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BRS Year 2 > Type 1 Diabetes > Flashcards

Type 1 Diabetes Flashcards

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1
Q

What causes type 1 diabetes?

What does type 1 diabetes result in?

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 different types of diabetes?

A 
Type 1 Diabetes
Type 2 Diabetes
Hybrid forms (starts in adulthood but presents like type 1)
Other
Unclassified
During pregnancy
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3
Q

What is LADA?

A

Latent autoimmune diabetes in adults

Autoimmune diabetes leading to insulin deficiency in, presenting in adults

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4
Q

Can T2DM present in childhood?

Can diabetic ketoacidosis be a feature of T2DM?

A

Yes

Yes - although more typical in type 1

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5
Q

What event might diabetes present after?

A

Following pancreatic damage or other endocrine disease

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6
Q

What challenges might clinicians face when trying to diagnose type 1 and type 2 diabetes?

A

Clinicians are faced with a challenge, trying to differentiate adult-onset type 1 diabetes from the much large numbers of cases of type 2 diabetes

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7
Q

What are the stages of development of type 1 diabetes?

A

Genetic predisposition

Potential precipitating event (a triggering event)

Overt immunological abnormalities; normal insulin release

Progressive loss of insulin release; glucose normal

Overt diabetes; C-peptide present

No C-peptide present

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8
Q

What do we measure when looking at beta cell function?

A

C-peptide cleaved from pro-insulin (C-peptide more stable in the blood)
Pro-Insulin is cleaved to make insulin and c peptide in a 1:1 ration

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9
Q

Why is the immune basis of T1DM 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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10
Q

Summarise immunology of T1DM?

A

Primary step is the presentation (by APC) of auto-antigen to autoreactive CD4+ T lymphocytes

CD4+ cells activate CD8+ T lymphocytes (cytotoxic)

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

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11
Q

Are all the beta cells destroyed in T1DM?

A

Not always, some beta cells escape the immune response

Some people with type 1 diabetes continue to produce small amounts of insulin and have C-peptide

Not enough to negate the need for insulin therapy

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12
Q

What is HLA?

What HLA is associated with diabetes?

A

Human Leukocyte antigen

HLA-DR = If you have these polymorphisms you are 6x more likely to develop T1DM

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13
Q

What are the environmental factors involved with T1DM?

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

When are auto-antibodies detectable?

Are auto-antibodies needed for diagnosis?

A

Detectable in the sera (serums) of people with Type 1 diabetes at diagnosis

Not generally needed for diagnosis in most cases

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15
Q

When are pancreatic auto-antibodies made?

A

Made when the beta cells content is exposed

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16
Q

What are the different types of pancreatic auto-antibodies ?

A 
Insulin autoantibodies (IAA)
Glutamic acid decarboxylase (GADA) – widespread neurotransmitter (prevents GABA production in pancreatic cell)
Insulinoma-associated-2 autoantibodies (IA-2A)
Zinc-transporter 8 (ZnT8) autoantibody
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17
Q

What are symptoms of T1DM?

A 
Excessive urination (polyuria)
Nocturia
Excessive thirst (polydipsia)
Blurring of vision
Recurrent infections eg thrush
Weight loss
Fatigue
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18
Q

Why does T1DM lead to blurry vision?

A

Glucose goes into eyeball

Causes osmotic change in lens

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19
Q

What are the signs of T1DM?

A 
Dehydration
Cachexia (wasting)
Hyperventilation (resp. compensation)
Smell of ketones
Glycosuria
Ketonuria
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20
Q

What are the 4 Ts of T1DM?

A

Toilet
Thirsty
Tired
Thinner

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21
Q

What is the mechanism of ketone body production in T1DM?

A
  1. Insulin deficiency- less suppression of fatty acyl-coa metabolism (Also stimulated by glucagon)
  2. NEFAs enter liver
  3. Fatty acyl-coa converts NEFA to Acetyl COA -> acetoacetate -> acetone + 3OH-B
  4. These are ketone bodies and are acidic so bad lead to diabetic ketoacidosis
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22
Q

What happens with insulin deficiency?

A

Proteolysis (inc. AAs)
Hepatic glucose output (inc. glucose)
Lipolysis (inc. Glycine and NEFA

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23
Q

What are the aims of treatment in type 1 diabetes?

A

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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24
Q

What is the only thing can prevent patients from taking insulin for life?

25
What are the acute complications of hyperglycaemia? What are the microvascular chronic complications of hyperglycaemia? What are the macrovascular chronic complications of hyperglycaemia?
Acute: Diabetic ketoacidosis Microvascular: Retinopathy Neuropathy Nephropathy Macrovascular: Ischaemic heart disease Cerebrovascular disease Peripheral vascular disease
26
How is T1DM managed?
Is self-managed with: Insulin Treatment Dietary support / structured educations Technology Transplantation
27
What are the main features of physiological profile of insulin?
Basal insulin has a flat profile Prandial (after eating) peak has two phases (the second phase is to break down remaining glucose- it's a much smaller peak) Insulin is never completely suppressed
28
What are the different types of insulin with meals?
short / quick-acting insulin ``` Human insulin – exact molecular replicate of human insulin (actrapid) Insulin analogue (Lispro, Aspart, Glulisine)- genetically altered in lab to be more rapid acting ```
29
What are the different types of long-acting insulin?
Background insulin ``` Bound to zinc or protamine (Neutral Protamine Hagedorn, NPH)- delay absorption of insulin Insulin analogue (Glargine, Determir, Degludec) ```
30
What is the typical regime for taking insulin?
Typical basal bolus regime Background once a day Short acting 3x a day (but can be more with snacks) OR Short acting (actrapid) 3x day Intermediate acting 2x day
31
What are the main features of insulin pump therapy?
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
32
What is CSII?
Alternative name for pump therapy | Continuous subcutaneous insulin infusion
33
What are the principles of dietary advice for T1DM? What are the NICE guidelines for diet and T1DM?
Dose adjustment for carbohydrate content of food. All people with type 1 diabetes should receive training for carbohydrate counting Where possible substitute refined carb containing food with complex carbs (low glycaemic index) NICE: 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
34
What substitutes should be made in diet?
Where possible, substitute refined carbohydrate containing foods (sugary / high glycaemic index) with complex carbohydrates (starchy / low glycaemic index
35
What is the closed-loop/artificial pancreas?
Real-time continuous glucose sensor- detects change in glucose Algorithm which uses glucose value to calculate insulin requirement Insulin pump delivers calculated insulin (basal insulin) Still need to log your carb intake so the pump can deliver short acting insulin Takes about 15 mins to detect glucose levels s pump acts 15 mins before time `Hybrid closed loop systems are available on the NHS
36
What are Hybrid closed loop systems?
Not quite closed loop The pump still needs to be told before a meal Available on NHS
37
What are the two types of transplant? What are the main features of these?
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
38
Why are transplants not more frequently used?
Limited organ availability Pancreas is not generally viable Risks of long-term immunosuppressants
39
What are the aims of transplantation?
Try to restore physiological insulin production to the extent that insulin can be stopped Even if incomplete, often results in better control
40
How do you measure glucose levels?
Capillary (finger prick) blood glucose monitoring Continuous glucose monitoring (HCL- restricted availability, NICE guidelines)
41
What are the main features of HbA1c? What are the limitations of HbA1c?
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 Not perfect Things affect it
42
What is used to guide insulin doses?
Using self-monitoring of blood glucose results at home and HbA1c results every 3-4 months Based on results, increase or decrease insulin doses
43
What are the main features of diabetic ketoacidosis?
Can be a presenting feature of new-onset type 1 diabetes Occurs in those with established type 1 diabetes. Causes: -Acute illness -Missed insulin doses -Inadequate insulin doses Life-threatening complication Can occur in any type of diabetes
44
How is diabetic ketoacidosis diagnosed?
pH <7.3, ketones increased (urine or capillary blood), HCO3- <15 mmol/L and glucose >11 mmol/L
45
What are the main features of hypoglycaemia?
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
46
What are the symptoms of a hypo?
Adrenergic - Tremors - Palpitations - Sweating - Hunger Neuroglycopaenic - Somnolence (drowsiness) - Confusion - Incoordination - Seizures, coma
47
When does hypoglycaemia become a problem?
Excessive frequency Impaired awareness (unable to detect low blood glucose) Nocturnal hypoglycaemia Recurrent severe hypoglycaemia
48
What are the 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 ```
49
What are the risk factors for a hypoglycaemia?
``` Exercise Missed meals Inappropriate insulin regime Alcohol intake Lower HbA1c Lack of training around dose-adjustment for meals ```
50
What are the 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
51
How do you acutely manage a hypoglycaemia when they are alert and orientated?
Oral carbohydrates Rapid acting juice/sweets Sandwich (longer acting)
52
How do you acutely manage a hypo when they are Drowsy / confused but swallow intact?
Buccal glucose e.g. Hypostop / glucogel Complex carbohydrate
53
How do you acutely manage a hypo when they are unconscious or concerned about swallow?
IV access | 20% glucose IV
54
What is monogenic diabetes?
A rare type of diabetes caused by mutation to a single gene Differs from type 1 and type 2 e.g. MODY, mitochondrial diabetes
55
What are the stages in development of T1DM?
Genetic risk: 15x increased risk of T1DM in those with relatives w/ disease Immune activation: Beta cells attacked Immune response: Development of single autoantibody Stage 1: Normal blood sugar: >/= 2 autoantibodies stage 2: abnormal blood sugar: >/= 2 autoantibodies Stage 3: clinical diagnosis: >/= 2 autoantibodies stage 4: Log-standing T1DM
56
Whats the problem with the basal bolus regime?
Short acting insulin doesnt replicate the 2 phases of the prandial peak Background insulin does not have the same flat basal profile
57
What factors can affect HbA1c?
Erythropoiesis: Inc. HbA1c- low iron, vit b deficiency Dec. - administration of erythropoietin, iron, vit b12 Altered Hb: haemoglobinopathies, HbF Glycation: Inc. - alcoholism, chronic renal failure dec. aspirin, vit C and E Erythrocyte destruction: Inc. HbA1c - increased erythrocyte life span (splenectomy) Dec. - splenomegaly, RA, drugs such as antiretrovirals
58
What should you do if a hypoglycemic person is deteriorating or its difficult to get IV access?
IM/SC insulin injection

BRS Year 2 (110 decks)

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