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Year2 Endo > Diabetes Type 1 > Flashcards

Diabetes Type 1 Flashcards

1
Q

What is 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

what are the 6 types of diabetes mellitus

A 
Type 1 Diabetes
Type 2 Diabetes
Hybrid forms
Other
Unclassified
During pregnancy
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3
Q

What causes type 1 diabetes

A

Environment and genetics

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4
Q

what does type 1 diabetes do and how is this different to type 2

A

1) autoimmune destruction of inlet
2) absolute insulin deficiency
3) hyperglycaemia

type 2

1) insulin resistance due to lifestyle
2) relative insulin defiance
3) hyperglycaemia

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5
Q

When does diabetes present in life for type 1 and for type 2

A

Autoimmune diabetes leading to insulin deficiency can present later in life = latent autoimmune diabetes in adults (LADA)
T1 normally present during childhood but now discovering that it can present at every stage of life
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

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6
Q

what is Monogenic diabetes

A

other type of DM but can present aw T1 or T2 diabetes ie ( MODY )

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7
Q

What are the stages of development of type 1 diabetes

A

1) genetic predisposition
2) Potential precipitating event –>
3) over immunological abnormalities( beta cells attacked and autoantibodies developed) , normal insulin release
4) progressive loss of insulin release, glucose normal
5) clinical diagnosis of overt diabetes, C peptide present
6) no c peptide
present
see google doc

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8
Q

What is C peptide

A

Side protein made by splitting of proinsulin –> c peptide + insulin

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9
Q

why is it important to find out if pateint has other immune diseases in T1 diabetes

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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10
Q

Describe the mechanism of how immune cells attack beta cells

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

Note not all beta cells are destroyed Some people with type 1 diabetes continue to produce small amounts of insulin
Not enough to negate the need for insulin therapy

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11
Q

Why do some ppl with T1 diabetes still prod insulin

A

not all beta cells are destroyed Some people with type 1 diabetes continue to produce small amounts of insulin
Not enough to negate the need for insulin therapy

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12
Q

which genes give you susceptibility to T1 diabetes

A

HLA-DR3 and HLA-DR4 deletions pose a significant risk to chance of getting T1DM (DR - human leukocyte ag)

see graph on docs

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13
Q

what environmental factors are established to cause T1

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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14
Q

What autoantibodies are tested for in ppl eiwth diabetes

A

In pancreas
Detectable in the sera of people with Type 1 diabetes at diagnosis.
Not generally needed for diagnosis in most cases
Insulin antibodies (IAA)

attackes:
Glutamic acid decarboxylase (GADA) – widespread neurotransmitter
Insulinoma-associated-2 autoantibodies (IA-2A)-Zinc-transporter 8 (ZnT8)

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15
Q

What are the symptoms of T1

A 
Excessive urination (polyuria) 
Nocturia
Excessive thirst (polydipsia) 
Blurring of vision
Recurrent infections eg thrush
Weight loss
Fatigue
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16
Q

what are the signs ( medical) of T1 diabetes

A 
dehydration 
cachexia
hyperventilation
smell of ketones
glycosuria 
ketonuria
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17
Q

How to diagnose diabetes T1

A

DIAGNOSIS IS BASED ON CLINICAL FEATURES and presence of ketones (in some cases pancreatic autoantibodies / C-peptide may be measured)

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18
Q

What are the effects of insulin deficiency

A

Proteolysis ( break down of muscle into AA)
stops hepatic glucose output ( HGO)
lipolysis ( fast –> gly + NEFA)

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19
Q

Why are ketone bodies formed in T1 diabetes

A

No insulin means no suppression of glucagon

1) glucagon acts on liver to turn fatty acyl coA –> acetyl co A –> acetoacetate –> acetone + 3OH-B –> ketone bodies

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20
Q

what should we aim for in the treatment of ppl with T1

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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21
Q

what are the complications of hyperglycaemia

A

1) Acute
Diabetic ketoacidosis

2) Chronic
Microvascular 
Retinopathy
Neuropathy
Nephropathy

3) Macrovascular
Ischaemic heart disease
Cerebrovascular disease
Peripheral vascular disease

4) Of treatment itself
Hypoglycaemia

22
Q

How can you manage T1

A

Insulin Treatment
Dietary support / structured educations
Technology
Transplantation

Type 1 diabetes is a condition that is ‘self-managed’

23
Q

when do you inject insulin

A

before a meal –> insulin has 2 phases

24
Q

what are teh 2 types of insulin and what are they used for

A 
1) With meals (short / quick-acting insulin)
Human insulin – exact molecular replicate of human insulin (actrapid)
Insulin analogue (Lispro, Aspart, Glulisine) 
2) Background (long-acting / basal)
Bound to zinc or protamine (Neutral Protamine Hagedorn, NPH)
Insulin analogue (Glargine, Determir, Degludec)
25
Q

When do you take short active vs long acting insulin

A

short acting 3x a day before meals

long acting in teh morning ( once a day or 2 daily intermediate to try to act like normal insulin)

26
Q

what is insulin pump therapy and what does it do

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

27
Q

extra

A

exra

28
Q

what dietary advice should be given to ppl with T1

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)

NICE Guidelines [NG17] for type 1 diabetes
All people with type 1 diabetes should be offered a Structured Education Programme
e.g. DAFNE but many others
5 day course on skills and training in self-management

29
Q

what happens with a closed loop / artificial pancreas

A

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

3) changes in glucose
4) real time continuous glucose sensor

Many advances in this field – some closed loop systems developed. Hybrid closed loop systems available on the NHS

30
Q

what are the 2 types of transplants for T1

and what are the limitations of this method of treatment

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

Aim: try to restore physiological insulin production to the extent that insulin can be stopped

Even if incomplete, often results in better control

Limitations: availability of donors, complications of life-long immunosuppression

31
Q

How do we monitor glucose levels

A

1) capillary finger prink blood glucose monitoring
2) continuous glucose monitoring using closed loop system ( restricted availability , Nice guidelines
3) HbA1C

32
Q

what is HbA1C and what do we use it for

A

Test for hyperglycaemia
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

N terminal valine residue B chain + glulose –> schiff base ( fast hrs) ( reversible reaction)

Schiff base –> amadori product ( slow days)

33
Q

Why is HbA1C not perfect

A

1) erythropoiesis
2) altered haemoglobin
3) glycation
4) erythrocyte destruction

34
Q

what is used to guide insulin doses

A

Using self-monitoring of blood glucose results at home and HbA1c results every 3-4 months

Based on results, increase or decrease insulin doses

35
Q

what are acute complications from T1

A

Diabetic ketoacidosis
Uncontrolled hyperglycaemia
Hypoglycaemia

36
Q

what is diabetes 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

37
Q

How to diagnose diabetic ketoacidosis

A

Diabetic ketoacidosis diagnosis

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

38
Q

what is hypoglycaemia and why does it happen in T1

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

39
Q

when does hypoglycaemia become a problem for T1

A

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

HbA1c itself may not be helpful in identifying hypoglycaemia

40
Q

What are the risks of hypoglycaemia

A

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
41
Q

Who is at risk of hypoglycaemia and what are some risk factors

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
42
Q

What management strategies can be used to combat hypoglycaemia

A

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

43
Q

how do you manage an acute hypoglycaemic episode

A

1) If alert and orientated :
oral carbohydrates that are rapid acting ie juice/ sweets or longer acting ie sandwich

2) drowsy / confused but can still swallow :
buccal glucose eg hypostop / glycogel
complex carbohydrates

3) unconscious / unable to swallow
Iv access –> give 20% glucose IV

Deteriorating /refractory /insulin induced /difficult IV access: consider IM /SC 1mg Glucagon

44
Q

What does a normal physiological insulin profile look like

A

Insulin is never 0 → prevents DKA and breakdown of muscle
Flat production of insulin between meals
When you eat you get a sharp rise in insulin production and then you get another peak afterwards

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Year2 Endo (13 decks)

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