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Urology > Balance Reg > Flashcards

Balance Reg Flashcards

1
Q

Regulation of sodium intake in brain

A

From lateral parabrachial nucleus

Normal sodium level -> inhibition of sodium intake through serotonin and glutamate

Decreased sodium level -> increased appetite for sodium through GABA and opioids

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2
Q

Sodium reabsorption in nephron

A 
67% PCT
25% thick ascending limb
5% DCT
3% collecting duct
<1% excretion
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3
Q

Increased tubular sodium and macula densa

A

Increased sodium chlorine uptake via triple transporter
Adenosine release from macula densa cells
Detected by extraglomerular mesangial cells
Reduces renin production of juxtaglomerular cells
Promotes afferent smooth muscle cell contraction
Reduces perfusion pressure and so GFR

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4
Q

Percentage of renal plasma entering the tubular system

A

20%

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5
Q

Renal plasma flow and GFR

A

Directly proportionally to MAP up to a certain point where it plateaus

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6
Q

Sympathetic activity and control of sodium excretion

A

Stimulates smooth muscle cell of afferent arteriole
Stimulates sodium uptake by cells of PCT
Stimulates juxtaglomerular apparatus to produce angiotensin 2

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7
Q

Angiotensin 2 and control of sodium excretion

A

Stimulate cells of PCT to increase uptake of sodium

Stimulate adrenal gland to make aldosterone to stimulate uptake in distal of DCT and collecting duct

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8
Q

Low tubular sodium and control of sodium excretion

A

Stimulate production of renin and so angiotensin II in juxtaglomerular apparatus

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9
Q

Atrial naturietic peptide and control of sodium excretion

A

Vasodilator
Decrease sodium reuptake in PCT, DCT, collecting duct
Suppress production of renin from juxtaglomerular apparatus

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10
Q

Aldosterone synthesised from

A

From adrenal cortex

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11
Q

Aldosterone release in response to

A

Angiotensin II

Decrease in blood pressure via baroreceptors

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12
Q

Angiotensin II function

A

Promote synthesis of aldosterone synthase

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13
Q

Aldosterone synthase function

A

Causes last two steps of aldosterone production from cholesterol

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14
Q

Aldosterone function

A

Increased sodium reabsorption
Increased potassium secretion
Increased hydrogen ion secretion

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15
Q

How does aldosterone work

A

Pass through cell membrane as hormones are lipid soluble
Bind to mineralcorticoid receptor which is inside cytoplasm and bound to protein HSP90
Once bound HSP90 is removed receptor will dimerise and translocate into nucleus, bind to DNA, and stimulate production of mRNA for genes that are under its control
Sodium epithelial channels, sodium potassium ATPase, regulatory proteins

Results in more channels and more active channels

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16
Q

Hypoaldosteronism

A

Reabsorption of sodium in distal nephron is reduced
Increased urinary loss of sodium
ECF volume falls
Increased renin, Ang II, ADH

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17
Q

Symptoms of hypoaldosteronism

A

Dizziness
Low bp
Salt craving
Palpitations

18
Q

Hyperaldosteronism

A 
Reabsorption of sodium in distal nephron is increased 
Reduced urinary loss of sodium 
ECF volume increase - hypertension 
Reduced renin, Ang II, ADH
Increased ANP and BNP
19
Q

Symptoms of hyperaldosteronism

A

High bp
Muscle weakness
Polyuria
Thirst

20
Q

Baroreceptors of low pressure

A

Heart - atria and right ventricle

Vascular system - pulmonary vasculature

21
Q

Baroreceptors of high pressure

A

Vascular system - carotid sinus, aortic arch, juxtaglomerular apparatus

22
Q

Detecting change in blood pressure on low pressure side

A

Low pressure - reduced baroreceptors firing - signal through afferent fibres to brain stem - sympathetic activity and ADH release

High pressure - atrial stretch - ANP, BNP release

23
Q

Detecting change in blood pressure on high pressure side

A

Low pressure - reduced baroreceptors firing - signal through afferent fibres to brainstem and JGA cells, (sympathetic activity and ADH release) and (renin released)

24
Q

ANP steps

A

Bind to guanylyl cyclase which causes conversion of GTP to cyclic GTP to activate protein kinase G which leads to cellular response (actions)

25
Q

Volume expansion leads to

A

Decreased sympathetic activity leading to reduces sodium reuptake in PCT
Also leading to decreased renin production and thus overall decreased aldosterone and increased sodium excretion

Increased ANP and BNP affecting GFR and sodium reabsorption

26
Q

Volume contractions causes

A

Increased sympathetic activity leading to increase in sodium reabsorption and increased renin

Increased AVP production in brain promoting water absorption

27
Q

Sodium excretion and ECF volume

A

Reducing sodium reabsorption reduces total sodium level, ECF volume and blood pressure

28
Q

ACE inhibitors

A

Diuretic

Prevent ACE to change angiotensin I to angiotensin II

29
Q

ACE inhibitor effects

A

Vasodilation
Reduced angiotensin II leads to increased vascular volume and decreased blood pressure

  • Direct renal effects - reduced sodium reuptake in PCT and increased sodium in distal nephron
  • Adrenal effects - reduced aldosterone
  • Indirect renal effects - decreased sodium uptake in collecting duct and increased sodium in distal nephron
  • all leading to decreased water reabsorption and thus decreased blood pressure
30
Q

Carbonic anhydrase inhibitor

A

Work in PCT as enzymes are most active in this region
Leads to sodium reabsorption and increased urinary acidity - inhibitor stops this
Enzyme turns bicarbonate into CO2, which is reconverted to bicarbonate inside cell which produces proton, thus allowing sodium proton exchange

31
Q

Loop diuretics

A

Furosemide
Thick ascending limb of loop of Henle
Triple transporter (sodium potassium chloride) inhibitor which reduces sodium reuptake in loop, increase sodium in distal nephron and reduce water reabsorption

32
Q

Thiazide diuretics

A

Work in DCT by blocking sodium chloride uptake transporter
Reduced sodium reuptake in DCT
Increased sodium in the distal nephron
Reduced water reabsorption

Increased calcium reabsorption - explanation

33
Q

Potassium sparing diuretics

A

Work in collecting duct
Inhibitor of aldosterone function
Bind to mineralcorticoid receptor and block its function like spironolactone
More potassium goes out to lumen

34
Q

What stimulates tissue uptake of plasma potassium

A

Insulin

Also aldosterone and adrenaline

35
Q

How does insulin stimulate potassium uptake

A

Indirectly by stimulating sodium proton exchange, thus increasing sodium concentration in cell , which is brought down through potassium sodium exchange

36
Q

Potassium depletion in kidney

A 
67% out in PCT
20% out in ascending limb
3% out in DCT
9% out in CD
1% excreted
37
Q

Normal and increased potassium in kidney

A 
67% out in PCT
20% out in ascending limb
10-50% in in DCT
5-30% in in CD 
15-80% excreted
38
Q

Potassium secretion stimulated by

A

Increased plasma potassium
Increased aldosterone
Increased tubular flow rate
Increased plasma pH

39
Q

Reason for potassium secretion increase from increased plasma potassium

A

Increased activity of sodium potassium ATPase
More potassium inside cell, thus more potassium going out
Also change in membrane potential which help to stimulate potassium secretion

40
Q

Reason for tubular flow rate affecting potassium secretion

A

Cells of distal cell have primary cilia
As there is increased flow, the cilia stimulate PDK1, which increases calcium concentrations in cells, and thus stimulates activity of openness of potassium channels, allowing potassium to be pumped in by sodium potassium ATPase and then out

41
Q

Hypokalaemia

A

Most common electrolyte imbalance
May be from inadequate dietary intake (too much processed food), diuretics (increase tubular flow rate), surreptitious vomiting (reduced intake), diarrhoea (reduced intake) and genetics (Gitelman’s syndrome, mutation in sodium chlorine transporter in distal nephron)

42
Q

Hyperkalaemia

A

Common electrolyte imbalance present in 1-10% hospitalised patients
In response to potassium sparing diuretics, ACE inhibitors
In elderly, severe diabetes and kidney disease

Urology (12 decks)

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