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BRS YEAR 2 > Uro - Renal regulation > Flashcards

Uro - Renal regulation Flashcards

1
Q

How do you calculate osmolarity

A

Number of dissociated solute particles x concentration - expressed as Osm/L or mOsm/L

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2
Q

How does osmotic pressure correlate with number of solute particles

A

Increase in solute particle number increases osmotic pressure - NOT SIZE

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3
Q

What is osmosis

A

Passive movement of water from an area of low solute concentration to high solute concentration across a semi-permeable membrane until they reach an equilibrium

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4
Q

How much of the body weight does fluid make up

A

60%

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5
Q

What is the split of ICF and ECF

A

2/3 ICF, 1/3 ECF - separated by cell membrane

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6
Q

What is ECF split into

A

3/4 extravascular, 1/4 intravascular (Plasma) - separated by capillary

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7
Q

What is extravascular split into

A

95% interstitial fluid, 5% transcellular fluid e.g. peritoneal fluid

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8
Q

What constitutes unregulated water loss

A

Sweat
Faeces
Vomiting
Water evaporation from the skin or respiratory lining

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9
Q

What makes up regulated water loss

A

Water loss from urine

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10
Q

How does osmolarity normalise in positive water balance

A
  1. Excess water intake
  2. ECF hit first - volume increases
  3. Dilution effect = sodium conc decreases
  4. Osmolarity decreases
  5. Hyposmotic urine production
  6. Osmolarity normalises
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11
Q

How does osmolarity normalise in negative water balance

A
  1. Low water intake
  2. ECF hit first - volume decreases
  3. Sodium concentration increases
  4. Osmolarity increases
  5. Hyperosmotic urine production
  6. Osmolarity normalises
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12
Q

Where is water reabsorbed in the nephron

A

67% reabsorbed in the PCT
It is then passively reabsorbed in the thin descending loop of henle (15%)
Then, variable amounts are reabsorbed in the DCT and CD - none is reabsorbed in the ascending LoH

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13
Q

What do we need in order for water to be passively reabsorbed in the loop of Henle and Collecting Duct

A

We need a hyperosmotic medullary interstitium

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14
Q

By what process do we create a hyperosmotic medullary interstitium

A

Countercurrent multiplication

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15
Q

Describe countercurrent multiplication

A

Tubular fluid arrives in the DLOH at 300 (arbitrary mOsm/L), and moves through until it reaches the thick ALOH where sodium is actively reabsorbed. This means that the tubular osmolarity decreases but medullary osmolarity increases. Due to the increase in medullary osmolarity e.g. to 400, tubular fluid now arriving in the DLOH will lose water passively to equalise osmolarity. Therefore the new tubular osmolarity in the DLOH = 400 too. AS tubular fluid moves through the LoH, Na is still actively reabsorbed in the thick ALOH, therefore we get multiplication of the process and a gradient will eventually form.
The reason as to why the top of the intersitum (outer) is less hyperosmotic is because when water first arrives in the DLOH it will move into the top of the interstium therefore the outer inertsitium will by more hypo osmotic

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16
Q

What gradient does countercurrent mutliplaction create

A

1200 in the inner medulla

300 in the outer medulla

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17
Q

What else occurs in the medulla to aid with water reabsorption

A

Urea recycling

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18
Q

How does urea leave the collecting duct

A

It can leave the collecting duct via UT-A1 and then UT-A3 - AVP boosts these transporters to concentrate urine

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19
Q

What is the medulla conc of urea

A

600mmol/L

20
Q

What are the 2 fates of urea having entered the medullary interstitum

A

It can either enter the DLOH via UT-A2 or it can enter the vasa recta via UT-B1 - this means that urea is recycled in the nephron to increase the osmolarity of the medulla

21
Q

What is the effect of urea recycling

A

Urea excretion requires less water

Urine concentration occurs

22
Q

Describe ADH

A

Short protein hormone produced in the magnoceullar neurones of the supraoptic and paraventricular nuclei of the hypothalamus, and then stored in the PPG. The main function is to promote water reabsorption in the CD and concentration urine

23
Q

What stimulates ADH

A 
Increase in plasma osmolarity
Decrease in blood volume
Decrease in blood pressure 
Nausea
Nicotine
Angiotensin II
24
Q

What inhibits ADH

A 
Decrease in plasma osmolarity 
Increase in blood pressure
Increase in blood volume
Atrial natriuretic peptide
Ethanol
25
Q

What is a healthy plasma osmolarity

A

275-290 mOsm/kg H2O

26
Q

What cells does ADH act on

A

Principal cells of the collecting duct

27
Q

What is the mechanism of action for ADH

A

Binds to v2 receptors in the basolateral membrane of cells. V2 = G-coupled - stimulates adenylate cyclase to produce cAMP and thus protein kinase A. This leads to the secretion of AQP2 channels which insert into the apical membrane
ADH also regulates AQP-3 channels which are found on the basolateral membrane

28
Q

How is sodium reabsorbed in the thick ascending limb

A

Active reabsorption whereby sodium is reabsorbed into the blood via Na/K ATPase, meaning that Na can enter the cells of the thick ascending limb passively through the triple pump - this provides energy for the entry of K and Cl too

29
Q

How is sodium reabsorbed in the DCT

A

Na/K ATPase in basolateral side again but there is a Na/CL symporter an apical side

30
Q

How is sodium reabsorbed in the principal cell of the CD

A

Na/K ATPase in basolateral, Na channel on apical side

31
Q

How does ADH affect Na reabsorption

A

ADH supports Na reabsorption in the thick ascending limb, DCT and CD

32
Q

Where does most water reabsorption happen in the CD

A

In the inner medulla due to the higher gradient as you move down

33
Q

How do we get net addition of metabolic acid and how much per day

A

Through metabolism and diet, there is net addition of bases and acids, however due to excretion of bases through feces, there is an overall net addition of acids by about 50-100mEq/ day

34
Q

How are metabolic acids neutralised

A

We have around 350mEq of HCO3 to neutralise H2SO4 and HCL which are the main metabolic acids

35
Q

What is the role of the kidneys

A

Secretion and excretion of H+
Reabsorption of HCO3
Production of new HCo3 ions

36
Q

What is the need to recycle HCO3 levels

A

Our body only has 350mEq // 24mEq/L therefore we only have a limited store that would run out in 4-7 days without replenishment therefore we need a way to conserve this

37
Q

Where is bicarbonate reabsorbed

A

80% in PCT
10% in TALOH
6% in DCT
4% in CD

38
Q

How is bicarbonate reabsorbed in the PCT

A

Co2 enters the cells of the PCT via diffusion
Co2 binds to water via carbonic anhydrase and then H+ +HCO3
H+ leaves the cell via H+ ATPase or via Na/H anti porter into the tubular fluid
HCO3 reabsorbed through the Na/HCO3 symporter

39
Q

How is bicarbonate reabsorbed in alpha cells of the DCT and CD

A

Co2 enters the cells of the PCT via diffusion
Co2 binds to water via carbonic anhydrase and then H+ +HCO3
H+ leaves either via H+ ATPase or via K/H anti porter into the tubular fluid
HCO3 reabsorbed by Cl/HCO3 anti porter into the blood

40
Q

How is bicarbonate secreted in the beta cells of the DCT and CD

A

H+ATPase allows H+ entry into blood

HCO3/Cl antiporter transports HCO3 into the tubular fluid

41
Q

How do we produce new HCO3 ions in the PCT

A

Glutamine is broken down into 2NH4 and A2- (divalent ion that gives 2HCO3).
2HCO3 are reabsorbed into the blood, whereas NH4 can be pumped out via NH4/Na anti porter. Or, it can be broken down to HN3 + H. NH3 is a gas that leaves via diffusion; H+ leaves via Na/H anti porter and then NH3 and h+ rejoin in the tubular fluid to form NH4

42
Q

How do we produce new HCO3 ions in the DCT and CD

A

HCO3/Cl anti porter allows HCO3 reabsorption whilst we have H+ secretion by HATPase or H/K ATPase and then neutralisation via the phosphate buffer system

43
Q

What is the compensatory response for metabolic acidosis

A

Increase in ventilation - increase in HCO3 reabsorption and production

44
Q

What is the compensatory response for metabolic alkalosis

A

Decrease in ventilation and increase in HCO3 excretion

45
Q

What is the compensatory response for respiratory acidosis

A

Acute: intracellular buffering whereby H+ formed in cells of nephron are neutralised by cellular proteins to cause net gain of HCo3
Chronic: increase in HCo3 reabsorption and production

46
Q

What is the compensatory response for alkalosis

A

Acute: intracellular buffering whereby we shift towards H2Co3 production so less HCo3 is also produced.
Chronic: decrease in HCo3 reabsorption and production

BRS YEAR 2 (37 decks)

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