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GERR > Lecture 24: Osmolarity and Blood Volume > Flashcards

Lecture 24: Osmolarity and Blood Volume Flashcards

1
Q

what is normal osmolarity

A

appx 280 mOsm

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2
Q

explain how hypertonic ECF causes release of ADH

A
  • aquaporin channels in hypothalamic neurons (osmoreceptors) allow water to exit cells by osmosis
  • osmoreceptors shrink
  • stretch sensitive channels open allowing entry of Ca and Na –> causes depolarisation and AP generated
  • AP passed to SONs and PVNs which then release ADH into post. pit.
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3
Q

explain the MoA of ADH

A
  • ^ water reabsorption at DCT and CD

- by ^ the aquaporins present in walls of CD and DCT

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4
Q

describe the effect a hypotonic ECF has on ADH release

A
  • aquaporins in hypothalamic neurons (osmoreceptors) allow water to enter cells by osmosis
  • osmoreceptors expand
  • stretch channels inactivate
  • decrease in Ca and Na entry therefore no AP
  • SONs and PVNs not activated
  • decrease in ADH release
  • less water reabsorption at CD
  • ^ ECF osmolarity
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5
Q

explain how normal blood pressure inhibits ADH release

A
  • baroreceptors in carotid sinus and aortic arch sense stretch of BV wall
  • baroreceptors activate w/ each heart beat allowing Ca and Na to enter and depolarise nerve cell
  • AP transmitted to hypothalamus
  • Normal BP inhibits SON and PVN dependent release of ADH
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6
Q

outline how reduced BP causes release of ADH and the effect ADH has on BP

A
  • reduced BP means reduced AP firing rate
  • SON and PVN not inhibited
  • ^ ADH release
  • ^ water reabsorption
  • ^ BP
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7
Q

what type of hormone is aldosterone and where is it released from

A

mineralocorticoid released from Zona Glomerulosa of adrenal cortex

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8
Q

what causes release of aldosterone

A
  • ^ plasma K+
  • ^ ACTH
  • ^ ang2 (renin)
  • dec. plasma pH
  • dec. atrial stretch
  • dec. BP
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9
Q

what does release of aldosterone cause

A
  • ^ Na+ and H2O reabsorption
  • ^ K+ secretion
    (via ^ Na/K ATPase expression)
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10
Q

describe action of aldosterone in response to hyperkalaemia

A
  • ^ expression of Na/K ATPase pump in DCT and CD
  • drives a net secretion
  • therefore more K+ excreted
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11
Q

what is Conn’s disease

A

primary hyperaldosteronism

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12
Q

what can cause Conn’s disease

A

adrenal adenoma

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13
Q

what is secondary hyperaldosteronism

A

over activity of RAAS

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14
Q

name a result of both primary and secondary hyperaldosteronism

A

arterial hypertension assc w/ hypokalaemia

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15
Q

name some causes of primary hypoaldosteronism

A
  • primary adrenal insufficiency
  • congenital adrenal hyperplasia
  • side effects of meds e.g. ACE inhibitors or some diuretics
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16
Q

describe some results of hypoaldosteronism

A
  • hyperkalaemia
    severe:
  • palpitations
  • muscle weakness
  • numbness
  • abnormal heart rhythms
  • cardiac arrest
  • death
17
Q

name types of hypo aldosteronism

A
  • primary
  • secondary
  • isolated
18
Q

what is isolated hypoaldosteronism

A

reduced aldosterone w/o corresponding changes in cortisol

19
Q

describe some cause of secondary hypoaldosteronism

A
  • disease of pituitary or hypothalamus (dec. ACTH)
  • dec. ang2 prod.
  • renal diseases e.g. diabetic nephropathy
  • drugs e.g. NSAIDs, cyclosporine
20
Q

how do you differentiate the cause of hypoaldosteronism

A
  • ACTH stimulation test for aldosterone
  • -> low aldosterone response = primary
  • -> normal/large response = secondary
21
Q

outline how dec. ECF osmolarity activates the RAAS

A
  • dec. ECF osmolarity = dec. plasma Na+
  • dec. plasma reabsorption
  • detected by kidneys which release renin
  • angiotensinogen converted to ang1
  • ACE in lungs conerts ang1 to ang2
  • ang 2 acts on adrenal cortex causing release of aldosterone
  • aldosterone ^ Na/K ATPase pump expression in DCT and CT
  • ^ Na+ reabsorption
22
Q

outline how ^ SNS activity activates RAAS

A
  • ^ SNS
  • renin released
  • angiotensinogen –> ang1
  • ang1 –> ACE (lungs) –> ang2
  • ang2 –> adrenal cortex
  • aldosterone release
  • pump expression ^
  • ^ Na+ reabsorption (and H2O)
  • ^ blood volume, BP and CO
23
Q

what can negatively feedback to ^ ECF osmolarity after activation of RAAS and how is it caused

A

^ blood volume

- ang2 acts on brain to release ADH which ^ H2O reabsorption causing ^ blood volume

24
Q

what can activate RAAS

A
  • dec. ECF osmolarity

- ^ SNS activity

25
Q

how is the negative feedback of ^ blood volume for dec. ECF osmolarity overcome

A

hypothalamus overrides effects of ang2 thus causing a dec. in ADH release therefore dec. H20 reabsorption

26
Q

explain regarding juxtaglomerular cells how low Na+, BP AND/OR SNS activity affects release of renin

A

low Na+

  • low Na+ in filtrate
  • low Na+ reabsorption into macula densa
  • sensed –> prod of PGE2
  • goes to juxtag. cell
  • renin prod by these cells and released into blood

SNS

  • SNS release noradrenaline onto B1 receptors on juxg. cell
  • prod of cAMP
  • prod renin

BP

  • ^ BP
  • stretch sensitive channels in juxg. cells
  • cause down regulation of cAMP
  • inhibits renin release
  • BP dec.
27
Q

how does ^ BP affect Na+ reabsorption

A

reduces reabsorption

28
Q

outline the effect of ^ ANP on renin release and blood volume

A
  • ^ ANP from atrial myocytes due to atrial distension
  • ANP inhibits renin release
  • -> dec. circulating ang2 and aldosterone (natriuresis and diuresis - K+ sparing as K reabsorption maintained)
  • ANP ^ GFR (diuresis)
  • ANP dec. Na transporter activity in loop (non K+ sparing natr/diuresis)
  • systemic vasodilation (directly and indirectly)
  • dec. blood volume, BP and CO
29
Q

name a natural counter regulatory system for RAAS

A

natriuretic peptides

30
Q

why is this mechanism useful in treatment of hypertension and CHF

A

doesn’t affect K+ levels in rest of body

31
Q

when is thirst activated

A

when blood osmolarity ^^

32
Q

when is thirst activated

A
  • when blood osmolarity ^^
  • inputs from blain (anticipation of food)
  • inputs from body (sensing salt in mouth, hypovolaemia)
33
Q

how does the kidney know what and how much to eliminate

A
  • imbalance of homeostasis (stimulus)
  • detected by sensor
  • info sent to control centre
  • effect produced
  • response
34
Q

which of these treatments for hypertension are working through RAAS and/or kidneys

  1. diuretics
  2. CCBs
  3. ACEi
  4. ang2 rec. antagonists
  5. B-adrenergic rec. antagonists
  6. vasodilators
  7. renin inhibitors
  8. aldosterone rec. antagonists
  9. A2 adrenergic rec. agonists
A

1, 3, 4, 5, 7, 8

2, 6 and 9 affect b.v.

GERR (46 decks)

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