Lecture 4 Renal Flashcards
what are the main uses of diuretics
to INHIBIT reabsorption of Na and WATER, thus causing an increase in urine volume and dropping blood volume thus dropping BP
reasons for use of diuretics
CHF: Leads to dec GFR, INC aldosterone, INC Na and H2o Reabsorption, INC ECV and edema
HYPERtension: INC ECV, INC plasma volume thus INC BP
Diuretics aim to treat these symptoms and thus dec the effects of these diseases
Osmotic diuretics action and site of action
Osmotic diuretics act in PCT and descending LoH
retain water by INC osmotic pressure, go in the tubule by filtration
CA inhibitors action and site of action
CA inhibitors DEC Na reabsorption and act in PCT
Loop diuretics action and site of action
loop diuretics act in THICK ASCENDING LIMB to inhibit Na reabsorption VIA NaKCl2 symporter
Thiazide action and site of action
thiazides act in DCT by blocking NaCl symporter
K sparing action and site of action
K sparing act in collecting ducts and DCT to inhibit Na reabsorption and INHIBIT K secretion
2 classes of K sparing diuretics
aldosterone antagonists
ENaC blockers
aqueretics site of action and action
aqueretics act in collecting duct and are aldosterone receptor antagonists
what is the only diuretic that gains access to the tubules thru filtration
Osmotic diuretics only one!
osmotic diuretics do what
2 examples
absorbed or poorly absorbed?
effects what part of tubule
results in excretion of how much filtered Na?
INC osmotic pressure in tubular fluid thus INHIBITING Na reabsorption
mannitol and elevated glucose
poorly absorbed
actions where tubule is permeable to water
10% INC in excretion of filtered Na
If osmotic diuretics DEC water reabsorption what happens to Ca absorption
Ca absorption is DEC due to solvent drag
CA inhibitors act how example gain access to tubule how? most of diuretic effect is where? INC Na excretion how much
CA inhibitors DEC Na absorption by INHIBITING CA thus reducing H for Na/H antiporter example: acetazolamide gain accès to PCT by secretion most of diuretic effect in PCT INC Na excretion 5-10%
Loop diuretics act how act where? example? secreted of filtered? INC Na excretion how much
loops: Inhibit Na absorption inhibiting Na K 2Cl symporter hus causing urine to leave loop diluted Loops act in THICK ascending limb example: furosemide (lasix) secreted! INC Na secretion by 25%!
what do loop diuretics prevent from forming causing urine to be diluted
Loops prevent osmotic gradient from forming in medullae interstitium so water is NOT reabsorbed in collecting duct
what is the most powerful diuretic?
LOOPS = most powerful for failing kidney and CHF
Thiazides act how act where? secreted or filtered example how much Na secreted bc of thiazides
Thiazides inhibit NaCl transporter thus inhibits Na absorption - diminishes kidneys ability to dilute urine
act in early DCT
example: chlorothiazide
INC Na secretion of 5-20%
K sparing diuretics act how
act where and on what specifically?
secreted or filtered
act by aldosterone antagonists or inhibiting ENaC this inhibiting Na absorption
secreted into fluid
act on principal cells in DCT and collecting ducts
what do aldosterone antagonist K sparing drugs do
blocks aldosterone ability to INC Na transporters in principal cells
what do ENaC inhibitor K sparing diuretics do
block Na absorption across apical membrane, act on membrane proteins
Aquatics developed why
act how
act where
aquatics developed to prevent loss of Na and only INC excretion of H2O
act by blocking action of ADH this INC secretion of water but allowing Na to be absorbed
act in DCT and collecting duct
explain the 2nd effect of diuretics called diuretic braking phenomenon
continued use of diuretics becomes less effective BC Volume contraction counteracts the effects of the diuretic
IE: diuretics DEC ECV so compensatory mechs involved
what compensatory mechanisms are involved with diuretic braking phenomenon (x4)
INC simp activity in RED BP > DEC GFR > INC PT and renin
DEC natruiretic peptides
DEC Na excretion bc INC Renin
INC ADH thus DEC water excretion
what does aldosterone do
INC Na reabsorption thus dec WATER excretion
another secondary effect of diuretics is INC secretion of K why? (2x)
what drug prevents K secretion and loss
diuretics INC flow of tubular fluid which INC K secretion
reduce ECV > INC aldosterone > INC K secretion
Use K sparing diuretics to dec K loss
how does acid base balance become affected by diuretics? specifically talk about 4 drugs
CA inhibitors= metabolic acidosis
Loops and Thiazide= DEC ECV > metabolic ALKALOSIS
K sparing= metabolic acidosis bc H secretion is inhibited
what drugs cause metabolic acidosis
CA inhibitors and K sparing = acidosis
what drugs cause metabolic alkalosis
Loops and thiazides= alkalosis
what is the only drug that does NOT alter Ca excretion?
K sparing diuretics has NO effect on Ca
What do osmotic and CA inhibitors due to Ca
Osmotic and CAIs RED Ca absorption this INC Ca excretion
what do loops do to Ca levels and how
Loops INC Ca excretion by affecting the transepithelial voltage
what do thiazides do to Ca levels?
Thiazides INC Ca REABSORPTION!!! reduce excretion of Ca
when is hemodialysis needed and what is it
Hemodialysis is the removal of waste products from blood when kidney is impaired. demand is on the rise!
how are dialysis fluid and plasma similar and what does the cause
both have similar concentrations of NaCl so urea, K, and phosphatase diffuse from blood into dialysis fluid
what is high in dialysis fluid to flow into blood to reduce blood acidity
dialysis fluid has high bicarbonate
methods to access blood for dialysis
pros and cons of the 3 methods
catheter: venous blood access for short term TX, scarring, vessel narrowing or occlusion can occur
AV fistula: Long term TX, creates an anastomosis between A and V, takes out arterial blood and returns blood to vein
AV graft: artificial vessel to join and A and V when there are vascular problems, cons: narrowing, clotting and infection
what can dialysis prescription be based on (3x)
typical TX
dialysis depends on frequency, type of fluid, size of dialyzer
typical TX: 3-4 hours per 3x a week
side effects of hemodialysis
short term
long term
vascular access problems
fatigue, chest pain, cramps, naussea, headaches due to acute change in blood chemistry
THE DIALYSIS HANGOVER
Long term: sepsis, endocarditis, osteomyelitis
amyloid deposits in joints from build up of minerals in dialysis fluid
patients with ESRD are always diagnosed with what and why
ESRD = anemia bc DEC secretion of EPO and DEC of RBCs
what is EPO
hormone produced by kidneys that stimulates bone marrow to make red blood cells
what is EPO made by and controlled by
EPO made by interstitial fibroblasts in renal cortex and is controlled at transcription level
when is EPO production INC?
EPO production stimulated when PO2 is low
what transcription factors regulate production of EPO in DEC PO2
hypoxia inducible factors 1 and 2
HIF 1 and HIF 2
Describe the life of HIF 1 and HIF2
HIF 1 and HIF 2 are continually made but degraded when PO2 is normal
what does EPO stimulate
EPO stimulates differentiation of RBC progenitor cells in bone marrow
treat of anemia by using EPO uses what
use Procrit to stimulate erythropoiesis
side effects of Procrit
flu like symptoms, headaches, high BP, cardio problems
