Type 1 Diabetes Mellitus Flashcards

1
Q

What is T1DM?
How does it differ from T2DM?
What is LADA?

A

Auto-immune condition that destroys pancreatic islet beta cells = reduced/no production of beta cells
T2 is insulin resistance leading to relative insulin deficiency
Latent Autoimmune Diabetes in Adults

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2
Q

What are the stages of T1DM development?

A

Genetic predisposition
Environment trigger leading to autoimmune abnormalities (and therefore production of antibodies)
Decreased insulin release
Decreased C-peptide

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3
Q

Why is C-peptide used over insulin levels as a marker for T1DM?

A

Insulin has a shorter half life and insulin medication will affect readings

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4
Q

What immune cells are involved in T1DM immune destruction?
What autoantibodies are produced?

A

CD4 t cells and CD8
Insulin Autoantibody

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5
Q

What are the 7 symptoms of T1DM?
What is the mechanism behind the blurry vision?

A

Nocturia, polyuria, polydipsia, blurred vision, recurrent infections in the urine, weight loss, fatigue
Blurred vision happens as a result of glucose being in the aqueous humour, causing water to be pulled in swelling the eye and distorting vision

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6
Q

Why do you get cachexia in T1DM?

A

The lower insulin promotes proteinolysis in order to make amino acids to use for energy
This causes the muscle wasting

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7
Q

What is the effect of T1DM of lipolysis?
What is the consequential effect of this?

A

Lipolysis is inhibited by insulin, so as insulin is low, lipolysis will increase
This causes non-esterified fatty acids to go through b-oxidation leading to more ketone bodies and therefore higher ketone levels into the blood
= ketoacidosis

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8
Q

What is the impact of low insulin levels on the liver?

A

More gluconeogenesis in order to produce more glucose

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9
Q

What are the acute and chronic complications of T1DM?

A

Acute- ketoacidosis, hyperglycaemia, hypoglycaemia (caused by treating T1DM)
Chronic-macrovascular and microvascular complications

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10
Q

How does diabetic retinopathy present?
What is the appearance a cause of?

A

Yellow exudate in retina of eyes due to the damage to the retina vessels

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11
Q

What is the difference between short acting and long acting insulin?

A

Short acting is given with meals- either human insulin or analogue
Long acting is given for background basal levels- insulin analogue

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12
Q

What is insulin pump therapy?
What is the biggest drawback for people when considering this line of treatment?

A

Continuous subcutaneous insulin infusion
Continuous delivery of short acting insulin (basal) via a pump into the subcutaneous space but can be programmed to give extra for bolus (meals)
People dont want to have the permanent pump

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13
Q

What dietary advice is given to patients with T1DM?

A

Dose adjustment of insulin per meal
Carbohydrate counting
Sub refined carbs for complex carbs- lower glycemic index

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14
Q

What is a closed loop?

A

An artificial pancreas is placed in the interstitial fluid of the subcutaneous fat, this allows for detection of change in glucose and calculates insulin dose required, and administers it without human assistance

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15
Q

What transplant options are available for T1DM?
How do they each work

A

Islet cell transplants- isolate donor islet cells and insert into hepatic portal vein
Must take immunosuppressants for rest of life
Pancreas & kidney transplant- use both for better chance of graft survival
Must take immunosuppressants for rest of life

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16
Q

Why is HbA1c used to monitor diabetes?
When can HbA1c not be used?

A

Reflects last 3 months of glycaemia
Glycated rather than glycosylated so it has a linear relationship

Affected by erythropoiesis (low iron or too much)
Altered genetic hb
Glycation from other causes such as alcoholism or CKD
Splenomegaly causing erythrocyte destruction

17
Q

What are the symptoms of DKA?

A

Blurred vision, nausea, vomiting, weight loss, recurring UTI

18
Q

How does T1DM cause hypoglycaemia?
How does it present?
What are its risk factors?

A

Tightly controlled insulin or adrenoreceptor become insensitive to hypoglycaemia
Présents: seizure, coma, death, driving- Contact DVLA
RF: alcoholism, exercise, missed meals

19
Q

How do you manage hypos in the following patients:
Alert and orientated
Drowsy but can swallow
Unconscious and can’t swallow
Deteriorating without IV access

A

Sweet/juice
Buccal glucose or glucose gel
Intravenous glucose 20% and saline
Intramuscular glucose