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Endocrinology > Diabetic Emergencies > Flashcards

Diabetic Emergencies Flashcards

1
Q

when does DKA occur

A

in absolute/ relative insulin deficiency accompanied by an increase in the counter regulatory hormones (glucagon, adrenaline, cortisol, growth hormone)

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2
Q

what is the biochemical triad of DKA

A

hyperglycaemia, ketonaemia, acidaemia

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3
Q

does DKA occur in T1 or T2 DM

A

can occur in both

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4
Q

why does stress hormone activation cause DKA

A

increased lipolysis
decreased glucose utilisation
increased proteolysis
increased glycogenolysis

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5
Q

how does hyperglycaemia cause decreased renal function

A

glycosuria
electrolyte loss
dehydration
decreased renal function

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6
Q

what increases lactate in DKA

A

dehydration

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7
Q

what causes increases ketogenesis in DKA

A

increases liplysis, increased free fatty acids= ketogenesis

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8
Q

what causes osmotic diuresis

A

glycosuria

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9
Q

what causes hyperosmolarity in DKA

A

dehydration (osmotic diuresis)

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10
Q

what are the biochemical diagnostic markers for ketacidosis

A

ketonaemia > 3mmol/L (or significant ketonuria)
blood glucose > 11.0mmol/L
bicarb<15 mmol/L or venous pH < 7.3

(ketones and acids rise, bicarb falls)

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11
Q

what causes death is DKA

A

adults: hypokalaemia, aspiration pneumonia, ERDS, co morbidities
children: cerebral oedema

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12
Q

what can precipitate DKA

A

newly diagnosed
infection
illicit drug and alcohol use
poorly managed diabetes (most common cause)

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13
Q

what are the typical symptoms and signs of DKA

A

osmotic related- thirst and polyuria, dehydration

ketone body related- flushed, vomiting, abdo pain and tenderness, breathlessness (kussmauls respiration), ketone smell of breath

associated conditions- underlying sepsis, gastroenteritis

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14
Q

what happens to potassium in DKA

A

is often raised > 5.5 mmol/K

BEWARE OF A LOW READING- treatment for DKA will further lower potassium

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15
Q

what happens to creatinine in DKA

A

often raised

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16
Q

what happens to sodium in DKA

A

often low or

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17
Q

what happens to lactate in DKA

A

common to be raised

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18
Q

why might amylase be raised in DKA

A

rarely pancreatitis

origin can be salivary

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19
Q

what happens to white cell count in DKA

A

often raised- not always due to infection

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20
Q

what do you lose in DKA

A

fluid
sodium
potassium
phosphate

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21
Q

what are the 4 main complications of DKA

A

cardiac arrest secondary to kypokalaemia
ARDS
cerebral oedema
gastric dilatation- risk of aspiration (aspiration pneumonia)

22
Q

what are the principles of management for DKA

A

manage in HDU
replace losses- fluid, insulin, potassium, (rare- phosphate and bicarbonate)
address risks- NG tube required?, monitor K+, prescribe LMWH (thrombo embolic risk), source sepsis (CXR, blood culture, MSSU)

23
Q

describe the process by which insulin deficiency causes DKA

A

insulin deficiency switches metabolic balance in a catabolic direction
liver produces gluconeogenesis (from proteins and glycogen)
fat in adipose is reduce to triglycerides and fatty acids
increasing levels of ketone bodies
rising level of glucose increases urine production- loss of electrolytes and ions
metabolic acidosis

24
Q

what is kussmaul respiration

A

involuntary attempt to remove carbon dioxide from the blood (would form carbonic acid and worsen the ketoacidosis)

25
Q

what is a normal level of ketones

A

<0.6 mmol/L

26
Q

what does urine ketone testing measure

A

acetoacetate - indivated levels of ketones 2-4 hours previously

27
Q

why does ketonuria persist after clinical improvement

A

mobilisation of ketones from fat tissue

28
Q

what is hyperglycaemic hyperosmolar syndrome

A

when hyperglycaemia results in osmolarity without significant ketoacidosis

29
Q

what are the biochemical markers of HHS

A

marked hypovolaemia, marked hyperglycaemia, no/mild ketonaemia, bicarbonate >15 mmol/L, venous pH >7.3
osmolarity > 320 mosmol/kg

30
Q

what are the features of HHS presentation

A

often older, or younger afro-caribbean

high refined COH intake beforehand

31
Q

what are the risk associations of HHS

A

CVD (MI and stroke), sepsis, medication (steriods/ thiazide diuretics)

32
Q

what has higher glucose DKA or HHS

A

HHS

33
Q

happens to renal function in HHS

A

significant renal impairment

34
Q

what is sodium like in HHS

A

normal or raised

35
Q

compare DKA to HHS:

age of presentation

A

DKA- younger

HHS- older

36
Q

compare DKA to HHS: type of diabetes

A

DKA- Type 1

HHS- type 2

37
Q

compare DKA to HHS:

causes

A

DKA- insulin deficiency

HHS- diuretics and/or steroids, Fizzy drinks

38
Q

compare DKA to HHS:

precipitant

A

DKA- insulin omission

HHS- new diagnosis, infection

39
Q

compare DKA to HHS:

mortality

A

DKA- <2%

HHS- 10-50%

40
Q

compare DKA to HHS:

treatment

A

DKA- insulin

HHS- diet/ oral hypoglycaemic agents/ (insulin)

41
Q

what are the differences in treating HHS rather than DKA

A
  1. fluids- more increased risk of fluid overload (caution)
  2. insulin- more sensitive, slower- may not require insulin
  3. sodium- avoid rapid flucuations
  4. co morbidities more likely- screen for vascular event (silent MI), sepsis, LMWH for all unless contraindicated
42
Q

what are the biochemical diagnostics of alcoholic/ starvation ketoacidosis

A

ketonaemia raised
biocarbonate low
venous pH <7.3
glucose normal, may be low

43
Q

do patients with diabetes stay in hospital longer

A

yes

44
Q

when should you admit someone with T1DM to hospital

A 
unable to tolerate oral fluids 
persisting vomiting 
persisting hyperglycaemia 
persisting positive/ increasing levels of ketones 
abdominal pain/ breathlessness
45
Q

what is the CPR in patient foot care

A

check, protect, refer

46
Q

what does clearance of lactate require

A

hepatic uptake, aerobic conversion to pyruvate then glucose

47
Q

what can lactic acidosis be caused by

A

type A- tissue hypoxaemia- sepsis, haemorrhage

type b- liver disease, leukaemic states, diabetes

48
Q

what are the clinical features of lactic acidosis

A

hyperventilation, mental confusion, stupor or coma if severe

49
Q

what are the biochemical features of lactic acidosis

A

raisaed bicarbonate, raised anion gap, abscence of ketonaemia, raised phosphate

50
Q

after diagnosing DKA what other blood tests should be done

A

U&Es as dehydration can cause renal failure and potassium disorders common

if you suspect infection FBC (for WBC) and CRP and possibly cultures

Endocrinology (46 decks)

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