Type 1, Clinical Features, Pathophysiology, Treatment Flashcards

1
Q

what used to be the biggest killer of diabetic and what is now

A

used to be coma

now thanks to insulin is cardiac/renal complications

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2
Q

what is the definition of type 1 diabetes

A

A state of absolute insulin deficiency probably caused by an environmental trigger in a genetically susceptible individual mediated by an auto immune response attacking the pancreatic B cells

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3
Q

how do you diagnose diabetes

A

fasting glucose >7
random >11.1
and symptoms OR repeat

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4
Q

how to diagnose type 1 or type 2 diabetes

A

Type 1 - history and presentation eg. DKA alone

If in doubt, GAD/IA2 antibodies (and C peptide) may help

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5
Q

what happens to a normal pancreatic islet in type 1 diabetes

A

it gets attacked by lymphocytes

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6
Q

what happens to a normal pancreatic islet in type 2 diabetes

A

as the B cells start to go into decline amyloid deposits start to form in the pancreas

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7
Q

what is the association between HLA and risk of type 1 diabetes

A

HLA genes represent 50% of the familial risk of T1DM

95% of those with T1DM under 30 have one or both of the HLA genotypes

Only 10% of people with susceptible HLA develop DM

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8
Q

what are some environmental triggers for the onset of T1DM

A

viral infection
maternal factors
weight gain

also a seasonal variation in date of diagnosis (more in winter)

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9
Q

What are the islet cell auto-antibodies

A

IA-2
IAA
GAD65
ZnT8

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10
Q

what are the autoantibodies seen in type 1 diabetes

A

GAD65Ab (targets glutamic acid decarboxylase)
IA-2AB (targets islet antigen 2)
IAA (targets insulin)
ZnT8Ab (targets ZnT8 transporter)

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11
Q

what are some foetal risk factors for type 1 diabetes

A

infection
age
ABO mismatch
Birth order

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12
Q

what are the histopathological disease markers of T1DM

A
raised glucose 
ketones 
decreased insulin 
decreased B cell mass 
decreased c peptide
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13
Q

what is the classical triad of presenting features of T1DM

A

Polyuria
-also enuresis in children
Polydipsia (thirst)
Weight loss

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14
Q

What are the clinical features other than the classic triad that present in T1DM

A
fatigue and somnolence 
blurred vision 
Candidal infection 
pruritus vulvae 
balanitis 
in established ketone-acidosiss
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15
Q

things to ask/think about in a newly presenting patient

A
has diabetes been confirm 
what type (antibody testing) 
is hospitalisation required 
-DKA 
-significant ketonaemia 
-vomiting 
are they at school/college/uni 
if not what's their employment 
do they drive
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16
Q

Management of a newly diagnosed T1DM patient

A
blood glucose and ketone monitoring 
Insulin usually basal (once daily) and bolus (with meals)
carbohydrate estimation 
regular dietitian contact 
appropriate medical clinic review
17
Q

what is the ideal HbA1c range for T1DM

A

48-58 mmol/mol

18
Q

what is checked in the annual review assessment

A
weight 
bp 
bloods - HbA1c, Renal function, Lipids 
retinal screening 
foot risk assessment
19
Q

what % of patients with cystic fibrosis will go on to develop T1DM

A

20%

20
Q

what intensified insulin therapy should be given for type 1 adults

A

human or rapid acting insulin analogues

21
Q

when are basal insulin analogues recommended

A

in patients with type 1 who are experiencing severe or nocturnal hypos

22
Q

what insulin regimen is given to children

A

insulin analogs (rapid or basal)
regular human insulin
NPH preparations (intermediate)
combination of all 3

23
Q

what are the overlap diabetes between types 1 and 2

A

MODY
LADA
Mitochondrial gene mutations
Amylin gene mutations

24
Q

how is insulin secreted normally

A

Biphasic secretion in response to a meal

  • rapid phase of preformed insulin lasts 5-10 mins
  • slow phase over 1-2 hours
25
Q

where is insulin secreted into naturally

A

portal vein

26
Q

what are children diagnosed under the age of 6 months most likely to have

A

monogenic diabetes

27
Q

what is LADA

A

later onset diabetes of adulthood

elevated pancreatic autoantibodies in a patient with recently diagnosed diabetes who does not require insulin

(also known as slow progressive type 1 or type 1.5)

28
Q

features of LADA

A
occurs in young adults 25-40 
males 
non-obese
auto-antibody positive 
associated autoimmune conditions 
non-insulin requiring at diagnosis 
sub-optimal control on oral agents
29
Q

what is DIDMOAD or Wolfram syndrome

A
diabetes insipidus
diabetes mellitus 
optic atrophy 
deafness 
neurological anomalies
30
Q

wha is barred bide syndrome

A
often seen in very obese 
polydactyly (extra fingers/toes) 
hypogonadal 
visual impairment 
mental retardation
diabetes 
consanguineous parents (inbred)
31
Q

common associated autoimmune conditions with T1DM

A
thyroid disease 
coeliac disease 
pernicious anaemia 
Addisons disease 
IgA deficiency
32
Q

what diseases are involved in type 1 polyglandular endocrinopathy

A
Addisons disease 
vitiligo 
primary hyponadism 
primary hypothyroidism 
coeliac disease