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BRS Phase 1b > Type 1 diabetes mellitus > Flashcards

Type 1 diabetes mellitus Flashcards

1
Q

What is type 1 diabetes?

A

An autoimmune condition in which insulin-producing beta-cells in the pancreas are attacked and destroyed by the immune system
The result is a partial or complete deficiency of insulin production, which results in hyperglycaemia
The resultant hyperglycaemia requires life-long insulin treatment

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2
Q

Why is the dichotomy of diabetes untrue?

A

There is significant overlap in the ways of presentation e.g Monogenic diabetes can present phenotypically as Type 1 or Type 2 diabetes (eg. MODY, mitochondrial diabetes)

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3
Q

When does type 1 diabetes present?

A

Traditionally thought to be childhood/ early adu;thoos but it can present at any age.

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4
Q

How does Type 1 diabetes develop?

A

Genetic predisposition
Immune Activation - Potential precipitating event ( e.g viral infection)
Immune Response - Development of single autoantibody
beta-cell mass degradation
progressive loss of insulin release
Overt diabetes; C-peptide present
No C-Peptide present

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5
Q

Why is the 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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6
Q

Describe the immunology in Type 1 diabetes?

A

Defect in both innate and active immune system.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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7
Q

Can people with type 1 Diabetes produce insulin?

A

Some have been found to be able to produce a small amount, but not enough to substitute the need for insulin therapy.

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8
Q

What mediates genetic susceptibility for type 1 diabetes?

A

HLA-DR Allele

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9
Q

What are possible environmental factors for Type 1 diabetes precipitation?

A

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

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10
Q

What Pancreatic autoantibodies can you measure to confirm type 1 diabetes?

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)

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11
Q

What are the symptoms of type 1 diabetes?

A 
polyuria
nocturia
polydipsia
Blurring of vision
Recurrent infections
Weight loss
Fatigue
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12
Q

What are the signs of type 1 diabetes?

A 
dehydration
cachexia
hyperventilation
smell of ketones
glycosuria
ketonuria
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13
Q

What affects the diagnosis of type 1 diabetes?

A

Diagnosis is based on clinical features and presence of ketones.

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14
Q

What happens when you don’t have enough insulin?

A

Breakdown of muscle protein
Increase glucose output from the liver
Break down fat cells (lipolysis)

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15
Q

What ketone bodies can lead to diabetic ketoacidosis?

A

Acetyl CoA
Acetoacetate
Acetone + 3OH-B

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16
Q

What are the main aims of treatment in type 1 diabetes

A

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

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17
Q

Why do you lose weight in type 1 diabetes?

A

Osmotic diuresis
become dehydrated
anything you eat cant be used due to lack of insulin

18
Q

Is type 1 diabetes monogenic or polygenic?

A

Polygenic - susceptibility spread amongst many genes

19
Q

Why do you get blurred vision in type 1 diabetes?

A

High glucose in the eyeball, water moves in to dilute increased solute concentration.

20
Q

What are the acute complications of type 1 diabetes?

A

Diabetes ketoacidosis
Uncontrolled Hyperglycaemia
Hypoglycaemia

21
Q

What are the chronic microvascular complications of type 1 diabetes?

A

Retinopathy
Neuropathy
Nephropathy

22
Q

What are the chronic macrovascular complications of type 1 diabetes?

A

Ischaemic heart disease
Cerebrovascular disease
Peripheral vascular disease

23
Q

What are the 4 tenets of type 1 diabetes treatment?

A

Insulin Treatment
Dietary support / structured educations
Technology
Transplantation

24
Q

What are the 3 features of insulins physiological profile?

A

Basal insulin has a flat profile
Insulin is never completely supressed
Prandial peak has two phases

25
Q

What are the short acting types of insulin?

A 
Human insulin – exact molecular replicate of human insulin (actrapid)
Insulin analogue (Lispro, Aspart, Glulisine)
26
Q

What are the long-acting types of insulin?

A 
Bound to zinc or protamine (Neutral Protamine Hagedorn, NPH)
Insulin analogue (Glargine, Determir, Degludec)
27
Q

Describe Insulin pump therapy?

A

Continuous delivery of short-acting insulin analogue e.g. novorapid via pump

Delivery of insulin into subcutaneous space

Programme the device to deliver fixed units / hour throughout the day (basal)

Actively bolus for meals

28
Q

What are the dietary principles for patients with type 1 diabetes?

A

Where possible, substitute refined carbohydrate containing foods (sugary / high glycemic index) with complex carbohydrates (starchy / low glycemic index)

29
Q

What is the artificial pancreas?

A

Real time glucose sensor, with an algorithm to use glucose value to calculate insulin requirement.

30
Q

What are the two types of transplantation?

A

Islet cell transplants

Isolate human islets from pancreas of deceased donor
Transplant into hepatic portal vein
Requires life-long immunosuppression

Simultaneous pancreas and kidney transplantBetter

survival of pancreas graft when transplanted with kidneys
Requires life-long immunosuppression

31
Q

How do we monitor glucose levels?

A

HbA1c

32
Q

Why do we measure Hb1Ac?

A

Reflect last 3 months (red blood cell lifespan) of glycaemia
Biased to the 30 days preceding measurement
Glycated NOT glycosylated (enzymatic)
Therefore linear relationship
Irreversible reaction
Glycated haemoglobin

33
Q

What guides insulin doses?

A

Using self-monitoring of blood glucose results at home and HbA1c results every 3-4 months

Based on results, increase or decrease insulin doses

34
Q

What is the diagnosis for diabetic ketoacidosis?

A

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

35
Q

What is the threshold hold for hypoglycaemia?

A

<3.6 mmol/L

36
Q

When does hypoglycaemia become a problem?

A

Excessive frequency
Impaired awareness (unable to detect low blood glucose)
Nocturnal hypoglycaemia
Recurrent severe hypoglycaemia

37
Q

What are the risks of hypoglycaemia?

A 
Seizure / coma/ death (dead in bed)
Impacts on emotional well-being
Impacts on driving
Impacts on day to day function
Impacts on cognition
38
Q

What are risk factors for hypoglycaemia?

A 
Exercise
Missed meals
Inappropriate insulin regime
Alcohol intake
Lower HbA1c
Lack of training around dose-adjustment for meals
39
Q

What is the acute management for hypoglycaemia?

A

Alert - Oral Carbs
Drowsy - Buccal glucose
Unconscious - IV glucose

40
Q

What is the treatment for Diabetic ketoacidosis?

A

Antiemetic
IV fluids for dehydration through a drip
Insulin to supress ketogenesis

BRS Phase 1b (80 decks)

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