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Endocrinology > Type 1 Diabetes Mellitus > Flashcards

Type 1 Diabetes Mellitus Flashcards

1
Q

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

Overlaps between diabetes

A

Autoimmune diabetes leading to insulin deficiency can present later in life = latent autoimmune diabetes in adults (LADA)

T2DM may present in childhood

Diabetic ketoacidosis can be a feature of T2DM

Monogenic diabetes can present phenotypically as Type 1 or Type 2 diabetes (eg. MODY, mitochondrial diabetes)

Diabetes may present following pancreatic damage or other endocrine disease

Type 1 diabetes can develop in adults

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3
Q

Stages of development of type 1 diabetes

A

Genetic predisposition

Potential precipitating event

Overt immunological abnormalities - normal insulin release

Progressive loss of insulin release - glucose normal

Overt diabetes, C peptide present (cleavage product of pro-insulin)

No C peptide present

From proinsulin to C peptide and insulin - C peptide measured over insulin as people are usually on insulin injection - not used for those not diagnosed

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4
Q

Immune response in type 1 diabetes

A

Increased risk of T1D for genetically susceptible

Immune activation - beta cells attacked

Immune response - development of single autoantibodies

Generate antibodies

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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

Immunology

A

Defect in innate and adaptive 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

Some people with type 1 diabetes continue to produce small amounts of insulin
Not enough to negate the need for insulin therapy

Genetic susceptibility related to HLA

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7
Q

Environmental factors

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

Pancreatic auto-antibodies

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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9
Q

Presentation of type 1 diabetes

A 
Excessive urination (polyuria) 
Nocturia
Excessive thirst (polydipsia) 
Blurring of vision
Recurrent infections eg thrush
Weight loss
Fatigue
dehydration 
cachexia
hyperventilation
smell of ketones
glycosuria 
ketonuria
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10
Q

Effects of insulin deficiency

A

Proteinolysis - amino acids
Hepatic glucose output (HGO) - glucose
Lipolysis - non esterified fatty acids and triglyceride

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11
Q

Ketone bodies

A

NEFA go into liver to undergo oxidation
Generate Acetyl CoA, Acetoacetate, Acetone + 3 OH-B (ketone bodies) - acidic, so accumulate to turn blood acidic - diabetic ketoacidosis

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12
Q

Aims of treatment in type 1 diabetes

A

People with type 1 diabetes, require insulin FOR LIFE

Aims:
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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13
Q

Complications

A

Acute
Diabetic ketoacidosis

Chronic
Microvascular 
Retinopathy
Neuropathy
Nephropathy
Macrovascular
Ischaemic heart disease
Cerebrovascular disease
Peripheral vascular disease

Hypoglycaemia

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14
Q

Management of type 1 diabetes

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

Physiological insulin profile

A

Insulin is never completely suppressed

Basal insulin has a flat profile

Prandial peak has two phases

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16
Q

Types of insulin

A 
With meals (short / quick-acting insulin):
Human insulin – exact molecular replicate of human insulin (actrapid)
Insulin analogue (Lispro, Aspart, Glulisine) 
Background (long-acting / basal):
Bound to zinc or protamine (Neutral Protamine Hagedorn, NPH)
Insulin analogue (Glargine, Determir, Degludec)

Three times short acting with once or twice daily long acting

17
Q

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

Variable basal rates
Extended boluses
Greater flexibility

18
Q

Dietary advice integral

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)

19
Q

Artificial pancreas

A

Real-time continuous glucose sensor
Change in glucose

Algorithm to use glucose value to calculate insulin requirement
Insulin pump delivers calculated insulin

20
Q

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

21
Q

How do we monitor glucose levels?

A

Capillary (finger prick) blood glucose monitoring

Continuous glucose monitoring (restricted availability, NICE guidelines)

22
Q

Glycated haemoglobin (HbA1c)

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

22
Q

Acute complications from type 1 diabetes

A

Diabetic ketoacidosis
Uncontrolled hyperglycaemia
Hypoglycaemia

23
Q

Diabetic ketoacidosis

A

Can be a presenting feature of new-onset type 1 diabetes
Occurs in those with established type 1 diabetes
Acute illness
Missed insulin doses
Inadequate insulin doses
Life-threatening complication
Can occur in any type of diabetes

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

24
Q

Hypoglycaemia

A

To some extent an inevitable feature of the self-management of type 1 diabetes
‘Lost normal physiology and homeostasis’

May become debilitating with increased frequency

Numerical definition (variable) <3.6 mmol/L

Severe hypoglycaemia: any event requiring 3rd party assistance

25
Q

Problematic hypoglycaemia

A

When does hypoglycaemia become a problem?
Excessive frequency
Impaired awareness (unable to detect low blood glucose)
Nocturnal hypoglycaemia
Recurrent severe hypoglycaemia

Risks of hypoglycaemia
Seizure / coma/ death (dead in bed)
Impacts on emotional well-being
Impacts on driving
Impacts on day to day function
Impacts on cognition
26
Q

Who is at risk of hypoglycaemia

A

All people with type 1 diabetes

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

Strategies to support problematic hypoglycaemia

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

27
Q

Acute management of hypoglycaemia

A

Alert & Orientated - Oral Carbohydrates (juice/sweets or sandwich)
Drowsy / confused but swallow intact - Buccal glucose (glucogel)
Unconscious or concerned about swallow - IV access

Endocrinology (13 decks)

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