Renal 1 Flashcards
what are the 3 main roles of the kidney
fluid, acid-base, electrolyte imbalance
what % of cadiac output goes to the kidneys
20%
what % of glomerular ultrafiltrate is reabsorbed
more than 99%
what is the functional unit of the kidney
nephron
how many nephrons in each kidney
bout a million’
what are the 5 main sections to the nephron
glomerulus, proximal tubule, loop of henle, distal convoluted tubule, collecting duct
what are glomerular capillaries permeable and not permeable to
permeable to water and many things, just impermeable to plasma proteins (eg. albumin)
how does the protein-free glomerular filtrate enter the bownmans capsule
hydrodynamic force
what do diurectics cause excretion of?
increased excretion of Na and Cl, causing a secondary loss of water
what are the main uses of diuretics (1)
alter the volume or composition of body fluids
where do diuretics act directly
on cells of the nephron in the kidney
where do diuretics act indirectly
by modifying the content of the filtrate
what are 6 classes of diuretics
osmotic diuretics, carbonyl anhydrase inhibitors, loop diuretics, thiazides, potassium sparing diuretics, antidiuretic hormone antagonists
what happens to osmotic diuretics when they pass through the nephron
they are not absorbed (if any, very minimal)
how do osmotic diuretics reduce water reabsorption
due to osmotic force of solute within the tubule
where do osmotic diuretics act
proximal tubule, descending loop of henle and collecting duct (where the nephron is most permeable to water)
what is the net effect of osmotic diuretics
increase in urine volume and urine flow rate, reduced Na+ reabsorption
what are therapeutic uses for osmotic diuretics
reduce intracranial pressure (brain injury or cerebral edema) or glaucoma
how/why can osmotic diuretics be used for brain injury and glaucoma
because they increase plasma osmotic pressure, which causes extraction of water from brain and eye
what is a serious adverse effect of osmotic diuretics and how can it happen
heart failure due to transient increase in extracellular fluid volume (sudden increase due to water leaving cells to follow osmotic force of blood-makes heart pump so hard)
can osmotic diuretics cause dehydration
yes
where does the majority of filtered Na+ and HCO3- reabsorption happen
early proximal tubule
how does Na+ enter the proximal tubule
Na+/H+ exchanger
how does Na+ enter the blood (proximal tubule)
Na+/K+ ATPase
what does carbonic anhydrase do in the lumen
turns H2CO3 into H2O and CO2
how is H2CO3 made in the lumen
HCO3- +H+
how does CO2 get into the early proximal tubule
diffusion
how is carbonic acid made in the proximal convoluted tubule
CO2 +H2O –> H2CO3 which is catalyzed by carbonic anhydrase
which reactions does carbonic anhydrase catalyze
H2CO3 –> CO2 +H2O
and
CO2 +H2O –> H2CO3
how does HCO3- exit the proximal tubule and into the blood
basolateral Na+/HCO3- co transporter
what happens in the late proximal tubule to HCO3-
low levels
what is the result of low levels of HCO3- in the lumen of late proximal tubule
H+ has no where to bind so the lumen is acidified
what happens when the lumen is acidic in the late proximal tubule
Cl-/base exchanger brings base to neutralize acid and Cl- enters the tubule
where do carbonic anhydrase inhibitors act on
proximal tubule
what does carbonic anhydrase inhibitors do to HCO3- reabsorption into blood
decrease
what do carbonic anhydrase inhibitors do to metabolic pH and how
decrease, causes metabolic acidosis because decreases HCO3- reabsorption into blood
what do carbonic anhydrase inhibitors do to Na+ reabsorption and how
decreases, because decreases supply of H+ for NHE3 (CA inhibitors prevents H2CO3 formation so H2CO3 cant be broken down into H+ and HCO3-)
what happens to water reabsorption with carbonic anhydrase inhibitors and how
decrease water reabsorption because there is decreased Na+ reabsorption (NHE3 not as active)
what happens to the pH of urine with carbonic anhydrase inhibitors
increases, becomes alkaline
what are 3 theraputic uses for carbonic anhydrase inhibitors
glaucoma
urinary alkalinisation
metabolic alkalosis
why are carbonic anhydrase inhibitors good for glaucoma
because carbonic anhydrase regulates formation of aqueous humor)
why are carbonic anhydrase inhibitors good for urinary alkalinisation treatment
because it increases the solubility of uric acid, good for gout (want urine alkaline for this)
what are some adverse effects of carbonic anhydrase inhibitors (3)
metabolic acidosis
renal stones
renal K+ wasting
how does carbonic anhydrase inhibitors cause metabolic acidosis
less HCO3- absorbed into blood
carbonic anhydrase inhibitors cause renal stones
Ca2+ and other salts precipitate in alkaline pH
how do carbonic anhydrase inhibitors cause renal K+ wasting
increased Na+ in collecting tubes causes increased K+ excretion
what does the SGLT2 do
reabsorb glucose and Na+ into tubule
where are the SGLT2 cotransporters
apical membrane of proximal convoluted tubule
what do SGLT2 inhibitos do
reduce absorption of glucose and Na+
when can SGLT2 inhibitors be used therapeutically
for diabetes type 2 because it reduces glucose reabsorption so its good to reduce glu in blood
do SGLT2 inhibitors have diuretic properties
yes but its not the main use. main use is for diabetes
