The kidney as a producer, regulator and excoriator

Question 1

what cells in the kidney secrete EPO

Answer 1

peritubular cells

Question 2

Vitamin D is made in the kidney too and this raises serum calcium by promoting GI absorption and decreasing renal excretion ( increased tubular reabsorption) and stimulating bone reabsorption what form of Vitamin D is made here

Answer 2

1,25 dihydroxycholecalciferol- calcitriol

Question 3

what is interstitial fluid

Answer 3

found in spaces around cells

aquaporins found each side of tubular cell

Question 4

role of golmerulus

Answer 4

filter plasma to produce glomerular filtrate - normal is about 120ml/min/hour
- primary maker of renal function
CKD stages with GFR above 90 then each stage reduce by 30 then last to 15

Question 5

what are podocytes

Answer 5

epithelial cells with extensive branching cytoplasmic processes ( pedicles and foot processes) prevent proteins in
cut off around 55,000-60,000

Question 6

what is net filtration pressure - 14mmHg

Answer 6

total pressure that promotes filtration - hydrostatic pressure gradient moves out and then oncotic gradient moves it back in

Question 7

creatinine is a product of muscle metabolism and maker of renal function
what other protein can be used as a marker of renal function that is produced by most cells that contain a nucleus and there is no tubular secretion

Answer 7

Cystatin C

Question 8

what two autoregualtion physiological changes occur when a drop is arterial pressure leads to fall in both RBF and GFR

Answer 8

afferent arteriole can dilate improving RBF at a lower arterial pressure or efferent arteriole constructs improving the GFR at a lower RBF therefore increasing the filtration fraction ( proprotion of fluid reaching the kidneys that passes into the renal tubules ( GFR/plasma flow))

Question 9

autoregulation of the arterioles can be controlled by myogenic mechanisms or bu tubulo-golmerular feedback what are they

Answer 9

Adenosine - produced in hydrated states constricted afferent arteriole reducing GFR and then is switched off with decreased filtrate flow

angiotensin II - constrict the efferent arteries to maintain pressure and therefore GFR - beware of ATII inhibition in hypovolaemia

PGE2 - produced in DCT in response to reduced filtrate flow. Dilates afferent arteriole to maintain RBF - antagonises vasopressin - NSAIDS in hypovolaemia
( also inhibits platelet aggregation and increase uterine stimulation)

Question 10

In the PCT reabsorption of sodium occurs by 2 main methods what are they

Answer 10

Sodium hydrogen antiporter ( sodium into tubular cell and hydrogen out into tubule lumen) - this has come from dissociation of carbonic acid - the sodium is then cotransported out into blood with the bicarbonate

sodium glucose symporter

( ATPASE pump moving more sodium into the blood)

transport maximum - divide by 1000

Question 11

in the PCT sodium leaves and water flows to save energy - how does water leave

Answer 11

through leaky junctions allowing easy passage between the tubular cells

Question 12

in diabetic situations in the pct like ketoacidosis - glycourias reusults leading to osmotic diuresis if the transport maximum is exceeded which is the GFR multiplied by the 4.5mmol of glucose divided by 1000 - this pull on the glucose and on sodium leads to what

Answer 12

dehydration of patients

Question 13

main role of loop on henle

Answer 13

hypotonic fluid is descending tubule

Question 14

as ions are lost and water retained tubular fluid becomes progressively more dilute whilst the interstitial fluid becomes more concentrated as ascending limb is impermeable to water is this due to the very tight junctions

Answer 14

yes

Question 15

Loop diuretics block the NKCC2 cotransporter what is an example of one

Answer 15

furosemide

Question 16

in the descending limb water is lost via aquaporins by osmosis and sodium retained tubular fluid becomes progressively more concentrated. The osmolarity ( conc of solution based on particles present) changes from 300-1200. Interstitial fluid in medulla is strongly….

Answer 16

hypertonic

Question 17

on DLOH what venue system takes away electrolytes in the blood

Answer 17

vasa recta - countercurrent system runs other way to nephron

Question 18

finish the sentence water pass from the descending LoH to ascending limb of what

Answer 18

vasa recta

opposite for ions - ascending LoH to descending vasa recta

Question 19

what cells in the DCT and CD reabsorb sodium and secret potassium controlled by aldosterone?

Answer 19

principal cells

Question 20

what cells reabsorb potassium and secrete hydrogen driven by ATPase

Answer 20

intercalated cells

Question 21

what channel is only found in the principal cells of the DCT

Answer 21

ENaC coupled channel - sodium and potassium contrnsporter - stimulated by aldosterone which also acs on the ATPase pump on the blood side
also a ROMK

Question 22

what channel are only found in the intercalated cells of the DCT

Answer 22

active proton potassium ATPase transport which acts to secrete hydrogen and reabsorb potassium stimulated by acidosis and hypokalaemia

Question 23

what is the main role of the medullary collecting duct

Answer 23

Main role in final regulation of water excretion and thereby urine conc
insertion of aquaporins into luminal membrane

Question 24

what are aquaporins

Answer 24

Transmembrane with narrow shaped and charged walls allowing only water to pass
Without them water moves slowly by osmosis

Question 25

what is the only aquaporin found in collecting duct on the luminal membrane( tubular cell and lumen) and inserted in response to ADH with variable water reabsorption

Answer 25

Aqu-2 1 - PCT and DLoH basal membrane ( closer to blood) and has constant presence with continuous rebasoptin 3,4 - collecting duct basal membrane side - constant presence and continuous water reabsorption Aquaporin 4 - miller fisher syndrome

Question 26

ADH bind to what receptor causing inserting of Aqu-2 into luminal surface

Answer 26

V2 receptor hypertonic interstitum - near complete water reabsorption when needed - ultra tight junctions imperabele to all

Question 27

morphine and hypoxia and nausea can stimulate increase ADH - what are the effects of this

Answer 27

increased plasma osmolarity( dehydration) decreased blood volume and decreased blood pressure resulting in increased water reabsorption, more concentrated urine and less concentrated blood plasma decrease ADH - opposite caused by Alcohol and antihypertensives

Question 28

what are the 3 types of receptors( where are they found and their roles) for ADH that all G protein coupled receptors

Answer 28

V1a - peripheral circulation - vasoconstriction V2- renal collecting duct and endothelium and Aqu-2 insertion and clotting factor release V3(V1b) - CNS - ACTH release

Question 29

final urine acidity is determined in the DCT by what cells

Answer 29

intercalated cells - protons acidosis increase proton excretion at the expense of potassium retention

Question 30

normal urine ph is 4.5-8 , where is the bulk of proton secretion and bicarbonate reabsorption taking place

Answer 30

PCT Acid constantly being produced - impaired renal elimination leads to acidosis

Question 31

what are the 3 cellular components of the juxtaglomerular apparatus

Answer 31

``` macula densa ( part of DCT) cells extraglomerular mesangial cells and juxtaglomerular cells( granular cells- secrete renin) ``` macula densa senses decreased pressure so granular cells then secrete renin to increase pressure

Question 32

Triggering of the JGA leads to

Answer 32

Dilations of the afferent arteriole - local action ( decrease adenosine and PGE2 ) Release renin ( granular cells) Note rennin action and release also triggered by sympathetic beta 1 stimulation Hypovolaemia - renin released, AG AG2 in lungs via ACE and then AG2 affects vasoconstriction on efferent arteriole ( maintain filtration rate as glomerular cap pressure maintained)

Question 33

aldosterone

Answer 33

increases sodium reabsorption ( variable) determines final urine sodium content LoH - creates are of interstitial hyperosmolarity