, HCO3 20mmol/L represent

  • Primary metabolic acidosis
  • Primary respiratory alkalosis
  • A picture consistent with diuretic abuse
  • Mixed respiratory acidosis, metabolic acidosis
  • Partly compensated metabolic acidosis
A

Partly compensated metabolic acidosis

Slightly acidotic so not completely compensated, but CO2 is reduced in an acidosis so is attempting compensation.

72
Q

Renal acid secretion is affected by all of the following except

  • pCO2
  • K
  • Carbonic anhydrase
  • Aldosterone
  • Ca
A

Ca

  • pCO2 - increases due to increased intracellular CA activity -> more H+ to secrete
  • K - Hypokalameia -> intracellular acidosis (H+ moves intracellularly to compensate for reduced K+), which leads to more H+ excretion
  • Carbonic anhydrase - inhibition reduces secretion, as less H+ can be produced intracellularly (also increases HCO3 excretion)
  • Aldosterone - increases activity of H+-ATPase in the DCT to increase excretion.
73
Q

Which of the following best describes the changes in uncompensated respiratory alkalosis

  • Low pH, HCO3 and PaCO2
  • High pH, low HCO3 and PaCO2
  • Low pH and HCO3 and normal PaCO2
  • High pH, low HCO3 and normal PaCO2
  • Low pH, high HCO3 and normal PaCO2
A

High pH, low HCO3 and PaCO2

Uncompensated respiratory alkalosis = pH >7.45, pCO2 low, bicarb normal/low

Low CO2 -> low intracellular levels -> less CA activity to convert H20 and CO2 into H+ + HCO3, so there is less H+ excretion and hence less HCO3 reabsorption, further lowering the already low biarb. This helps to reduce the pH towards normal.

74
Q

Regarding H+ excretion

  • H+ is secreted in the PCT via an ATPase.
  • P cells in the collecting duct actively excrete acid.
  • The limiting urine pH is approximately 5.5.
  • For each H+ secreted in the PCT, one Na and one HCO3 enters the interstitium
  • Carbonic anhydrase in the DCT luminal membrane facilitates H+ buffering and the formation of H2CO3
A

For each H+ secreted in the PCT, one Na and one HCO3 enters the interstitium

  • H+ is secreted in the PCT via Na/H exchange
    • ​In the DCT it is an ATPase
  • I cells in the collecting duct actively excrete acid
  • The limiting urine pH is approximately 4.5
  • Carbonic anhydrase in thePCT luminal membrane facilitates H+ buffering and the formation of H2CO3
    • Then H2CO3 -> H20 + CO2 which diffuse into cells
75
Q

Acid secretion is not increased in the following

  • Aldosterone
  • Hypokalaemia
  • Carbonic anhydrase inhibitors
  • High arterial pCO2
  • Chronic acidosis
A

Carbonic anhydrase inhibitors

Reduces H+ excretion, and creates a metabolic acidosis

76
Q

Renal acid secretion is independent of

  • K
  • Intracellular CO2
  • Carbonic anhydrase level
  • Aldosterone
  • ADH
A

ADH

  • Hypokalaemia -> increased H+ excretion*
  • Increased CO2 -> increased excretion*
  • CA inhibiton -> Decreased excretion*
  • Aldosterone -> increased excretion (increased ATPase in DCT)*
77
Q

With respect to buffers in the blood

  • Plasma is rich in carbonic anhydrase.
  • Oxyhaemoglobin is better buffer than deoxyhaemoglobin.
  • Phosphate is an important buffer in plasma.
  • 80% of the acid load in metabolic acidosis is buffered in plasma.
  • the most effective buffers have pK values close to the pH of the environment they operate in
A

the most effective buffers have pK values close to the pH of the environment they operate in

The closer to the pK, the more they can buffer without a change in pH

  • RBC, kidneys, and lungs are rich in carbonic anhydrase
  • Deoxyhaemoglobin is better buffer than oxyhaemoglobin.
    • ​Thus once Hb has offloaded O2 into the tissues, it is better able to buffer products of metabolism etc on the way back to the lungs
  • Phosphate is an important buffer in intracellular fluid, along with protein.
    • Blood buffers are bicarb, protein and Hb. Bicarb is an interstitial buffer
  • Metabolic acidosis buffering load is 20% in ECF, 80% ICF.
    • For metabolic alkalosis, the ratio is closer to 1:2 (ECF:ICF)
78
Q

In metabolic alkalosis

  • A common cause is the ingestion of aspirin.
  • Respiratory compensation can fully restore pH to normal.
  • Base excess is positive
  • Treatment with NaHCO3 restores pH to normal.
  • There is more renal excretion of H ions.
A

Base excess is positive

Because there is more base than acid (hence the alkalosis)

  • the ingestion of aspirin causes a metabolic ACIDOSIS - (Fixed acid)
  • Respiratory compensation cant restore pH to normal
    • There is only so much hypoventilation possible before hypoxia stimulates respiratory drive.
  • Treatment with NaHCO3 will make this worse, as it is a weak base itself
  • There is less renal excretion of H ions, as the body wants to conserve acid
79
Q

Compensatory mechanisms in metabolic acidosis include

  • A fall in pH
  • Decreased CO2 formation
  • Decreased minute volume
  • An alkaline urine
  • Reduction in the pCO2 of alveolar gas
A

Reduction in the pCO2 of alveolar gas

  • Fall in pH is not compensatory, it is the thing.*
  • There will be increased CO2 production likely (increased H+ + HCO3-) to try and remove H+*
  • Minute volume will increase to remove CO2*
  • Urine will be acidic as the body excretes acid*
80
Q

Urinary buffers

  • Carbonic anydrase in the DCT increases the buffering capacity.
  • Dibasic phosphate plays a role in buffering in the distal tubule and the collecting ducts
  • The conversion of glutamate to glutamine in the renal tubular cells provide NH3 for buffering.
  • The largest pH difference between the tubular cells and the lumen occurs across the PCT
  • The NH4+ content of the urine increases with serum HCO3 concentrations above 28mmol
A

Dibasic phosphate plays a role in buffering in the distal tubule and the collecting ducts

Adds H+ to become monobasic phosphate

  • Carbonic anydrase in the PCT increases the buffering capacity.
  • The conversion of glutamine to glutmate in the renal tubular cells provide NH3 for buffering.
  • The largest pH difference between the tubular cells and the lumen occurs across the DCT or CD
  • The HCO3- content of the urine increases with serum HCO3 concentrations above 28mmol
81
Q

With respect to the following ABG taken on 24% O2 – pH - 7.56, pO2 – 135, pCO2 – 28, HCO3 – 26

  • The person would be expected to have a lower pO2
  • The person has an acute metabolic alkalosis
  • The person is demonstrating respiratory compensation
  • The person has a chronic respiratory alkalosis
  • In a few days time they would compensate by lowering HCO3 concentrations
A

In a few days time they would compensate by lowering HCO3 concentrations

Acute uncompensated respiratory alkalosis, will be compesated with a metabolic acidosis

82
Q

The most important buffer in intracellular fluid is

  • Bicarbonate
  • Ammonia
  • Diphosphate
  • Albumin
  • Myoglobin
A

Diphosphate

  • As well as protein*
  • ECF = bicarbonate*
  • Blood = bicarb, protein, Hb*
83
Q

In relation to acid base balance in the body

  • Respiratory compensation in metabolic alkalosis is limited by carotid and aortic chemoreceptor response.
  • HCO3 concentration will decrease in compensated respiratory acidosis.
  • The rate of renal H secretion is not affected by pCO2 in respiratory acidosis.
  • Cl excretion is decreased in respiratory acidosis
  • Hepatic glutamine synthesis is decreased in chronic metabolic acidosis.
A

Respiratory compensation in metabolic alkalosis is limited by carotid and aortic chemoreceptor response.

Hypoventilation to compensate for alkalosis can not go so far as to cause hypoxia

  • HCO3 concentration will increase in compensated respiratory acidosis, as HCO3 is absorbed in exchange for H+ secretion
  • The rate of renal H secretion increases due to increasing pCO2 in respiratory acidosis.
  • Cl excretion is increased in respiratory acidosis
  • Hepatic glutamine synthesis is increased in chronic metabolic acidosis, t**o produce more NH4+ and HCO3- to act as buffers
84
Q

Regarding renal compensation in respiratory acidosis and alkalosis

  • The rate of HCO3 reabsorption is inversely proportional to the arterial pCO2.
  • In respiratory acidosis, HCO3 reabsorption is reduced.
  • Changes in plasma Cl concentration are proportional to HCO3 concentrations
  • In respiratory alkalosis, renal H secretion is increased.
  • HCO3 reabsorption depends upon the rate of H secretion by the renal tubular cells
A

HCO3 reabsorption depends upon the rate of H secretion by the renal tubular cells

  • The rate of HCO3 reabsorption is proportional to the arterial pCO2 - increased pCO2 -> increased HCO3 reabsorption/H+ excretion
  • In respiratory acidosis, HCO3 reabsorption is Increased (see above)
  • Changes in plasma Cl concentration are ?inversely proportional to HCO3 concentrations
  • In respiratory alkalosis, renal H secretion is Decreased
85
Q

the main buffer in the interstitium is

  • protein
  • Hb
  • Phosphate
  • Ammonia
  • HCO3
A

HCO3

  • ICF = protein + phosphate*
  • Plasma = protein, bicarb, Hb*
86
Q

Regarding the anion gap

  • It is the difference between cations including Na and anions including Cl and HCO3
  • It is increased in hyperchloraemic acidosis secondary to ingestion of NH4Cl.
  • It is decreased when Ca/Mg is decreased.
  • It consists mostly of HPO42-, SO42- and organic acids.
  • It is decreased when the albumin is increased
A

It consists mostly of HPO42-, SO42- and organic acids.

Increases with increasing negative charge (eg proteins), decreasing positive charge (eg Ca/Mg), or organic anions such as lactate are present (eg lactic acidosis, ketoacidosis)

  • It is the difference between cations other than Na and anions other than Cl and HCO3
  • It is normal in hyperchloraemic acidosis secondary to ingestion of NH4Cl, as the Cl is measured in the AG
  • It is increased when Ca/Mg is decreased
  • It is increased when the albumin is increased
87
Q

The ratio of HCO3 ions to carbonic acid at pH of 7.1 is

  • 1
  • 10
  • 0.1
  • 100
  • 0.01
A

10

pKa of HCO3 is 6.1. At this level HCO3 = carbonic acid. An increase of 1 equates to a 10-fold increase in HCO3 (more basic = more bicarb)

88
Q

hypokalaemic metabolic acidosis may be associated with

  • carbonic anhydrase inhibitors
  • diuretic use
  • chronic diarrhea.
A

carbonic anhydrase inhibitors

  • Inhibit CA in the cells -> less H+ secretion, so there is less exchange with K+ so it is excreted*
  • diuretics cause a hypokalaemic metabolic alkalosis (this happens because there is increased Na delivery to the DCT, increasing aldosterone stimulation of the Na-K-ATPase, which acts to increase Na reabsorption in exhange for K and H secretion)*
89
Q

All of the following represents an acid load to the body except

  • DKA
  • CRF
  • Fruit.
  • Ingestion of acid salts
A

Fruit.

Mainly alkali load

CRF causes an acid load by ????

90
Q

What is the H ion concentration at a pH of 7.4

  • 0.0001meq/L
  • 0.00004meq/L
  • 0.0004meq/L
  • 0.0002meq/L
  • 0.00002meq/L
A

0.00004meq/L

4 zeroes and then a 4

91
Q

Hypokalaemic metabolic alkalosis is associated with

  • Carbonic anhydrase inhibition
  • Diuretic use
  • Chronic diarrhea
A

Diuretic use

Carbonic anhydrase inhibition -> Hypokalaemic metabolic acidosis (due to incresased HCO3 loss in urin, and reduced H+ secretion -> increased K+ excretion )

Chronic diarrhea -> Hypokalaemic acidosis due to K and HCO3 loss in the stools

92
Q
  1. Regarding renal handling of hydrogen ion, which of the following is INCORRECT?
  • a. Acetazolamide decreases tubular secretion
  • b. Aldosterone increases distal tubular secretion
  • c. Much more acid secretion occurs in proximal than distal tubule
  • d. Lowest tubular fluid pH achievable is 4.5
  • e. Secondary active transport mechanism operates in distal tubule
A

e. Secondary active transport mechanism operates in distal tubule

DCT H+ loss is due to an ATPase (stimulated by aldosterone)

  • a. Acetazolamide decreases tubular secretion (by reducing the formation of H2CO3 in the lumen -> increased HCO3 loss)
  • b. Aldosterone increases distal tubular secretion (see above)
  • c. Much more acid secretion occurs in proximal than distal tubule (due to Na-H exchanger)
  • d. Lowest tubular fluid pH achievable is 4.5 (hence buffering needed)