osmolality Flashcards
When blood pressure drops what are the two main systems that come into play?
-RAAS
-prostaglandins
what 3 main things cause the release of renin
- increases sympathetic innervation: granular cells produce renin
- wall tension in arterioles fall: lower wall tension stimulates granular cells
- reduces Na to macula densa cells: they will release prostaglandins and granular cells release renin
what does RAAS do to help with low blood pressure?
- direct vasoconstriction in glomerulus: increase perfusion pressure
- release aldosterone: increase EnaC and more sodium reabsorption so more water reasorbed
- release ADH
- thirst
what role do prostaglandins have in reduced blood pressure
- reduced blood pressure means reduced perfusion to organs
- they cause vasodialation (prevent excessive vasoconstriction from the renin)
- so more perfusion to the organs
flow chart of the bodies response to reduced BP
what occurs when there is an increased blood pressure?
- ANP released (atrial natureric peptide)
- tries to increase extracellular fluid
- inhibit NA/K ATPase and close Na channels to prevent reabsorption of Na
- so reduced water reabsorption
- vasodialate afferent arterioles: increase GFR and reduce Na reasborption
- inhibit aldosterone
- inhibit ADH
- reduce renin
starlings forces in the PCT reducing blood pressure
- high hydrostatic pressure in peritubular capillaries
- reduced oncotic pressure
- water reabsorption reduces
what is pressure natriuresis?
increased sodium excretion
what is pressure diuresis
increased water excretion
how congestive cardiac failure effect the kidneys
- reduced CO
- reduced perfusion to kidney
- see this as hypovolemia (even tho its not, still normal volume heart is just weak)
- kidney will reabsorb more Na and H20
- odema and increased circulating fluid volume
congestive heart failure effect on the lungs
- kidneys mistake low CO as hypovolemia
- they increase NA and H20 reabsorption
- odema
- backs up into lungs
- pulmonary odema
managment of congestive heart failure
as it can cause pulmonary odema and odema in general must reduve fluid:
- diuretics (furezmide)
- ACE inhibitor (reduce RAAS)
- nitrates
- vasodialator (so blood vessels can compenstate foe extra fluid)
where commonly causes hypervolemia ?
- kidney retention of sodium and water
- excessive sodium intake
- cirrhosis
- hyperaldosteronism ( more aquaporins, more reabsorption of na and water)
what is hypovolemic shock
- vital organs are inadequately perfused
- anaerobic respiration
- tiredness and dizziness and thirst
- vasodialation to maintain blood supply
- tissue necrosis
in severe circumstances when there is a low BP what are the body response
- tachycardia
- peripheral vasoconstriction
- increase in myocardial contractility
during execssive vasoconstriction what are secereted in the kidneys
- prostaglandins to maintain some dialation
- to maintain blood flow
- suffiecient GFR
what are some common causes for hypovolemia
- burns
- haemmorage
- vomiting and diarrhoea
hypertensive renal disease
- high BP is transferred to the kidney
- arteriosclerosis of renal arteries
- hylanization (scarring and thickening) of small vessels
- can lead to chronic renal damage
what are some renal causes of secondary hypertension?
- impaired Na and water excretion
- stimulation of renin
- renal artery stenosis ( kidneys constantly think there is reduced perfusion to the kidney and stimulate RAAS which increases the blood pressure)
what is osmolality and osmolarity a rough measure of
amount of solute in the solvent (how dilute or concentrated)
which two systems are involved in regulating osmolarity
what are osmorecpetors and where are they made
- found in the hypothalamus
- made from the supraoptic nucleus
- sense change in plasma osmolarity
- can either change: conc of urine or thirst
how does ADH work
- anti-diuretic hormone released when there is high plasma osmolarity
- synthesized in the supraoptic nucleus of the hypothalamus
- causes more H20 to be reabsorbed
- bind to V2 receptors -> causes fusion of 2 aquaporin channels for water to pass
how does release of ADH
- High BP:
ADH has a higher set point so less water is reabsorbed - Low BP:
ADH has a lower setpoint so that more water can be reabsorbed
what is the ultimate compensation for reduced water
drinking water
what is diabetes insipidus
inability to reabsorb water from the distal tubule, due to the failure of ADH secretion
what are some symptoms of diabetes insipidus
polyuria
polydipsia
but the wee wont be sweet and full of glucose like diabetes mellitus as its not to do with insulin and glucose
what is central diabetes inspidus and how can you treat?
- impaired ADH synthesis or secretion due to damage of the hypothalamus due to:
- brain injury
- tumour
- anerysm
treat: administer ADH
nephrogenic diabetes insipidus? how to treat
- insensitivity of the kidney to ADH
- water inadequately reabsorbed and too much urine
TREAT:
- low salt, low protein
what is SIADH
- inappropriate seceretion of ADH (too much seceretion)
what are some causes of execssive ADH
- dilutional natremia (lots of water in plasma)
- low sodium in plasma
- body fluid increased
4.
what are some symptoms of SIADH
- hyponatremia and low plasma
- inappropriate NA in urine: body tries to remove Na to remove excess water
summary of if plasma osmolality is decreased
summary if plasma osmolality increased
