session 4 Flashcards
response to raise in BP
-release in ANP to inhibit NaKATPase and ENaC
response to reduction in BP
- prostoglandin release to remove systemic vasoconstriction
- RAAS activated
when does congestive cardiac failure occur
the heart muscle pump cannot cope with its qorkload
how does congestive cardiac failure cause oedema
- 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
management congestive heart failure
diuretics, ACE inhibitors, nitrates, vasodilators
causes hypervolaemia
kidney retention of Na+ and water, excessive sodium intake, cirrhosiis
what is hypertensive renal disease
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
where are osmoreceptors located
hypothalamus, OVLT
how do osmoreceptors work
fenestrated leaky epithelium exposed to systemic circulation, sense changes in plasma osmolarity. lead to changes in ADH and thirst
how is ADH formed
synthesised in supraoptic nucleus of hypothalamus as large precursos. transported to posterior pit where its syntehsis is completed
effects of ADH
V1 receptor- blood vessel vasoconstrition
V2 receptor- reduced water excretion. create more aquaporims.
diabetes insipidus
the inability to reabsorb water from nephron due to failure of secretion or action of ADH
symptoms diabetes insipidus
polyuria, polydypsia, low urine osmolality
2 types of DI
nephrogenic, central
causes central DI
damage to hypothalamus or pituitary causing impaired ADH secretion or synthesis. caused by brain injury or tumour.
