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ENDOCRINOLOGY 2 > TYPE 1 DIABETES MELLITUS > Flashcards

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
Q

What are some ways to monitor glucose levels?

A

Capillary (finger prick) blood glucose monitoring

Continuous glucose monitoring

26
Q

What is glycated haemoglobin (HbA1c)?

A

Reflects the last 3 months of glycaemia (RBC lifespan)

Has a linear relationship with glucose levels as it is irreversible

27
Q

What are 4 reasons why HbA1c may not be perfect?

A

Erythropoiesis
Altered Haemoglobin
Glycation
Erythrocyte destruction

Each reason can cause an increase of decrease in HbA1c

28
Q

Causes for erythropoiesis affecting HbA1c?

A

Increased HbA1c: iron, vitamin B12 def, decreased erythropoiesis

Decreased HbA1c: EPO admin, iron, vitamin B12, reticulocytosis, chronic liver disease

29
Q

Causes for altered haemoglobin affecting HbA1c?

A

Genetic or chemical alterations in haemoglobin: haemoglobinopathies… may increase or decrease HbA1c

30
Q

Causes for glycation affecting HbA1c?

A

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
Q

Causes for erythrocyte destruction affecting HbA1c?

A

Increased HbA1c: splenectomy (increased erythrocyte life span)

Decreased HbA1c: splenomegaly, haemoglobinapathies, rheumatoid arthritis (decreased erythrocyte life span)

32
Q

What is used to help guide insulin doses?

A

Self monitoring of blood glucose results at home and HbA1c results every 3 months

33
Q

What are the acute complications from T1DM?

A

Diabetic ketoacidosis
Uncontrolled hyperglycaemia
Hypoglycaemia

34
Q

Which types of diabetes can ketoacidosis present in?

A

All types

Can be presenting feature in new-onset type 1 diabetes
Occurs in established T1DM (missed/inadequate insulin doses, acute illness)

35
Q

What is the diagnosis of diabetic ketoacidosis?

A

ph < 7.3
Increased ketones in urine or capillary blood
HCO3- < 15 mmol/L
Glucose > 11 mmol/L

36
Q

Why does hypoglycaemia occur in T1DM?

A

Inevitable feature of the self-management of T1DM

37
Q

What glucose level indicates hypoglycaemia?

A

< 3.6 mmol/L

38
Q

Why can repeated hypoglycaemic instances be bad?

A

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
Q

When does hypoglycaemia become a problem?

A

Excessive frequency
Impaired awareness
Nocturnal hypoglycaemia
Recurrent severe hypoglycaemia

40
Q

What are some strategies to support problematic hypoglycaemia?

A

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

41
Q

What is the acute management for a hypoglycaemic patient who is alert and orientated?

A

Oral carbohydrates
Juice/sweets (rapid acting)
Sandwich/bread (long acting)

42
Q

What is the acute management for a hypoglycaemic patient who is drowsy/confused but intact swallow?

A

Buccal glucose e.g. Hypostop/glucogel

Complex carbohydrate

43
Q

What is the acute management for a hypoglycaemic patient who is unconscious or concerned swallow?

A

20% glucose IV

ENDOCRINOLOGY 2 (12 decks)

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