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Year 2 BRS > Type 1 Diabetes Mellitus > Flashcards

Type 1 Diabetes Mellitus Flashcards

1
Q

What is type 1 diabetes?

A

Autoimmune disease where beta cells in pancreas are attacked and destroyed by immune system.
Partial or complete insulin deficiency causing hyperglycemia.
Requires life long insulin treatment.

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2
Q

What is the best treatment for type 1 Diabetes

A

Individualize to clinical status and preferences

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3
Q

What is autoimmune diabetes presenting later in life called

A

Latent autoimmune diabetes in adults (LADA)

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4
Q

Can T2DM present in childhood ?

A

Yes

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5
Q

Can ketoacidosis be a feature of T2DM

A

Yes

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6
Q

What can monogenic diabetes present as?

A

Type 1 or type 2 e.g MODY , mitcohondiral diabetes

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7
Q

Can diabetes present following pancreatic damage or other endocrine disease.

A

Yes

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8
Q

What is a challenge for clinicians with diabetes in adults

A

differentiating between adult onset Type 1 and much larger cases of diabetes type 2

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9
Q

Stages of Development of Type 1 Diabetes

A

Genetic predisposition -> potential precipitating event -> overt immunological abnormalities, normal insulin release –> progressive loss of insulin -> overt diabetes c peptide still present -> no c-peptide present

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10
Q

Why is C-peptide used as a marker for insulin

A

Has a longer half-life as insulin goes though hepatic first pass metabolism.
If on insulin treatment don’t know if insulin is from pancreas or injection

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11
Q

stages of T1DM autoimmune

A

after immune activation beta cells attacked.
Development of single autoantibody.
Normal blood sugar –> abnormal blood sugar ( >/ 2 autoantibodies–> clinical diagnosis –> Long standing T1DM

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12
Q

Why is immune basis important

A

Increased prevalence of other autoimmune disease
Risk of autoimmunity in relatives
More complete destruction of B-cells
Auto antibodies can be useful clinically
Immune modulation offers the possibility of novel treatments
Not there yet

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13
Q

Overview of immunology

A

Primary step is the presentation of auto-antigen to autoreactive CD4+ T lymphocytes
CD4+ cells activate CD8+ T lymphocytes
CD8+ cells travel to islets and lyse beta-cells expressing auto-antigen
Exacerbated by release of pro-inflammatory cytokines
Underpinned also, by defects in regulatory T-cells that fail to supress autoimmunity

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14
Q

Why is it good that sometimes not all beta cells are destroyed

A

If heading towards hypo then pancreas can buffer insulin production.
Less likely to have vascular problems in future

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15
Q

Which HLA-Dr allele have the highest risk

A

DR3 and DR4

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16
Q

What factors may be implicated (no causality established)

A

Enteroviral infections
Cow’s milk protein exposure
Seasonal variation
Changes in microbiota

17
Q

What are pancreatic auto-antibodies

A

Detectable in the sera of people with Type 1 diabetes at diagnosis.
Not generally needed for diagnosis in most cases
Insulin antibodies (IAA)
Glutamic acid decarboxylase (GADA) – widespread neurotransmitter
Insulinoma-associated-2 autoantibodies (IA-2A)-Zinc-transporter 8 (ZnT8)

18
Q

Presentation of type 1 diabetes

A

SYMPTOMS
Excessive urination (polyuria)
Nocturia
Excessive thirst (polydipsia)
Blurring of vision
Recurrent infections eg thrush
Weight loss
Fatigue

SIGNS
dehydration
cachexia
hyperventilation
smell of ketones
glycosuria
ketonuria

19
Q

Effects of insulin deficiency

A

Proteinolysis
increased HGO
increased lipolysis –> glycerol and NEFA

20
Q

how are Ketone bodies made

A

Acetyl coA –> acetoacetate –> acetone + 3OH B – > ketone bodies

21
Q

What causes smelly breath

A

acetone

22
Q

treatment of type 1

A

People with type 1 diabetes, require insulin FOR LIFE

Aims:
Maintain glucose levels without excessive hypoglycaemia
Restore a close to physiological insulin profile
Prevent acute metabolic decompensation
Prevent microvascular and macrovascular complications

23
Q

Management of type 1 diabetes

A

Insulin Treatment
Dietary support / structured educations
Technology
Transplantation

Type 1 diabetes is a condition that is ‘self-managed’

24
Q

complication of hypergycaemia

A

Acute
Diabetic ketoacidosis
Chronic

Microvascular
Retinopathy
Neuropathy
Nephropathy

Macrovascular
Ischaemic heart disease
Cerebrovascular disease
Peripheral vascular disease

25
Q

short acting insulin

A

With meals (short / quick-acting insulin)

Human insulin – exact molecular replicate of human insulin (actrapid)
Insulin analogue (Lispro, Aspart, Glulisine)

26
Q

Background insulin

A

Background (long-acting / basal)

Bound to zinc or protamine (Neutral Protamine Hagedorn, NPH)
Insulin analogue (Glargine, Determir, Degludec)

Year 2 BRS (1 decks)

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