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Endocrine > Type 1 diabetes > Flashcards

Type 1 diabetes Flashcards

1
Q

What is the pathophysiology of type 1 diabetes?

A

-Autoimmune response against pancreatic B cells
-causes infiltration of pancreatic islets by mononuclear cells = insulitis
=absolute insulin deficiency

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2
Q

What is the Aetiology of type 1 diabetes?

A

HLA-assoc. immune-mediated organ specific disease:

  • genetic susceptability is polygenic with greatest contribution from HLA region
  • Auto-antibodies directed against pancreatic islet constituents appear in circulation in 1st few years of life and often predate onset for many years
  • Environmental factors then act as a trigger: viral/infection/maternity/weight gain
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3
Q

Describe the epidemiology of T1DM?

A

Peak incidence around the time of puberty

  • highest incidence Finland and northern european contries
  • incidence increasing
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4
Q

What is the diagnosis of T1DM?

A

Diagnosis of diabetes:
Random glucose 11.1mmol/l or more
Fasting glucose 7.0mmol/l or more
and symptoms or repeat test

Diagnosis of type 1 diabetes:

  • often on history and presentation alone e.g. DKA
  • GAD/IA2 antibodies and C peptide may help

(discriminatory tests: GAD/anti islet cell abodys, ketones, c-peptide)

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5
Q

What is C-peptide

A

This is a biproduct of insulin synthesis and it’s level indicates insulin levels - if low =insulin is low

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6
Q

Describe the risk factrors and disease markers for T1DM in the:

  • Foetus
  • Pre-diabetes
  • Clinical diabetes
A

Foetal risk factors (maternal factors):

  • infection
  • age
  • ABO mismatch
  • Birth order

Foetal disease markers:
-HLA or non-HLA

Pre-diabetes risk factors (autoimmune trigger factors):

  • viral infection
  • vit D deficiency
  • Dietary factors
  • environ. toxins

Pre-diabetes disease markers:

  • autoantibodies
  • candidate antigens
  • insulitis

Clinical diabetes risk factors (accelerating factors):

  • infection
  • insulin resistance
  • puberty
  • diet/weight
  • stress

Clinical diabetes disease markers:

  • raised blood glucose
  • ketones
  • low insulin levels
  • decrease in B cell mass
  • decrease in C peptide
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7
Q

Type 1 diabetes symptoms:

  • Triad?
  • others?
A

Triad:

  • polyuria (enuresis in children)
  • polydipsia
  • weight loss
  • fatigue and somnolence
  • blurred vision
  • candida infection
  • ketoacidosis
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8
Q

Describe the general management principles of Type 1 diabetes

A
  • blood glucose and ketone monitoring
  • insulin: usually basal/bolus regime
  • carbohydrate estimation
  • regular DSN + dietician contact
  • appropriate medical clinic review
  • HbA1c monitoring (ideal range is 48-58 mmol/L)
  • annual review
  • record severe hypoglycaemic episodes or admission with diabetic ketoacidosis
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9
Q

What is included in an annual diabetic review?

A
  • weight
  • BP
  • bloods
  • HbA1c
  • Renal function
  • Lipids
  • Retinal screening
  • foot risk assessment
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10
Q 
insulin - What is:
-humalog
-humulin S
-insulatard
-lantus/levermir
-humalog mix 25
-humulin M3
examples of?
A
  • humalog: rapid acting
  • humulin S: short acting
  • insulatard: intermediate acting
  • lantus/levermir: long acting
  • humalog mix 25: rapid/intermediate mix
  • humulin M3: short/intermediate mix
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11
Q

What are the blood glucose targets:

  • pre-prandial
  • post-prandial
A

Pre-prandial: 4-7mmol/L

post-prandial: <10mmol/L

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12
Q

What are the main aims of insulin treatment?

A
  • prevent hyperglycaemia (too little insulin)
  • avoid hypoglycaemia (too much insulin)
  • reduce chronic complications
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13
Q

What symptoms are associated with hyperglycaemia?

A
  • Thirst
  • tiredness
  • blurred vision
  • weight loss
  • polyuria
  • nocturia
  • fungal infections
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14
Q

What signs are associated with hyperglycaemia?

A
  • mood state
  • information processing
  • working memory
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15
Q

What is the risk of hyperglycaemia in type 1 diabetes? What could precipitate this?

A

Diabetic ketoacidosis

  • non-compliance with treatment
  • newly diagnosed DM
  • alcohol
  • illicit drugs
  • infection
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16
Q

Describe the pathogenesis of diabetic ketoacidosis in the absence of insulin?

A

in the absence of insulin:

  • hepatic glucose production accelerates (glycogenolysis and glucneogenesis) and peripheral uptake glucose is reduced.
  • rising glucose levels leads to an osmotic diuresis = loss of glucose in urine drags salt/electrolytes with it which water follows
  • plasma osmolarity rises and renal perfusion falls

simultaneously:

  • rapid lipolysis occurs which leads to raised levels of free fatty acids
  • these are broken down in the liver = ketone bodies

This leads to:
-renal perfusion has fallen and therefore ketones can’t be excreted
= build up
=ketoacidosis

17
Q

What other biochemistry is deranged in ketoacidosis?

A
  • hyperkalaemia (insulin usually drives potassium into cells)
  • Creatinine often raised
  • hyponatraemia
  • raised lactate common
  • bicarb <10 in most severe cases
  • amylase often raised
  • WCC raised due to effect of acidosis on bone marrow
18
Q

What symptoms are experienced in ketoacidosis?

A

Osmotic related:

  • thirst/polyuria
  • dehydration

Ketone body related:

  • flushed
  • vomiting
  • abdo pain and tenderness
  • kussmauls resp. (breathless as trying to blow off CO2)
  • ketone smell

Assoc. conditions:

  • gastroenteritis
  • underlying sepsis
19
Q

How is diabetic ketoacidosis diagnosed?

A

Ketonaemia >3mmol/L
Ketonuria >2+ on dipstick
Blood glucose >11mmol or known DM
Bicarbonate <15mmol/L or venous pH <7.3

20
Q

What is the management of diabetic ketoacidosis?

A

In HDU following hospital protocol

Replace losses:

  • fluid (initially 0.9% NaCl, if glucose falls to 15 use dextrose)
  • insulin 0.1unit/kg/hour
  • potassium
  • phosphate rarely
  • HCO3- almost never
21
Q

Describe ketone monitoring

A

Ketone monitoring, this is attached to the glucometer in T1DM to prevent ketoacidosis as can allow preventative action:

Blood ketone monitoring - <0.6mmol/L normal

Urine ketone testing - indicates ketone level 2-4hrs ago

22
Q

What hormone effects are seen in insulin deficiency?

A

Growth hormone:
-promotes lipolysis and reduces hepatic uptake glucose

Adrenaline:
-stimulates glucagon release and lipolysis

Cortisol:
-stimulates glucneogenesis in liver from amino acids, glycerol, lactate and pyruvate

23
Q

Describe what symptoms are seen in hypoglycaemia?

A

Symptoms - typically below 3mmol/L develop over minutes:

  • pallor
  • sweating
  • tremor
  • palpitations
  • confusion
  • nausea
  • hunger
  • irritable/angry
  • pounding heartbeat
  • weakness/fatigue
  • heachae
24
Q

What signs are seen in hypoglycaemia?

A
  • pallor

- cold sweat

25
Q

What does hypo-unaware mean? what does this predispose to?

A

= unaware of warning signs and are more at risk of neurogylcopenia

  • altered behavior/concious level
  • pale/drowsy/detached
  • irritable/aggressive
  • can slip into coma
  • can have convulsions during coma
26
Q

What increases the risk of becoming hypo-unaware?

A
  • Low blood glucose episodes are common
  • long duration T1/T2DM
  • intensively treated T1DM (low HbA1c)
27
Q

what is the immediate treatment of hypoglycaemia?

A
  • consume 15-20g glucose or simple carb (s)
  • recheck after 15mins
  • if still hypo repeat
  • on BG normal, eat a small snack if next planned food is >1hr away

If severe:

  • glucagon 1mg injection IM
  • 100mls 10% glucose IV
28
Q

What are the risk factors for developing hypoglycaemia in type 1 diabetes and in other scenarios?

A

Exaggerated mismatch of insulin and nutrient absorption

Prolongation of insulin effects:

  • renal impairment
  • hypothyroidism
  • liver failure

Primary failure hormones to raise glucose:

  • hypopituitarism
  • adrenal cortical failure
  • isolated GH deficiency

Lifestyle contributors:

  • acute increase in glucose uptake with excersize
  • depletion of liver glycogen with vigorous or prolonged exercise
  • alcohol suppresses glucneogenesis
29
Q

What factors affect insulin absorption at site/action?

A
  • pen accuracy
  • leakage at site
  • temp of site
  • excersize
  • injection depth
  • injection site itself (diff. tissues absorb insulin diff.)
30
Q

What is lipohypertrophy and why does this occur in insulin treatment?

A

lump of fat at injection site

-reuse of needles or injection site not rotated

31
Q

Describe the initial approach to T1DM therapy

A
  • treat with a multiple dose insulin regimen or continuous subcutaneous infusion (CSII)
  • educate people in how to match prandial insulin to carb intake, pre-meal glucose and anticipated activity
32
Q

A 60KG 16yo male presents with new onset T1DM. You are asked to start subcut insulin injections, what do you do?

A

start at 0.3U/kg of body weight = 18 units

Divide this by 50% prandial and 50% basal

  • 9 units prandial (3/3/3 units before meals)
  • 9 units basal (before bed)
33
Q

if a patient is unable to manage a basal bolus regimen - what is recommended?

A

2 X long acting analogue

34
Q

What is the difference between onset action, peak action and duration of analogues vs soluble insulins for prandial insulin?

A

Analogue (novarapid/humalog):

  • onset 10-15mins
  • peak action 60-90mins
  • duration 4-5hrs

Soluble (actarapid/humulin S):

  • onset 30-60mins
  • peak action 2-4 hours
  • duration 5-8hours
35
Q

How does the continuous subcut insulin infusion work?

A
  • pump
  • pumps continuous short acting insulin delivering background insulin indicated by basal rates in advance
  • bolus of prandial insulin is delivered manually (calculated via CHO counting)
36
Q

What is HbA1c? what are the limitations?

A
  • glycalated haemoglobin
  • increases as blood glucose increases
  • measures BG average over 6-8weeks
  • reference range 4-6%

only tells you an average so if someone is fluctuating wouldn’t know

37
Q

What can be used to overcome the limitation of HbA1c?

A

continous blood glucose monitoring

-device constantly attached and shows levels throughout day

38
Q

What different pancreas transplants exist? what are the indications?

A
  • Kidney - pancreas auto-transplantation
  • islet-autotransplantation

Indications:

  • iminents or ESRD due to recieve or with kidney transplant
  • severe hypoglycaemia/metabolic complication
  • incapacitating clinical/emotional problems

Endocrine (18 decks)

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