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Endo > T1DM > Flashcards

T1DM Flashcards

1
Q

What is T1DM?

A

Autoimmune condition that destroys pancreatic beta cells, leading to a reduced or no production of insulin

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2
Q

What is the key difference between T1DM and T2DM?

A

T1DM is autoimmune destruction of islets leading to total insulin insufficiency,
T2DM is insulin resistance leading to relative insulin deficiency (however some overlap)

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3
Q

What is it called when T1DM presents later in life?

A

LADA - latent autoimmune diabetes in adults

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4
Q

What is an example of monogenic diabetes?

A

MODY - maturity onset of diabetes of the young

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5
Q

What are the stages of T1DM development?

A

Genetic predisposition,
environment trigger leading to immune abnormalities (production of autoantibodies),
decreased insulin release,
decreased C-peptide

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6
Q

Why is insulin not used as a marker for assessing T1DM?

A

Shorter half life than C-peptide (hepatic metabolism) // insulin medication will affect readings

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7
Q

How will you be able to observe immune infiltration of the islets on a microscope?

A

Macrophages surrounding islets, low density of cells within islets (destruction)

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8
Q

What immune cells are involved in T1DM immune destruction?

A

CD4 T cells and CD8 T cells

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9
Q

Do patients with T1DM lose all beta cells?

A

No - some continue to make small amounts of insulin just insufficient levels

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10
Q

Which alleles are responsible for genetic susceptibility to T1DM?

A

HLA-DR allele: DR3 and DR4 (human leukocyte allele)

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11
Q

What are 4 environmental triggers that can cause T1DM?

A

Enteroviral infections,
gut microbiota,
seasonal variation,
cow milk protein

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12
Q

What are 4 autoantibodies in the pancreas and how are they detected?

A

Sera is used for detection -
Insulin Autoantibodies (IAA) ,
Glutamic acid decarboxylase (GAD-65) , (widespread NT)
insulinoma - associated 2 autoantibodies (IA-2A) ,
Zinc-transporter 8 (ZnT8)

Measure antibodies at diagnosis as that is when they are most likely to be positive.

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13
Q

What are 7 symptoms of T1DM?

A

Polyuria, Nocturia, Polydipsia, Blurred Vision, Recurrent Infections, Weight Loss, Fatigue

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14
Q

Why would you get blurring of vision in T1DM?

A

Glucose in the aqueous humour, water pulled in, the eye swells distorting light, blurry

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15
Q

What are 6 signs of T1DM?

A

Dehydration,
Cachexia (muscle wasting),
Hyperventilation,
Ketone Smell,
Glycosuria,
Ketonuria

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16
Q

Why do you get cachexia in T1DM?

A

Lower insulin stimulates proteinolysis (for amino acids and energy), so muscle wasting occurs

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17
Q

What is the effect of T1DM on lipolysis?

A

Lipolysis is inhibited by insulin, as insulin is low, lipolysis will increase

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18
Q

What is lipolysis and what is the consequential effect of it?

A

Non-esterified fatty acids go through beta-oxidation pathway leading to the production of ketone bodies (higher ketone levels in blood)

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19
Q

What is the impact of insulin deficiency in the liver?

A

Increased hepatic glucose output (gluconeogenesis) - because low insulin usually means more glucose needed

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20
Q

What are the 4 therapeutic objectives of T1DM?

A

Maintain glucose levels without excessive hypoglycaemia, restore physiological insulin profile,
prevent acute metabolic decompensation,
prevent microvascular and macrovascular complications

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21
Q

What is the best treatment method for T1DM? (with examples)

A

Individualised plans (insulin injections, insulin pump, islet cell transplantation)

22
Q

What are three acute complications of T1DM?

A

Diabetic Ketoacidosis, Uncontrolled Hyperglycaemia, Hypoglycaemia

23
Q

What are the two groups of chronic complications of T1DM?

A

Microvascular and Macrovascular

24
Q

Microvascular complications examples

A

Retinopathy
Neuropathy
Nephropathy

25
Q

Macrovascular complications examples

A

Ischaemic heart disease
stroke - cerebrovascular disease
peripheral vascular disease

26
Q

What is the limitation of all T1DM managements?

A

Self-managed condition, regardless of treatment type it will require 24 hour awareness from patient

27
Q

Describe a physiological insulin profile

A

Basal insulin is flat but never 0, after food there will be a prandial peak (two phases of insulin release)
If insulin reaches 0 this will lead to DKA

28
Q

When is short-acting insulin given and name two examples?

A

With meals, prandial peak
Human insulin (exact molecular replicate - actrapid) ,
Insulin analogue (recombinant - Lispro)

29
Q

When is long-acting insulin given and name two examples

A

For background basal levels
Bound to zinc or protamine (NPH) ,
Insulin Analogue (glargine)

30
Q

What is insulin pump therapy?

A

Continuous delivery of short acting insulin analogue via a pump into subcutaneous space. Can programme levels to give extra for bolus (meals)
can vary the basal rate

31
Q

What is a closed loop and how does it work?

A

Artificial Pancreas - real-time glucose sensor placed in interstitial fluid of subcutaneous fat. Algorithm detects change in glucose and calculates insulin dose required, and administers without human assistance
reduces risk of hypoglycaemia

32
Q

What are the two types of transplantation used in T1DM?

A

Islet cell transplants
Pancreas & Kidney Transplant

33
Q

How does islet cell transplantation work?

A

Isolate human islet cells from donor and transplant to hepatic portal vein.
Requires lifelong immunosuppression

34
Q

How does pancreas and kidney transplantation work and why do you need to remove the kidneys?

A

Remove both pancreas and kidney to lower the chnace of rejection
life-long immunosuppression

35
Q

What blood tests helps us monitor diabetes?

A

Glycated Haemoglobin (HbA1c)

36
Q

Why is this test used?

A

Reflects the last 3 months of glycaemia. This is glycated not glycosylated (which requires enzymes), and hence a linear relationship. It is also irreversible

37
Q

When can HbA1c not be used?

A

Affected erythropoiesis (iron deficiency or excess)
Altered Haemoglobin (genetic)
Glycation from other causes (alcoholism, chronic renal failure)
Erythrocyte destruction (splenomegaly or opposite splenectomy)

Not useful in identifying hypos

38
Q

Why is the HbA1c test not perfect?

A

The variation in mean glucose and mean HbA can vary greatly between patients

39
Q

How can we monitor glucose levels?

A

Capillary finger prick test // Continuous glucose monitoring machine

40
Q

What is the presentation of DKA?

A

Blurred vision, vomiting/nausea, weight loss, recurrent UTI (T1DM specifically)

41
Q

Why is recurrent UTI associated with DKA?

A

High glucose concentration in renal areas breeds a better survival environment for bacteria

42
Q

DKA diagnosis

A

pH <7.3
Increased ketones
HCO3 <15
glucose > 11

43
Q

How can hypoglycaemia occur in T1DM and what is the consequence of this?

A

Tightly controlled glucose intake
Recurrent - adrenergic receptors build up insensitivity to hypoglycaemia
May need to contact the DVLA as it can impact driving

44
Q

Hypoglycaemia triad

A

Low glucose - <3.5
Relief of symptoms with glucose administration
Symptoms

45
Q

Hypoglycaemia symptoms

A

Adrenergic - tremors, palpitations, sweating, hunger
Neuroglycopenic - confusion, seizures, coma, incoordination, somnolence

46
Q

Problematic hypoglycaemia

A

Excessive frq
Impaired awareness (unable to detect low glucose)
Nocturnal hypo
Recurrrent severe hypo

47
Q

What are 5 impacts of hypoglycaemia?

A

Seizure/Coma/Death in Bed
Emotional effects
Driving impacted
Day to Day affected
cognition effects

48
Q

What are the risk factors for hypoglycaemia in T1DM?

A

Exercise, missed meals, inappropriate insulin dose, alcohol

49
Q

How do you manage hypoglycaemia in alert & orientated patients?

A

Oral carbohydrates or sweets/juice

50
Q

How do you manage hypoglycaemia in drowsy but swallowing patients?

A

Buccal glucose or glucogel

51
Q

How do you manage hypoglycaemia in unconscious and non-swallowing patients?

A

Intravenous 20% glucose & saline

52
Q

How do you manage hypoglycaemia in deteriorating patients without IV access?

A

Intramuscular glucagon

Endo (13 decks)

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