Diabetic Ketoacidosis Flashcards

1
Q

In what population does DKA arise?

A

T1DM

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2
Q

In DKA there is insulin -___ with ___ counter regulatory hormone

A

In DKA there is insulin -Deficiecny with increased counter regulatory hormone

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3
Q

How does pseudohyponatraemia arise in DKA?

A

Hyperglycaemia induces osmotic diuresis

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4
Q

How does glycosuria and ketonuria arise?

A

glucose and ketones exceed the renal threshold

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5
Q

Compare the changes between total body and serum K+

A

Total body is depleted

Serum K+ is normal/elevated

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6
Q

Why does K+ shift from ICF to ECF

A

Increased plasma osmolaltiy

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7
Q

What happens to total body PO4?

A

Depleted

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8
Q

What are the clinical features of DKA that start with P

A

Polyuria, Polyphagia, polydipsia

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9
Q

What can cause decreased level of consciousness in DKA?

A

Hyperglycaemia or dehydration

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10
Q

What are the GI symptoms of DKA?

A

Abdominal pain

Fruity breath

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11
Q

How does respiration change in DKA

A
Initially = Hyperventilation
Late = Kussmaul's breathing
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12
Q

What do ABGs show for DKA

A

HAGMA with respiratory alkalosis

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13
Q

Key features of DKA on EUC

A

Increased BGL
Increased ketones
Decreased PO4

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14
Q

Should you use Arterial gas, BGL or serum ketones for monitoring ketoacidosis?

A

Arterial gases

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15
Q

What saline for rehydration?

A

0.9% NaCl

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16
Q

When do you implement Dextrose?

A

When the BGL has reduced to <14mmol/L

17
Q

What is critical to resolve acidosis?

A

Insulin therapy

18
Q

How should insulin be administered?

A

IV 3.3mmol/L Insulin

19
Q

When do you administer HCO3-

A

If pH <7.0 or pH <7.1 + Arrhythmia or coma

20
Q

What is the prognosis of DKA?

A

2-5% mortality

21
Q

What is most likely to kill someone with DKA? (5)

A

Sepsis, hypokalaemia, respiratory complication, TE complication or cerebral oedema

22
Q

What are the 4 principles of managing DKA?

A

Fluids
Insulin
Potassium
Treat precipitant

23
Q

Name the 5 Is precipitating DKA

A
Infection
Ischaemia
Iatrogenic (glucocorticoids)
Intoxication
Insulin missed
Initial presentation
24
Q

In who does HHS typically arise?

A

T2DM

25
Q

What is HHS often precipitated by?

A
Vascular: Stroke/MI
Infection: Sepsis
Trauma: Trauma, burns
Metabolic: Renal
Iatrogenic: glucocorticoids, immunosuppressants, diureeics
Degenerative: CHF
26
Q

Pathophys behind HHS?

A

Increased SNS with decreased Insulin prevents glucose into muscles –> leads to increased omsolality and hyperglycaemia –> dehydration

27
Q

Is the dehydration more severe in DKA or HHS?

A

HHS - due to more gradual onset

28
Q

How does coma arise in HHS?

A

High osmolality causes a shift in fluid from the Intra-celluar neutrons to the ECF

29
Q

How does HHS present?

A

insipid onset of weakness, polyuria, polydipsia

30
Q

What are key history components for DKA?

A

Preicpiating events

Reduced fluid intake

31
Q

Why does Ketosis not arise in HHS?

A

Due to partial insulin presence

32
Q

Is kussmaul’s breathing present in HHS?

A

No - As no acidosis

33
Q

What dos the serum osmolality for HHS illustrate?

A

BGL +++ (>50mmol/L)

Dehydration and increased osmolality

34
Q

Whereas glucose is ____ in the urine in HHS, ketones are ___ in the urin

A

Whereas glucose is present in the urine in HHS, ketones are absent in the urine

35
Q

What are the principles of treatment of HHS

A

Same as DKA- Fluid, K+ replacement, treat precipitating event

36
Q

Should insulin be applied in HHS?

A

No

37
Q

What is the mortality for HHS?

A

approaches 50%

38
Q

Which population is HHS most common in?

A

Elderly