regulation of homeostasis via the kidney Flashcards
what is fluid balance?
the amount of water gained by the body each day equals the amount lost
what is electrolyte balance?
the ion gain each days equals ion loss
what is acid-base balance?
H+ gain is offset by H+ loss
what do acids do?
release H+ into solution
what do bases do?
remove H+ from solution
what are the 2 groupings of acids and bases?
strong or weak
what do buffers do?
- resist changes in pH
- when H+ added, buffer removes it
- when H+ removed, buffer replaces it
what are the 3 types of bugger systems?
- carbonic acid/bicarbonate
- protein
- phosphate
what is the optimal pH window?
7.2-7.4
what happens when the lungs excrete a large amount of CO2?
- potential acid is formed by metabolism
- CO2 reacts with water to form carbonic anhydrase
what must the kidneys do to maintain acid-base balance?
- excrete non-volatile acids produced form normal metabolism
- reabsorb virtually all filtered HCO3-
what does HCO3- do?
acts as a physiological buffer
what is the average blood pH?
7.4
what is the average urine pH?
6.0
what is the average concentration of HCO3- in the blood?
24mM
wha is the average partial pressure of CO2 in the blood?
40mmHg
what happens when the partial pressure of CO2 increases?
pH decreases
what happens when the partial pressure of CO2 decreases?
pH increases
what detects the changes in pH levels?
peripheral chemoreceptors
what happens to adjust respiration rates?
the peripheral chemoreceptors act on respiration centres in the brain
how does renal tubular acidosis occur?
when there is insufficient reabsorption of HCO3- and H+ secretion
what happens if pH or ECF falls?
acidaemia
what needs to happen to reverse acidaemia?
- more secretion of H+ into filtrate
- reabsorption of HCO3- back into ECF
when is secretion of H+ inhibited?
when urine pH falls below 4.5
what happens if pH or ECF increases?
alkalaemia
what needs to happen to reverse alkalemia?
- secretion of H+ into filtrate
- reabsorption of HCO3- declines extracellular
what is acidosis?
when the pH of body fluids falls below 7.35
what is alkalosis?
when the pH of body fluids goes above 7.45
how do you reverse acidosis?
- get rid of H+ out of the body
- excrete H+ via the lungs as CO2 and in the kidneys as H+
- generate more buffer (HCO3-) in the kidneys
how do you reverse alkalosis?
- increase H+ levels in the body
- reduce excretion of CO2 via the lungs
- increase excretion of HCO3- buffer via kidneys
- increase generation of H+ via kidneys
what causes respiratory acidosis?
- caused by inadequate ventilation
- can be acute or chronic
what causes metabolic acidosis?
- results from all conditions other than respiratory that decrease pH
- always chronic
how can you gain H+?
- CO2 in blood (combines with H2O to form carbonic acid)
- non-volatile acids from metabolism
- loss of HCO3- in diarrhoea or non-gastric GI fluis
- loss of HCO3- in urine
how do you treat metabolic acidosis?
- give IV isotonic HCO3-
- give IV lactate solution
how do you treat respiratory acidosis?
- restore ventilation
- treat underlying dysfunction or disease
- give IV lactate solution
what causes respiratory alkalosis?
- caused by hyperventilation
- can be acute or chronic
what causes metabolic alkalosis?
- results from all other conditions other than respiratory that increase pH
- always chronic
how ca you suffer a loss of H+?
- use of H+ in metabolism of organic ions
- loss of H+ in vomit
- loss of H+ in urine
- hyperventilation
how do you treat metabolic alkalosis?
- give electrolytes to replace those lost
- give IV Cl- containing solution
- treat underlying disorder
how do you treat respiratory alkalosis?
- treat underlying cause
- breathe into paper bag
- give IV Cl- containing solution
what are some causes of respiratory acidosis?
- reduced elimination of CO2 from the body fluids
- asphyxia
- hypoventilation
- advanced asthma
- severe emphysema
what are some causes of metabolic acidosis?
- elimination of large amounts of HCO3- resulting from mucous secretion
- direct reduction of the body fluid pH as acid is absorbed
- production of large amounts of fatty acids and other acidic metabolites such as ketone bodies (untreated diabetes mellitus)
- inadequate oxygen delivery to tissue resulting in anaerobic respiration and lactic acid build up
what are some causes of respiratory alkalosis?
- reduced CO2 levels in the extracellular fluid
- decreases atmospheric pressure reduces oxygen levels, which stimulates the chemoreceptor reflux causing hyperventilation
what are some causes of metabolic alkalosis?
- elimination of H+ and reabsorption of HCO3- in the stomach or kidney
- ingestion of alkaline substances
how does ADH work?
- interacts with V2 receptors on the basolateral surface of principal cells in the collecting duct
- results in increased permeability of collecting duct to H2O by insertion of aquaporin-2 water channels on apical surface
- maximal ADH leads to production of low amounts of concentrated urine
how is volume regulated by ADH?
- ADH released in response to changes in plasma osmolarity and effective circulating volume
- these changes are detected by osmoreceptors and baroreceptors
what happens in dehydration?
- increased plasma osmolarity stimulates osmoreceptors in the hypothalamus which trigger ADH release
- more water reabsorbed from collecting ducts in kidney back into circulation leading to increased ECV
- increased osmolarity also stimulates a second group of osmorecetpors in the hypothalamus which triggers thirst
- promotes water intake which enters circulation which also increases ECV
how does urea play a part in the countercurrent multiplication?
- active transport of NaCl contributes 600-1000mOsm
- urea is freely filtered at glomerulus
- some reabsorption in proximal tubule, but LOH and distal tubule relatively impermeable to urea
- urea can diffuse out of collecting drug into medulla down its concentration gradient
- this adds to the osmolarity of medullary interstitium
what are the 2 main types of central vascular sensors?
- low pressure blood volume receptors
- high pressure arterial stretch receptors
where are the low pressure blood volume receptors found?
- large systemic veins
- cardiac atria
- pulmonary vasculature
where are the high pressure arterial stretch receptors found?
- carotid sinus
- aortic arch
- renal afferent arteriole
what is the feedback control of ECV mediated by?
baroreceptor stimulation
what are the 4 parallel effector pathways that act on the kidney?
1) RAAS
2) sympathetic nervous system
3) ADH release
4) ANP release
what are the 3 ways that decreased ECV stimulates Reni release?
1) decreased renal perfusion pressure detected in the afferent arteriole the ‘renal baroreceptor’
2) decreased Na+ concentration in the distal tubule detected by the macula densa cells the ‘renal Na+ sensor’
3) decreased sympathetic BP also triggers effects of the sympathetic nervous system supplying the JGA
what are the 3 actions of AngII that increase ECV?
1) enhances tubular Na+ transport in the kidney: promotes Na+ and water reabsorption from tubule
2) stimulation of aldosterone release from adrenal cortex: more Na+ and water is reabsorbed from distal tubule/collecting duct
3) acts on hypothalamus to stimulate thirst and ADH release into circulation: water intake adds to ECV and ADH increases water reabsorption from the collecting duct
what is a long term effect of AngII?
causes renal hypertrophy so more protein synthesis of Na+ transporters and channels
what are the 3 actions of aldosterone that increase ECV?
1) stimulates Na+ reabsorption in the distal tubule and collecting duct
2) aldosterone also exerts indirect negative feedback on the RAAS by increasing ECV and lowering plasma K+ concentrations
3) important in conserving Na+ and water but also important in preventing large variation in plasma K+ levels
what is the RAAS volume regulation pathway?
1) decreased ECV
2) detected by renal baroreceptors and renal Na+ sensors
3) activation of the RAAS
4) AngII and aldosterone
5) reduced Na+ excretion by the kidney and increased renal Na+ reabsorption
6) increased ECV
what is the ANS volume regulation pathway?
1) decreased ECV
2) detected by peripheral baroreceptors
3) signals to hypothalamus in brain
4) activation of the ANS
5) direct effets on renal haemodynamics and activation of RAAS
6) reduced Na+ excretion by the kidney and increased renal Na+ reabsorption
7) increased ECV
what are the 2 ADH volume regulation pathways?
FIRST ONE
1) decreased ECV
2) detected by peripheral baroreceptors
3) signals to hypothalamus in brain
4) release of ADH into circulation
5) increased water reabsorption in the kidney
6) increased ECV
SECOND ONE
1) decreased ECV = increased plasma osmolarity
2) detected by osmoreceptors in hypothalamus
3) release of ADH into circulation
4) increased water reabsorption in kidney
5) increased ECV
how does ANP work?
- designed to lower ECV
- atrial myocytes synthesise and store ANP
- increased ECV causes atrial stretch which leads to ANP release into circulation
- ANP promotes natriuresis
- also causes renal vasodilation so increased blood flow leads to increased GFR so more Na+ excreted
- more Na+ reaches the macula densa so rent release by JGA is reduced: reduces the effects of AngII
what is the overall effect of ANP?
inhibits actions of renin and opposes effects of AngII
