complications of diabetes Flashcards

1
Q

who/when can diabetic ketoaacidosis occur

A

those with T1DM or the 1st presentation of it
- rare + only under extreme stress does it affect T2DM

precipitating factors
- infection
- missed insulin
- myocardial infarction

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2
Q

features of DKA

A

abdo pain
polyuria, polydipsia, dehydration
acetone breath - “peardrops” smell

Kussmaul respiration (deep hyperventilation)

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3
Q

diagnostic criteria of DKA

A

glucose > 11 mmol/l or known diabetes mellitus

pH < 7.3
bicarbonate < 15 mmol/l

ketones > 3 mmol/l or urine ketones ++ on dipstick

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4
Q

key points of DKA management

A
  1. fluid replacement - isotonic saline
  2. insulin
    - once BM <14, infusion of 10% dextrose should be started in addition to the 0.9% sodium chloride regime
  3. correct electrolyte disturbances

long acting insulin should be continued, short acting should be STOPPED

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5
Q

management of electrolye disturbances in DKA

A

serum potassium often high despite total body potassium being low
- this often falls quickly following treatment with insulin resulting in hypOkalaemia

potassium may therefore need to be added to the replacement fluids
if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required

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6
Q

who needs slower fluid resus in DKA? Why?

A

young adults (18-25yrs)

–>greater risk of cerebral oedema

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7
Q

DKA resolution definition

A

pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L

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8
Q

complications of DKA

A
  • gastric stasis
  • VTE
  • arrythmias - 2nd to potassium
  • iatrogenic due to poor fluid therapy - cerebral oedema, hypokalaemia

acute resp distress syndrome
AKI

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9
Q

Hyperosmolar hyperglycaemic state

A

hyperglycaemia results in osmotic diuresis, severe dehydration + electrolyte deficiencies

typically = elderly with T2DM

med emergency + 20% mortality

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10
Q

pathophysio of DKA

A

caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

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11
Q

pathophysio of Hyperosmolar hyperglycaemic state

A

hyperglycaemia → ↑ serum osmolality → osmotic diuresis → severe volume depletion

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12
Q

Hyperosmolar hyperglycaemic state precipitating factors

A

intercurrent illness
dementia
sedative drugs

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13
Q

differences between DKA + HHS

A

DKA
- T1DM
- presents within hours
- ketones ++
- rapid breathing, N+V

HHS
- T2DM
- comes on over days (metabolic disturbances more extreme)
- minimal/no ketones
- confusion, lethargy

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14
Q

features of HHS

A
  • comes on over days
  • lethargy
  • dehydrated, polyuria/dipsia
  • N+V
  • confused
  • blood hyperviscous - MI, stroke
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15
Q

diagnostic criteria HHS

A

no precise criteria but-

  • hypovolaemia
  • hypergkycaemia >30
  • raised serum osmolarity >320
  • no significant ketones <3
  • no significant acidosis >7.3
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16
Q

management of HHS

A

fluid replacement
- IV 0.9% sodium chloride
- monitor potass, add depending on level

insulin - should NOT be given unless blood glucose stops falling while giving IV fluids

VTE prophylaxis

17
Q

complications of HHS

A

vascular complications due to hyperviscosity of blood
- MI
- Stroke

(due to extreme dehydration)

18
Q

causes of hypoglycaemia

A
  • insulinoma (increased ratio of proinsulin to insulin)
  • self-admin of insulin/sulphonylureas
  • liver failure
  • addisons
  • alcohol
  • nesidioblastosis - beta cell hyperplasia
19
Q

why can alcohol cause a hypo

A

causes exaggerated insulin secretion

mechanism is thought to be due to the effect of alcohol on the pancreatic microcirculation → redistribution of pancreatic blood flow from the exocrine into the endocrine parts → increased insulin secretion

20
Q

hypoglycaemia presentation based on blood glucose levels

A

<3.3 autonomic sx (due to release of glucagon + adrenaline)
- sweating, shaking
- anxiety, nausea

<2.8 neuroglycopenic sx (due to low glucose supply to brain)
- weakness, vision changes
- confusion, dizziness

severe/rarely -
- convulsion
- coma

21
Q

hypoglycaemia investigations

A

if cause not clear, a combo of serum insulim + c-peptide levels can be measured

(insulin + C-peptide are release in equimolar amounts from pancreas –> C-peptide is a marker of endogenous insulin production)

22
Q

what might high insulin levels + high C-peptide levels tell you in hypoglycaemia

A

endogenous insulin production

causes
- insulinoma
- sulfonylurea use/abuse

23
Q

what might high insulin levels + low C-peptide levels tell you in hypoglycaemia

A

exogenous insulin administration

  • exogenous insulin overdose
  • factitious disorder
24
Q

what might low insulin levels + low C-peptide levels tell you in hypoglycaemia

A

non-insulin related cause

  • alcohol induced
  • critical illness - sepsis, adrenal insufficiency, growth hormone deficiency
  • fasting/starving
25
Q

management of hypoglycaemia in the community

A
  • oral glucose 10-20g - liquid, gel or tab

Px may be given “hypokit” contains syringe + vial of glucagon IM or SC

26
Q

management of hypoglycaemia in hospital setting

A

if patient alert -> quick acting carbohydrate/glucogel

unconscious/unable to swallow -> SC / IM glucagon

or IV 20% glucose