Tutorial: DKA Flashcards
Primarymdefect in T1DM
Deficient insulin from B cell
What could precipitate diabetic ketoacidosis (DKA)
- New diagnosis of T1DM
- Not taking insulin
- Intercurrent stress (pneumonia, heart attack)
- Fasting and not taking enough insulin WHY–> stress hormones
What will happen with deficient [insulin]
High HGO and deficient muscle glucose uptake
What will happen with high plasma [glucose]
2.Glucose exceeds proximal convoluted tubule ability for reabsorption
Pathophysiology in DKA
Insulin deficiency, and high stress hormones (cortisol, catecholamines and GH)
Leads to hyperglycaemia
Leads to osmotic diuresis and dehydration
DEHHYDRATION CENTRAL TO DKA
Fever also increases dehydration
Which is statement is incorrect when [insulin] low
Increased lipolysis rate
Glycerol used to produce glucose in liver
Fatty acids to produce glucose in liver
Fatty acids to produce ketone bodies in liver
Fatty acids to produce glucose in liver…
They don’t produce glucose (this is the glycerol from TAGs)…. they produce ketones whichncause a metabolic acidosis
Acid base, which is correct
- Low insulin causes reduced bicarbonate production
- Bicarbonate production linked to H+ excretion
- Excess urinary filtrate inhibits H+ excretion
- Bicarbonate is primarily generated in PCT
- All of above
- None of above
2
- Needs adequate glomerular filtration for the acid base system to function
- Carbonate dehydratase is important in acid base homeostasis
- Na excretion is linked to H or K excretion
- Acid ketone bodies require increased HCO3 buffering
- All correct choose 5
5
What is the cause of metabolic acidosis with DKA
Reduced [HCO3] in blood because -
- impaired production
- increased H+ buffering
What happens to the anion gap in ketoacidosis
HIGH ANION GAP….
same amount of acids and bases in blood, as blood is neutral….
The reason for the anion gap (i.e. the fact that less anions are recorded than cations) is that some of the anions are not measured in the anion gap eqaution… these are the unknown anions… including phosphate, and ORGANIC ACIDS.
These organic acids dissociate into H+ and an anion (e.g. for lactic acid it splits into lactate and H+). The serum remains neutral because the excess H+ from this organic acid is mopped up, but an increased amount of the negative ion (e.g. lactate) is left behind. So the anion gap will increase, despite same overall amount of anions and cations.
https://www.youtube.com/watch?v=sQnEFVNrY74
FANTASTIC video! (He’s annoying but still!)
What happens to the following ions in DKA:
- Water
- Na
- K (total body levels, plasma levels and urine)
- Lost in urine (osmotic diuresis)
- Lost in urine (during the osmotic diuresis)
- Usually, insulin stimulates Na+/K+ ATPase…. so drives K+ into cells. With insulin decifiency in DKA, K+ isn’t driven into cells, so hyperkalaemia. Additionally, H+/K+ ATPase on cells increases activity to bring H+ into cells and neutralise blood, but in doing so forces more K+ out.
THUS:
HIGH SERUM
LOW total body K+ (as it’s all being removed from cells)
INCREASED K+ removal in urine
As well as insulin decifiency what else causes increase sugar levels during DKA
Stress hormones
From the flow diagram, what leads to dehydration in DKA
Osmotic diuresis due to hyperglycaemia
Hyperventilation loses water as compensation for metabolic acidosis (Kussmaul’s breathing)
fever causes dehydration
so does vomoiting due to acidosis
Clincal features of DKA
Dehydration Insulin, deficiency Total body potassium deficiency, although plasma [potassium] high Acidotic Risk of arrhythmia, infection and dilated stomach Polyuria and polydipsia due to osmotic diuresis dehydration hyperventilation (Kussmaul) abdominal pain, vomiting coma look for precipitating factor glycosuria and ketonuria
Inverstigsations for DKA
Capillary glucose Plasma glucose creatinine, K+, Na+ FBC Arterial blood gases amylase (triglyceride) ECG CXR Septic screen
