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Genitourinary > Renal physiology > Flashcards

Renal physiology Flashcards

1
Q

Where do you find water in the body?

A

Inside cells - intracellular fluid
Outside cells - extracellular fluid
- which includes interstitial fluid and plasma

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2
Q

Low osmolality solution

A

Lots of water, not many osmotically active molecules

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3
Q

High osmolality solution

A

Not much water, many osmotically active molecules

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4
Q

Which membranes are not permeable to water?

A

Ureter, kidney and bladder membranes

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5
Q

Osmolality and osmolarity units

A

Osmolality: milliosmoles per kilogram
Osmolarity: milliosmoles per litre

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6
Q

Hypotonic

A

More osmolalic particles

A cell in a hypotonic solution will take in water to dilute osmolalic particles - the cell will swell

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7
Q

Hypertonic

A

Less osmolalic particles
A cell in a hypertonic solution will expel water to dilute osmolalic particles in extracellular fluid - the cell will shrink

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8
Q

Osmolality

A

Number of osmotically active particles per unit weight of solvent
Property of a particular solution independent of a membrane

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9
Q

Tonicity

A

Osmotic pressure a solute exerts across a cell membrane, causing movement of water
Accounts only for osmotically active impermeable solutes
Property of a solution in reference to a particular membrane

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10
Q

Gibbs-Donnan equilibrium

A

Charged particles separated by a semi-permeable membrane can fail to distribute evenly across the membrane in the presence of a non-diffusible ion, e.g. a protein
Mismatch between electrical equilibrium and concentration equilibrium

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11
Q

How is a voltage gradient formed?

A

At equilibrium, the side with the proteins is more negatively charged because of the competing electrical and concentration gradients

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12
Q

Oncotic pressure

A

More osmotically active molecules are on the protein side of the membrane, so water will flow to the protein side causing an oncotic pressure
Cells need to balance the osmotic pressures across the membrane, otherwise they will burst, therefore transporters are utilised to actively push osmotically active particles out of the cell so water will follow

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13
Q

How do we regulate ECF osmolality?

A

By altering water levels

Stable ECF osmolality is crucial for survival

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14
Q

What does ECF volume depend on?

A

Primarily the amount of Na+ which is the dominant particle in the ECF
Volume is less tightly controlled than osmolality

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15
Q

Oedema process

A

Changes in Starling forces in the plasma cause movement of fluid into the interstitial space which causes abnormal expansion of the compartment

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16
Q

pH in the renal corpuscle

A

7.4

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17
Q

pH in the proximal tubule

A

6.7

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18
Q

Particle reabsorption in the proximal tubule

A

Na+: 67%
Cl-: 67%
K+: 70%
H2O: 67%

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19
Q

Particle reabsorption in the loop of Henle

A

Na+: 18%
Cl-: 11%
K+: 25%
H2O: 15%

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20
Q

pH in the distal tubule

A

6.0

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21
Q

Particle reabsorption in the distal tubule

A

Na+: 10%
Cl-: 6%
K+: 5% secreted
H2O: 8%

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22
Q

pH in the collecting duct

A

4.5

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23
Q

Particle reabsorption in the collecting duct

A

Na+: 4%
Cl-: 10%
K+: 5% secreted
H2O: 9%

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24
Q

Starling’s forces

A

Governs movement of water and solute between plasma and ISF

Plasma proteins not filtered, so exert inward oncotic pressure

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25
Q

Hydrostatic pressure

A

Forces water and solute out of blood

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26
Q

Net filtration pressure of the glomerulus

A

Glomerular hydrostatic pressure - oncotic pressure - capsular hydrostatic pressure = net filtration pressure
in mmHg

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27
Q

Average glomerular filtration rate

A

125 mL/min for both kidneys

Constant GFR vital for kidneys to tightly regulate ECF osmolality and pH

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28
Q

Primary regulation of GFR

A

Via changes in glomerular hydrostatic presure

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29
Q

Renal autoregulation

A

Feedback mechanisms that causes dilation or constriction of afferent arteriole or constriction of efferent arteriole
Results in stopping systemic blood pressure change from affecting GFR

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30
Q

Effect of afferent arteriole vasoconstriction

A

Decreased blood flow —>
Decreased glomerular hydrostatic pressure —>
Decreased GFR

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31
Q

Effect of afferent arteriole vasodilation

A

Increased blood flow —>
Increased glomerular hydrostatic pressure —>
Increased GFR

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32
Q

Effect of efferent arteriole vasoconstriction

A

Increased glomerular hydrostatic pressure —>

Increased GFR

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33
Q

3 extrinsic mechanisms of renal autoregulation

A

Renin-Angiontensin II
Atrial natriuretic peptide
Sympathetic nervous system

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34
Q

2 intrinsic mechanisms of renal autoregulation

A

Myogenic

Tubuloglomerular feedback

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35
Q

Renin-Angiontensin II renal autoregulation

A

In low GFR, too little NaCl passes macula dense cells so paracrine signals are released
JG cells activated to release renin
Angiotensin II produced which constricts the efferent arteriole, increasing glomerular hydrostatic pressure and increasing GFR
Aldosterone prodcued which increases Na+ uptake from distal nephron and increases blood volume

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36
Q

Atrial natriuretic peptide renal autoregulation

A

Dilation of the afferent arteriole increases glomerular hydrostatic pressure and increases GFR

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37
Q

Sympathetic nervous system renal autoregulation

A

Constriction of the afferent arteriole decreases glomerular hydrostatic pressure and decreases GFR

38
Q

Myogenic renal autoregulation

A

Increased arterial pressure stretches the afferent arteriole which makes it constrict
Offsets pressure increase and keeps GFR stable

39
Q

Tubuloglomerular feedback

A

Macula densa cells monitor NaCl levels in distal tubule
If high, paracrine signals released, telling afferent arteriole to constrict
Decreased glomerular hydrostatic pressure and decreased GFR

40
Q

Proximal tubule reabsorption

A

66% water and inorganic ions
100% glucose and amino acids
90% bicarbonate

41
Q

Transport mechanisms in proximal tubule

A 
Transcellular:
1) Primary active transport
- ATP driven
2) Secondary active transport
- driven by another gradient
Paracellular
- passive, in response to osmotic gradients
42
Q

Active transport in the early proximal tubule

A
  • Na+ gradient established by Na+/K+/ATPase drives active solute uptake
  • Na+ moves down concentration gradient and pulls glucose with it
  • Water follows Na+ paracellularly, K+ dragged with it
  • Osmolality in the lumen remains constant
43
Q

To diffuse across a cell membrane, bicarbonate must:

A

Be converted to H2CO3, then CO2 via carbonic anhydrase

CO2 can freely diffuse across proximal tubule membranes, but bicarbonate can’t

44
Q

The pH drop in the proximal tubule is due to:

A

Loss of HCO3- as it’s converted to carbonic acid

45
Q

Reabsorption of bicarbonate by the proximal tubule

A

Uptake of Na+ drives H+ into the lumen which lowers to pH of the lumen
To neutralise, HCO3- uptaken as CO2
HCO3- reabsorbed by proximal tubule

46
Q

Proximal tubule mediated acidosis

A

Proximal tubule dysfunction

HCO3- not reabsorbed, therefore it’s lost in the urine leading to metabolic acidosis

47
Q

Generation of new bicarbonate in proximal tubule

A

Proximal tubule cells metabolise glutamine to ammonium and bicarbonate
Ammonium secreted into lumen
Bicarbonate transported into blood

48
Q

Fanconi syndrome

A

Impaired ability of proximal tubule to reabsorb bicarbonate and other things which are excreted in the urine instead

49
Q

Chloride reabsorption in the late proximal tubule

A

Chloride concentration in the lumen is higher than the concentration in the ECF due to prior reabsorption of water and solutes
Cl- moves into ECF via paracellular tight junctions
Lumen becomes electropositive as Cl- moves out which induces paracellular Na+ reabsorption to counter

50
Q

Loop of Henle main job

A

Water reabsorption and concentration of urine

51
Q

Short loop nephron transporters

A

NKCC2 (Na+ to ECF)
Na/K ATPase (Na+ to ECF)
Tight junctions (watertight)

52
Q

Countercurrent mechanism of water reabsorption in the loop of Henle

A

Between the thin descending limb and the thick ascending limb is a hypertonic interstitium
Water moves from thin descending limb to dilute hypertonic interstitium, making descending limb a higher osmolality
Thin ascending limb is not permeable to water, so the balance the osmolality of the thin ascending and the interstitium, solute moves into the interstitium
This process repeats with the most concentrated urine at the junction of the thin ascending and thin descending limbs forming a Na Cl gradient in the outer mudella

53
Q

Vasa recta

A

Carries blood counter to direction of tubular fluid flow
Prevents wash out of the gradient
As blood descends, water goes out and solute comes in
As blood ascends, water comes in and solute goes out

54
Q

How does the speed of the blood flow affect substance exchange?

A

Slow blood flow favours optimal exchange

Increased flow causes washout and lowers urine concentrating ability

55
Q

Early distal convoluted tubule

A

Tubular fluid leaving the thick ascending limb is dilute, and further dilution occurs in the distal tubule as NaCl is removed via the Na/Cl transporter

56
Q

What is the target of thiazide diuretics?

A

The Na/Cl transporter in the early distal convoluted tubule

57
Q

Gittleman syndrome

A

Mutation in the Na/Cl transporter results in Na+ and Cl- wasting, hyperaldosteronism and hypokalaemic metabolic alkalosis
Also comes with hypocalcaemia and hypomagnesemia

58
Q

Two types of cells in the late distal convoluted tubule, connecting tubule and collecting duct

A

Principal cells and intercalated discs

59
Q

Principal cells

A

Reabsorb sodium and secrete potassium

Occurs via electrogenic sodium channel

60
Q

ENac

A

Electrogenic sodium channel
Reabsorbs sodium into principal cells which makes lumen electronegative
Potassium secreted to balance the charge

61
Q

How do thiazide diuretics cause hypokalamia?

A

They block the Na/Cl transporter so more Na is delivered to the late distal tubule
To balance the charge, more potassium is secreted

62
Q

Potassium-sparing diuretics target

A

ENacs e.g. amiloride

63
Q

Liddle’s syndrome

A

Mutation causes incerased ENacs

Too much NaCl reabsorbed leading to increased ECF volume and hypertension

64
Q

Aldosterone and principal cells

A

Aldosterone binds nuclear receptors, is brought into the nucleus where it upregulates and opens ENac channels
More ENac channels means increased sodium reabsorption and potassium secretion

65
Q

Intercalated cells

A

Secrete protons via H+ ATPase and H+/K+ ATPase
Rebasorbs HCO3- and K+
H+ freely secreted which generates new HCO3-

66
Q

Diffusion trapping of ammonium

A

Occurs in the collecting duct
NH3 can freely diffuse so combines with H+ to make NH4+ which is trapped in the urine and excreted, therefore getting rid of excess H+

67
Q

ADH in the cortical collecting duct

A

ADH causes aquaporin-2 channels to be inserted into the apical membrane which reabsorbs water rather than excreting it
Same mechanism in outer medulla

68
Q

Passive hypothesis

A

Urea at very high concentration in cortical collecting duct when ADH present
ADH increases urea and water permeability
Urea deposited in interstitium
Water causes NaCl concentration to drop
NaCl moves out of thin AL down it’s concentration gradient

69
Q

How does dehydration cause water retention?

A

Water deficit causes increased extracellular osmolality, which is sensed by osmoreceptors
Osmoreceptors cause ADH secretion from posterior pituitary which increases plasma [ADH]
ADH deposits aquaporin-2 channels in the distal tubules and collecting ducts, increased water permeability
Water is reabsorbed and retained

70
Q

ADH

A

Anti-diuretic hormone
Synthesised as part of precursor protein in supraoptic neurons of hypothalamus and stored in granules in the nerve terminals in the posterior pituitary

71
Q

Physiological stimuli of ADH

A

Small increase in plasma osmolality

Larger decrease in ECF volume

72
Q

Non-physiological stimuli of ADH

A

Pain, stress, drugs, carcinomas, CNS and pulmonary disorders

73
Q

Diabetes insipidus

A

Overproduction of urine due to decreased ADH or ADH receptors
Water not reabsorbed leading to massive urine production and dehydration
Can be central or nephrogenic

74
Q

Central diabetes insipidus

A

Problem with ADH itself - not enough secreted

Can be from a problem with hypothalamus or posterior pituitary due to brain injury, tumour or infection

75
Q

Treatment of central DI

A

Synthetic ADH analog

76
Q

Nephrogenic diabetes insipidus

A

Problem with ADH receptors
Collecting tubule unresponsive to ADH so concentrated urine can’t be produced
Can be cause by certain drugs e.g. lithium
Can also be hereditary
Not treatable

77
Q

Water deprivation test

A

Distinguishes between central and nephrogenic DI
Deny patient water for short period of time, then give ADH substitute
If there is an increase in urine osmolality then it’s central, because the kidneys are now reabsorbing H2O

78
Q

SIADH

A

Syndrome of inappropriate ADH secretion
Plasma ADH levels higher than normal for persons plasma osmolality and volume
Patient retains water inappropriately
Can be caused by brain injury, tumour, anti-cancer drugs and small cell carcinoma of the lung
Treated by restricting water intake

79
Q

3 things that promote renin secretion

A

Decrease afferent arteriolar pressure
Increase sympathetic activity
Decrease macula densa NaCl delivery

80
Q

Renin-angiotensin summary

A

Factors stimulate renin secretion from JG cells to convert angiontensinogen into angiotensin I
Angiotensin I is converted to angiontensin II by ACE
Angiotensin II acts on AT1 receptors and AT2 receptors

81
Q

AT1 receptor roles

A 
Increase aldosterone
Increase vasoconstriction
Increase proximal Na+ reabsorption
Increase thirst
Increase ADH
Decrease renal blood flow
Maintain GFR
82
Q

AT2 receptor roles

A

Vasodilation

83
Q

3 main roles of angiotensin II

A

1) Increased aldosterone production
2) Constriction of efferent arteriole
3) Stimulates Na+/K+ ATPase

84
Q

If the right renal artery becomes abnormally constricted, what will happen to renal secretion by the right kidney and left kidney?

A

Baroreceptors in the kidney sense decreased blood flow and macula densa sense decreased NaCl flow
Right kidney secretes renin to produce angiontensin II to increase renal perfusion pressure
Increased renin from the right kidney provides negative feedback mechanism via systemic blood pressure to inhibit renin secretion from the left kidney

85
Q

Aldosterone

A

Circulates in bloodstream and binds mineralocorticoid receptors
Inserts ENacs on tubulolumen side and activates Na+/K+ ATPase on renal interstitial side

86
Q

Spironolactone

A

Treatment for hyperaldosteronism

Blacks aldosterone binding mineralocorticoid receptor

87
Q

Regulation of osmolality

A

Regulated by changes in renal water handling

Mediator is ADH

88
Q

Regulation of ECF volume

A

Regulated by changes in renal Na+ handling

Mediators are R-A system and sympathetic nervous system

89
Q

Most important thing for increasing Na+ reabsorption

A

RAAS

90
Q

Most important thing for decreasing Na+ reabsorption

A

Atrial natriuretic peptide

91
Q

ANP

A

Released from atria in response to increased filling pressure and increased atrial stretch
ANP binds receptors to increase cGMP
Decreases Na+ reabsorption in distal tubule and outer medullary connecting tubule by blocking ENac and inhibiting Na+/K+ ATPase

92
Q

3 major actions of ANP

A

Inhibits aldosterone release
Inhibits renin release
Vasodilates afferent arteriole to increase GFR

Genitourinary (6 decks)

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