renal - lecture 6 Flashcards
what is alkalosis
low [h+] = high ph
resp alkalosis results from altered respiration
metabolic alkalosis results from other causes
what is acidosis
high [h+] = low ph
resp acidosis results from altered respiration
metabolic acidosis results from other causes
name 3 responses to acidosis
1 - sufficient h+ are secreted to reabs all filtered bicarb
2 - still more h+ secreted and contributes to new bicarb to the plasma as h+ excreted are bound to non bicarb buffer like hpo4 2-
3 - tubular glutamine metabolism and ammonium excretion are enhanced = contributes to new bicarb to plasma
all 3 active to try to help
what is net result when acidosis
more new hco3 - than usualy added to plasma = compensates for acidosis
urine highly acidic
lowest ph = 4.4
name 3 responses to alkalosis
1 - rate of h+ secretion inadequate to reabs all filtered bicarb = so lots of bicarb excreted in purine - not complete reabs anymore
2 - little/no h+ secretion on nonbicarb buffers
3 -tubular glutamate metabolism and ammonium excretion decreased so that little or no new bicarb contributed to plasma from this source
describe net result when alkalosis
plasma bicarb will decrease = compensates for alkalosis
urine high alkaline ph >7.4
describe classification of acidosis and alkalosis
resp = primary abnormality =co2
metabolic = primary abnormality hco3-
primary and compensatory = same direction
what happens when resp acidosis
Pco2 = increase co2 so reaction shifts right and h
+ increases
H+ = increase
HCO3 - = since [bicarb]/[co2] = then bicarb must go up to compensate
what happens when resp alkalosis
Pco2 = decrease
H+ = decrease
HCO3 - = decrease
what happens when metabolic acidosis
HCO3 - = decrease
H+ = increases
Pco2 = decreases
what happens when metabolic alkalosis
HCO3 - = increases
H+ = decreases
Pco2 = increases
describe clinical ex of resp acidosis
resp failure with co2 retention
compensates = increase bicarb
describe clinical ex of resp alkalosis
hyperventilation eg high altitudes
also pregnant women
bicarb compensates by decreasing
what are diuretics
drugs used to clinically increase vol of urine excreted
describe clinical ex of metabolic acidosis
diarrhea = loss of bicarb in poop
renal failure = accumulation of inorganic acids
so body naturally hyperventilates so co2 goes down
describe clinical ex of metabolic alkalosis
less common
vomiting = loss of hydroen ion in vomit
hyperaldosteronism= primary aldol= increased h
+ secretion in dct and ccd, loss of h+
so tries to retain more co2 to compensate
what do diuretics act on
tubules to inhibit reabs to sodium along with chloride and or bicarbonate
Results in increased excretion of these ions
water excretion increased too
sodium and water excretion in urine
describe loop diuretics
acts on thick ascending limb
most common
inhibits cotransport of sodium, chloride and potassium = Na -K -2Cl cotransporter
furosemide
stops na reabs at tal
describe potassium sparing diuretics
other diuretics lead to hypokalemia
inhibit na reabs in ccd and also inhibits k secretion here
unlike other diuretics, plasma conc of k doesnt dcrease
either block action of aldosterone or block aldosterone regulated epithelium na channel in ccd
amiloride, spironolactone
describe action of potassium sparing diuretics - figure
block aldosterone and k secretion
spironolactone blocks aldosterone = which controls channels and nakatpase
amiloride = blocks sodium channel channel similar to blocking aldosterone
= k+ secretion coupled
what is clinical use of diuretics
renal retention of salt and water = abnormal expansion of ecf = edema
what is clinical use of diuretics ex 1 and 2
congestive heart failure = cardiac failure leading to lowered co, kidney sense by baroreceptors and reabs salt and water back = edema and wet lungs = bad
hypertension = in some patients with hypertension, renal retention of salt and water contribure to high bp, use less powerful diuretics
name many common features of kidney disease or failure
proteinuria = protein in urine
accumulation of waste products in blood = urea, creatinine, phosphate, sulfate
high k conc in blood = hyperkalemia
metabolic acidosis
anemia = decreased secretion of epo - so no good rbcs but now = recombinant epo can be administered
decreased secretion of 1,25-hydroxylated vit d = leads to hypocalcemia = final hydroxylation in kidneys
when do kidneys need replacement therapies
when more than 90% of nephrons stop working= cannot sustain life
one must have renal replacement therapies
name 3 renal replacement therapies
- Hemodialysis
- Peritoneal dialysis
- Kidney transplantation
describe hemodialysis - gen
surgically enlarged veins = blood flows to hemodialyzer and gets filtered then returned to body via vein = 3-4 hrs per day a few times a week= need it to live
describe hemodialysis - specifics
arterial blood from patient –> blood pump 350-400ml/min –> anticoagulants added –> dialyzer= strands of tubings removes waste products from blood and gets rid of extra water , fresh dialysis fluid (concentrate and purified water) added in –> air trap an air detector –> venous blood returned to patient
describe peritoneal dialysis
lining of patients own abdominal cavity - peritoneuem used as dialysis membrane
fluid injected into cavity via tube inserted through abdominal wall
solutes diffused into fluid from persons blood
fluid exchanged several times per day
cycler automatically does it over night = good at home
brain bad = after a few hours = many times a day
do not have to stay attached
describe kidney transplantation
best replacement
either from deceased person (cadaveric transplant) or from living related/unrelated donor - altruistic donor
anti rejection treatments have improved lots in recent years
organ shortage a problem
donors can function quite normally with one kidney
best = if twin donates kidney since no chance of rejection
