Diabetes mellitus type I Flashcards

1
Q

drug induced diabetes can be caused by what drugs?

A
glucocorticoids 
atypical antipsychotics (clozapine)
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2
Q

definition: T1DM

what are the different types?

A

destruction of pancreatic beta cells - absolute insulin deficiency

type 1a - autoimmune etiology
type 1b - no evidence of autoimmunity

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3
Q

what are the major susceptibility genes for T1DM? which chromosome?

A

HLA region on chromosome 6
HLA-DR3 and DR4 haplotypes

MHC II molecules on macrophages

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4
Q

genetic T1DM is highest in what relationship?

A

monozygotic twins - 50%

offspring with both parents - 30%

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5
Q

the immune response in T1DM is mediated by what process?

A

inappropriate ADAPTIVE immune response that targets and destroys the beta cells (“mistaken identity”)

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6
Q

what is the immune response in type 1a? type 1b?

A

type 1a - chronic, progressive T cell mediated immune destruction of pancreas with HLA association

type 1b - no evidence of autoimmunity with NO HLA association

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7
Q

what cell type mediates the beta cell destruction?

A

T cells

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8
Q

do beta cells undero necrosis or apoptosis in T1DM?

A

apoptosis

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9
Q

what is the antibodies see in T1DM?

A
  • glutamic acid decardoxylase (GAD65) - 80%
  • insulin
  • islet cell
  • tyrosine phosphatase
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10
Q

when does the disease process begin in T1DM?

A

months to years before clinical diagnosis

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11
Q

what are hypotheses for environmental factors in T1DM?

A
  • hygiene
  • perinatal
  • viruses
  • diet
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12
Q

what vitamin is thought to play a protective role in T1DM?

A

vitamin D

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13
Q

diagnosis of T1DM

A
  • formal oral glucose tolerance test
  • classical presentation with DKA
  • evidence of antibodies
  • C peptide
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14
Q

what glucose physiology is occurring during ketoacidosis?

A
  • glucose cannot be taken up by cells

- gluconeogenesis is not suppressed

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15
Q

what protein / fatty acid physiology is occurring during ketoacidosis?

A

catabolic pathways are activated leading to amino acids and free fatty acids, which further stimulates the process and leads to ketone production

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16
Q

what are the signs of DKA?

A
  • dehydration
  • acidosis
  • low BP
  • orthostasis
  • tachycardia
  • acetone
  • decreased body temperature
17
Q

what are the biochemical findings of DKA?

A
  • hyperglycemia
  • low bicarb
  • low serum pH
  • serum ketones
18
Q

DKA - treatment

A
  • aggressive volume resuscitation
  • correct the hyeprglycemia with insulin
  • replete the electrolytes
  • treat any underlying cause
19
Q

DKA - treatment GOALS

A
  • normoglycemia
  • normal A1C
  • normal growth in children
  • treatment of cardiac risk factors (BP, lipids, smoking)
20
Q

what is always involved in the treatment of T1DM?

A

insulin

21
Q

which diabetes drugs meet basal, baseline insulin needs?

A

glargine

detemir

22
Q

what are the bolus / rapid insulin drugs? what are the indications?

A
  • lispro
  • aspart
  • glulisine

used for meal or stress

23
Q

what is pramlitide? what does it do?

A

mimics amylin

  • slows GI transit
  • decreases glucagon
  • decreases appetite
  • net effect: better post meal control and often weight loss
24
Q

what tool allows monitoring glucose every few minutes, and is useful to define problems with glucose management?

A

CGMS (continuous glucose monitoring)

25
Q

what does acanthosis indicate in the context of insulin physiology?

A

insulin resistance

26
Q

what is the mainstay treatment for T1DM? what is an additional treatment for the insulin resistant T1DM?

A

insulin

pramlitide