acute complications of diabetes - other W6 Flashcards

1
Q

what type of diabetes does diabetic ketoacidosis develop in? what is it more usual to develop in the other type?

A

diabetic ketoacidosis develops in type 1 diabetes mellitus

more likely to develop a hyperosmolar hyperglycaemic state in type 2 diabetes

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2
Q

pathogenesis of DKA?

A

profound insulin deficiency leads to inability of body to utilise glucose, accumulates in blood, hyperglycaemia. inability to utilise leads to free fatty acid mobilisation, used as energy source, leads to increased levels of ketone bodies. -> ketonuria. weak acids but as they build up, leads to acidosis, severe illness.

progression of DKA leads to osmotic diuresis, hypovolaemia (exacerbated by vomiting). can lead to reduced consciousness, death.

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3
Q

which other pathway exacerbates DKA?

A

decreased peripheral glucose causes increase in gluconeogenesis, glycogenolysis. counter regulatory hormone release, exacerbates hyperglycaemia.

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4
Q

consequence of osmotic diuresis and profound hypovolaemia?

A

reduction in GFR, therefore glucose not efficiently cleared from the kidneys

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5
Q

pathogenesis of HHS?

A

relative insulin deficiency, inability for peripheral glucose to be taken up by tissue. persisting hyperglycaemia, worsens from continuous glucagon release and increased glucose formation. causes osmotic diuresis, hypovolaemia, reduced GFR.

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6
Q

management of DKA?

A

fluids - faster then slower
iv insulin - switch off ketone production
monitor potassium - metabolic acidosis shifts K+ to extracellular space, as you give insulin K+ moves into the cells and K+ falls.

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7
Q

how often is DKA the first presentation of T1DM?

A

10% of cases

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8
Q

DKA diagnosis?

A

polyuria, polydipsia
hypovolaemia
abdo pain, N&V
Kussmaul resps, ketotic breath
muscle cramps
precipitant evidence (eg sepsis)

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9
Q

DKA - after the event?

A

swap to s/c insulin once patient is eating and drinking
ensure basal insulin given >1h before iv insulin stops
try identify precipitant
educate patient
look out for complications

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10
Q

HHS findings?

A

marked hyperglycaemia, raised osmolality

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11
Q

epidemiology of HSS?

A

2/3 cases in previously undiagnosed DM
affects middle-aged or elderly T2DM
mortality up to 33%

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12
Q

diagnosis of HHS?

A

hyperglycaemia (>30mmo/l, often 60-90mmol/l)
serum osmolality >320mmol/kg
no/mild ketoacidosis
severe dehydration and pre-renal failure common

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13
Q

HHS features?

A

insidious onset
profound dehydration (double amount found in DKA)
hypercoagulability
confusion, coma, fits
gastroparesis, N&V, haematemesis

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14
Q

management of HHS?

A

similar to DKA but:
slower, prolonged rehydration
gradual reduction in Na+
gentler glucose reduction
anticoagulation vital - prophylactic sc heparin
seek the precipitation (infection, MI etc)

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15
Q

metformin safety - pragmatic suggestions?

A

stop MF if eGFR <30 or worsening fast
withdraw during tissue hypoxia (but an reinstate later)
withdraw for 3 days after iodine-containing contrast (reinstate 48h later)
withdraw 2 days before giving general anaesthetic

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16
Q

what is raised lactate generally a consequence of?

A

tissue hypoxia