Urology and renal Flashcards
what are the mechanisms to regulate sodium intake (2)
central
peripheral
how central mechanism regulate sodium intake
- increase appeptite for na+
- lateral parabrachial nucleus suppress desire for Na+ intake
- euvolemia
- inhibition of Na+ intake by serotonin glutamate
how peripheral mechanism regulate sodium intake
taste
where is sodium reabsorbed in nephron
PCT
thick ascending limb
DCT
collecting duct
what happens when there is increased tubular sodium and GFR
- higher tubular sodium
- increased Na/Cl uptake via triple transporter
- Adenosine release from Macula Densa cells
- Detected by extraglomerular mesangial cells
- reduces renin production
- promote afferent SMC contraction
- reduces perfusion pressure and GFR
role of juxtaglomerular cells
secrete renin
how increased SNS activity control sodium excretion
increased reabsorption at collecting duct, PCT, LOH, DCT
reduce GFR rate
stimulate JGA produce more renin
how Angiotensin ll control sodium excretion
increased reabsorption at PCT
increase aldosterone from adrenal gland to increase reabsorption at collecting duct
what is the main vasodilator to control sodium excretion
atrial naturietic peptide (ANP)
ANP role on decrease Na reabsorption
inhibit PCT, LOH, JGA, DCT, CT
when low sodium, will there be more angiotensin l or less
more
when low sodium, will there be more vasoconstriction or less
more
where is aldosterone made and released
adrenal cortex zona glomerulosa
what is aldosterone release in response to
angiotensin ll when decrease in BP via baroreceptors
function of aldosterone for ions (3)
increase Na reabsorption
increase K+ secretion
increase H+ secretion
what happens when aldosterone excess
hypokalaemic alkalosis
why steroid can pass through membrane
steroid hormone
lipid soluble
how aldosterone work in cells
aldosterone bind to mineralcorticoid receptor
translocate into nucleus
then bind to DNA for transcription
what happens when aldosterone increase in cortical collecting duct
increase active na+ channel
what happens in hypoaldosteronism
reduced Na reabsorption in distal nephron
increase urinary Na+ loss
ECF volume falls
increased renin and angiotensin ll and ADH
symptoms of hypoaldosteronism
dizzy
low BP
salt craving
palpitations
what happens in hyperaldosteronism
increased reabsorption of Na in distal nephron
reduced Na urinary loss
ECF volume increases
reduced renin, angiontensin ll and ADH
increase ANP, BNP
what increases in hyperaldosterone
BP
ANP
BNP
symptoms of hyperaldosteronism
high BP
muscle weakness
polyuria
thirst
what is Liddle’s syndrome
inherited disease of high BP
cause of Liddle’s syndrome
mutation in aldosterone activated sodium channel and the channel is always on
results of Liddle’s syndrome
Na retention
hypertension
which parts have high baroreceptor conc
carotid sinus
aortic arch
JGA
how low pressure side detect reduced in BP and counteract
low pressure
reduced baroreceptor firing
signal through afferent fibres to brainstem
SNS and ADH release
how low pressure side detect increase in BP and counteract
high pressure
atrial stretch
ANP and BNP release
how high pressure side detect reduced in BP and counteract
reduce BP
reudced baroreceptor firing
a) signal thru affernet fibres to brainstem to stimualte SNS and ADH release
b) stimulate JGA cells and release renin
when are ANP and BNP released
in respond to atrial stretch and high BP
actions of ANP
vasodilation of renal blood vessels
inhibit Na reabsorption in PCT and CT
inhibit release of renin and aldosterone
reduce BP
what are the direct effects of ACEi
reduce angiotensin ll
vascular effects of ACEi
vasodilation
increase vascular volume
reduce BP
reduce water reabsorption
direct renal effects of ACEi
reduce Na uptake in PCT
increase Na in distal nephron
adrenal effects of ACEi
reduce aldosterone
indirect renal effects of ACEi
reduce Na uptake in cortical CT
increase Na in distal nephron
where does loop diuretics act on
thick ascending LOH
where does thiazides diuretics act on
DCT
mechanism of carbonic anhydrase inhibitors
inhibit H2O+CO2 –> H2CO3
reduce Na reuptake in PCT
increase Na in distal nephron
reduce water reabsorption
effects of carbonic anhydrase inhibitors
increase urinary acidity
reduced Na+ reabsorption
example of loop diuretics
furosemide
mechanism of furosemide
triple transporter inhibitor
reduce Na reuptake in LOH
increase a in distal nephron
reduce water reabsorption
mechanism of thiazides
block Na+ Cl- uptake transporter
reduce Na+ reuptake in DCT
increase Na+ in distal nephron
increase Ca2+ reabsorption
reduce water reabsorption
mechanism of Potassium sparing diuretics
inhibits aldosterone function
example of potassium sparing diuretics
spironolactone
what is the main intracellular ion
K+
is K+ high or low in ECF
low
what is K+ uptake stimulated by after meal
insulin and aldosterone and adrenaline
what is K+ secretion stimulated by
aldosterone
increase tubular flow
increase plasma pH
increase [K+]
what cells secrete K+
principal cells
in principal cells what is the mechanism of K+ secretion
Na+ K+ ATPase uptake K+ and secrete Na+
K+ secretes out via K+ channel
causes of hypokalaemia
diet (too many processed food)
duretics
surreptitious vomiting
diarrhoea
genetics (mutation in Na/Cl transporter in distal nephron)
where is water reabsorped
PCT
descending limb of LOH
collecting duct
what is countercurrent multiplication
used to concentrate urine in the kidneys by the nephrons of the human excretory system.
most concetrated at bottom of LOH
where are UT-A2 found in nephron
think descedning LOH
where are UT-A1 and UT-A3 found in nephron
inner medullary collecting duct
UT-A1: apical membrane
UT-A3: basolateral membrane
what increases UT-A1 and UT-A3 numbers
vasopressin
role of UT-A2
transports urea across the apical membrane into the luminal space of cells in the thin descending loop of Henle of the kidneys.
role of UT-A1
urinary concentrating mechanism
what are the roles of urea transporter
facilitate urea reabsorption and concentration in the interstitium
what stimulates ADH production and release
increased plasma osmolarity
hypovolemia
decreased BP
nausea
angiotensin ll
nicotine
what inhibits ADH production and release
decreased plasma osmolarity
hypervolemia
increased BP
ethanol
ANP
mechanism of action of ADH
ADH release into blood vessels
bind to V2 receptor + G protein
cause adenylate cyclase to turn ATP to cAMP
cAMP + protein kinase A stimulates aquaporein 2 to insert onto membrane of collecting duct
what is diuresis
increased dilute urine excretion
where hv isomotic fluid
PCT
as excreted equal water and NaCl
where hv hypoosmotic fluid
end of LOH
which transporter helps with NaCl reabsorption at thick ascending LOH
basolateral:
Na+K+ ATPase (3Na out 2 K + in)
K+Cl- symporter (K+ and Cl- out)
apical membrane:
Na+K+2Cl- symporter (Na, K, 2Cl in)
K+ channel (K+ out)
where has NaCl reabsorption
thick ascending LOH
DCT
which transporter helps with NaCl reabsorption at DCT
basolateral:
Na+K+ ATPase (3Na out 2 K + in)
K+Cl- symporter (K+ and Cl- out)
apical membrane:
Na+Cl-symporter (Na and Cl in)
where is principal cells
collecting duct
which transporter helps with Na reabsorption at collecting duct
basolateral:
Na+K+ ATPase (3Na out 2 K + in)
apical membrane:
Na+transporter (Na in)
where does ADH support Na+ reabsorption (3)
- thick ascedning limb (increase Na+ K+2 Cl- symporter)
- DCT (increase Na+ Cl- symporter)
- Collecting duct increase Na+ channel)
what is central diabetes insipidus
decreased production and release of ADH
clinical features of Central Diabetes insipidus
polyuria
polydipsia
treatment for central diabetes insipidus
extrenal ADH
what is Syndrome of Inappropriate ADH syndrome (SIADH)
increased production and release of ADH
clinical features of SIADH
hyperosmolar urine
hypervolemia
hyponatramia
treatment of SIADH
non peptude inhibitor of ADH
what is nephron diabetes insipidus
less or mutant AQP2
mutant V2 receptor
clinical features of nephron diabetes insipidus
polyuria
polydipsia
treatment for nephron diabetes insipidus
thiazide diuretics and NSAIDs
role of kidney for acid-base balance
secretion and excretion of H+
reabsorption of HCO3-
production of new HCO3-
where do we have reabsorption of HCO3- (4)
PCT (main)
thick ascending LOH
DCT
collecting duct
how reabsorption of HCO3- works at PCT
Na+HCO3- symporter
role of alpha intercalated cell at DCT and CT
HCO3- reabsorption
H+ secretion
role of Beta intercalated cell at DCT and CT
HCO3- secretion
H+ reabsorption
how alpha intercalated cells at DCT and CT healp HCO3- reabsorption
and H+ secretion
Cl-HCO3- antiporter at basolateral : HCO3- reabsorption
H+ATPase and H+K+ATPase and apical: H+ secretion
how beta intercalated cells at DCT and CT healp HCO3-secretion
and H+ reabsorption
H+ATPase at basolateral : H+ reabsorption
Cl-HCO3- antiporter at apical: HCO3- secretion
where does new bicarbonate production occur
PCT
DCT CT
which transporter helps production of bicarbonate at PCT
Na+ H+ antiporter
which transporter helps production of bicarbonate at DCT and CT
at alpha intercalated cells
H+ATPase, H+K+ATPase at apical
Cl-HCO3- antiporter at basolateral
what is metabolic acidosis
lowered [HCO3-]
compensatory response for metabolic acidosis
increase ventilation
increase [HCO3-] reabsorption and production
what is metabolic alkalosis
increase [HCO3-]
compensatory response for metabolic alkalosis
decrease ventilation
increase [HCO3-] excretion
what is respiratory acidosis
increase PCO2
compensatory response for respiratory acidosis
increase [HCO3-] reabsorption and production
what is respiratory alkalosis
reduce PCO2
compensatory response for respiratory alkalosis
reduce [HCO3-] reabsorption and production
