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Hormones > Endo 16: Type 1 diabetes > Flashcards

Endo 16: Type 1 diabetes Flashcards

1
Q

T/f DKA only occurs in T1DM

A

F, also feature of T2DM

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2
Q

t/f monogenic diabetes is only ever t1dm

A

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

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3
Q

Patietns presenting with T1DM in adult life may have what

A

latent autoimmune diabetes in adults (LADA)

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4
Q

Basic mechanism of type 1 and type 2

A

1:
Environmenta trigger+ genetics –> autoimmune destruction of islet cells –> insulin deficiency –> hyperglycaemia

2:
Genetics+obesity –> insulin resistance –> b cell failure (due to long term hyperglycaemia, so need insulin eventually) –> hyperglycaemia

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5
Q

Components of type 1 diabetes cause

A

Immune dysregulation, environmental triggers and regulators

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6
Q

Why is there a relapsing/remitting stage

A

Increase in effector T cells is followed by increase in regulatory T cells, over time effector T cells increases to a greater extent than the regulatory T cells, at which point hyperglycaemia occurs ….

READ: Model for type 1 diabetes as a relapsing-remitting disease.

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7
Q

What is the honey moon phase

A

beta cells temporarily recover then switch off

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8
Q

Which disease can occur due to immune basis of T1DM

A

B12 deficiency, ONE MORE
Hashimotos
Addison’s disease

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9
Q

Ideas of novel treatment

A

Immune modulation offers the possibility of novel treatments

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10
Q

What can be seen on histology with t1dm

A

Inflammation in islets of langerhans

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11
Q

Where is HLA located

A

Chr 6

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12
Q

Which HLA-DR allele increases risk of T1DM

A

DR3/DR4

Increases likelihood of immune cell interaction with these antigens

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13
Q

Incidence of DKA occurring

A

Less in summer times compared to other times of year (possible more infection in winter?)

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14
Q

Which markers can confirm type 1 DM (not always needed)

A

Islet cell antibodies (ICA)- grp O human pancreas

Glutamic acid decarboxylase (GADA) – widespread nuerotransmitter

Insulin antibodies (IAA)

Insulinoma-associated-2 autoantibodies (IA-2A)-receptor like family

but doesn’t effect treatment

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15
Q

T1DM presentation SYMPTOMS

A 
polyuria 
nocturia
polydipsia 
blurring of vision
‘thrush’ 
weight loss
fatigue
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16
Q

T1DM SIGNS

A 
dehydration 
cachexia
hyperventilation (due to metabolic acidosis, to blow off CO2.... kussmauls breathing)
smell of ketones
glycosuria 
ketonuria
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17
Q

Metabolic effects of insulin

A

Glucose regulated through liver, muscle and fat cells

3 checks to prevent hyperglycaemia:

  1. Insulin prevents gluose from getting out of the limit
  2. Unsluin causes glucose to get into muscle
  3. Prevents fat from getting out of adipose cells as glycerol and used in gluconeogenesis
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18
Q

How are the ketone bodies produced

A

Breakdown of adipocytes leads to glycerol (–>liver for gluconeogenesis)

AND

fatty acids (–>liver making ketones)

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19
Q

Are ketones a good wa to determine insulin deficiency

A

Y, Ketones define insulin deficiency

20
Q

Aims of t1m treatment

A

Reduce mortality

Prevent long term complications (micro and macrovascular issues)

- retinopathy
- nephropathy
- neuropathy
- vascular disease
21
Q

What is recommended in t1dm for diet (less important than t2dm, but sitll)

A

reduce calories as fat
reduce calories as refined carbohydrate
increase calories as complex carbohydrate
increase soluble fibre

balanced distribution of food over course of day with regular meals and snacks

22
Q

T/f insulin is only produced after meals

A

F: there is a basal amount of insulin, makes up 50% of what you need

23
Q

What does insulin treatment involve

A

With meals
Short acting
Human insulin
Insulin analogue (Lispro, Aspart, Glulisine)

+

Background
Long acting
Non-c bound to zinc or protamine
Insulin analogue (Glargine, Determir, Degludec)

24
Q

What kind of insulin is used

A

Genetic engineering to alter absorption,

distribution, metabolism and excretion

25
Q

Slide 27

A

Short acting insulin after meals and then background insulin (blue) works for 14 houra

26
Q

Slide 28

A

if 3 short acting ones, then give 1 background insulin per day

Point is that you tailor regime to how often they eat, and how much they eat each tim

27
Q

When is insulin pump given

A

Often when pens don’t work (i.e. they keep getting HYPOS)

28
Q

T/F insulin pump gives only short acting insulu

A

F… it’s background, then they can inform it when there are food bolus

29
Q

When are islet cells transplanted

A

if they keep getting hypos with pens and pumps….

islet cells injected into portal system and produces insulin… must give suppressants

30
Q

How can the success of treatment be measured

A

Capillary monitorying/ hba1c

31
Q

What is capillary monitorig

A

tests glucose levels… can give electroic device which can measure the glucose pver long period of time which you can use to inform the treatment regime

32
Q

What is hba1c

A

Relies on RBCs.. glucsose molecules attach to Hb… RBC half life is 120 days, so can measure glucose over 3 month period

33
Q

When is hba1c not relaible

A

Haemolysis, or Fe deficiency anaemia

34
Q

Why is Hba1c useful

A

Forms ideal measure of long term glycaemic control and has been shown to be related to risk of complications.
Furthermore lowering HbA1c associated lower risk of complication particularly microvascular complication

35
Q

What is ketosis

A

rapid decompensation of type 1 diabetes…. involving hyperglycaemia nad metabolic acidosis

36
Q

Metabolic disturbances in ketoacidosis

A

hyperglycaemia

	- reduced tissue glucose utilisation
	- increased hepatic glucose production

metabolic acidosis

  • circulating acetoacetate & hydroxybutyrate
    - osmotic dehydration and poor tissue perfusion
37
Q

Why do diabetics get hypogylcaemia

A

occasional hypos inevitable as a result of treating diabetes
major cause of anxiety in patients & families
source of major misconceptions in medi

38
Q

Define hypoglycaemia vs sever hypoglycaemia

A

hypoglycaemia - plasma glucose of < 3.6 mmol / l

severe hypoglycaemia - any hypo requiring help of another person to treat

39
Q

What happebs at glucose:
<3mmol/l
<2mmol/l

A

most mental processes impaired at <3 mmol/l
consciousness impaired at <2 mmol/l
severe hypoglycaemia may contribute to arrhythmia and sudden death

40
Q

Long terms effects of hypoglycaemia

A

may have long-term effects on the brain

recurrent hypos result in loss of warnings= HYPOGLYCAEMIC UNAWARENESS

41
Q

Who is at risk of hypo

A
  • main risk factor is quality of glycaemic control

- more frequent in patients with low HbA1c (i.e. well controlld)

42
Q

When does hypo occur

A

can occur at anytime but often a clear pattern

  • pre-lunch hypos common
  • nocturnal hypos very common and often not recognised
43
Q

Why do hypos occur

A 
unaccustomed exercise
missed meals
inadequate snacks
alcohol
inappropriate insulin regime
44
Q

Symptos due to hypoglycaemia

A
  1. Due to increased autonomic activation
palpitations (tachycardia)
tremor
sweating
pallor / cold extremities
anxiety
  1. Due to impaired
    CNS function
drowsiness
confusion
altered behaviour
focal neurology
coma
45
Q

Hypolycaemia treamtent

A

ORAL
feed the patient!
glucose
- rapidly absorbed as solution or tablets
complex CHO
- to maintain blood glucose after initial treatment

PARENTERAL
give if consciousness impaired
IV dextrose e.g 10% glucose infusion
1mg Glucagon IM
avoid concentrated solutions if possible (e.g 50% glucose)
46
Q

Why may glucagon not be given (it can usualyl be but why not)

A

Glucagon is reliant on there being adequate store of sugar in the liver… if they have been really unwell may not work

47
Q

Give names of 2 short acting and 2 long acting insulin analogues

A

short: Lispro, Aspart, Glulisine)
long: (Glargine, Determir, Degludec)

Hormones (23 decks)

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