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FHB > RENAL 04: BODY WATER > Flashcards

RENAL 04: BODY WATER Flashcards

1
Q

Vasopressin alternate names

A

ADH (antidiuretic hormone) , arginine vasopressin

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2
Q

Where is vasopressin SYNTHESIZED?

A

Hypothalamus

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3
Q

Where is vasopressin RELEASED FROM?

A

it travels down the axons of the cells in the hypothalamus where it was synthesized to the posterior pituitary gland, and from there it is released into the circulation

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4
Q

Under what conditions is vasopressin released

A

Extracellular hyperosmolality and volume depletion (via baroreceptor, osmolality, and pressure of body)

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5
Q

Where are the osmosensors that sense high osmolality?

A

OVLT and SFO (organum vasculosum of lamina terminalis; subfornical organ) ; these are in the hypothalamus

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6
Q

Where are the baroreceptors

A

Carotid sinus and aortic arch

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7
Q

Activation of the OVLT and SFO osmolality receptors in the hypothalamus indicate what?

A

High osmolality

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8
Q

Aortic arch and carotid baroreceptors lead to what effect of ADH release?

A

Inhibition of ADH release; this makes sense, when you consider the fact that aortic arch and carotid sinus will sense high blood pressure and therefore, if these are firing we would want to STOP the release of ADH so we do NOT keep as much water.

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9
Q

What is the “effector” mechanism of Adh release

A

Exocytosis of ADH from terminal axons of supraoptic and paraventricular neurons into blood of posterior pituitary

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10
Q

What is the target of ADH release?

A

We have a lot of ADH reeptors in the body, but we are most interested in the ones in the collecting ducts and distal tubules of the kidneys.

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11
Q

what happens upon binding of vasopressin/ADH to its receptor in the distal tubules/collecting ducts?

A

You get an increase in the amount of water being reabsorbed ; this is due to aquaporins

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12
Q

What affect does angiotensin II have on ADH release?

A

Stimulation of ADH release (this is a product of the RAAS pathway, so we know we are looking for ways to raise volemia)

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13
Q

ANP (atrial natriuretic peptide) effect on ADH release?

A

Inhibitory

This is released upon stretch of the heart; so this may indicate you have too much volume, so you want to inhibit ADH release because ADh encourages water reabsorption.

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14
Q

As we increase the osmolarity of the blood, what is the effect on ADH

A

Bigger release to dilute blood

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15
Q

What is a physiological condition in which you may see an increase in ADH

A

dehydration ; if you are dehydrated, salts get concentrated. Body wants to hold onto water, and does so by producing AVP/ADH

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16
Q

after we’ve started holding onto water, what else are our brains going to do if we’re dehydrated?

A

Tell us we’re fuckin thirsty

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17
Q

As soon as you start drinking water, what happens to ADH release? Why?

A

it turns off; you don’t want to become hypervolemic.

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18
Q

Result of a drop in blood pressure, with regard to AVP/ADH release?

A

A drop in blood pressure would lead to an increase in AVP (you want to hold onto water to raise bP back to normal)

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19
Q

What is the aquaporin responsive to ADH?

A

Aquaporin 2

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20
Q

What is the vasopressin receptor responsible for responding to ADH and leading to the ADH-specific responding aquaporin?

A

Vasopressin receptor type 2

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21
Q

Molecularly speaking, what general signaling cascade occurs upon ADH binding to its receptor?

A

generation of cAMP, activation of PKA, and then

  1. you encourage already-made aquaporins to be inserted into the membrane
  2. you stimulate activation of transcription factors that allow more aquaporin to be synthesized and inserted into the membrane
22
Q

Where is the ADH sensitive aquaporin inserted? What does it do?

A

it is inserted into the lumen side apical side) and lets water go into the cell of late distal tubule and collecting duct , then that water will pass through the basolateral (blood side) through DIFFERENT aquaporin types, and move into the blood

23
Q

If we are in a state of dehydration, what is the order of events which follows?

A

Osmolarity of plasma goes up, which stimulates osmoreceptors in hypothalamus and allows ADH secretion from posterior pituitary gland. This goes into the blood supply and will activate the vasopressin receptor, which will result in the insertion of aquaorin type 2 into distal tubule and collecting duct which facilitates water to be coming in and brought back into blood (reabsorbed). The result is a decrease in osmolarity, and a trend toward normal.

At the same time, if osmolarity is high enough we trigger thirst and drink water. this will also trend body osmolarity toward normal.

24
Q

What happens if we are in a state of water overload? What is the general order of events?

A

You inhibit osmoreceptors in hpothalamus due to plasma osmolarity being decreased which turns off production and release of ADH. This means in the kidneys in the late distal tubule and collecting duct there will be less aquaporins inserted into the apical (lumen) membrane and therefore the distal tubule does not pull water back in, leading toward a net fluid loss and osmolarity of plasma increases toward normal.

At the same time, thirst receptors will be shut off and this will also trend an increase in plasma osmolarity.

25
Q

CENTRAL DIABETES INSIPIDUS:

  • How does it manifest?
  • What is causing it?
  • Basic mechanism of what’s physiologically happening to the individual as a result of the ADH disorder?
A

This manifests in terms of polyurea and the desire to drink (polydipsia).
It is caused by an impairment of vasopressin in the brain
You don’t have a lot of AVP so you’re not taking water back from kidneys and you piss a lot and are thirsty as a result

26
Q

NEPHROGENIC DIABETES INSIPIDUS

  • Manifestation
  • What is affected / what is the cause
  • basic mechanism of what’s happening due to ADH disoder
A
  • Polyuria (piss lots) and polydipsea (thirst lots)
  • vasopressin receptor type 2 is fucked up (this can often be due to family mutations or damage of kidneys due to drug toxicity)
  • you have ADH but it can’t bind to the receptor. No binding = no Aquaporin 2 = no water reabsorption (so you piss it out)
27
Q

SIADH

  • Manifestation
  • What causes it?
  • basic mechanism of what’s going to happen to you as a result
A
  • too much water , reduced osmolality of plasma
  • you over produce ADH (syndrome of inappropriate ADH secetion)
  • reduced osmolality, hyperconcentrated urine and high water retention
28
Q

Total body water is approximately what percentage of body weight

A

60%

29
Q

Of the total body water, what proportion is intracellular and what is extracellular?

A

most is intracellular (2/3), remaining 1/3 is extracellular

30
Q

What makes up intracellular fluid

A

fluid in cells

31
Q

What makes up cells

A

interstitial fluid and plasma

32
Q

What is high in intracellular fluid (5)

A 
Potassium
magnesium
proteins
phosphates
chloride
33
Q

What is found in the extracellular fluid? (3)

A

Sodium
chloride
bicarb

34
Q

If we have a disruption of body fluids what compartment is affected first when we draw a darrow yannet diagram

A

ECF

35
Q

How do we measure TBW?

A

D2O

36
Q

How do we measure ECF?

A

Radiosodium/radiosulfate

37
Q

Example of isosmotic volume contraction

A

Diarrhea

38
Q

Example of hyperosmotic volume contraction

A

Water deprevation (dehydration)

39
Q

Example of hyposmotic volume contraction

A

Adrenal insufficiency

40
Q

Example of Isosmotic volume expansion

A

Infusion of isotonic NaCl (nromal saline infusion)

Blood transfusion of someone with similar osmolality

41
Q

Example of hyperosmotic volume expansion

A

high NaCl intake from a high concentration saline infusion

Drink sea water

42
Q

Example of hyposmotic volume expansion

A

SIADH

43
Q

3 steps to solving a darrow yannet digram

A
  1. construct the diagram
  2. draw the disturbance (this only happens to the ECF)
  3. Equilibrate the ICF and ECF by moving water from the hpotonic to hypertonic (water shift may be ECF -> ICF, or from ICCF to ECF)
44
Q

Darrow yannet diagram representing someone who has had isotonic volume contraction

A
45
Q

Darrow yannet diagram representing someone who has had hypertonic volume contraction

A
46
Q

darrow yannet diagram of someone who has experienced hypotonic volume contraction

A
47
Q

Darrow yannet diagram that represents someone who has had an isotonic volume expansion

A
48
Q

Darrow yannet diagram that represents someone who has had hypertonic volume expansion

A
49
Q

Darrow yannet diagram that represents someone who has had hypotonic volume expansion

A
50
Q

What is the anion gap?

A

If you measure cations in plasma (primarily Na) and compare to anions that are in plasma, you compare to anions present (should be equal). This is primarily chloride and bicarb, but there’s some missng - this is really sulfate, phosphate, albumin, and other proteins.

51
Q

Why do we care about the anion gap?

A

It is important when considering metabolic acidosis ; bicarbonate is key when we consider buffering and pH - therefore, if gap is greater than normal some kind of metabolic acidosis may be diagnosed

52
Q

From where do we measure the anion gap?

A

plasma/serum - NOT urine

FHB (54 decks)

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