Unit 3 - Kidneys & Osmoregulation Flashcards

1
Q

How is our body fluid compartments divided?

A
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)
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2
Q

what is the difference between osmolarity and osmolality?

A
osmolarity = osmoles/ 1L solution
osmolality = osmoles/ 1 Kg solvent
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3
Q

what is tonicity?

A

ability of an extracellular solution to move water into/out of cell by osmosis

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4
Q

how is free movement of water controlled?

A

osmotic and hydrostatic pressure

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5
Q

if there is a higher oncotic pressure than hydrostatic pressure what will happen?

A

absorption of fluid from interstitium into capillaries

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6
Q

what is oncotic pressure?

A

colloid osmotic pressure -pressure exerted by proteins in blood = albumin

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7
Q

what regulates the distribution of water between cells and interstitial fluid?

A

osmotic pressure

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8
Q

what is the GFR?

A

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

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9
Q

what is net filtration pressure?

A

glomerular hydrostatic pressure - bowman’s capsule pressure - glomerular oncotic pressure
(approx 10mmHg)

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10
Q

what is Kf?

A

filtrate coefficient - measure of membrane’s permeability to water determined by surface area and hydraulic pressure

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11
Q

how can GFR be measured clinically?

A

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)
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12
Q

how can GFR be altered?

A
  • 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
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13
Q

how does kidney sense changes in GFR?

A

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
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14
Q

what else does angiotensin stimulate?

A
  • 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
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15
Q

which hormone opposes the effect of aldosteron and ADH?

A

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

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16
Q

what are the three components that restrict the passage of fluid from glomerular capillaries?

A
  • capillary wall contains fenestrae
  • basement membrane - fibrils of negatively charged proteins
  • podocytes extend pedicels over basement membrane - provides filtration slits
17
Q

why does albumin retain inside capillaries?

A

barrier more permeable to neutral/ positively charged molecules
albumin is negatively charged so retained due to mutual repulsion as well as its size

18
Q

what is the function of the PCT? describe the cells

A

function: selective reabsorption of water, glucose and amino acids
simple cuboidal epithelial cells - tight junctions between cells
microvilli on surface: brush border - increase SA

19
Q

what is the function of the ascending limb? describe the cells

A

function: concentration gradient between cortex and medulla

squamous epithelial cells with few mitochondria in thin limb/ cuboidal rich in mitochondria in thick limb

20
Q

what is the function of the distal convoluted tubule? describe the cells

A

function: ion balance

cuboidal wall - no brush border but initially has macula densa where distal tubule meets ascending limb and glomerulus

21
Q

what is the function of the collecting duct? describe the cells

A

function: concentrating urine/ water absorption/ urea
P cells - regulate sodium balance
I cells - acid-base balance

22
Q

what are the three main buffers in the body?

A

bicarbonate buffer
haemoglobin buffer
phosphate buffer

23
Q

what is the isohydric principle?

A

when a buffer reacts with H+ ions the change in H+ affects other buffer reactions in the same body compartments

24
Q

what is acidaemia and alkalaemia? why do they occur

A

pH <7.35 - due to respiratory/ metabolic acidosis

ph >7.45 - due to respiratory/ metabolic alkalosis

25
Q

what are the causes of respiratory acidosis and how does it affect pH?

A
  • impaired gas exchange/ hypoventilation
  • inhalation of CO2
  • decreased respiratory drive

increased pCO2 in plasma = increased carbonic acid so increased H+ and HCO3- = decreased pH

26
Q

what are the causes of respiratory alkalosis and how does it affect pH?

A
  • hyperventilation
  • hypoxia
  • increased respiratory drive

decreased pCO2 in plasma = decreased carbonic acid so decreased H+ and HCO3- = increased pH

27
Q

what are the causes of metabolic acidosis?

A

loss of base from gut (due to diarrhoea)
diabetic ketoacidosis
impaired acid secretion from renal tubules

28
Q

what are the effects of metabolic acidosis?

A

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
29
Q

what are the causes of metabolic alkalosis and how does it affect pH?

A
  • loss of HCl from vomiting
  • excess base ingestion
  • aldosterone excess

low pH causes increase in non-volatile base (bicarbonate)

30
Q

what renal compensation occurs in the proximal tubule when chronic respiratory acidosis?

A

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)

31
Q

what renal compensation occurs in the distal tubule when chronic respiratory acidosis?

A

excess h+ excretion by type A I cells via H+-ATPase against pH gradient so increases HCO3- pH returns to normal

32
Q

what renal compensation occurs in the proximal/distal tubule when chronic respiratory alkalosis?

A

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

33
Q

what compensation occurs for metabolic acidosis?

A

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)

34
Q

what compensation occurs for metabolic alkalosis?

A

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