Lecture 12 - Renal Physiology: Salt and Water Flashcards
Proximal tubule?
majority (75%) of water reabsorption
Loop of henle?q
free reabsorption of water in descending limb, and 20% of sodium reabsorption at ascending limb
Anti-diruetic hormone/vasopressin?
made in hypothalamus and secreted by pituitary, increased in response to BP drop or osmolarity increase, increases absorption of water to restore BP and osmolarity
Aldosterone?
adrenal gland release, increases Na reabsorption and K excretion @ distal CT and CD; stimulated by K and angiotensin II
Renin angiotensin?
juxtaglomerular apparatus senses decreased renal perfusion and secretes renin -> increases angiotensin production
Drug targets?
carbonic anhydrase inhibitors (PCT), loop diuretics (LoH), thiazide diruetics (DCT), K+ sparing diuretics (CD)
Hypernatraemia?
impaired thirst/level of consciousness, no access, burns/diarrhoea/blood loss caused, solute diuresis
Diabetes insipidus?
reduction in amount or efficacy of ADH, polyuria and water loss, dilute urine, can’t drink to compensatory level, increased plasma osmolarity, hyper-natraemia, dehydration
Types of D.I?
central (common, linked to brain injury) and nephrotic (rare, resistance to ADH, failure to produce aquaporin channels in CD)
Hypovolaemic?
dehydrated, low urine sodium, sodium loss w relatively less water, caused by: diarr/vomiting, bowel obstruction, skin losses, urinary losses (diuretics, addison’s)
Hyper volaemic?
fluid overloaded, Na retention BUT relatively higher water retention, caused by: cirrhosis, nephrotic syndrome, heart or renal failure
Euvolaemic?
SIADH, hypothyroid/low cortisol, diuretics, fluid replacement
SIADH?
body accumulates too much water, not low urine Osmol, urine sodium not low, low plasma osmol
Causes of SIADH?
trauma, surgery, cancer, chronic lung disease, head injury, medications
Symptoms of hyponatraemia?
brain adaptations, confusion (in slow development); cerebral oedema causing seizures, confusion or coma (in fast development)
