Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IMED3002 > Lecture 7 Salt and water balance > Flashcards

Lecture 7 Salt and water balance Flashcards

1
Q

What are the hormones that regulate tubular reabsorbtion?

A

Aldosterone

Angiotensin II

Antidiuretic hormone

Atrial natriuretic peptide

Parathyroid hormone (not yet needs to be known)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does Aldosterone do?

A

Increases NaCl and H2O reabsorption and K+ secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does Angiotensin II do?

A

NaCl and H2O reabsorption and H+ secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does ADH do?

A

Reabsorbs water at distal tubule and collecting tubule+duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does Atrial Natriuretic Peptide do?

A

Decreases NaCl reabsorbtion at distal tubule and collecting tubule+duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where does parathyroid hormone act?

A

Acts on proximal tubule, thick ascending loop of henle, and distal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does parathyroid hormone do?

A

PO2 reabsorption and increased calcium absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does water loss get controlled?

A

An increase in plasma osmolarity causes the ECF osmolarity to increase. This results in osmoreceptor cells shrinking which results in action potential which are relayed to posterior pituitary gland and this results in ADH release.

ADH results in water reabsorption and in turn an increase in plasma water which dilutes the plasma and the ECF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is ADH released?

A

In the posterior pituitary gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which brain regions are responsible for ADH release?

A

Supraoptic (5/6)

Paraventricular (next to 3rd ventricle of brain) (1/6)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is ADH produced in response to?

A

Plasma osmolarity increase

Medullary BP centers (drop in BP)

Drop in blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What factors decrease ADH release?

A

Low blood osmolarity

High blood volume

High blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does aquaporin expression work?

A

The interstitial side aquaporins are always expressed and open and unregulated these maintain the cell’s osmolarity.

On the tubular side there are aquaporin 2 channels which get exocytosed into vesicles.

Vasopressin binds to the membrane receptor which activates cAMP secpnd messenger system.

Cell inserts AQP2 water pores into apical membrane.

Water is then absorbed into blood via osmosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is salt reabsorption controlled?

A

atII and aldosterone, these hormones have little effect on Na+ concentration except under extreme conditions.

This is called RAAS (Renin-angiotensin-aldosterone-system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When is renin typically produced?

A

In the kidney by the juxtaglomerular apparatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is renin produced?

A

In response to low GFR (i.e low BP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does the renin angiotensin pathway work?

A

Kindeys produce renin

Liver produces angiotensinogen

renin converts angiotensinogen into angiotensin I

Surface of pulmonary and renal endothelium contains Angiotensin Converting Enzyme which converts AtI into AtII which has systemic effects to raise BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does the renin angiotensin pathway work?

A

Kindeys produce renin (rate limiting part of process)

Liver produces angiotensinogen constantly

renin converts angiotensinogen into angiotensin I

Surface of pulmonary and renal endothelium contains Angiotensin Converting Enzyme which converts AtI into AtII which has systemic effects to raise BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does AtII raise BP?

A

Increases sympathetic activity

Increases tubular reabsorption of Na Cl and H2O. It also increases excretion of K+ (through sodium potassium pump activity increase)

Adrenal gland and cortex produce more aldosterone which increases H2O reabsorption as well as salts

Areteriolar vasoconstriction increases TPR which increases MAP and in turn blood pressure

ADH secretion resulting in more H2O reabsorption at collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where is aldosterone produced?

A

Adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the negative feedback of the Renin Angiotensin Aldosterone System?

A

Renin release is slowed down in response to the increase in BP

22
Q

How does renin get secreted?

A

Granular cell of the juxtaglomerular apparatus produces it in response to salt receptors in the macula densa cells which sense change in electric potential and respond.

a decrease in salt concentration

23
Q

What are the triggers for increased renin release?

A

Drop in NaCl concentration at DCT.

Decrease in stretch on the afferent arterioles

Increase in sympathetic stimulation (as a result of the baroreceptor reflex)

24
Q

What is the most potent sodium retaining hormone?

A

AtII

25
Q

What does AtII do that makes it so powerful at retaining sodium?

A

Directly stimulates basolateral Na+/K+-ATPase and Na+/H+ exchange in PCT.

Increases reabsorption by peritubular capillaries.

Stimulates aldosterone secretion

26
Q

Where is aldosterone produced?

A

Adrenal cortex zona glomerulosa

27
Q

What mediates adrenal secretion of aldosterone?

A

Mostly AtII

And local potassium concentration

also ACTH

28
Q

Why is aldosterone produced when its effects are similar to AtII?

A

It is a steroid and its effect is more long term.

29
Q

What does aldosterone do in cells to increase BP?

A

Increases sodium reabsorption and secretion of potassium and hydrogen

Increases active reabsorption of sodium (water follows)

Increases BP and blood volume

30
Q

Where are principle cells located?

A

Towards end of nephron so in collecting tubule

31
Q

What does aldosterone bind?

A

Mineralocorticoid receptor which activates signal transduction and gene transcription and non-genomic activation.

Acts on principle cells of cortical convoluted tubule by stimulating the basolateral sodium potassium pump

It also increases the sodium permeability of luminal membrane

and sodium potassium + sodium hydrogen counter transporters.

32
Q

Why is potassium secreted?

A

To maintain electrochemical gradient and H+ cant be released to maintain pH

33
Q

What does Atrial Natriuretic peptide do?

A

Decreases Na+ and H2O reabsorption and inceases urinary loss and drops blood volume

increases GFR by dilating afferent arteriole and constricting efferent arteriole

34
Q

What does ANP get released in response to?

A

High atrial pressure indicates high venous pressure and in turn high venous volume

35
Q

What is the response of cells to ANP?

A

Decreases ADH release

Decreases renin release and in turn aldosterone

Decreases GFR

Decreases aldosterone directly as well

Stimulates medulla to decrease BP

AS A RESULT INCREASES NACL AND H2O EXCRETION

36
Q

Where is potassium stored?

A

98% is stored in the ICF (prevents it from becoming problematic)

37
Q

Why is potassium regulated so precisely?

A

High blood potassium results in heart problems and nervous system problems.

38
Q

How is potassium regulated?

A

Excreted from kidneys

ECF:ICF distribution (store some in the cells)

39
Q

What factors shift K+ into cells?

A

Insulin

Aldosterone

Beta-adrenergic stimulation

Alkalosis

40
Q

What factors shift K+ out of cells?

A

Insulin deficiency

Aldosterone deficiency

Beta-adrenergic blockade

Acidosis

Cell lysis

Strenuous exercise

Increased extracellular fluid osmolarity

41
Q

How is potassium secreted?

A

Principle cells

42
Q

How is potassium secretion determined?

A

Sodium potassium ATPase activity. More sodium reabsorption means more potassium excretion.

Potassium electrochemical gradient

Potassium permeability.

There is also a H+/K+ ATPase co transporter which has minimal effect but alkalosis can result in loss of potassium

43
Q

How is potassium controlled by feedback?

A

Increase in extracellular potassium concentration increases potassium secretion in 3 ways

Na+/K+-ATPase stimulation
Increase in K+ gradient towards tubule
Increase in aldosterone secretion

44
Q

What is drinking threshold determined by?

A

Osmolarity changes .

45
Q

How is blood volume regulated?

A

Low P baroreceptors in great veins and right atrium detect low volume

Hypotension is detected by high P baroreceptors.

AtII is a very potent dipsogen

All these symptoms feed into hypothalamus

46
Q

How does AtII cause thirst?

A

AtII is a neurotransmitter in the hypothalamus used to influence thirst

47
Q

What controls thirst?

A 
Thirst increased by:
Increase in osmolarity
Drop in Blood volume
Drop in BP
Rise in AtII
Dryness of the mouth
Thirst decreased by:
Decrease in osmolarity
Increase in blood volume
Increase in blood pressure
Drop in AtII
Gastric distention
48
Q

What region of the brain controls water balance?

A

Thirst center in the anteroventral 3rd ventricle region. Lesion causes acute adypsia (absence of thirst)

49
Q

Where are the osmoreceptors located?

A

AV3V (anteroventral 3rd ventricle region.)

50
Q

What is the stimulus in hunger for salt?

A

Drop in sodium concentration in extracellular fluid

BP drop increases salt appetite

IMED3002 (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions