Balance Reg

Question 1

Regulation of sodium intake in brain

Answer 1

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

Question 2

Sodium reabsorption in nephron

Answer 2

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

Question 3

Increased tubular sodium and macula densa

Answer 3

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

Question 4

Percentage of renal plasma entering the tubular system

Answer 4

20%

Question 5

Renal plasma flow and GFR

Answer 5

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

Question 6

Sympathetic activity and control of sodium excretion

Answer 6

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

Question 7

Angiotensin 2 and control of sodium excretion

Answer 7

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

Question 8

Low tubular sodium and control of sodium excretion

Answer 8

Stimulate production of renin and so angiotensin II in juxtaglomerular apparatus

Question 9

Atrial naturietic peptide and control of sodium excretion

Answer 9

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

Question 10

Aldosterone synthesised from

Answer 10

From adrenal cortex

Question 11

Aldosterone release in response to

Answer 11

Angiotensin II

Decrease in blood pressure via baroreceptors

Question 12

Angiotensin II function

Answer 12

Promote synthesis of aldosterone synthase

Question 13

Aldosterone synthase function

Answer 13

Causes last two steps of aldosterone production from cholesterol

Question 14

Aldosterone function

Answer 14

Increased sodium reabsorption
Increased potassium secretion
Increased hydrogen ion secretion

Question 15

How does aldosterone work

Answer 15

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

Question 16

Hypoaldosteronism

Answer 16

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

Question 17

Symptoms of hypoaldosteronism

Answer 17

Dizziness
Low bp
Salt craving
Palpitations

Question 18

Hyperaldosteronism

Answer 18

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

Question 19

Symptoms of hyperaldosteronism

Answer 19

High bp
Muscle weakness
Polyuria
Thirst

Question 20

Baroreceptors of low pressure

Answer 20

Heart - atria and right ventricle

Vascular system - pulmonary vasculature

Question 21

Baroreceptors of high pressure

Answer 21

Vascular system - carotid sinus, aortic arch, juxtaglomerular apparatus

Question 22

Detecting change in blood pressure on low pressure side

Answer 22

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

High pressure - atrial stretch - ANP, BNP release

Question 23

Detecting change in blood pressure on high pressure side

Answer 23

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

Question 24

ANP steps

Answer 24

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

Question 25

Volume expansion leads to

Answer 25

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

Question 26

Volume contractions causes

Answer 26

Increased sympathetic activity leading to increase in sodium reabsorption and increased renin Increased AVP production in brain promoting water absorption

Question 27

Sodium excretion and ECF volume

Answer 27

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

Question 28

ACE inhibitors

Answer 28

Diuretic | Prevent ACE to change angiotensin I to angiotensin II

Question 29

ACE inhibitor effects

Answer 29

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

Question 30

Carbonic anhydrase inhibitor

Answer 30

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

Question 31

Loop diuretics

Answer 31

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

Question 32

Thiazide diuretics

Answer 32

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

Question 33

Potassium sparing diuretics

Answer 33

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

Question 34

What stimulates tissue uptake of plasma potassium

Answer 34

Insulin | Also aldosterone and adrenaline

Question 35

How does insulin stimulate potassium uptake

Answer 35

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

Question 36

Potassium depletion in kidney

Answer 36

``` 67% out in PCT 20% out in ascending limb 3% out in DCT 9% out in CD 1% excreted ```

Question 37

Normal and increased potassium in kidney

Answer 37

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

Question 38

Potassium secretion stimulated by

Answer 38

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

Question 39

Reason for potassium secretion increase from increased plasma potassium

Answer 39

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

Question 40

Reason for tubular flow rate affecting potassium secretion

Answer 40

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

Question 41

Hypokalaemia

Answer 41

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)

Question 42

Hyperkalaemia

Answer 42

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