TYPE 1 DIABETES MELLITUS Flashcards

1
Q

What is type 1 diabetes mellitus?

A

Autoimmune condition where beta-cells in pancreas destroyed causing partial/complete deficiency of insulin production resulting in hyperglycaemia

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2
Q

What is LADA?

A

Latent autoimmune diabetes in adults

Autoimmune diabetes leading to insulin deficiency can present in later life

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3
Q

Which type of diabetes does ketoacidosis present in?

A

Type 1 and type 2

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4
Q

What are the stages of development of type 1 diabetes?

A

Genetic predisposition

  • potential precipitating event (e.g. viral)

Overt immunological abnormalities with normal insulin release

Progressive loss of insulin release (glucose normal)

Overt diabetes (C-peptide present)

No c-peptide present

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5
Q

What difference can be seen when looking at the islet of beta-cells and surrounding between an early type 1 and long duration type 1?

A

In the long duration type 1 a lot of the immune cells which have crowded around the islet will have burnt off

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6
Q

Are all beta-cells destroyed in type 1 diabetes?

A

In some patients not all
- still continue to produce small amount of insulin

However not enough to negate insulin therapy

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7
Q

Which allele is the genetic susceptibility of type 1 diabetes most associated with?

A

HLA-DR

Human leukocyte antigen

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8
Q

List environmental factors associated with type 1 diabetes

A

Enteroviral infections
Cow’s milk protein exposure
Seasonal variation (more in winter)
Changes in microbiota

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9
Q

What pancreatic auto-antibodies could you test for in type 1 diabetes (not generally required for diagnosis because of how type 1 presents)

A
Insulin antibodies (IAA)
GADA (widespread neurotransmitter)
Insulinoma-associated-2 autoantibodies (IA-2A)
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10
Q

What are the symptoms of type 1 diabetes?

A
Polyuria
Nocturia
Polydipsia
Blurring of vision (osmotic shift in eyeball due to hyperglycaemia)
Recurrent infections e.g. thrush
Weight loss
Fatigue
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11
Q

What are the clinical signs of type 1 diabetes?

A
Dehydration
Cachexia (loss of weight)
Hyperventilation
Smell of ketones
Glycosuria
Ketonuria
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12
Q

What are the effects of insulin deficiency?

A

Proteinolysis
Increased HGO
Lipolysis into triglycerides and NEFA

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13
Q

Why are more ketone bodies made in insulin deficiency?

A

Glucose can’t enter cells so fat is burnt instead causing the formation of ketones (acetyl CoA, acetoacetate, acetone)

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14
Q

What are the aims in treatment for type 1 diabetes?

A

Maintain glucose levels without excessive hypoglycaemia
Restore close to physiological insulin profile
Prevent acute metabolic decompensation (e.g. ketoacidosis)
Prevent microvascular and macrovascular complications

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15
Q

What are the complications of hyperglycaemia?

A

Diabetic ketoacidosis

MICROVASCULAR

  • Retinopathy
  • Neuropathy
  • Nephropathy

MACROVASCULAR

  • Ischaemic heart disease
  • Cerebrovascular disease
  • Peripheral vascular disease
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16
Q

What are the 4 ways type 1 diabetes mellitus is managed?

A

Insulin treatment
Dietary support/structured education
Technology
Transplantation

“Self-managed”

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17
Q

What are the 2 categories of insulin that can be given?

A

Short/quick-acting insulin with meals

long-acting/basal insulin as background

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18
Q

What insulin is short/quick-acting and taken with meals?

A
Human insulin (identical to own insulin)
Insulin analogue (Lispro, Aspart, Glulisine)
19
Q

What insulin is long-acting/basal and is used as background?

A
Insulin bound to zinc or protamine (NPH)
Insulin analogue (Glargine, Determir, Degludec)
20
Q

Describe the typical basal insulin bolus regime

A
3 times a day short acting post-prandial
and
Once daily long-acting injected
or
twice daily intermediate acting insulin
21
Q

What is insulin pump therapy and describe how it works

A

Continuous delivery of short acting insulin analogue into subcutaneous space. Device is programmed to deliver fixed units/hour (basal) and a bolus for meals

22
Q

Give reasons why insulin pump therapy is used

A

Variable basal rates
Extended boluses
Greater flexibility

23
Q

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

A

Dose adjustment for carbohydrate content of food

All people with type 1 diabetes should receive training for carbohydrate counting

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

24
Q

What are the 2 transplantations you can carry out to cure type 1 diabetes?

A
  • Islet cell transplantation (transplant into hepatic portal vein, patient requires life-long immunosuppression)
  • Simultaneous pancreas and kidney transplants (better survival of pancreas graft when transplanted with kidneys, requires life-long immunosuppression)
25
What are some ways to monitor glucose levels?
Capillary (finger prick) blood glucose monitoring | Continuous glucose monitoring
26
What is glycated haemoglobin (HbA1c)?
Reflects the last 3 months of glycaemia (RBC lifespan) | Has a linear relationship with glucose levels as it is irreversible
27
What are 4 reasons why HbA1c may not be perfect?
Erythropoiesis Altered Haemoglobin Glycation Erythrocyte destruction Each reason can cause an increase of decrease in HbA1c
28
Causes for erythropoiesis affecting HbA1c?
Increased HbA1c: iron, vitamin B12 def, decreased erythropoiesis Decreased HbA1c: EPO admin, iron, vitamin B12, reticulocytosis, chronic liver disease
29
Causes for altered haemoglobin affecting HbA1c?
Genetic or chemical alterations in haemoglobin: haemoglobinopathies... may increase or decrease HbA1c
30
Causes for glycation affecting HbA1c?
Increased HbA1c: alcoholism, chronic renal failure, decreased intra-erythrocyte pH Decreased HbA1c: aspirin, vitamin C/E, increased intra-erythrocyte pH, certain haemoglobinopathies Variable HbA1c: genetic
31
Causes for erythrocyte destruction affecting HbA1c?
Increased HbA1c: splenectomy (increased erythrocyte life span) Decreased HbA1c: splenomegaly, haemoglobinapathies, rheumatoid arthritis (decreased erythrocyte life span)
32
What is used to help guide insulin doses?
Self monitoring of blood glucose results at home and HbA1c results every 3 months
33
What are the acute complications from T1DM?
Diabetic ketoacidosis Uncontrolled hyperglycaemia Hypoglycaemia
34
Which types of diabetes can ketoacidosis present in?
All types Can be presenting feature in new-onset type 1 diabetes Occurs in established T1DM (missed/inadequate insulin doses, acute illness)
35
What is the diagnosis of diabetic ketoacidosis?
ph < 7.3 Increased ketones in urine or capillary blood HCO3- < 15 mmol/L Glucose > 11 mmol/L
36
Why does hypoglycaemia occur in T1DM?
Inevitable feature of the self-management of T1DM
37
What glucose level indicates hypoglycaemia?
< 3.6 mmol/L
38
Why can repeated hypoglycaemic instances be bad?
May become debilitating with increased frequency | If it occurs too many times, the patient can become unable to detect the symptoms and not notice it
39
When does hypoglycaemia become a problem?
Excessive frequency Impaired awareness Nocturnal hypoglycaemia Recurrent severe hypoglycaemia
40
What are some strategies to support problematic hypoglycaemia?
Indication for insulin-pump therapy (CSII) May try different insulin analogues Revisit carbohydrate counting/structured education Behavioural psychology support Transplantation
41
What is the acute management for a hypoglycaemic patient who is alert and orientated?
Oral carbohydrates Juice/sweets (rapid acting) Sandwich/bread (long acting)
42
What is the acute management for a hypoglycaemic patient who is drowsy/confused but intact swallow?
Buccal glucose e.g. Hypostop/glucogel | Complex carbohydrate
43
What is the acute management for a hypoglycaemic patient who is unconscious or concerned swallow?
20% glucose IV