transport mechanism 2 Flashcards
(20 cards)
describe potassium balance ?
Potassium concentration ECF is 4.2 and 140 ICF ( MORE INSIDE THE CELLS )
Regulation of K is difficult because 98% of potassium is concentrated inside the cells and 2% outside —> Maintenance of internal potassium balance is difficult
External balance is maintained by rapid adjustment to excretion through the kidney
Failure to get rid of extracellular fluid of potassium ingested each day could result in life threating hyperkalemia
A small loss of potassium from extracellular fluid could cause severe hypokalemia in absence of rapid compensatory response
Potassium is ESSENTIAL for excitable tissue
Precise control is required
increase in plasma concnetration can cause cardiac arrhythmias and higher can lead cardiac arrest/fibrillation
what are causes of hyperkalemia?
Diabetes ( cuz insuline increases cell uptake = when missing no uptake )
Deficiency of aldosterone ( aldosterone increases cell uptake )
BB
Acidosis ( cuz it make kidney reabsorb potassium )
Cell lysis
Strenuous exercise
Hyperosmolarity –> causes cell dehydration - raises intracellular potassiuum . promotes diffusion of potassium from cells
what are causes of hypokalemia
Insulin ( cuz increases potassium uptake )
Aldosterone ( secrete K and absorb Na )
B adrenergic stimulation
Alkalosis ( cuz kidney will secrete potassium )
describe external potassium balance?
High potassium intake = Increased secretion of potassium
Low potassium intake = increased absorption and decreased secretion
Day to day regulation of potassium excretion occurs by changes in K secretion in LATE DISTAL and collecting Tubules
In thick ascending limb = we have N/K/2cl pump for K regulation
reabsorption of potassium is not affected much except in late DCT and collecting tubules with intercalacted cells which are very important in variability ( secretion and reabsorption ) of potassium cells
Describe potassium secretion?
Principal cells reabsorb sodium and excrete potassium under ALDOSTERONE
Water is influenced and regulated by ADH
Electrochemical gradient created by Na/K atpase
High K INTRACEULLULARY secreted into lumen via BK and ROMK channels
K+ secretion regulated by here aldosterone activity by increasing Na/K atpase activity BK ROMK expression
High potassium diet = high potassium excretion
Increased urine rate = Increased K secretion
Acute acidosis : Hyperkalemia without increased potassium excretion ( cuz in acidosis K is reabsorbed )
Chronic acidosis : Reabsorption of soidum and water is at PCT is distorted = more sodium and water lost = urine flow rate increases = increased urine excretion of potassium = hypokalemia
what is the role of type A intercalated cells ?
in acidosis they secrete H outside to reduce acidosis
via H/k ATPASE and H atpase
will secrete H outside and bring a K inside ( Hyperkalemia )
It also PREVENTS HYPOKALEMIA by reabsorbing K
what is the role of type B intercalated cells?
function in ALKALOSIS
they reabsorb H
they reabsorb H but secrete K
function in hyperkalemia as well by secreting K
using the same channels: H/K atpase and H atpase but on opposite sites
Regulation of increased potassium secretion ?
High Potassium diet
Increased Aldosterone
Alkalosis (cuz we take in H and release K )
Diuretics ( INCRREASE SECRETION ARE ONE SPECIFIC FOR K ions )
Regulation of decreased secretion of K?
Low potassium diet
Decreased aldosterone
Acidosis
Potassium sparing diuretics
Describe glucose absorption ?
All glucose reabsorbed in PCT
Normally No glucose in urine
Facilitated diffusion on the basolateral side and secondary active transport on the luminal side by :
GLUT1—> LATE PCT ( 1 am = late )
GLUT2—-> EARLY PCT ( 2 is early )
Secondary active transport channels as SGLT ( Na/glucose cotransporter )
SGLT1—>LATE PCT ( 10% of glucose ) ( 1 am = late )
SGLT2—> EARLY PCT ( 90% of glucose ) ( 2 pm is early )
Describe glucose titration curve and transport maximum?
Filtered load is the quantity of substance that is filtered per unit time
Glucose is freely filterable
filtered load = GFR x solute plasma conc
Filtered load increases with increased plasma concentration of the solutes
at plasma conc LESS than 200 all filtered load is reabsorbed
at plasma conc above 200 curve bends
at above 350 carries are saturated so theres platuea or transport maximum
Maximum tubular reabsorptive capacity or tubular maximum for glucose :
Maximum amount of glucose that can be absorbed per unit time = approx is 375
at 375 = no more reabsorption increasing
describe glycosuria ?
Normally no measurable glucose appears in urine
All filtered glucose is reabsorbed in proximal tubule
Plasma conc of glucose above 200 = small amount of glucose in urine
appearance of glucose in urine occurs before T maximum is reached
Threshold and Tm are different because all nephron dont have same Tm for glucose
The overall T maximum for nephrons is 375
healthy person no excretion of glucose in urine
In uncontrolled diabetes mellitus glucose levels become high causing filtered load of glucose to exceed the T maximum urinary excretion of glucose
describe urea reabsorption ?
usually by simple diffusion
in Thin descending limb ,theres higher conc of urea in interstitium = Urea is secreted into the tubule
So its secreted to tubule in thin descending limb
THEN REABSORPTION AT :
Medullary collecting ducts cuz of UT1 transporter which create hyperosmolar interstitial environment in the medulla for urine conc
ADH cause water reabsorption in the distal tubule increasing the concentration of urea ( so water doesnt reach medullary only urea does ) = more urea reabsorption
describe PAH secretion? PARA AMINOHIPPURIC ACID
at low concentration of plasma PAH, excretion is filtration plus secretion
at high concentration there is SATURATION because T maximum ( saturation of carriers )
transporters get saturation in SECRETION so secretion is decreased ( cant secrete more cuz no carrier )
Describe what types of TF/P?
TF/P = freely filtered
TF/P less than 1 = reabsorption of solutes more than water
TF/P more than 1 = either net secretion of solute or more water absorption than solutes substances
TF = tubular fluid
Describe phosphate handling in nephrons ?
Phosphate secreted in PCT and DCT
most of phosphate is reabsorbed by Na/Phosphate cotransporters ( Transcellular )
Critical for urinary buffering of H and constituent of bones
PTH increases phosphate secretion in urine by :- phosphate trashing hormone
Inhibits Na/PO3 cotransporter in PCT ( Resulting in inhibited reabsorption )
The decrease the transport max which leads to a way faster occupation of transporter
most of phosphate unbound and 90% IS FILTERED
Phosphate also follows transport maximum Tm like glucose cuz its absorbed by carrier T=0.1
when less than this amount is present in the GFR all filtered phosphate is reabsorbed and when more than this excess is excreted
Pseudohypoparathyroidism :
Defect in receptors for PTH, PTH is normal but receptor defective so no phosphate in urine
describe calcium handling in the nephron?
99% of calcium in body is contained in bones
only free clacium is ultrafilterable 60%
Decreased ECF calcium —- Increased secretion of PTH = increased calcium reabsorption occurs through the thick ascending loop of henle and distal tubule which reduces urinary excretion of calcium
80% of calcium is reabsorbed Paracellularlly mostly dissolved in water
Transcellular route only 20% calcium diffuse through luminal membrane down the gradient exist through basolateral membrane via :
Calcium atpase pump
Na-Ca counter transporter
describe magneium handling in then nephron?
Small % is reabsorbed in DCT
Overall absorption is 95% and 5% is excreted and primary site for reabsorption is the loop of henle
Furosemide = loop diuretics inhibit reabsorption and increase excretion
describe bicarbonate handling nephron?
Indirectly through H secretion
H leaves by Na/H channels to luminal side
Then H units with HCO3 in the lumen
H + HCO3 = H2CO3 = CO +H2O —-> Go inside the cell REFORM to HCO3 AND H and then HCO3 is reabsorbed and H goes back n cycle repeat –> VIA CARBONIC ANHYDRASE
mechanism for reabsorption of filtered HCO3 in cell of the proximal tubule
90-95% OF filtered bicarbonate reabsorbed
Carbonic anhydrase inhibitor reduces H secretion and bicarbonate reabsorption
What to expect to happen if carbonic anhydrase inhibited?
Less H excreted / Less HCO3 = reabsorbed = Acidosis
Less Na is reabsorbed and extra sodium is lost in urine ( cuz Na/H exchanger inhibited )
Less water reabsorbed - more water excreted , increased urine volume ( cuz less sodium )
response to water and drinking and dehydraiton?
Dehydration —> Increased Plasma osomlarity —> Hypothalamus —> Increased thirst + ADH secretion —-> Principal cells express aquaporin —> Increase water reabsorption
Opposite happen when plasma is osmolarity is decreased ( High fluid )
