renal

Question 1

Total body water

Answer 1

60% of weight, average of 42L but more in younger people.

25-30% intracellular
38% ECF

Question 2

ICF and ECF ions

Answer 2

ICF - K+ = 148mM , Na+ = 10mM, Cl- = 4mM, proteins = 55mM

ECF -K+ = 5mM , Na+ = 140mM, Cl- = 103mM, proteins = 15mM

Question 3

Na role and how we obtain it

Answer 3

input by diet av. 150mM a day, lose 140mM in urine and 10mM i sweat and stool
if not excretion increase in Na+ leads to increase h20 reabsorption to increase BP

Question 4

Kidney structure ;

Answer 4

150g, 12th thoracic to 3rd lumbar, 10cm tall, 5.5 cm wide

cortex - outer layer, paler
medulla - inner layer, dark, medullary rays, striated
capsule - fibroule for protection
nephron - functional unit 1-1.5million per kidney

Question 5

2 types of nephron>

Answer 5

superficial - glomerolus dlose to cortec surface, and Lof H in outer medulla

Juxtamedullary - henle is in inner medulla too , key in urine concentration

Question 6

renal faliure -

Answer 6

drop in GFR leads to increase serum urea and creatine
progressive thickening of the glomerular membrane so filtration is slowed damage and scarring as inflammation so reduced renal size and fibrosis occurs.

causes - diabetes, hypertension, polycystic kidney

Treat - diuretics, Na bicarbonate to reduce acidosis and change diet

in US RF kidney small and bright

Question 7

uraemia symptoms -

Answer 7

hypertension
acidosis as cannot excrete salt and water 
vomiting
protein in urine
pericarditis

Question 8

Bowmans capsule -

Answer 8

20 % plasma into bowman the rest goes back into circulation via the renal vein. blood cells and protein remain apart from 1% (albumin)

Question 9

types of transport across renal cells

Answer 9

paracellular - between tight junctions

transcellular - through cell via exocytosis and endocytosis

Question 10

Proximal tubule reabsorption -

Answer 10

reabsorb 70% of filtrate
70% water and Na+
100% glucose and amino acids
90% HCO3-

Question 11

Porximal tubule cell

Answer 11

rich in mitochondria for ATP, high SA

Na+/K+ ATPase so 3Na+ out and to K+in on baso
multiple sodium coupled transporters eg.

SGLT1 - sodium glucose protein
NaPi2 - sodium and phosphate transport
NHE3 - sodium and hydrogen exchanger so H leaves and bind to form HCO3- that dissociates into CO2 and H2O t move into cell and then H+ is recycled and HCO3-leaves cell to maintain ph of blood

Question 12

NHE3 knock out in mice causes -

Answer 12

Ph to drop so BP drop as less H20 reabsorbed

Question 13

isosmotic meaning

Answer 13

loss of ions followed by h20 via aquaporins

Question 14

Familial Renal Glycosuria -

Answer 14

increase glucose in urine if SGLT1 and 2 are lost

more glucose in plasma the mor is reabsorbed until blood is saturated around 375mg/min so then in urine

Question 15

Loop of hence role ;

Answer 15

reabsorb Na+,cl-,h2o,ca2+mg2+

thin descending = loss of H20 yet impermeable to Na+ and CL- so osmotic gradient to h20 to leave into interstitial

thin ascending = permeable to cl- and Na+ but imp to h20
thick ascending = same as thin

Question 16

CLCK and barttin role in TAL

Answer 16

on basolateral of cell, CLCK removes Cl - and barttin is the accessory protein. I not there none reabsorbed
e.g. in barrtinns syndrome

Question 17

ROMK role in TAL

Answer 17

recycle K+ out of cell for NKCC2 to work

Question 18

NKCC2 role in TAL

Answer 18

transports Na+, 2Cl- and K+ int the TAL cell so Na + can be removed on baso into the blood and CL-

too much cl- stops it from working

Question 19

Bartters sysndrone

Answer 19

recessive mutation , loss of salt in urine so polyuria (increase flow) low BP and Hypokaleamia as K lost in urine, not as much calcium reabsorbed so clarification in kidney = stones

if ROMK,NKCC2 or CLCK bartin are mutated

Question 20

Loop diuretics :

Answer 20

eg. furosemide and bumetamide - treat high BP as block NKCC2 so loose H20 as little ions reabsorbed

Question 21

Early distal tubule reabsorption -

Answer 21

Na+, cl- and mg2+

NCC - Na and Cl transporter on apical
Mg cahnnels on apical not known how lost on baso
Na/K atpase on baso
K+ lost out of baso through channel
CLCK and Barttin - lose CL- into blood

Question 22

Gitelmanns syndrome

Answer 22

recessive, loss of salt, polyuria, hypotension, hypokalaemia, alkalosis as NCC mutation

Question 23

thiazide diuretics -

Answer 23

inhibit the NCC in early distal tubule

Question 24

2 cell types in distal tubule

Answer 24

prinicpal 
and intercalated (alpha and beta)

Question 25

Principal cell

Answer 25

ENaC - Na+ channel which is regulated by phosphrylation
ROMK - K+ out of apical, secreted into tubular fluid

The more Na+ in the more K+ out , Na+ drives ROMK

Aquaporin 2 - H20 into apical and out via AQP2,3

Question 26

Diabetes insipidus cause

Answer 26

if AQP2 in principle cell mutated

Question 27

Liddles syndrome

Answer 27

autosomal dominant, high blood pressure associated with low plasma renin activity, metabolic alkalosis, low blood potassium as increased activity of ENaK in principal cell

Question 28

Amiloride Diuretics -

Answer 28

block ENaK in Principal cell , treats high BP

Question 29

Alpha IC cell role in distal tubule

Answer 29

H+ secretion & HCO3- reabsorption

AE1 - BASOLATERAL SIDE - HCO3- out and Cl- in to regulate Ph
Cl- is pumped out by own channel to continue to allow HCO3- to b pumped out, it is recycled
H+ into tubular fluid by atpase pump

make blood more alkali

Question 30

Beta IC cell role in distal tubule

Answer 30

HCO3- secretion and H+ reabsorption

AE1 on apical membrane - HCO3- out and Cl- inCl- is pumped out by own channel to continue to allow HCO3- to b pumped out, it is recycled
H+ into blood by atpase pump

make blood more acidic

Question 31

Distal renal tubular acidosis

Answer 31

mutation in AE1 so pH drops

Question 32

Medullary collecting duct permeability:

Answer 32

low Na+ permeability but high H20 and urea in presence of vasopressin

Question 33

Hypovolamia :

Answer 33

low GFR so high BP

Question 34

Hyperkalaemia

Answer 34

lack of K+ secretion so cardiac excitability - increase arrhythmia

Question 35

Vasopressin -

Answer 35

posterior pituitary
regulates body fluid, conserve H20
osmoreceptor in hypothalamus sensitive to chance by 1%
If plasma osmolarity high - release vasopressin, thirsty
can increase due to high salt in food, drugs, stress

Acts on AQP2 in principal cells, binds to V2 receptor on basolateral, activates protiein kinase A, phosphorylates proteins on vesicle with AQP2 so fuse with membrane and increase of channels in the apical

if Vasopressin low, channels back to vesicle s

Question 36

Aldosterone -

Answer 36

adrenal glads in zona glomerulosa the outermost layer
a mineralocorticoid, regulates plasma Na+ and K+ volume
Released if K+ is high
acts on DT and CD causes Na+ reabsorption so k+ secreted

is a steroid hormone so cytosolic receptor as diffuses into cell
receptor stimulates RNA transcription of ENaC

Question 37

Renin -

Answer 37

in juxtaglomerular apparatus, released if low ECF volume. Causes angiotensin 1 to convert to 2 which is the acvtive form that causes the release of aldosterone and vasoconstriction to increase BP