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Year 2 - Endocrinology > T1DM > Flashcards

T1DM Flashcards

1
Q

T1DM Classification?

A

COMPLETE LACK of insulin

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2
Q

T2DM Classification?

A

RELATIVE LACK of insulin & INSENSITIVITY

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3
Q

How is the Classification of Diabetes ambiguous?

A

o Autoimmune T1DM can present later in life
- as LADA (latent autoimmune diabetes in adults)

o T2DM can present in childhood (however more common in adult life)

o DIABETIC KETOACIDOSIS (DKA) is only a feature of T1DM
- In T2DM, insulin production is sufficient to supress ketone production (although can present)

o Monogenic diabetes can present as T1 or T2 (e.g. MODY)

o Diabetes may present

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4
Q

Classification of diabetes based on aetiology?

A

Genetics can play a role in BOTH

BUT
o T2 is more hereditary (genetic play a larger role)
o T1 is usually autoimmune

The beta-failure in T2 is RELATIVE
- the cells still make lots of insulin, it just is NOT enough to stimulate the insulin receptors

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5
Q

What is the pathogensis of T1DM?

A

There are multiple relapse-remitting processes

o including Abs destroying beta-islet cells

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6
Q

Honeymoon Phase?

A

Last instance where the beta-cells produce a NON-hyperglycaemic response with just enough insulin

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7
Q

Role of T-cells in T1DM?

A

Effecter T-cells are destructive
AND
the T-reg cells are supposed to keep them in check

EVENTUALLY the T-effector cells overcome the T-reg cells = DESTRUCTION OCCURS

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8
Q

How does patient w. T1DM have an immune background?

A

o Increase prevalence of other autoimmune disease
o Risk of autoimmunity in relatives
o More destruction of B-cells
o Auto-Abs to confirm T1DM
o Immune modulation offers possibility of novel treatments

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9
Q

HLA-DR allele?

A

HLA-DR is an MHC class II cell surface receptor encoded by the human leukocyte antigen complex on Chr6

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10
Q

Genetic susceptibility in regards to HLA-DR?

A

HLA-DR3/4 deletion

o provides significant risk

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11
Q

Envrionmental triggers for T1DM?

A

More T1DM patients present in winter/autumn months

POSSIBLE INFECTIOUS CAUSE

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12
Q

Markers for T1DM?

A

Normally do NOT need to measure

o Islet cell Abs
o Insulin Abs
o Glutamic acid decarboxylase (GADA)
 -NTs
o Insulinoma-associated-2 autoAbs (IA-2A)
 - Receptor
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13
Q

C-peptide and first phase insulin?

A

C-peptide marker of insulin production
o If C-peptide REDUCES = Insulin deficient

Auto-Abs make patient lose their first phase insulin
o indicator of diabetes in later life

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14
Q

Symptom presentation of T1DM?

A 
o Polyuria
o Nocturia
o Polydipsia
o Blurring of vision
o 'Thrush'
o Weight loss
o Fatigue
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15
Q

Sign presentation of T1DM?

A 
o Dehydration
o Cachexia - muscle wasting/weakeness
o Hyperventilation - have metabolic acidosis so Kussmahl breathing
o Ketone smell
o Glycosuria
o Ketonuria
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16
Q

Liver, muscles and adipoytes?

A

o Liver is a large source of glucose
- mainly from GLYCEROL

o Aa from muscle goes OUT into circulation
- can be taken up by the liver

o Adipocytes have TGs
- can be broken down into glycerol + FAs

17
Q

Negative effects of insulin on body?

A

o HGO

o Protein breakdown in the muscle

o GLYCEROL being taken out from fatty tissue into the periphery

18
Q

Positive effect of insulin on body?

A

o Glucose being taken UP by muscle

19
Q

What does insulin deficiency mean then?

A

A lot of glucose goes OUT into circulation
BUT
is NOT taken up by tissues

ALSO enables GLYCEROL to leave cells
o and TGs breakdown
o SO are THIN!!

20
Q

Mechanism of DKA?

A

Diabetic Ketoacidosis

Normally:
o glycerol leaves adipocytes + enters liver

BUT in insulin deficiency:
o FAs come out of adipocytes + enter liver
o converted to KETONES (normally inhibited by insulin)

21
Q

Link between insulin deficiency & ketone bodies?

A

Deficient in insulin = MORE ketone bodies produced by liver

Casues ketonuria

22
Q

What are the aims of T1DM treatment?

A

o Reduce early mortality
o Avoid acute metabolic decomposition
o Prevent long-term complications
- e.g. retino/neuro/nephropathy, vascular disease

23
Q

What type of treatment to T1DM patients require?

A

EXOGENOUS Insulin!

Ketones define the insulin deficiency

24
Q

What are the diet changes required in those w. T1DM?

A

o Reduce calories as fat
o Reduce calories as refined carbs

o Increase calories as complex carbs
o Increase soluble fibre

Distribute food evenly throughout the day with regular meals and snacks

25
Q

What is important to consider when giving insulin treatment?

A

There is ALWAYS a BASAL LEVEL of INSULIN in a non-diabetic person

SO

treatment must try to retain this!

26
Q

When must insulin treatment be given?

A
  1. WITH meals
    o short-acting
    o can be human OR an analogue (lispro, aspart, glulisine)
  2. Background (intermediately)
    o long-acting
    o ‘non-c bound to zinc or protamine’ OR an analogue (glargine, determir, degludec)

These insulin shots can be altered depnding on lifestyle & habit

27
Q

What are alternatives to insulin treatments?

A

Can be time-consuming to give it so many times a day so:

  1. Insulin pump
    o continuous delivery
    o pre-programmed basal rates & bolus for meals
    o does NOT measure glucose (so no completion of feedback loop)
  2. Islet cell transplant
    o donor donates pancreas islet cells - inserted into diabetic’s liver portal vessels to release insulin
    o patient must be on continuous immunosuppressants
    o only available for those w erratic control of diabetes
28
Q

Treatment options for MONITORING T1DM?

A
  1. Capillary monitoring
    o either via. continuous monitor attached to belly OR finger-pricks (BMs)
    o allows adjustment of insulin dose
  2. HbA1C RBC monitoring
    o glucose binds to RBCs irreversibly so can give long-term view of glucose control (3month)
    o loweing HbA1C is associated w. a lower risk of microvascular complications!!
29
Q

2 main acute complication of T1DM?

A
  1. Metabolic acidosis (ketoacidosis)

o due to circulating acetoacetate/hydroxybutyrate
o due to osmotic dehydration & poor tissue perfusion
o CAN occur in T2DM and new onset diabetes BUT more common in T1DM

  1. Hyperglycaemia

o reduced tissue glucose utilisation
o INCREASED HGO
o patients MAY become hypoglycaemic when treating

30
Q

Why can hypoglycaemia occur?

A

Due to TREATING diabetes - defined as <3.6mmol/L glucose

o most mental processes impaired at <3mmol/L

o Coma at <2mmol/L
- severe hypoglycaemia may contribute to arrhythmia & sudden death

o Reccurrent hypos. result in a LOSS of warning to the body
- hypoglycaemia unawareness

31
Q

Who may hypoglycaemia affect?

A
  • Low quality glycaemic control patients

- More common in patients with LOW HbA1C

32
Q

When may hypoglycaemia strike?

A
  • ANYTIME but often a clear pattern (e.g. pre-lunch hypos common)
  • Nocturnal hypos are common BUT not often recognised
33
Q

Why may hypoglycaemia strike?

A 
o Unaccustomed exercise
o Missed meals
o Inadequate snacks
o Alcohol
o Inappropriate insulin regime
34
Q

Signs & Symptoms of hypoglycaemia?

A 
1. INCREASED ANS Activation
 o palpitations
 o tremor
 o sweating
 o pallor/clod extremities
 o anxiety
2. IMPAIRED CNS Function
 o drowsiness
 o confusion
 o altered behaviour
 o focal neurology
 o coma
35
Q

How can you treat hypoglycaemia?

A
  1. ORAL - FEED the patient!
    o Glucose - tablets/solution
    o Complex CHO - maintain blood glucose after initial treatment
  2. PARENTERAL - if consciousness impaired

o IV DEXTROSE!!!! (avoid concentrated solutions i.e. 50% glucose)
o 1mg glucagon IM (if patient cacextic will NOT work as not enough glucose reserve!)

Year 2 - Endocrinology (19 decks)

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