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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
Where is ADH stored
In granules in the posterior pituitary
26
What is the plasma half life of ADH
10-15 mins
27
How is ADH released into the circulation
Action potentials cause calcium dependent exocytosis of the hormone to be released
28
What does ADH bind to
type 2 vasopressin receptors found on the basolateral membrane of the tubular cells
29
What does the binding of ADH to the type 2 vasopressin receptors do?
this initiates cell response where there is an increase in the cyclic AMP
30
What type of receptors are the type 2 vasopressin receptors
G protein coupled receptors
31
What does an increase in cyclic AMP result in
an increased expression of the water channels (aquaporins) at the apical membrane
32
Describe what happens when we are dehydrated
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
33
Describe what happens when we are overhydrated
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
34
What happens o the collecting duct in the presence of minimal ADH
It is impermeable to water and so no water is reabsorbed
35
What are the 2 main factors that allow us to produce varying amounts of concentration of urine
ADH levels | corticomedullary concentration gradient
36
How does ADH affect the solute excretion
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
What happens to the urine osmolarity as the plasma ADH increases (dehydration)
It increases
38
What receptors senses our hydration status and what do they do
hypothalmic osmoreceptors - they signal to the hypothalamic neurones and stimulate the release of ADH / decreased release of ADH
39
What receptors are activated if there is a substantial decrease in the circulating plasma volume (e.g. Haemorrhage)
The left atrial volume receptors
40
How does ADH work if there is a severe loss of circulating plasma volume
It promotes vasoconstriction which will increase total peripheral resistance which acts in a negative feedback fashion to increase arterial blood pressure
41
What are the 2 classifications of diabetes insidious
Central or nephrogenic
42
What are the main symptoms of diabetes insipidus
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
What is the treatment for central diabetes insipidus
ADH replacement
44
What is the treatment for nephrogenic diabetes insipidus
Drug treatment to reduce the urine output
45
Diabetes insipidus is a common side effect of what drug
lithium
46
What happens in central diabetes insipidus
Unable to produce or secreteADH from the posterior pituitary
47
What happens in nephrogenic diabetes insipidus
ADH is produced as normal but it does not exert its effect on the target cells
48
What is the most important stimulus for ADH release
Hypothalamic osmoreceptors
49
What substances inhibit ADH release
alcohol and ecstasy
50
What substance stimulates ADH release
Nicotine
51
What is aldosterone
Steroid hormone secreted by the adrenal cortex
52
When is aldosterone secreted
In response to risking K+ concentration or falling Na+ concentration in the plasma Activation of the renin-angiotensin system
53
What does aldosterone do
Stimulates Na reabsorption and K+ secretion
54
An increase in K+ results in what
Direct stimulation of the cells in the adrenal cortex to release aldosterone
55
An decrease in Na results in what
the indirect release of aldosterone thought the activation of the juxtaglomerular apparatus (renin-angiotensin system, a
56
What would happen if we did not have aldosterone in our body
We would continue to secrete salt i the urine - this would have a knock on effect on plasma volume and therefore arterial BP
57
What enzyme concerts angiotensin 1 to angiotensin 2
Angiotensin converting enzyme (expressed on endothelial cells of capillaries primarily in the pulmonary circulation
58
Give an overview of how the renin-angiotensin system works
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
What are the 3 ways in which renin release from granular cells in JGA is controlled
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
What does aldosterone increase in the distal and collecting tubule
The sodium reabsorption
61
Most patents with hypertension have some issues with what
The renin-angiotensin system
62
what is the treatment for hypertension
Low salt diet, diuretics | ACE inhibitors: stop fluid and salt retention and arteriolar constriction
63
What type of diuretics are best in the treatment of hypertension
Loops - specifically target and inhibit the triple cotransporter in the ascending limb of the loop f Henle
64
Where is Atrial natruretic peptide (ANP) produced
The heart (stored in atrial muscle cells
65
When is ANP released
When the atrial muscle cells in the heart are stretched due to an increase in the circulating plasma volume
66
What does ANP promote and what does this achieve
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
What are the two mechanisms in which micturition or urination is governed by
Micturation reflex | Voluntary control
68
What is the difference between water diuresis and osmotic diuresis
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
What are the two contirbuting components of the medullary osmolality
NaCl and urea (50% each)
70
What is the purpose of the countercurrent multiplication
To concentrate the medullar interstitial fluid
71
Why do we need the countercurrent multiplication
TO enable the kidney to produce urine of different volume and concentration according to the amount of circulating antidiuretic hormone (ADH)
72
What is the range of Volume of urine that can be produced
1-25ml/min
73
How does capillary blood equilibrate with interstitial fluid
Across the leaky endothelium
74
What happens to the blood osmolality as it dups into the medulla
It increases | water loss and solute gain
75
What happens to the blood osmolality as it rises back up into the cortex
It falls | Water gained and solute loss
76
What structure acts as the countercurrent exchanger
Vasa Recta
77
What structures act as a countercurrent system
Loop of Henle and Vasa recta
78
In what 3 ways is the blood flowing through the medulla that would wash away NaCl and urea prevented
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
What ensure that solute is not washed away
Passive exchange across the endothelium preserves medullary gradient
80
Where does most of the reabsorption occur
In the proximal tubule of the kidney
81
What makes up the medullary osmotic gradient
The countercurrent multiplier and the urea cycle
82
What preserves the medullary osmotic gradient
The countercurrent exchanger
83
What does a high medullary osmolarity allow
The production of hypertonic urine in the presence of ADH

SM Renal (23 decks)

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