physiology Flashcards
what is the horizontal gradient between levels of the loop of Henle
200 mOsmol
how do stretch receptors in the bladder control micturition (babies/ spinal injuries)
become distended as the bladder fills (300- 350mls) until their output is large enough to stimulate parasympathetic system and relax external sphincter by inhibiting somatic neurones
what effect does hyperkalaemia/ hypokalaemia have on the body cells
hyperkalaemia - >5.5 - lower r.m.p –> ventricular fibrilation
hypokalaemia - <3.5 - increase r.m.p –> hyper polarise cells –> cardiac arrythmias
when the renal artery constricts what hormone is released
Renin
what is the HCO3 in blood
24 mmoles/ L (22- 26)
what is the pH of blood and how many H ions are free
7.4 (7.37 - 7.43)
4 x 10-6 mmoles/L free H - contribute to pH
what is the henderson hassebalch equation for pH
pH = HCO3/ PCO2
if a substance has a lower clearance that inulin what will happen
filtered and reabsorbed
[Ux] lower, [Px] higher
how do changes in osmolarity affect osmoreceptors
increases osmolarity - water out the cells, cells shrink, increased neural discharge
decreased osmolarity - water in the cells, cells swell, decreased neural discharge
what is the anion gap
difference between the sum of principal cations (Na and K) and principle anions (Cl and HCO3) in the plasma
normally 14-18 mmoles/L
what is the filtration fraction of the kidneys
19%
GFR/ Renal plamsa flow (55% of BV) x 100 = 125/660 x 100
when the mean arterial blood pressure increases, what happens to the afferent arteriole?
constricts - prevent rise in glomerular pressure
describe the process of ammonium excretion
in renal tubule cells - deamination of glutamine by renal glutaminase enzyme produces NH3
NH3 moves out tubule to combine with secreted H (fro CO2 in blood)
NH4 is formed in lumen which combines with Cl and NH4Cl is excreted in distal tubule
how does a metabolic alkalosis occur
HCO3 increase
what is the minimum and maximum pH of urine
min - 4.5-5
max - 8
what is used to estimate GFR
creatinine clearance
eGFR = 1/ [PCr]
in antidiuresis, how is urea retained to save water
reabsorbed from collecting duct into interstitium where it reinforces the interstitial gradient in the loops of Henle
if molecules X has filtration < excretion what will be the renal handling of X
net secretion
how do osmoreceptors regulate ADH secretion
increased osmolarity increased neural discharge mediated by osmoreceptors in the anterior hypothalamus
what is the mechanism for reabsorption of HCO3
active H secretion from tubule cells coupled to passive Na reabsorption
filtered HCO3 reacts with H to form H2CO3
with carbonic anhydrase this is converted into CO2 and H20
CO2 freely permeable and enters the cell
within the cell CO2 forms H2CO3 which dissociates to H and HCO3
the HCO3 ions pass into the peritbular capillaries with Na
(1 for 1 - no net gain)
how does increased sympathetic nerve activity impact renin release
increase release (B1 effect)
why can a big blood transfusion cause a metabolic alkalosis
bank blood contains citrate to prevent coagulation which is converted to HCO3
in the absence of ADH, what happens to water in the collecting duct
impermeable to H20 so large volumes of dilute urine are lost (compensate for H20 excess)
where does the majority of respiratory acid get buffered
97% within cells
rest within plasma proteins
what is the function of ANP
promotes Na excretion
what is the kidney regulation of HCO3 dependent on
active H ion secretion from the tubule cells into the lumen
how does the body respond to a low ECF to reduce blood pressure
reduced; ECF –> plasma volume –> venous pressure –> venous return –> atria pressure –> end diastolic volume –> systolic volumes –> cardiac output –> BP –> carotid sinus baroreceptor that normally inputs sympathetic discharge
increased sympathetic discharge
why is the oncotic pressure in peritubular capillaries so high
very concentrated plasma proteins
why is knowing GFR important in drug prescribing
if drug is excreted by the kidneys reduced GFR will increase drug concentration which may lead to toxicity
(adjust dose to appropriate renal function)
what factors affect serum creatinine
muscle mass
dietary intake
drugs
when is ANP released from he atria of the heart
response to expansion of ECF volume - causes natriuresis, loss of Na and H20 in urine
how do pudendal nerves control micturation
somatic motor neurones - innervate skeletal muscle of external sphincter, keeping it closed against strong bladder contractions (s2,3,4)
for micturition they must be inhibited by interneurones
how long do respiratory compensations take to occur
minutes
how does the kidney regulate HCO3
reabsorbing filtered HCO3
regenerating new HCO3
what blood pressure range is auto regulation effective in
60- 130 mmHg
filtration ceases <50 mmHg
how do juxtaglomerular cells act as renal baroreceptors
increase renin release when increased pressure in afferent arteriole
what can cause a metabolic alkalosis
- H ions lost in vomiting
- renal H lost in excess aldosterone/ liquorice (glycyrrhizic acid)
- excess HCO3 administration in renal impairment
- big blood transfusions
what is the equation for the buffer of plasma proteins
Pr + H –> HPr
what is the osomotic concentration of the fluid that leaves the proximal tubule
300 mOsmoles/ L - same as the plasma
what is used to measure renal plasma flow (RPF) and why
para-amino hippuric acid (PAH)
- freely filtered and actively secreted so plasma content is cleared of it
what is the net filtration pressure of the glomerulus
10 mmHg OUT
what is the vertical gradient of the loop of henle
300 -1200 mOsmol
what drug abolishes the the active transport of NaCl in the loop of henle
diuretics - furesmide
NaCLa nd H20 are no longer absorbed and concentration differences are lost - kidney produces a large amount of isotonic urine
what is oncotic pressure
osmotic force exerted on fluids by presence of proteins in the blood and tissue
where are the low and high pressure receptors
low - L and R atria and great veins
high - carotid and aortic baroreceptors
how does the body respond to a chronic metabolic acidosis
Renal correction increase H excretion and generate new HCO3 by ammonium excretion - need renal glutiminase (4-5 days)
how long does the kidney take to adapt to acid loads
4-5 days (chronic)
requires protein synthesis of renal glutiminase
how would the posterior pituitary respond to dehydration
increase ADH
what molecules share the same carrier molecule as Na
glucose, AA, HCO3
where is Angiotensin Converting Enzyme (ACE) found
throughout vascular endothelium
Where are the Na pumps in the proximal tubule
basolateral membrane
is the urea clearance higher or lower than inulin
lower - reabsorbed
which bladder sphincter is under voluntary control
external
how would low P receptors in atria respond to a reduction in ECF
decreased receptor discharge increases ADH released
In hypovolaemia, what affect does a reduction of atrial pressure have
Increases ADH secretion (low P receptors)
what is the normal decline of GFR
1ml/ min/ year after 30
how do pelvic nerves control micturation
parasymapthetic supply - increase contraction of detrusor muscle to increase pressure/ micturition (S2,3,4)
what would the ingestion of a hypertonic solution e.g seawater do to urine flow
Increase urine flow leading to dehydration
what 3 components on the glomerulus prevent solutes passing
fenestrations - RBC
basal lamina - larger proteins
still membrane between pedicles - medium sized proteins
what happens in the ascending limb of the loop of henle
fluid flows up
Na and Cl actively transported out of lumen into interstitium
impermeable to water
how does the body responf to metabolic acidosis
Increase PCO2 by decreasing ventilation
HCO3 lost in urine
If the pressure of the glomerular capillaries increases, what happens to filtration?
also increases
what are the main symptoms of diabetes insidious
polydipsia and polyuria (very large volumes of very dilute uric - >10 L day)
what is the maximum concentration of urine produced by the kidneys
1200- 1400 mOsmoles/L
what is the renal threshold for glucose
10 mmoles/l
way above plasma level of 5 mmoles/L - all is reabsorbed
how does a hyperglycaemic coma occur
- glucose remains in tubule retaining water with it
- decreased Na concentration in lumen as it is more diluted
- reduced glucose and Na reabsorption (symport)
- reduced movement of water in DESCENDING loop of henle (retain water)
- fluid delivered to ascending limb is less concentrated
- lower medullary interstitial gradient
- macula densa detects high NaCl delivery so inhibits renin
- ADH has no function can’t conserve H20
- large volume of isotonic urine lost
- inadequate brain flow of blood
in a drastic ECF volume change that affects MBP which receptors contribute to ADH secretion
carotid and aortic
how does ADH control the permeability of the collecting duct to water
aquaporins on the luminal membrane
cAMP secondary messenger system tell cells to insert pores into membrane
what happens to urea in the collecting duct in the presence of ADH
becomes more concentrated due to the removal of water
what does the activity of renal glutaminase depend on
pH - if pH falls, activity increases - more NH4 formed and excreted
what is a major source of alkali
oxidation of organic anions such as citrate
which receptors do moderate decreases in ECF affect
low P receptors in atria
what blood vessels are responsible for reabsorption
peritubular capillaries
what percentage of the filtrate is removed by the loop of henle
15-20% - up to 36L
what is the equation of the plasma clearance of X
Cx = [Ux} x V / [Px] in mls/ min
what causes urine to flow from kidneys to ureters
peristaltic contraction
what is the function of ACE
converts angiotensin I into angiotensin II
what is renal threshold
plasma threshold at which saturation occurs
what are the differences between central and peripheral diabetes insidious (ADH deficiency)
central - hypothalamic area is diseased from tumour, meningitis etc, treat with ADH
peripheral - collecting duct insensitive to ADH
how can acidosis lead to ventricular fibrillation and death
K is moved out of cells with H, leading to hyperkalaemia
if you increase the blood pressure of the glomerular capillaries, what happens to filtration
increases
what is the respiratory source of H
CO2 + H20 –> H2CO3 –> H + HCO3
ie formation of carbonic acid - in a healthy person this will be adjusted by an increase in ventilation
what fraction of the concentration of H in comparison to Na
one millionth
what allows the kidney to produce urine of varying concentrations
counter current multipliers of juxtamedullary nephrons
describe the efferent arterioles of the glomerulus
long and narrow, increasing friction and resistance for fluid (causing a build up of pressure in the glomerulus and inhibiting free outflow of blood)
in hypovolaemia what happens to the hydrostatic pressure in peritubular capillaries
reduced - efferent arteriole constriction by angiotensin II
what is the equation for the buffer dibasic phsophate
HPO4 + H –> H2PO4 (monobasic)
once urien has left the kidneys, does its composition change
no
what can cause a metabolic acidosis
- increased H production eg DKA, lactic acidosis, acetoacetic acid
- failure to excrete normal load of H eg renal failure
- loss of HCO3 eg diarrhoea
in hypovolaemia what happens to the oncotic pressure in peritubular capillaries
increased - loss of salt and water increases the concentration of plasma proteins
where is the hypertonic medullary gradient established
loop of henle in the medulla