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Endocrinology > Type 1 Diabetes Mellitus > Flashcards

Type 1 Diabetes Mellitus Flashcards

1
Q

What are the 3 different types of diabetes you can have?

A
  1. Type I
  2. Type II
  3. Monogenic diabetes (e.g. MODY “maturity onset diabetes of the young”, mitochondrial diabetes)
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2
Q

What is type I diabetes mellitus?

A
  • An autoimmune condition in which insulin-producing beta-cells in the pancreas are attacked and destroyed by the immune system
    -Can have predisposed genetic risks, and contributed by environmental triggers
  • The result is a partial or complete deficiency of insulin production, which results in hyperglycaemia
  • The resultant hyperglycaemia requires life-long insulin treatment (still responds to insulin)
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3
Q

What are the stages of development of type I diabetes?

A

a. Genetic predisposition
b. Potential enviornmental precipitating event/ trigger
c. Immunological response
- Destruction of the beta cells (progresses with time):
- Development of at least 1 autoantibody
Stage 1. Development of 2 or more autoantibodies but blood sugar still normal- glucose normal, no symptoms
Stage 2. Overt diabetes, abnormal blood sugar, but still no symptoms (C peptide still detectable)
Stage 3. Clinical diagnosis: significant beta cell loss + Symptoms of T1D
(no C-peptide detectable)

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4
Q

What causes the destruction of the beta cells?

A
  • Usually in the body if there are auto-antigens: (attempting to suppress autoimmunity) T reg cells inhibit T cell proliferation and cytokine production

However, in Type I diabetes there are defects in regulatory T-cells that fail to suppress autoimmunity, so instead:

  1. presentation of auto-antigen to autoreactive CD4+ T lymphocytes
  2. CD4+ cells activate CD8+ T lymphocytes
  3. CD8+ cells travel to islets and lyse beta-cells expressing auto-antigen
  4. Exacerbated by release of pro-inflammatory cytokines
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5
Q

Some people with type I diabetes still have some undestroyed beta cells, why do they still require insulin therapy?

A

-Continue to produce small amounts of insulin but it is not enough to negate the need for insulin therapy

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6
Q

What increases the genetic susceptibility of having type I diabetes mellitus?

A
  • HLA-DR allele increases the risk (how significant the risk is, depends on where the allele is found/ the locus)
  • NOTE: this just increases susceptibility- still need a trigger
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7
Q

What are potential environmental triggers of type I diabetes mellitus?

A

(Multiple factors implicated, but causality has not been established)

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

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8
Q

What are the symptoms of Type I diabetes mellitus?

A

Excessive urination (polyuria)
Nocturian (getting up in the night to pee)
Excessive thirst (polydipsia)
Blurring of vision
Recurrent infections eg thrush
Weight loss
Fatigue

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9
Q

What are some signs of Type I diabetes mellitus?

A

dehydration
cachexia
hyperventilation
smell of ketones
glycosuria
ketonuria

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10
Q

What effect does insulin deficiency have on the organs of the body?

A
  • Increased proteinolysis (breakdown of muscle) to gain amino acids- used for fuel
  • Increased hepatic glucose output (HGO)- Counterintuitive- blood glucose is high but it is not being used, so the body gets confused and increases production
  • Increased lipolysis (breakdown of fat/ adipose tissue) to gain non-esterified fatty acids/ NEFA’s for fuel
    -Formation of ketone bodies
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11
Q

Why are ketone bodies formed as a result of insulin definicency?

A

-Breakdown of fat:
- Fatty Acyl-Co A into the ketone bodies
- Used as fuel during starvation
- Acidic: accumulation= acidosis

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12
Q

What are the aims with Type 1 Diabetes Mellitus treatment?

A

People with type 1 diabetes, require insulin FOR LIFE
Aims:
Maintain glucose levels without excessive hypoglycemia
Restore a close to physiological insulin profile
Prevent acute metabolic decompensation (e.g. ketoacidosis or severe hypoglycemia)
Prevent microvascular and macrovascular complications

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13
Q

What are the complications of hyperglycaemia?

A
  1. Acute:
    Diabetic ketoacidosis
  2. Chronic:
    Microvascular (Retinopathy, Neuropathy, Nephropathy- damage to kidney)
    Macrovascular (Ischaemic heart disease, Cerebrovascular disease, Peripheral vascular disease)
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14
Q

What is the management of Type I diabetes mellitus?

A

Insulin Treatment
Dietary support / structured educations
Technology
Transplantation
(Type 1 diabetes is a condition that is ‘self-managed’)

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15
Q

What are 3 facts about plasma insulin levels?

A
  • Insulin is never completely suppressed (levels on a profile never at 0)
  • Insulin has a 1st phase release (estimate for how much you’ll eat) and 2nd phase release (more accurate to meet the amount of food)= 2 peaks
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16
Q

What are the 2 types of insulin?

A
  1. Short/ quick acting insulin
    (Human insulin – exact molecular replicate of human insulin (actrapid)
    Insulin analogue (Lispro, Aspart, Glulisine))
    GIVEN THREE TIMES A DAY
  2. Long-acting/ basal
    (Bound to zinc or protamine (Neutral Protamine Hagedorn, NPH)
    Insulin analogue (Glargine, Determir, Degludec))
    GIVEN ONCE A DAY
17
Q

What is 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

pros:
Variable basal rates (replicates the true response more accurately)
Extended boluses
Greater flexibility

18
Q

How is dietary advice given for Type I diabetes mellitus?

A
  • Dose adjustment for carbohydrate content of food
  • All people with type 1 diabetes should receive training for carbohydrate counting (known as a Structured Education Programme- 5 day course on skills and traning in self-management
  • Where possible, substitute refined carbohydrate containing foods (sugary / high glycaemic index) with complex carbohydrates (starchy / low glycaemic index
19
Q

How does a closed loop/ artificial pancreas work?

A
  • Change in glucose
  • Real-time continuous glucose sensor
  • Algorithm to use glucose value to calculate insulin requirement
  • Insulin pump delivers calculated insulin
20
Q

How would a transplantation treat Type I diabetes mellitus?

A
  1. Islet cell transplants:
    Isolate human islets from pancreas of deceased donor
    Transplant into hepatic portal vein
    Requires life-long immunosuppression
  2. Simultaneous pancreas and kidney transplants
    Better survival of pancreas graft when transplanted with kidneys
    Requires life-long immunosuppression

Even if incomplete, often results in better control
Limitations: availability of donors, complications of life-long immunosuppression

21
Q

How are glucose levels monitored?

A
  1. Capillary (finger prick) blood glucose monitoring
  2. Continuous glucose monitoring (restricted availability, NICE guidelines)
  3. Glycated haemoglobin (HbA1c)
22
Q

What are pros and cons of using HbA1c to monitor glucose levels?

A

Pros:
- Reflect last 3 months (red blood cell lifespan) of glycaemia

cons:
- Biased to the 30 days preceding measurement
- Anything that affects the haemolglobin in the body will affects HbA1c (e.g. anaemia, haemolysis)

23
Q

What are some acute complications from type 1 diabetes

A

Diabetic ketoacidosis
Uncontrolled hyperglycaemia
Hypoglycaemia

24
Q

What can cause diabetic ketoacidosis to occur as a complication of treatment/ management?

A

Acute illness
Missed insulin doses
Inadequate insulin doses

25
Q

How do you diagnose diabetic ketoacidosis?

A

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

26
Q

How do you diagnose Hypoglycaemis?

A

Numerical definition (variable) <3.6 mmol/L glucose level
Severe hypoglycaemia: any event requiring 3rd party assistance
Symtpoms:
Adrenergic: (tremors, palpitations, sweating, hunger)

27
Q

When does hypoglycaemia become a problem?

A

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

28
Q

What are the complications that can be caused from 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

29
Q

What are the risk factors of hypoglycaemia?

A

Risk factors:
Exercise
Missed meals
Inappropriate insulin regime
Alcohol intake
Lower HbA1c
Lack of training around dose-adjustment for meals

30
Q

How can you support problematic hypoglycaemia?

A

Indication for insulin-pump therapy (CSII)
May try different insulin analogues
Revisit carbohydrate counting / structured education
Behavioral psychology support
Transplantation

31
Q

What factors determine the acute management of hypoglycaemia?

A

If the patient is alert and orientated:
- oral carbohydrates
- Juice/ sweets (rapid acting)
- Sandwich (longer acting)

If the patient is drowsy/ confused but still able to swallow:
- Buccal glucose
- Hypostop/ glucogel
- Complex carbohydrate

If the patient is unconscious/ unable to swallow
- IV access/ glucose

Endocrinology (14 decks)

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