renal volume 1 Flashcards
recommended intakes for patients (NA,K,Glucose)
water 25ml/kg/day
Na- 1 mmol/kg/day
K- 1mmol/kg/day
glucose- 50g a day.
what should vs should not be used for vascular space resusitation.
dextrose- only 7% stays in intravasc space, distributes accross all cells. used to maintain hydration without sig electrolites.
normal saline- isotonic- contains na, cl. 25% stays in vasc space. Used for resus and maintainance. (can result in hyperchloraemic acidosis.)
Heartmans- isotonic- Na+, Cl–, K+, HCO3– (as lactate), Ca2+, and water. both resuscitation and fluid maintenance. considered more physiological, has bicarb too to help. use in acidosis.
discusss body fluid composition
2/3 body wt is water
2/3 of that is extracellular
1/3 is intracellular.
what can happen in sepsis in regard to fluid distribution
discuss normal control of blood flow in the kidney
2 mechanism enable a steady flow of blood to kidney
Bayliss myogenic response: if BP raises (e.g exercise) afferent arteriole constricts, reducing amount of blood- keeping GFR the same. opposite also happens as needed
tubulo glomerular feedback/ macular densa. –> BP inc, flow through efferent inc, Na inc–> macular densa detects this, constricts afferent tubule + reduced renin. vice versa also happens when needed.
how does chronic hypertension cause pathology
bayliss mechanism no longer works. –> hyper filtration (causing proteinuria)–> inflammation –> mesanglial cell expansion –> glomerular sclerosis.
you also get hyaline arteriosclerosis –> renal artery sclerosis –> lower blood flow to the kidney.
ischaemia results in nephron death + immune cells to react –> releasing TGF-B1–> glomerular hardening and scarring. = reduction in GFR.
upregulation of the RAAS occurs due to the sclerosis- reduced blood flow. generally increasing the HTN problem.
signs and symptoms of hypertensive nephropathy + management
proteinuria, albuminuria, decreased eGFR,
General CKD signs are:
loss of appetite, nausea, vomiting, itching, sleepiness or confusion, weight loss, and an unpleasant taste in the mouth
management:
ACE inhibitor –> vasodilate efferent arteriole–> improve blood flow + filtration + BP mgt
keep checking K+ to ensure maintaining function.
ACEi good in CKD, bad in AKI
diagnosis of hypertensive nephropathy + prognosis
definitive diagnosis requires morphological examination, preceded by lab investigations e.g
albumin/ protein presence in urine, reduced GFR etc.
1/3 of all people who are on HD is due to HTN nephropathy.
if on HD then prognosis is 25% die each year.
more likely to develop nephropathy if African American,
action of ADH
acts on renal collecting ducts to make them permeable- allows free water absorbtion, production of concentrated urine.
secretion stimed by- inc in plasma osmolality
dec plasma volume
pain,stress,nausea,drugs,angoi 2
ECF volume overrides osmolar controls.
what should blood pressure do on standing.
urinary sodium values and indications
urinary osmolality indicators
blood should increace in pressure
a drop indicates fluid depletion.
is more than 20 - loosing
if less than 20- gaining.
urine osmolality - more than 1 = conversin
less than 1 = loss (water)
what happens is the body is acidotic-i.g what is associated with it on abg
it becomes hyperkalaemia- it preferentially gets rid of H ions.
alkalosis and hypokalaemia go together.
why is H+ secreted and lines of defence for this
H+ created by ATP formation.
need to maintain to prevent denaturation of proteins.
H+ ions are lost renally
bicarb is lost renally
co2 is lost resp
1st line of def- bicarb system (need carbonic anhydrase)
phosphate and Hb can also mop up some as can bone
2nd line- resp system blowing off Co2
3rd- the kidneys - retains bicarb but a slow response. (PCT is where the majority are reabsorbed)
causes of disruption to acid base balance
resp acidosis- Co2 retention
resp alkylosis- hyperventilation
met acidosis- inc in H= prod/ reduction in in buffer capacity (e.g diarrhea)
Met alkalosis- excessive H+ loss, or exogenous alkalai consumption. (vom)
resp compensation is rapid, met compensation is long
what is the anion gap
diff between positive and negative plasma anions
(Na + K) - (Cl + Hco3)
normal diff is 10-18
causes of raised are KUSMAL
Ketoacidosis
uraemia
Salicylate poisoning
methanol ingestion
aldehydes
lactic acidosis
hyponatraemia algorithm for aetiology
Hypertonic hypo – high plasma osmolality–> water drawn in from cells diluting Na (think high glucose)
pseudohyponatraemia -> patients have normal plasma osmol but low Na. - high protein (myeloma) triglicerides (artificially low Na)
Hypotonic hyponatraemia (low plasma osmolality) -
assess volume status
hypovolaemic - assess urine salt losses (higher or lower than 20) - if less than- salt loss is extra renal (GI, burn, Haemmorhage)
if more than 20- renal salt loss (addisons, diuretic)
Euvolaemic-
urine NA< 20 - acute H20 overload. (e.g beer)
urine Na > 20- chronic h20 overload, impaired excretion (SIADH)
Hyper volaemia - urine Na < 20 => oedema
