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SM Renal > Physiology 5 and 6 > Flashcards

Physiology 5 and 6 Flashcards

1
Q

Describe the osmolarity of the tubular fluid leaving the loop of Henle

A

Hypo-osmotic to plasma

100mosmol/L

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2
Q

What is the osmolarity of the surrounding interstitial fluid of the renal cortex

A

300mosmol/L

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3
Q

What causes the osmotic gradient between the interstitial fluid and the tubular fluid

A

The tubular fluid leaving the loop of Henle is 100 and the cells that make up the wall of the nephron have an osmolarity of 300

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4
Q

Describe the concentration of surrounding fluid as the collecting duct descends through the medulla

A

It is progressively increasing (300-1200)

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5
Q

Where do all of the tubules empty into

A

Cortical collecting ducts

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6
Q

What is very important for salt balance in the distal tubule

A

The residual load

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7
Q

What mainly controls the regulation of fluid and NaCl

A

Hormones

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8
Q

Name the 4 main hormones involved in the the regulation of water and ion balance

A

ADH (vasopressin)
Aldosterone
Atrial natriuretic hormone
Parathyroid hormone

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9
Q

How does ADH work

A

It makes the cells more or less permeable to water to increase water resorption and decrease urine production

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10
Q

What does aldosterone do

A

It promotes Na reabsroption and promotes K ion secretion

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11
Q

What type of hormone is Atrial natriuretic hormone

A

Peptide

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12
Q

What is the function of Atrial natriuretic hormone

A

decreases Na resorption

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13
Q

What is the function of PTH

A

Increases Ca reabsorption by tubular cells and decreases phosphate ion reabsorption.

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14
Q

When is PTH released

A

When we become hypocalcaemic

This causes more calcium to be reabsorbed and bring calcium back to normal

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15
Q

Describe the permeability of the distal tubule

A

It has a low permeability to water and urea

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16
Q

Urea is concentrated and diluted in the tubular fluid

A

Concentrated

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17
Q

What does the concentrated urea help to establish

A

The osmotic gradient within the medulla

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18
Q

What are the two segments of the distal tubule

A

Early and Late

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19
Q

What do the cells of the early distal tubule express

A

A triple co-transporter (Na-K-2Cl)

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20
Q

Where else is the triple co-transporter found

A

In the apical membrane of the thick ascending limb of Henle

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21
Q

What do the cells of the late distal tubule do

A

They will increase potassium secretion and Na reabsorption

PTH stimulates them to also increase Ca reabsorption

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22
Q

Describe the properties of the early collecting duct

A 
Similar to the late distal tubule:
increased Ca reabsorption 
increased K secretion 
Increased Na reabsorption
Increased H+ secretion
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23
Q

Describe the features of the late collecting duct

A

A low ion permeability
Permeability to water (and urea) influenced by ADH
The cells are more sensitive to ADH here

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24
Q

How is ADH synthesised and secreted

A

By neurones in the supraoptic and paraventricular nuclei in the hypothalamus (
Synthesised by nerve cells in the cell body and released by here terminal of the nerve cells

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25
Q

Where is ADH stored

A

In granules in the posterior pituitary

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26
Q

What is the plasma half life of ADH

A

10-15 mins

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27
Q

How is ADH released into the circulation

A

Action potentials cause calcium dependent exocytosis of the hormone to be released

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28
Q

What does ADH bind to

A

type 2 vasopressin receptors found on the basolateral membrane of the tubular cells

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29
Q

What does the binding of ADH to the type 2 vasopressin receptors do?

A

this initiates cell response where there is an increase in the cyclic AMP

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30
Q

What type of receptors are the type 2 vasopressin receptors

A

G protein coupled receptors

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31
Q

What does an increase in cyclic AMP result in

A

an increased expression of the water channels (aquaporins) at the apical membrane

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32
Q

Describe what happens when we are dehydrated

A

There is an increase in ADH released which binds to the type 2 vasopressin G protein coupled receptor. This causes an increase of intracellular cyclic AMP = increased number of aquaporins = more water reabsorbed

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33
Q

Describe what happens when we are overhydrated

A

There is an decrease in ADH released which binds to the type 2 vasopressin G protein coupled receptor. This causes a decrease of intracellular cyclic AMP = decreased number of aquaporins = less water reaborped

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34
Q

What happens o the collecting duct in the presence of minimal ADH

A

It is impermeable to water and so no water is reabsorbed

35
Q

What are the 2 main factors that allow us to produce varying amounts of concentration of urine

A

ADH levels

corticomedullary concentration gradient

36
Q

How does ADH affect the solute excretion

A

It has no affect at all - it only influences the water reabsorption.
It has an effect on the volume and water concentration of urine

37
Q

What happens to the urine osmolarity as the plasma ADH increases (dehydration)

A

It increases

38
Q

What receptors senses our hydration status and what do they do

A

hypothalmic osmoreceptors - they signal to the hypothalamic neurones and stimulate the release of ADH / decreased release of ADH

39
Q

What receptors are activated if there is a substantial decrease in the circulating plasma volume (e.g. Haemorrhage)

A

The left atrial volume receptors

40
Q

How does ADH work if there is a severe loss of circulating plasma volume

A

It promotes vasoconstriction which will increase total peripheral resistance which acts in a negative feedback fashion to increase arterial blood pressure

41
Q

What are the 2 classifications of diabetes insidious

A

Central or nephrogenic

42
Q

What are the main symptoms of diabetes insipidus

A

Large volumes of dilute urine (up to 20 litres per day)

constant thirst - makes the patient want to drink more and has a knock on effect

43
Q

What is the treatment for central diabetes insipidus

A

ADH replacement

44
Q

What is the treatment for nephrogenic diabetes insipidus

A

Drug treatment to reduce the urine output

45
Q

Diabetes insipidus is a common side effect of what drug

A

lithium

46
Q

What happens in central diabetes insipidus

A

Unable to produce or secreteADH from the posterior pituitary

47
Q

What happens in nephrogenic diabetes insipidus

A

ADH is produced as normal but it does not exert its effect on the target cells

48
Q

What is the most important stimulus for ADH release

A

Hypothalamic osmoreceptors

49
Q

What substances inhibit ADH release

A

alcohol and ecstasy

50
Q

What substance stimulates ADH release

A

Nicotine

51
Q

What is aldosterone

A

Steroid hormone secreted by the adrenal cortex

52
Q

When is aldosterone secreted

A

In response to risking K+ concentration or falling Na+ concentration in the plasma
Activation of the renin-angiotensin system

53
Q

What does aldosterone do

A

Stimulates Na reabsorption and K+ secretion

54
Q

An increase in K+ results in what

A

Direct stimulation of the cells in the adrenal cortex to release aldosterone

55
Q

An decrease in Na results in what

A

the indirect release of aldosterone thought the activation of the juxtaglomerular apparatus (renin-angiotensin system, a

56
Q

What would happen if we did not have aldosterone in our body

A

We would continue to secrete salt i the urine - this would have a knock on effect on plasma volume and therefore arterial BP

57
Q

What enzyme concerts angiotensin 1 to angiotensin 2

A

Angiotensin converting enzyme (expressed on endothelial cells of capillaries primarily in the pulmonary circulation

58
Q

Give an overview of how the renin-angiotensin system works

A

A decrease in circulating NaCl causes decreased ECF volume and Arterial BP
These act to increase the secretion of renting from the granular cells
Renin acts as an enzyme to cleave angiotensinogen (protein secreted by cells i the liver) that is then converted to angiotensin 1. Angiotensin converting enzyme then causes angiotensin 1 to angiotensin 2

Angiotensin 2 stimulates cells of the adrenal cortex to release aldosterone which will act on distal cells of the collecting duct to increase Na ion reabsorption to allow passive reabsorption of chloride ions, conserve salt, which also exerts an osmotic effect.

Angiotensin 2 also stimulates the release of ADH and contributes to arterial vasoconstriction

59
Q

What are the 3 ways in which renin release from granular cells in JGA is controlled

A
  1. Reduced pressure in afferent arteriole (more renting, (more Na reabsorbed increased BP, BP restored)
  2. Macula densa cells sense the amount of NACl in the distal tubule (salt sensitive cells)
  3. Increased sympathetic activity as a result of reduced arterial blood pressure stimulates more renin secretion
60
Q

What does aldosterone increase in the distal and collecting tubule

A

The sodium reabsorption

61
Q

Most patents with hypertension have some issues with what

A

The renin-angiotensin system

62
Q

what is the treatment for hypertension

A

Low salt diet, diuretics

ACE inhibitors: stop fluid and salt retention and arteriolar constriction

63
Q

What type of diuretics are best in the treatment of hypertension

A

Loops - specifically target and inhibit the triple cotransporter in the ascending limb of the loop f Henle

64
Q

Where is Atrial natruretic peptide (ANP) produced

A

The heart (stored in atrial muscle cells

65
Q

When is ANP released

A

When the atrial muscle cells in the heart are stretched due to an increase in the circulating plasma volume

66
Q

What does ANP promote and what does this achieve

A

excretion of Na and diuresis, thus decreasing plasma volume (opposite effect of aldosterone )
causes a decrease in the cardiac output which also decreases arterial blood pressure

67
Q

What are the two mechanisms in which micturition or urination is governed by

A

Micturation reflex

Voluntary control

68
Q

What is the difference between water diuresis and osmotic diuresis

A

Water –> there is an increased urine flow but not an increased solute excretion
Osmotic diuresis –> increased urine flow as a result of a primary increase in salt excretion

69
Q

What are the two contirbuting components of the medullary osmolality

A

NaCl and urea (50% each)

70
Q

What is the purpose of the countercurrent multiplication

A

To concentrate the medullar interstitial fluid

71
Q

Why do we need the countercurrent multiplication

A

TO enable the kidney to produce urine of different volume and concentration according to the amount of circulating antidiuretic hormone (ADH)

72
Q

What is the range of Volume of urine that can be produced

A

1-25ml/min

73
Q

How does capillary blood equilibrate with interstitial fluid

A

Across the leaky endothelium

74
Q

What happens to the blood osmolality as it dups into the medulla

A

It increases

water loss and solute gain

75
Q

What happens to the blood osmolality as it rises back up into the cortex

A

It falls

Water gained and solute loss

76
Q

What structure acts as the countercurrent exchanger

A

Vasa Recta

77
Q

What structures act as a countercurrent system

A

Loop of Henle and Vasa recta

78
Q

In what 3 ways is the blood flowing through the medulla that would wash away NaCl and urea prevented

A

Vasa recta capillaries follow hairpin loops
vasa recta capillaries freely permeable to NaCl and water
Blood flow to vasa recta is low (few juxtamedullary nephrons

79
Q

What ensure that solute is not washed away

A

Passive exchange across the endothelium preserves medullary gradient

80
Q

Where does most of the reabsorption occur

A

In the proximal tubule of the kidney

81
Q

What makes up the medullary osmotic gradient

A

The countercurrent multiplier and the urea cycle

82
Q

What preserves the medullary osmotic gradient

A

The countercurrent exchanger

83
Q

What does a high medullary osmolarity allow

A

The production of hypertonic urine in the presence of ADH

SM Renal (23 decks)

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