Diabetes Mellitus Flashcards

1
Q

Type 1 DM

A

beta cell destruction
absolute insulin deficiency
T cell mediated pancreatic islet B cell destruction
patients become symptomatic once 90% pancreatic B cells destroyed

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2
Q

Symptoms DM T1

A
polyuria 
polydipsia 
blurred vision 
weight loss 
in association with - glycosuria and ketonuria
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3
Q

Diagnosis DM T1

A

fasting glucose > 7 mmol/l OR
2 hour post prandial glucose > 11.1 mmol/l
confirm need measure specific antibodies
= islet antigen 2 antibodies and glutamic acid decarboxylase GAD antibodies

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4
Q

Diabetic ketoacidosis

A

CATABOLIC STATE
increased levels of counter regulatory hormones: catecholamines, cortisol, glucagon, growth hormone
absolute insulin deficiency = previously undx diabetic OR insulin injection omitted
relative insulin deficiency = stress situations, counter regulatory hormones increase response stress

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5
Q

Clinical features of DKA

A
Acidotic breathing 
Nausea 
Vomiting 
Abdominal Pain 
LOC 
Coma
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6
Q

Biochemical criteria for DKA

A

Diabetic with Hyperglycaemia >11mmol/l
Ketonuria
Acidotic with - Venous pH < 7.3 and Serum bicarb < 15 mmol/l

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7
Q

Management of DKA

A

IV fluids 0.9% saline (IV of 10-20ml/kg over hour) - degree fluid deficit 7.5-10% of body weight
use 0.45 or 0.9% saline depending corrected Na
insulin - 0.1unit/kg/hr
glucose to 11mmol/l = dextrose added IV fluids

movement of K+ form EC into IC space
K+ should added IV fluids - if renal fx is adequate

in HCU with frequent monitoring of vital signs and hourly glucose and electrolytes

First maintenance Insulin dose should be given 2 hours before discontinuing IV insulin infusion

NB - only give saline fluid boluses if pt is shocked (tachycardia and decreased BP)

K potassium
I insulin
N NGT in comatose
G glucose administration once serum level drops
F fluid infusion - corrected Na
U urea and creatinine mentoring every 4 hours
DO NOT GIVE BICARB

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8
Q

Cerebral oedema

A

serious but rare complication of DKA

  • headache
  • altered mental status
  • vomiting
  • hypertension
  • inappropriate bradycardia
    management: IV mannitol 1-2g/kg
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9
Q

Maintenance insulin dose

A

0.5 x total weight in kg = total daily insulin requirement (in units of insulin)

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10
Q

Dawn phenomenon

A

DOWN INSULIN
normal glucose until 3am then starts rise
hyperglycaemia on awakening due release counter regulatory hormones in pre-dawn hours - GH
reduced tissue sens to insulin 5-8am
endogenous insulin secretion decreased

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11
Q

Symogyi effect

A

SO MOch insulin
nocturnal hypoglycaemia leads surge of counter regulatory hormones (glucagon and epinephrine) that produce early morning hyperglycaemia - rebound hyperglycaemia
due excessive amounts exogenous insulin

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12
Q

Causes of Hypoglycaemia

A
stacking insulin 
excessive basal insulin 
delayed eating after takin mealtime insulin 
taking wrong insulin by mistake 
increased insulin sensitivity 
eating less carb than anticipated 
increased activity or exercise 
delayed gastric emptying 
fear of complications
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13
Q

Hypoglycaemia management

A

BG < 3.0 mmol/l - below 2.5 is pathological and requires investigation
child alert and fully conscious
- 10-20g given by mouth either in liquid (200ml milk) or as granulated sugar (2tsp)
- recheck glucose in 10-15 min and repeat if necessary
- further food prevent recurrence

unconscious or fitting
- Glucagon IMI or s/c <12 years 0.5mg; > 12 years 1mg
- if not effective in 10 minutes, IV glucose should be given
2-5ml/kg of 10% glucose iV infusion

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14
Q

Long term complications of DM

A
coronary artery disease 
diabetic myonecrosis 
peripheral vascular disease 
ischaemic stroke 
retinopathy 
neuropathy 
nephropathy 
cardiomyopathy 
encephalopathy
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15
Q

DM T2 - Features of insulin resistance

A
Hyperlipidaemia 
Hypertension 
Acanthosis Nigricans 
Non-alcoholic fatty liver disease 
Polycystic ovarian hyperandrogegism 
NB - can also present in DKA
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16
Q

Treatment options for DM T2

A

insulin requirements decrease as diabetes is controlled
lifestyle and dietary adjustments
oral medications - Metformin
insulin

17
Q

MODY - maturity onset diabetes of the young

A

hereditary forms of DM caused mutations in AD gene disrupting insulin production
Presentation
- mild - moderate hypoglycaemia - < 30
- 1st degree relative similar degree diabetes
- absence antibodies or other AI in pt + fam
- persistence of low insulin requirements
- absence of obesity/ other problems associated T2, metabolic syndrome
- Cystic kidney disease in pt or close relatives
- non transient neonatal diabetes or apparent T1 DM with onset < 6m age

advantages of dx

  • insulin may not be necessary
  • prompt screening relatives
18
Q

Neonatal DM

A

monogenic form
first 6 months of life
rare disease
do not produce enough insulin - increase BG
NDM can mistaken for much more common T1 DM (which occurs >1st 6m of life)
50% condition lifelong
rest - transient and disappears during infancy - BUT can reappear later in life