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BRS YEAR 2 > Type 1 Diabetes > Flashcards

Type 1 Diabetes Flashcards

1
Q

What is type 1 diabetes

A

Autoimmune disease
Beta cells affected in pancreas causing partial/complete deficiency in insulin thus hyperglycemia

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2
Q

Difference in type 2

A

Acquired insulin resistance

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3
Q

What is MODY

A

mature onset diabetes of the young
Usually monogenic diabetes

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4
Q

What is LADA

A

latent autoimmune diabetes in adults

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5
Q

When does type 1 DM develop

A

Usually in youth

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6
Q

Cleavage product with insulin

A

Proinsulin cleaved into c peptide and insulin

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7
Q
  • steps of type I DM development?
A

genetic predisposition → environmental trigger → immune abnormalities but normal insulin → progressive loss of insulin release → overt diabetes with c-peptide → no c-peptide

  • stage I: normal blood sugar, more than one autoantibodystage II: abnormal blood sugarstage III: clinical diagnosisstage IV: long standing type 1 diabetes
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8
Q

Stages of type 1 dm

A

stage I: normal blood sugar, more than one autoantibody

stage II: abnormal blood sugar

stage III: clinical diagnosis

stage IV: long standing type 1 diabetes

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9
Q

Where are beta cells located

A

Pancreatic islets of langerhanss, cytological changes after immune infiltration

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10
Q
  • clinical relevance of immune basis of disease?
A

other autoimmune conditions more common in self + relatives

more complete destruction of beta cells

possible immune modulation treatment in the future

Risk of autoimmunity in relatives

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11
Q

Primary step in immune deficiency

A

autoantigen presented to autoreactive CD4+ T-lymphocytes

  • CD4+ → activate CD8+ → lyse beta cells expressing auto-antigen

Exacerbated by pro inflammatory cytokines

Underpinned also by defects in T regulatory cells

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12
Q

What happens after the autoantigen is presented to auto reactive CD4+ T lymphocytes

A

CD4+ → activate CD8+ → lyse beta cells expressing auto-antigen

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13
Q

what aids this process?

A

Pro inflammatory cytokines expression and defects in T reg cells
Some beta cells can be ,left thus some insufficient insulin made

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14
Q

What is the HLA-DR gene responsible for

A

MHC II

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15
Q

Significance of different alleles

A

associated with different risk levels for diabetes, some dependent also on ethnicity

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16
Q

possible environmental factors?

A

enteroviral infection, cow’s milk protein exposure, seasonal variation, microbiota changes

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17
Q

what is the significance of pancreatic autoantibodies?

A

detectable in sera of those with type I at diagnosis. recommended as diagnostic tool

18
Q

Different types of autoantibodies include

A

insulin antibodies IAA
GAD-65 glutamic acid decarboxylase
IA-2 insulinoma associated 2 antibodies ZnT8 zinc transporter 8

19
Q

what is the diagnosis of diabetes based on?

A

presence of clinical features + ketones

20
Q

various effects of insulin deficiency?

A

protein lysis in muscles → amino acid metabolism

increased hepatic glucose output

lipolysis in adipocytes → glycerol + non-esterified fatty acids

21
Q
  • how and where are ketone bodies usually formed?
A

from fatty acyl-CoAs in liver e.g. → acetyl-CoA, acetoacetyl-CoA

22
Q

hormonal regulation how?

A

upregulated by glucagon and suppressed by insulin usually

23
Q

Principal aims of diabetes treatments

A

maintain glucose levels, avoid excessive hypoglycaemia

restore physiological insulin profile or close

avoid micro and macrovascular complications

prevent acute metabolic decompensation

24
Q

acute complications of diabetes?

A

diabetic ketoacidosis

hypoglycaemia from treatment

25
Q

chronic complications?

A

microvascular → retinopathy, nephropathy, neuropathy

macrovascular → ischaemic heart disease, cerebrovascular disease, peripheral vascular disease

26
Q

physiological insulin profile characteristics?

A

prandial peak (i.e. after meals) with two phases (peak and mini peak)

baseline insulin steady but not zero. This prevents ketoacidosis

27
Q

different types of insulin?

A

human insulin (actrapid), insulin analogues e.g. Lispro, Aspart, Glulisine → short acting, take with meals

zinc or protamine bound e.g. NPH, insulin analogues e.g. Glargine, Determir, Degludec → long acting, background/basal

  • short-acting = 3x a day after mealslong acting - 1x a day
28
Q

When to take different types of insulin

A

short-acting = 3x a day after meals

long acting - 1x a day
Or twice daily intermediate acting insulin

29
Q

What do insulin pumps do

A

continuous delivery of short acting insulin into subcutaneous space

30
Q

principles of dietary education in diabetes?

A

carb counting, adjusting dosage based on food carbohydrate content, try sub refined carb foods with complex carb foods

  • insulin pump that can detect glucose intake → calculate and adjust insulin dose
31
Q

what are closed loop systems?

A

insulin pump that can detect glucose intake → calculate and adjust insulin dose

32
Q
  • how does transplantation work as a treatment option?
A

islet cell transplants → islets isolated from deceased donor → transplant into hepatic portal vein

simultaneous pancreas and kidney transplants

However require lifelong immunosuppresion

33
Q

How are glucose levels monitored

A

capillary blood glucose

continuous glucose monitoring via pump

HbA1c

34
Q

What is HbA1C

A

glycated haemoglobin → reflects last 3 months of glycaemia

35
Q

what factors can throw off HbA1c accuracy?

A

altered erythropoiesis e.g. increased in iron/B12 deficiency. Decrease in high epo,iron,b12,reticulocytosis

haemoglobinopathies/altered haemoglobin may increase/decrease

variable glycation e.g. increased in excess alcohol,chronic renal failure and decreased Intra erythrocyte pH variable in genetic factors, and low in aspirin, vit C/E,certain haemoglobinopathies

erythrocyte destruction increased HbA1c in splenectomy and increased erythrocyte life span, decreased in haemoglobinopathies,splenimegaly,drugs such as antiretroviral ribavirin and dapsone

36
Q

how is diabetic ketoacidosis diagnosed?

A

blood pH < 7.3, ketones (urinary or capillary) increased, HCO3- < 15 mmol/L, glucose > 11 mmol/L

37
Q

numerical definition of hypoglycaemia?

A

glucose less than 3.6 mmol/L

38
Q

what defines severe hypoglycaemia?

A

situation requires 3rd party assistance

39
Q

When can severe hypoglycemia become a problem

A

excessive frequency (can get worse), impaired awareness, nocturnal/recurrent severe hypoglycaemia

Leads to seizures/coma/death
Impacts cognition,driving,day to day function and emotional wellbeing

40
Q

Who is at risk of hypoglycemia

A

everyone with type I DM, especially if:

meals missed, exercise too much, alcohol, inappropriate insulin regime/dose adjustment

41
Q
  • how is hypoglycaemia acutely managed?
A
  • if concerned about swallow?IV access → 20% glucose
    If unable to give via iv then subcutaneous injection of glucagon
  • if swallow intact?oral carbs → buccal glucoserapid acting e.g. hypostop, glucogellonger acting → complex carbs

If aware and swallow intact
Rapid acting give sweets or juice
Long acting give sandwiches

BRS YEAR 2 (43 decks)

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