session 4 Flashcards

1
Q

response to raise in BP

A

-release in ANP to inhibit NaKATPase and ENaC

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2
Q

response to reduction in BP

A
  • prostoglandin release to remove systemic vasoconstriction

- RAAS activated

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3
Q

when does congestive cardiac failure occur

A

the heart muscle pump cannot cope with its qorkload

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4
Q

how does congestive cardiac failure cause oedema

A
  • heart cannot pump blood leading to kidney hypoperfusion, and so oedema
  • kidneys sense this as hypovolemia. retain NaCL and water to increase circulating volume, increasing oedema firther
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5
Q

management congestive heart failure

A

diuretics, ACE inhibitors, nitrates, vasodilators

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6
Q

causes hypervolaemia

A

kidney retention of Na+ and water, excessive sodium intake, cirrhosiis

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7
Q

what is hypertensive renal disease

A

when increase in BP is transferred to the kidney/glomerulus.
- arteriosclerosis of major renal arteries
- hyalinisation of small vesssels
leads to chronic renal damage and reduction in kidney size

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8
Q

where are osmoreceptors located

A

hypothalamus, OVLT

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9
Q

how do osmoreceptors work

A

fenestrated leaky epithelium exposed to systemic circulation, sense changes in plasma osmolarity. lead to changes in ADH and thirst

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10
Q

how is ADH formed

A

synthesised in supraoptic nucleus of hypothalamus as large precursos. transported to posterior pit where its syntehsis is completed

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11
Q

effects of ADH

A

V1 receptor- blood vessel vasoconstrition

V2 receptor- reduced water excretion. create more aquaporims.

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12
Q

diabetes insipidus

A

the inability to reabsorb water from nephron due to failure of secretion or action of ADH

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13
Q

symptoms diabetes insipidus

A

polyuria, polydypsia, low urine osmolality

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14
Q

2 types of DI

A

nephrogenic, central

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15
Q

causes central DI

A

damage to hypothalamus or pituitary causing impaired ADH secretion or synthesis. caused by brain injury or tumour.

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16
Q

how to treat central DI

A

administering ADH (desmopressin) or ADH injections/nasal spray

17
Q

what is nephrogenic DI

A

acquired insensitivity of kidney to ADH. water inadequately absorbed from collecting ducts so large quantity of urine produced.

18
Q

how to manage nephrogenic DI

A

low salt, low protein diet

19
Q

what is SIADH

A

syndrome of innapropriate ADH secretion. excessive reelease.

20
Q

symptoms SIADH

A
  • dilutional hyponatremia causing lowered plasma sodium and raised total body fluid
  • innapropriate urine osmolality
  • inappropriate Na+ secretion
21
Q

cause SIADH

A

stroke, malignancy, lung disease

22
Q

what is hypernatremia

A

plasma [Na] > 146mmol/L, increased solute:water ratio in body fluids and increased serum osmolality.

23
Q

causes hypernatremia

A

osmotic diuresis, fluid loss, DI, incorrect IV, primary aldosteronism

24
Q

what is hyponatremia

A

serum concentration of Na below 130/135mmol/L

25
symptoms hyponatremia
agitation, nausea, focal neurology, coma
26
causes hyponatremia
diuretics, water overload, increased ADH. D+V, burns
27
normal serum osmolality
275-295mosm/kg
28
what is hypovolemic hyponatremia
low volume, low sodium (not caused by increased fluid)
29
causes of hypovolemic hyponatremia
Gi losses eg. vomiting, excessive sweating, cerebral sat wasting syndrome
30
treatment hypovolemic hyponatremia
fluid restriction
31
effect of aldosterone on bp, where produced and where act
increase BP, adrenal gland, DCT
32
what class of hormone is aldosterone
steroid
33
action of ADH
upregulation of aquaporin channels in CD
34
which part of loop of henle is impremeable to water
thin and thick ascending limbs