4- Na, Osmolality, Fluid volume Flashcards

1
Q

What is renin and what are its effects

A

Enzyme
Made and stored in JGA
Causes conversion of angiotensinogen to angiotensin 1

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

How is renin production activated

A

Increased sympathetic innervation (granular cells of JGA innervated by sympathetic system)
Wall tension in afferent arterioles falls
Decrease Na at macula densa leads to prostaglandins being release

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

What does angiotensin 2 do

A

Vasoconstricts efferent>afferent arterioles

Stimulates the zona glomerulosa to release aldosterone

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

What does aldosterone do

A

Increases Na reabsorb from PCT
Release ADH
Stimulates thirst

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

What factors affect Na reabsorb

A

Starlings force in PCT
Prostaglandins
ANP

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

What is Starlings force

A

Reabsorption depends on rate and amount of uptake from intercellular spaces into capillaries
Changes in body fluid volume alter plasma hydrostatic and oncotic pressure
If increase hydro and decreased oncotic in ECF it means NaCl reabsorbed by PCT decreases

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

Where are prostaglandins made

A

Cortex
Medullary interstitial cells
Collecting duct epithelial cells

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

What is the result of prostaglandins

A

Vasodilators- prevent excessive vasoconstriction

Renin release

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

Atrial natriuretic peptide produced from ? and work by ?

A

Produced by cardiac atrial cells in response to increased ECF
Inhibits Na/K atpase and closes ENAC of PCT
Reduced Na absorption and hence water
Vasodilation afferent arterioles = increase GFR
Inhibit aldosterone secretion
Inhibit ADH release
Decrease renin release

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

What cells do aldosterone target

A

Principal cells of DCT and CD

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

How does the descending limb of vasa recta reabsorb

A

Isosmotic blood enters hyperosmotic milieu of medulla

Na, Cl, urea diffuse into lumen

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

Why is the flow slow in the vasa recta

A

To allow it to equilibrate at each stratified level
To not compromise delivery of nutrients
Maintain medullary hypertonicity

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

How does the ascending limb of vasa recta reabsorb

A

Ascends towards cortex
Higher solute conc that interstitium
Water moves from descending limb of loop of Henle

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

Where are osmoreceptors located and what do they do if they sense change

A

Brain - hypothalamus.
Concentration of urine
Thirst

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

What is ADH and its effects

A

Peptide hormone
Name from supraoptic nucleus of hypothalamus
Stored in posterior pituitary
Increase osmolality = release
1. reduced water excretion
2. vasoconstriction
3. aquaporins fuse with luminal membrane - V2 receptor

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

In a state of reduced ECV does the set point for ADH get higher or lower

A

Lower
Relationship steeper
Volume trumps osmolarity

17
Q

What is Diabetes insipidus

A

Inability to reabsorb water from distal part of nephron

Failure of secretion/ action of ADH

18
Q

What causes Diabetes insipidus

A

Nephrogenic - failure to secrete ADH

Central - resistance to ADH

19
Q

Central Diabetes insipidus

A

Impaired ADH secretion or synthesis
Damage to hypo or pituitary
Brain injury, sarcoidosis, aneurysm, tumour

20
Q

How to treat Central DI

A

Desmopressin (ADH injection)

21
Q

Nephrogenic DI

A

Acquired insensitivity of kidneys to ADH

ADH levels normal

22
Q

How to manage nephrogenic DI

A

Low salt, low protein diet to reduce urine output

23
Q

Causes of Nephrogenic DI

A

Chronic pyelonephritis, polycystic kidneys, lithium

24
Q

What is SIADH

A

Excessive release of ADH from posterior pituitary

25
Q

What are signs of SIADH

A

Dilutional hyponatremia
due to increase body fluid
Hyperosmotic urine
Inappropriate Na secretion despite decrease in plasma Na.

26
Q

What causes SIADH

A
CNS disorder
drugs
lung disease
metabolic disease
malignancy
27
Q

What is loss of large amount of hypo osmotic urine called

A

Diuresis

28
Q

What will occur if osmolality increases by 10%

A

Thirst response

29
Q

What is hypernatremia

A

> 140mmol/L
Increase solute:water ratio
Increased serum osmolality

30
Q

Causes of hypernatremia

A
Osmotic diuresis- diabetes 
Fluid loss 
Diabetes insipidus
IVI inappropriate
Primary aldosteronism- too much = ENAC on
31
Q

What is the main cause of hyponatremia

A

Too much fluid- dilutional

<130mmol/L

32
Q

Symptoms of hyponatremia

A

Agitation
Focal neurology
Coma
Nausea

33
Q

Causes of hyponatremia
Fluid reasons
True Na loss

A
FR:
Diuretics
Water overload or retention 
Increased ADH secretion - HF, kidney dx, liver dx, tumour, meds- anti epileptic 
Increases plasma osmolality (glucose)
TNL:
Burns
Peritonitis
Diuretics/ renal failure
D and V
34
Q

Normal serum osmolality

A

275-295 mOsm/kg

35
Q

How is osmolality calculated

A

2 Na + glucose + urea (mmol/L)

36
Q

Treatment of Na imblance

A

Fluid restriction good

Hypertonic saline + furosemide in those symptomatic

37
Q

What is Pontine demyelination

A

Rapid correction of hyponatremia

Leads to demyelination and neuron swelling