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PBL case Brief

Mary 23rd year old women brough in by ambulance from a music festival presenting with
drowsiness, slurred speech, dyspnea and has vomited three time. She has had two beers and
claims to not have taken any drugs. Mary has Type 1 Diabetes and has lost her insulin and blood
glucose monitor earlier today. For the past few years she has had a runny nose and cough
possibly due to viral infection and also a pruritic rash in her vulva region. The rash has not
resolved from antifungal cream.

Mary is a 23 year old women brought in by ambulance from a muscle festival presenting with
drowsiness, slurred specch, dyspnea at rest and vomiting on a background of Type 1 diabetes.
She reports of thirst polyuria but no pain on urination, has not vomited any blood or bile but has
intermittent abdominal cramps. She has had some food intake including 2 beers today but has
missed her previous evening insulin dose and her morning dose as well. She also has not
measured her BGL
She also complains of general unwellness over the last three days with running nose, sore throat,
cough in addition to a itchy vulva rash for the last 4 months with thick vaginal discharge. It has
been partially relief with topical clotrimazole cream.
Mary was diagnosed with diabetes at the age of 19 due to complants of urinary frequency. Initially
she was treated with twice daily injection of insulin and has difficult with regular meal and
carbohydrate intake complance due to work and social activities. She has had a number of
hypoglycaemic attacks before she stopped taking the insulin. During this period she experience
general unwellness with thirst, polyuria, blurred vision and vaginal irritation. The diabetes Centre
re-commence therapy with a lower insulin dose and her BGL and HbA1c stabalised.
Mary self tests her blood glucose and calculates her own insulin dose and does admit to irregular
insulin use and BGL testing.
She is concerned about her friends and colleages knowing about her diabetes due to social and
employment implications. She needs to maintain her drivers license to transport students. Only
her boyfriend knows about her diabetes as she has difficulties communicating this to her parents.
Mary is a social smoker starting at the age of 15 and has a quarter of a pack a week. She has 2-3
standard drinks on weekends only.
Upon examining Mary, she is tachycardic with increased respiratory rate. Her BMI is in the lowest
range of normal (18.3). Mary is orientated but slow ot answer questions and appear sleeping (GCS
of 14). She has dry skin and tongue with acetone breath suggestive of ketone acidosis.
Examination of the chest founds right basal crackles. Tis is consistent with a eryhtmatous pharynx
however no tonsiular exudate was present. Her CRT was delayed at 3 seconds but she had normal
peripheral sensation and equal pulses. Her retinal examination was unremarkable. Vaginal
examination found red scaly plaque on the labia and thick white vaginal discharge.
In summary, Mary is a 23rd female presenting with a possible hyperglycaemia and diabetic
ketoacidosis due to missing previous two insulin injections.
Hyperglycaemia ddx
Mechanism of diabetes

How does diabetes impair immunity (complications)


What is optimal diabetes in young people
History for initial rapid assessment
Physical exam
Investigations
Insulin complication
Explain symptoms
Explain results

Mechanism of Type 1
-

Autoimune beta cell deustrction (mostly)


o Some have clinical phenotype of type 1 but lack immunologic markers of
autoimmune process. Development of insulin deficiency by unknown process and are
ketosis prone (African American or Asian heritage)

This graph shows the function of beta cell mass


70-80% before diabetic features, the residual functional beta cells cannot maintain glucose
tolerance.
There is a honeymoon phase post diagnosis which is the phase in which the patient may not
require that much insulin. This goes away but some patients can be seen with C peptide
production = small amounts of insulin production.

Genetics
HLA complex Chromosome 6 involing MHC. Most indivudlas have HLA DR3 or DR4
However the risk of low for first degree relatives
Pathogenesis of DM1
-

Insulitis with T lymphocyte infiltration


Autoantibodies do not generally react with cell surface of islet cells
THUS the islet dustruction is mostly mediate by T lymphocytes rather than islet
autoantibodies.
B cells are particularly suspectible to toxic effects of TNFa, IFNy and Il1

DKA pathophysiology
-

Insulin deficiency with counterregulatory hormone excess (glucagon, catecholamine,


cortisol, growth hormone)
Insulin:glucagon ratio decreases resulting in gluconeogenesis, glycogenolysis and ketone
body formation
Glucagon decreases activity of pyruvate kinase
Insulin deficiency increases phosphoenolpyruvate carboxykinase = glucose synthesis and
less glycolysis.

Ketosis
-

Marked increase in free fatty acid release from adipocytes


This is due to reduced insulin, increased catecholone and growth hormone
Increase lipolysis and release free fatty acid

When can DKA occur?


-

Increased insulin requirement when there is concurrent illness


Complete or inadequate insulin

DKA diagnosis
-

Hyperglycaemia, ketosis and metabolic acidosis (increased anion gap)


However BGLl can be minimally elevated
Serum bicarb is <10 and pH ranges 6.8 to 7.3 depending on the severity
Potassium can be mildly elevated secondary to acidosis
Sodium, chloride, phosphorus and magnesium and reduced in DKA
Increased BUN and creatinine serum = volume depletion
Increased lipid profile (risk of pancreatitis)

Treatment of DKA

IV fluid replacement and insulin therapy (haemodynamic stability and adequate urine
output)
o Use of short acting insulin
o Mild can use SC but IV insulin used for those with acidosis and metabolic unstability
If vomiting = nasogastric tube to prevent aspiration

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