type 1 diabetes mellitus Flashcards

1
Q

describe the difference between type 1 and type 2

A
  • 1: complete lack of insulin
  • 2: relative lack of insulin and insensitivity
  • diabetic ketoacidosis is only a feature of T1DM
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2
Q

why is there no ketacidosis in T2DM?

A

insulin production is sufficient to supress ketone production

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3
Q

in pathogenesis, what is the honeymoon phase?

A

last instance where the beta cells produce a non-hyperglycaemic response with just enough insulin

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4
Q

how do T cells cause destruction?

A
  • effector T cells are destructive
  • T-reg cells are supposed to keep effector T-cells in check
  • eventually T-effector cells overcome T-reg cells and destruction occurs
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5
Q

as patients with T1 have an immune background, what does this mean?

A
  • inc. prevalence of other AI disorders
  • risk of AI in relatives
  • more destruction of beta cells
  • can measure auto-antibodies to confirm T1DM and can treat autoimmunity
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6
Q

which gene mutations pose a significant risk to getting T1DM?

A

HLA-DR3 and HLA-DR4 deletions

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7
Q

what are the markers for T1DM?

A
  • islet cell antibodies
  • insulin antibodies
  • glutamic acid decarboxylase
  • insulinoma-associated-2 autoantibodies receptor like family
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8
Q

what are the symptoms of T1DM?

A
  • polyuria, nocturia
  • polydipsia
  • blurring of vision
  • thrush
  • weight loss
  • fatigue
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9
Q

what are the signs of T1DM?

A
  • dehydration
  • cachexia (muscle wasting, weakness)
  • hyperventilation
  • ketone smell
  • glycosuria, ketonuria
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10
Q

what is the action of insulin?

A
  • released post-prandial
  • acts to absorb glucose into cells
  • creates stores of energy
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11
Q

what is the effect of insulin on adipocytes?

A
  • insulin inhibits glycerol leaving adipocytes

- deficiency of insulin enables glycerol to leave cells and TGs break down

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12
Q

what does the lack of insulin do?

A
  • allows FFAs to escape adipocytes and so are turned into ketone bodies inside liver
  • ketone bodies are then taken up by muscle and brain but also cause ketonuria
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13
Q

what are the aims of treatment?

A
  • reduce early mortality
  • avoid acute metabolic decompensation
  • prevent long term complications
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14
Q

what diet changes?

A
  • reduce calories as fat and refined carbohydrate
  • inc. calories as complex carbs and inc. soluble fibre
  • distribute food evenly throughout day with regular meals and snacks
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15
Q

when should insulin treatment be given?

A
  • meals: short acting insulin

- background: long acting insulin and can be non c-bound to zinc/protamine

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16
Q

what are insulin pumps?

A
  • give continuous delivery
  • have pre-programmed basal andbolus rates
  • do not measure glucose feedback
17
Q

what are islet cell transplants?

A
  • donor can donate some pancreas islet cells
  • inserted into diabetic’s liver portal vessels to release insulin
  • pt must be on continuous immunosuppression
  • treatment is only reserved for those with erratic control of diabetes
18
Q

what is capillary monitoring?

A

either via a continuous monitor attached to belly

or through finger pricks

19
Q

what is HbA1C red cell monitoring?

A
  • glucose binds to RBCs irreversibly so can give a long-term view of glucose control
20
Q

what are 3 acute complications?

A
  • metabolic acidosis (keotacidosis)

- hyperglycaemia (reduced tissue glucose utilisation and inc. HGO)

21
Q

what is metabolic acidosis due to?

A
  • circulating acetoacetate/hydroxybutyrate and osmotic dehydration and poor tissue perfusion
22
Q

what is hypoglycaemia?

A

<3.6mmol/L glucose
mental processes impaired at <3mmol/L
coma <2mmol/L

23
Q

who do hypos affect?

A
  • low quality hypoglycemic control patients

- more common in patients with low HbA1C

24
Q

why do hypos strike?

A
  • new exercise
  • missed meals
  • inadequate snacks and alcohol
  • bad insulin regime
25
Q

what are the symptoms of hyperglycaemia?

A

inc. autonomic activation:
- palpitations
- tremor
- sweating
- pallor/cold extremities
- anxiety
impaired CNS functions:
- drowsiness
- confusion
- altered behaviour
- coma

26
Q

what is the hypoglycaemia treatment?

A
  • oral: glucose, complex carbs

- parenteral (give if consciousness impaired): IV dextrose, 1mg glucagon IM