diabetic ketoacidosis Flashcards
what could precipitate diabetic ketoacidosis *
new diagnosis of t1dm - complete insulin deficiency
not taking insulin eg if vomiting and not eatibg much people think they dont have to take insulin - but still need the basal level and more than that becasue ill so should increase dose
intercurrent stress- pneumonia, mi, gi/urinary infection, stroke, pvd
fasting and not taking enough insulin
what are the metaboilic effects of low insulin
*
high hgo - cant be stopped
deficient muscle glucose uptake
therefore increase in glucose in serum
why is there glucose in urine in t1dm *
glucose exceeds pct ability for reabsorption - too much glucose means the transport system is oversaturated
effect of sglt2 receptor in pct *
increase glucose reabsorption from kidney
why do you give an sglt2 inhibitor in t2dm *
to prevent reabsorption of glucose in kidney and fascilitate loss in urine
why can you get dehydrated in dm *
insulin deficiency and stress cause hyperglycaemia
this causes osmotic diuresis - when cant drink enough or vomit cause dehydration - worsened by sepsis
where are ketones produced *
liver
effect of fasting on ketosis *
make it worse
why do you lose weight in t1dm *
deficient in insulin - cant take glucose into muscle
protein breaks down
what happens to ketone bodies after they are released from the liver *
taken into the muscle and used in the krebs cycle
describe acid base regulation on the kidney with respect to dm *
bicarbonate is important and is linked to h+ excretion - more h excreted means more co2 enter pct epi from the filtrate and so is converted to bicarb by carbonate dehydratase which then enters blood and buffers acids
it needs adequate glomerular filtration = if dehydrated, gfr is reduced and acidosis is worse - less bicarb enter the blood
low insulin causes increased bicarb production
na excretion is linked to h or k excretion - via an antiporter (h enters epi from filtrate and na enters filtrate from epi)
acid ketone bodies require increased bicarb buffering - in attempt to neutralise the ph
therefore to treat ketoacidosis you need to hydrate to increase gfr and bicarb secretion into blood
what are the blood gases in metabolic acidosis eg dka *
ph low
bicarb low - it is being used to buffer the high h+ also there is reduced production
co2 is low - blown off to compensate for the metabolic acidosis - this is kussmaul’s breathing
what is the anion gap and how is it affected in dm*
the anion gap is te difference between positive and negative ions
positive - na and k
negative - bicarb and cl
in dka - the increased glucose causes a discrepancy between positive and -ve ions - the bicarb is used up to mop up the ketones to compensate for the acidosis so bicarb levels decrease, increasing the anion gap
water is lost in the urine, na lost in urine k lost in urine - acidosis shows high k but total body level is low
describe the pathophysiology of diabetic ketoacidosis*
insulin def and increased stress hormones cause hyperglycaemia and ketosis
hyperglycaemia means glucose conc exceeds the amount able to be reabsorbed in kidney so enters urine which causes osmotic diuresis which causes dehydration and loss of electrolytes
fasting worses ketosis
ketosis causes acidosis becausse ketones are acids
acidosis causes hyperventilation to blow of co2 and vomiting which is result of acid on gi tract
hyperventilation, vomiting, osmotic diuresis, and fever cause dehydration
dehydration causes renal hypoperfusion = reduced gfr = impaired h+ excretion rate = worsening of acidosis because bicarb cant interact with h+
what are the clinical features of diabetic ketoacidosis *
dehydration
insulin def
low potassium because there is an increased renal excretion of potassium because of osmotic diuresis induced by hyperglycaemia, and hypovolaemia induced hyperaldosteronism. however, the insulin def means k leaves cells so serum k is high. when you give insulin as treatment, all k will go back into cells and people become hypokalaemic.
acidotic
risk of arrhythmia from acidosis and low k, infection and dilated stomach from acidosis which would worsen vomiting and hence acidosis because it would increase dehydration and loss of electrolytes
polyuria and polydipsia because of the osmotic diuresis
abdo pain
coma
glucosuria or ketonuria
need to look for the precipitating factor
