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Glomerular disease - week 1 > Salt and water handling > Flashcards

Salt and water handling Flashcards

1
Q

Renin angiotensin aldosterone system

A
  1. Renin released from kidneys n response to stimuli
  2. Converts angiotensinogen to Ang I in liver
  3. Ang I converted by ACE to ang II which has effect in body both directly and via aldosterone
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2
Q

Angiotensin II

A
  1. Na+ reabsorption in the proximal tubule and lielyi distal sites as well
  2. At higher concentration causes vasoconstriction
  3. releases aldosterone
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3
Q

What is the function of aldosterone

A

Allows Na+ reabsorption in the DCT/collecting duct in exchange for K+

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4
Q

Prostaglandins -formation

A

arachidonic acid released from phospholipids, is metabolized to PGs by cyclooxgenase

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5
Q

Prostaglandin action in the kidney

A

-main PG is PGI2 (i.e. prostacyclin)

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6
Q

PGI2 role

A

=afferent arteriole vasodilation and natriuress

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7
Q

Prostaglandins in healthy

A

-little or no basal PGI12 syntheiss

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8
Q

When do prostaglandin levels rise

A

-in low ECGV states (CHF or cirrhosis) PGI2 levels rise to maintain renal perfusion in the setting of high AII, SNS activity ect

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9
Q

NSAIDS in certain people -safety

A

NSAIDS will remove the counteregulation…

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10
Q

How renal sympathetic nerves regulate kidney function

A
  • increase SNS activity leads to renin secretion

- greater activity of SNS also directly causes increase Na+ /H2O reabsorption

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11
Q

Kidney transplant patients - effect SNS

A

-lack renal innervation (cant attach sympathetic nerves during surgery) and therefore seem to be prone to ECF volume depletion

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12
Q

Natriuretic peptides

A

-atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP)

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13
Q

Renal effects of natriuretic peptides

A

-increase GFR and natriuresis (latter effect similar to the poss)

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14
Q

Uroguanylin production

A

gut natriureti peptide

-produced in intestines in response to salt intake (probably as a prohormone)

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15
Q

Uroguanylin effect

A
  • reduces renal sodium reabsorption, helping to compensate for ingestion of dietary sodium
  • not a target for pharmacological intervention yet
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16
Q

Nitric oxide effect

A

-appears to have diuretic properties (separate from its vasodilatory powers) and NO deficiency or resistance has been implicated in some models of hypertension

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17
Q

Salt reabsorption –> major sites in nephron

A
  • total 27000 mmol Na+ is filtered per day excreting 150 mmol of Na+ in a day
    1. Proximal convolutedd tubule filter 27000 mmol –> takes back 18,00 and 9000 travelling more distally
    2. Loop of henle –> reabsorbs 6000, 3000 goes more distally
    3. In cortical collecting duct 700 reabsorbed, 300 remains
    4. In medullary collecting duct 150 reabsorbed 150 remains
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18
Q

Water regulation -purpose

A

-regulated to maintain a physiological [Na+]
-disturbances of Na+ lead to change in ADH secretion
-loss of water = increase Na+ concentration = increase osmolarity leading to cell shrinkage in hypothalamus = increase release of arginine vasopressin (ADH) by posterior pituitary
+ increase thirst (same osmotic stimulus in hypothalamus leads to increased thirst)

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19
Q

Effect loss pituitary function

A

-can lead to loss of adh = central diabetes insipidus –> does not usually impair thirst so can still survive?

20
Q

ADH receptors

A

2 main vasopressin receptors
V1
V2
(V3)

21
Q

V1 receptor

A
  • located in arterioles, glomerular mesangila cells, and the brain
  • mediates vasoconstriction
22
Q

V2 receptor

A

-located on the blood side…

23
Q

ADH and V1 receptor activation

A

physiological adh nnot sufficient to cause activation of V1 receptor

24
Q

Non osmotic stimuli of ADH

A
  1. Volume depletion
  2. Nausea/vomiting
  3. Pain
  4. Medications (narcotics, chlorpropamide, carbamazepine)
  5. Exercise
25
Q

Half life of endogenous vasopressin

A

t1/2 of minutes

26
Q

MOA of vasopressin drug

A

-a selective V1 agonist which can be used in the treatment of shok in the ICU setting

27
Q

DDVP

A

??

28
Q

What determines the extracellular fluid volume

A

The serum sodium content (number of Na+ particles)

29
Q

What determines the serum sodium concentration

A

Determines the intracellular fluid volume (not under direct physiological control due to water permeability of cell mebranes)
-no hormones involved in this (automatic)

30
Q

What does serum [Na+] reflect

A
  • the ratio of Na+ to water

- it does not correlate wtih ECFV (volume status) or body sodium content

31
Q

What do alteration in Na+ concentration reflect

A
  • imbalances in the ratio of salt to water

- almost always this is because of disturbance in water content

32
Q

Main intracellular ion vs. extracelluar

A

Na+ main extracellular, K+ main intracellular

33
Q

What do change in body salt content result in

A

-corresponding change in body wter content such that ECF volume changes but sodium concentration…

34
Q

MOA cerebral edema/coning

A

1) Loss Na+ (hyponatremia) –> decrease Na+ content in same volume of fluid = lower Na+ concentration
2) Water therefore flows into the cells to reach a new euiqlibrium (low extracellular osmolality compared with the intracellular space)
3) Water flows into cells to reach new equilibrium
4) Water expands in cells –> edema (conning why??)

35
Q

CHF

A

1) Reduced CO
2) Decreased presure loading of arterial sensors =decreased effective circulating volume
3) Initiates several processes leading to Na+ retention
4) If the extracellular fluid becomes salty other signals act to retain water as well

36
Q

Effect Na+

a) increased
b) decreased

A

a) edema

b) hypovolemia or shock

37
Q

Effect H2O

a) increased
b) decreased

A

a) cerebral edema

b) osmotic demylination

38
Q

How low sodium content leads to low Na+ concentration via ADH

A

1) Decreased Na+

2) Decreased sodium concentration (via ADH induced H2O retention)

39
Q

What is being sensed

a) osmoregulation
b) volume regulation

A

1) plasma osmolarity

2) volume regulation

40
Q

Sensors

a) osmoregulation
b) volume regulation

A

X

41
Q

X

A

X

42
Q

X

A

X

43
Q

How to change the concentration of urine

A

X

44
Q

x

A
  1. Prox tubule = lots of isotonic reabsorption
  2. Descending lumb = concentrating segment = water reabsorbed but salt isnt
  3. Ascending limb = diluting segment = solutes reabsorbed
  4. Distal tubule = some additional salt/H2O reabsorbtion but in general urine remains diluted (relative to the blood):
  5. Collecting duct: if ADH acting, water reabsorbed down its gradient, otherwise urine remains dilute
45
Q

Diluting the urine - requirements

A

TAL must be functioning in order to create.

46
Q

Concentrating the urine MOA

A

Water must be removed to leave behind a concentrated urine

Glomerular disease - week 1 (12 decks)

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