Unit 3 - Kidneys & Osmoregulation Flashcards
How is our body fluid compartments divided?
intracellular fluid (2/3 of body fluid) extracellular fluid (1/3 of body fluid) - plasma (1/4 of ECF) - interstitial fluid (3/4 of ECF)
what is the difference between osmolarity and osmolality?
osmolarity = osmoles/ 1L solution osmolality = osmoles/ 1 Kg solvent
what is tonicity?
ability of an extracellular solution to move water into/out of cell by osmosis
how is free movement of water controlled?
osmotic and hydrostatic pressure
if there is a higher oncotic pressure than hydrostatic pressure what will happen?
absorption of fluid from interstitium into capillaries
what is oncotic pressure?
colloid osmotic pressure -pressure exerted by proteins in blood = albumin
what regulates the distribution of water between cells and interstitial fluid?
osmotic pressure
what is the GFR?
glomulerular filtration rate - rate at which kidneys form glomerular filtrate (ultrafiltration)
GFR =Kf x net filtration pressure (usually 180L/day)
GFR = (concentration of urine x amount of urine produced per minute)/ plasma concentration
what is net filtration pressure?
glomerular hydrostatic pressure - bowman’s capsule pressure - glomerular oncotic pressure
(approx 10mmHg)
what is Kf?
filtrate coefficient - measure of membrane’s permeability to water determined by surface area and hydraulic pressure
how can GFR be measured clinically?
cannot measure directly so can measure rate of excreted substances which are not secreted/ absorbed by tubules= filtered load
- inulin clearance - not convenient does not have steady conc
- creatinine clearance - most common (<100 healthy)
how can GFR be altered?
- decrease in afferent tone - increases diameter of afferent arteriole/ increase in efferent tone - decrease diameter of efferent arteriole = increases glomerular hydrostatic pressure - more filtration
- change in Kf
- change in oncotic pressure
how does kidney sense changes in GFR?
tubuloglomerular feedback
- decrease in arterial pressure = decrease in GFR (detected by baroreceptors in carotid sinus)
- decreased filtrate NaCl concentration to macula densa stimulates juxtaglomerular cells to release renin
- renin cleaves decapeptide -angiotensin I which is converted to angiotensin II
- increase in efferent tone - vasoconstriction - increase in hydrostatic pressure = increase in GFR
what else does angiotensin stimulate?
- release of aldosterone from zona glomerulosa: increases NaCl and water reabsorption - increas in blood volume - increase in blood pressure
- release of ADH: - stimulates water reabsorption from final 1/3 of distal tubule and collecting ducts of kidneys (into plasma) urine volume decreases and is more concentrated = urine osmolality increases and plasma osmolarity decreases
which hormone opposes the effect of aldosteron and ADH?
ANP/ANF - atrial natriuretic peptide - released from heart during atrial stretch
acts on receptors that increase GFR to decrease NaCl reabsorption in distal nephron so decrease in blood pressure - decrease volume - increased sodium excretion - smaller cardiac output
what are the three components that restrict the passage of fluid from glomerular capillaries?
- capillary wall contains fenestrae
- basement membrane - fibrils of negatively charged proteins
- podocytes extend pedicels over basement membrane - provides filtration slits
why does albumin retain inside capillaries?
barrier more permeable to neutral/ positively charged molecules
albumin is negatively charged so retained due to mutual repulsion as well as its size
what is the function of the PCT? describe the cells
function: selective reabsorption of water, glucose and amino acids
simple cuboidal epithelial cells - tight junctions between cells
microvilli on surface: brush border - increase SA
what is the function of the ascending limb? describe the cells
function: concentration gradient between cortex and medulla
squamous epithelial cells with few mitochondria in thin limb/ cuboidal rich in mitochondria in thick limb
what is the function of the distal convoluted tubule? describe the cells
function: ion balance
cuboidal wall - no brush border but initially has macula densa where distal tubule meets ascending limb and glomerulus
what is the function of the collecting duct? describe the cells
function: concentrating urine/ water absorption/ urea
P cells - regulate sodium balance
I cells - acid-base balance
what are the three main buffers in the body?
bicarbonate buffer
haemoglobin buffer
phosphate buffer
what is the isohydric principle?
when a buffer reacts with H+ ions the change in H+ affects other buffer reactions in the same body compartments
what is acidaemia and alkalaemia? why do they occur
pH <7.35 - due to respiratory/ metabolic acidosis
ph >7.45 - due to respiratory/ metabolic alkalosis
what are the causes of respiratory acidosis and how does it affect pH?
- impaired gas exchange/ hypoventilation
- inhalation of CO2
- decreased respiratory drive
increased pCO2 in plasma = increased carbonic acid so increased H+ and HCO3- = decreased pH
what are the causes of respiratory alkalosis and how does it affect pH?
- hyperventilation
- hypoxia
- increased respiratory drive
decreased pCO2 in plasma = decreased carbonic acid so decreased H+ and HCO3- = increased pH
what are the causes of metabolic acidosis?
loss of base from gut (due to diarrhoea)
diabetic ketoacidosis
impaired acid secretion from renal tubules
what are the effects of metabolic acidosis?
decreased pH leads to decrease in bicarbonate
- ketoacidosis - production of acetoacetic and B-hydroxybutyric acid (non-volatile acid) which decrease pH so H+ ions react with bicarbonate and CO2 is excreted
- in bony skeleton shift in pH ions from crystallites displaced by protons so crystallities used for buffering - ions excreted in urine - significant loss in calcium=bone dissolution
what are the causes of metabolic alkalosis and how does it affect pH?
- loss of HCl from vomiting
- excess base ingestion
- aldosterone excess
low pH causes increase in non-volatile base (bicarbonate)
what renal compensation occurs in the proximal tubule when chronic respiratory acidosis?
increased H+ excretion via NHE3: Na+-H+ antiporter
more carbonic acid which dissociates and then increase in pCO2 so reforms in tubular cells
bicarbonate formed leaves basolateral membrane (reabsorbed) in exchange for chlorine (excreted)
what renal compensation occurs in the distal tubule when chronic respiratory acidosis?
excess h+ excretion by type A I cells via H+-ATPase against pH gradient so increases HCO3- pH returns to normal
what renal compensation occurs in the proximal/distal tubule when chronic respiratory alkalosis?
reverse of acidosis
proximal: decreased H+ excretion/ increased bicarbonate excretion
distal: decreased H+ excretion by type A I cells/ increased bicarbonate excretion by non-type A intercalated cells
what compensation occurs for metabolic acidosis?
respiratory compensation - increased respiration to decrease pCO2 which returns pH almost to normal but not exact because as it approaches 7.3 there is less stimulus to central/ peripheral chemoreceptors so pH is within 0.1 of range
renal compensation - corrects pH via ammoniagenesis= excretion of ammonia (slow adjustment)
what compensation occurs for metabolic alkalosis?
similarly respiratory compensation -as high pH impairs respiration so higher pCO2 decreases pH but not to exact pH so renal compensation occurs via retention of Cl- and excretion of bicarbonate
