mcq bridging course: endocrinology

MCQ Bridging Course 2019 ENDOCRINOLOGY Dr O.Pronyakova Slide #1

ＭCQ BRIDGING COURSE:

ENDOCRINOLOGY

Dr Oksana PRONYAKOVA

24 July 2019,

Melbourne, Australia

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Diabetes Mellitus type I:

Clinical features: Acute onset of polydipsia, polyuria, polyphagia, weight loss, fatigue. Secondary enuresis. Ketoacidosis.

Investigations: next step – urine dipstick for sugar;

best step – random glucose equal or more than 11.1 mmo/L.

TPO a/b, tissue transglutaminaze a/b.

Management: admit to hospital for insulin therapy.

Follow-up: HbA1c every 3 months (target equal or less than 7 %).

Late complications.

Vaccination: Pneumococcal, Influenza, dTPA.


Diabetes Mellitus type II:

Clinical features: Asymptomatic, Metabolic syndrome, Acanthosis

nigricans, skin tags, hirsutism.

Recurrent skin/genital infections.

Chronic fatigue.

Late complications.

Positive family history.

Investigations: next step – random blood glucose – equal or >11.1 mmol/L;

best step – fasting blood glucose – equal or > 7.0 mmo/L.

HbA1c equal or more than 6.5% (on two occasions).

OGTT if uncertain level of blood glucose.

Management: Life style modification. Consider hypoglycemic drugs.

Follow-up: HbA1c every 3 months (target equal or less than 7 %).

Monitor late complications.

Vaccination: Pneumococcal, Influenza, dTPA.


Follow-up for late complications:

Nephropathy: albumin/creatinine ratio in spot urine sample every year;

Microalbuminuria 3 to 29 mg/mmol. Start ACE inhibitors.

Macroalbuminuria > or equal 30 mg/mmol. 24 - hours proteinuria. RFT.

eGFR yearly. If eGFR less than 30 mL/min refer to nephrologist.

Retinopathy: not later than 5 years after diagnosis – if no retinopathy is present repeat at least every two years by optometrist/trained GP/ophthalmologist;

nonproliferative retinopathy is identified – annual eye examination by optometrist/trained GP/ophthalmologist;

proliferative retinopathy/macular oedema – urgent referral to ophthalmologist.

Vitreous hemorrhage – same day by specialist.

Foot care: if no neuropathy – annual foot assessment, if neuropathy – podiatry review every 3- 6 months.


Screening for general population:

The risk assessment for Type 2 Diabetes should be done every 3 years in people over the age 40.

Screening should take place if:

1. Have Intermediate Hyperglycaemia;

2. Previous GD;

3. Have Polycystic Ovarian Syndrome;

4. Have Clinical Cardiovascular Disease (acute MI, angina, stroke);

5. Are Taking Antipsychotic Medication;

6. Are Taking Long-Term Steroids;

7. Age >30 years with: family history (first degree relative with type 2) plus obesity (BMI >30) plus hypertension.

People from high prevalence ethnic groups (e.g. ATSIs, Pacific Islanders) should start screening from 18 years.


VENOUS FASTING BLOOD GLUCOSE:

If fasting glucose < 5.5 mmol/L – diabetes unlikely, follow-up in 3 years.

If fasting glucose 5.5 – 6.9 mmol/L – uncertain level – do OGTT with 75 g of glucose. Check the glucosaemia in 2 hours:

If < 7.8 mmol/L – impaired fasting glucose, follow-up in 1 year;

If 7.8 – 11.0 mmol/L – impaired OGTT – follow-up in 1 year;

If > or equal 11.1 mmol/L – Diabetes type 2.

If fasting glucose 7.0 mmol/L or higher – Diabetes type 2 likely.

If asymptomatic – repeat fasting glucose twice.


Secondary Causes of Hyperglycemia:

I Diseases of Pancreas

- Pancreatitis

- Neoplasia

- Cystic fibrosis

- Haemochromatosis

II Endocrinopathies

- Cushing’s

- Acromegaly

- Pheochromocytoma

- Hyperthyroidism

III Drug-induced: antipsychotic, thiazide diuretics, oestrogen, GCS

IV Genetic syndromes: Turner Syndrome, Down Syndrome, Klinefelter’s


Q A 4-year-old girl is brought by her mother

with complaints that for one week her daughter

has woken up in the night to pass urine. She

also noticed that there was an increase in the

child’s milk intake. Weight loss despite

increased appetite.

What is the next step in the management?

1. Give 10 days oral penicillin

2. Do a glucose tolerance test

3. Do urine dip-stick for sugar

4. Urine culture

5. Mid-stream urine analysis


Q The most appropriate investigation for a

diabetic patient with very tanned skin is:

WOF would be the best investigation?

1. Transferrin saturation

2. Serum iron

3. Serum ferritin

4. Blood glucose

5. HbA1c


• Bronze diabetes = haemochromatosis

diabetes

• Hereditary haemochromatosis is a disorder of

iron overload. Iron deposits in pancreas causing

diabetes.

• Serum transferring saturation is more then 70%.


Q Patient present at your practise with DM type

1 and bone fracture.

What type of investigation should you consider

in this patient?

1. Tissue transglutaminase a/b

2. Thyroid a/b

3. Serum Ca level

4. Bone X-ray


An Endoscopic Jejunal Biopsy

Courtesy: Shaun McCann, Robin Foa, Owen Smith, Eibhlin Conneally,

"Haematology", Willey-Blackwell, 2005. - 190pp.

Fig.36 & Fig.35, p.41.

Biopsy showing normal villi

(N) and no lymphocytic

infiltrate

Biopsy showing blunted villi

(V) and an inflammatory

infiltrate of lymphocytes (L)


Coeliac Disease

• IgA Antigliden antibodies

• IgA Anti-endomysial a/b

• IgA Tissue transglutaminase a/b are more preferable in

screening for coeliac disease.

• Prevalence 5-10% in DM type I.


Q A 12 – year – old girl with acantosis

niagricans over her axilla. Her HbA1c is 8%.

Her mother and grand mother are diabetic.

What is your management?

1. Do OGTT

2. Start her on Metformin

3. Start her on Insulin


Image Courtesy:

Badiu C, Verzea S, Picu M, Pencea C.

Autoimmunity puzzle in Down

syndrome. Down Syndrome Research

and Practice. 2010;12(2);98-102.

Image Courtesy:

Juvenile acanthosis nigricans. Smeeta

Sinha, MD, Robert A. Schwartz, MD,

MPH. JAAD, Volume 57, Issue 3, Pages

502-508 (September 2007).

Acanthosis Nigricans


Various skin conditions are associated with insulin resistance including acanthosis

nigricans, hirsutism, acne, hidradenitis suppurativa, oiliness, alopecia, papulosis of

the fingers and skin tags.

Image Courtesy:An. Bras. Dermatol. vol.85 no.1 Rio de Janeiro Jan./Feb. 2010

Skin Tags


Q A 46-year-old female no significant past

history, BMI 24, FBS 5.8 mmol/L.

What to do?

1. FBS 1 yearly

2. FBS 3 yearly

3. OGTT now

4. RBS 2 yearly


Q Apatient presented with fasting blood glucose 5.7

mmol/L

What is your advice?

1. OGTT now

2. No investigations needed

3. Screen 3 yearly

4. Others


Q A 62-year-old lady with a family history of DM

came to you for routine test. All tests are

normal.

What is the test of choice?

1. OGGT every year

2. OGTT every 2 years

3. Venous plasma glucose every 3 years

4. Venous plasma glucose every year

5. HbA1c every 2 years


Q A 45 year old woman came for screening for

diabetes as her friend has been dx DM few days

earlier.

wts the best to be done ?

1. Fasting blood glucose every 3 years

2. Random blood glucose every 3 years

3. OGTT every year

4. Fasting blood glucose every year

5. HB A1C now


Treatment targets in diabetes

Blood glucose fasting 4 – 8 mmol/L

Blood glucose postprandial Less than 10 mmol/L

HbA1c Less than 7%

BMI 20 – 25

LDL Less than 2 mmol/L

HDL More or equal 1 mmol/L

Triglycerides Less than 2.0 mmol/L

Total cholesterol Less than 4.0 mmol/L

Blood pressure (no albuminuria) Equal or < 140/90 mm Hg

Blood pressure (plus albuminuria) Equal or <130/80 mmHg


Treatment targets in diabetes

Urinary albumin excretion < 20 mcg/min

Albumin/creatinine ratio < 2.5 mg/mmol – men

< 3.5 mg/mmol - women

Alcohol Less or equal 2 standard

drinks

Exercise At least 30 minutes walking

BMI 18 – 25


• Biguanides (Metformin)

• Treatment of choice in those that are overweight.

• Improves lipid profile.

• No hypoglycaemia. Save in pregnancy and children.

• Side effects: gastrointestinal intolerance.

• Contraindicated: renal failure, chronic heart failure, severe

anaemia, COPD due to risk of lactic acidosis.

• Monitor vit B12, Folic acid.

• Omit Metformin on the morning of surgery.

• Contrast study - 24 hours before procedure.

• Recommence 24 hours after major surgery provided that

there has been no deterioration in serum creatinine.


• Metformin immediate release 500 mg orally twice daily

with food as an initial dose, increasing the daily dose up to

maximum of 1 g, 3 times daily.

• Metformin extended-release 1 g orally daily with evening

meal as an initial dose, increasing the daily dose up to 2 g

daily.


• Sulfonylureas (Glibenclamide, Gliclazide, Glimepiride,

Glipizide) increase insulin secretion via the pancreatic

sulfonylurea receptor.

• Longer-acting sulfonylureas (Glibenclamide and

Glimepiride) should be avoided in older people with type 2

diabetes due to an increased risk of severe prolonged

hypoglycaemia, especially those with deteriorating kidney

function.

• Short-acting sulfonylureas (Gliclazide, Glipizide) can be

given to elderly patients with impairment of renal function

because they are converted to inactive metabolites by the

liver.


• Thiazolidinediones (Pioglitazone, Rosiglitazone)

improve glucose utilisation in peripheral tissues, supress

gluconeogenesis in the liver and reduce adipocyte lipolysis.

• They cannot be prescribed in heart failure due to fluid

retention;

• They increase the risk of fracture in postmenopausal

women;

• They increase the risk of bladder cancer associated with use

of pioglitazone;

• They increase risk of macular oedema.


Q A patient with DM type 2 came for review. His

blood glucose (fasting) is 6.2, HbA1c is 6.9%.

He is taking Metformin 500 mg/day.

What will you do?

1. Increase the dose of Metformin

2. Reassure

3. Add Insulin

4. Add Gliclazide


Q A patient with type 2 diabetes on Metformin 500

mg came to routine health check-up. Blood

pressure 135/80 mmHg. Lab investigation was

done and showed HBA1c 6.9% (normal <6.5%), total

cholesterol is 3.5 mmol/L, HDL 1.3 mmol/L.

WOF is most appropriate next step in management?

1. Commence Insulin

2. Increase Metformine

3. Commence Ramipril

4. Add Simvastatin

5. Continue same treatment


Q Around 47-year-old diabetic patient on metformin

extended release 1 g bd. HbA1c 8, FBG 9.

What is next?

1. Add perindopril

2. Glipizide

3. Insulin

4. Increase Metformine


Q A 68-year-old woman has had DM type 2 for 15 years.

She has hypertension, IHD, congestive heart failure,

renal impairement, prolipherative retinopathy and

peripheral neuropathy. Her diabetic control was good

untillthe past twelve months. She walks 1km three times

per week. She takes gliclazide, provastatin, lisinopril,

metoprolol, aspirin and GTN. Her BMI is 32, proteinuria

++, HbA1c 11%, serum creatinin 0.20 (0.06-0.12).

What is the most appropriate next step?

1. Commence insulin

2. Commence metformin

3. Commence rosiglitazone

4. Refer her to a dietitian

5. Advise increase in exercise


Q A 30-year-old female patient has been taking

Olanzapine for 8 months. She complains of 10

kg weight gain. On investigation: HbA1c 10%,

Lipid profile normal. BP 140/90 mmHg. Urine

test glucosuria, ketones negative.

What is the most appropriate management?

1. Add Metformin

2. Recommend life style modification

3. Switch to Aripiprazole

4. Switch to Quetipine

5. Reduce the dose of Olanzapine


Q A hypertensive patient suffering from DM

type 2.

What medication is the most suitable for him?

1. Beta blockers

2. Methyldopa

3. Thiazide

4. ACE inhibitor


Diabetic Nephropathy


Diabetic Neuropathy

I. Symmetrical mainly sensory/motor

polyneuropathy (distal)

Sensory nerve involvement:

• Loss of vibration

• Pain sensation

• Temperature sensation

• Light touch

• Unsteadiness

Motor nerve involvement:

• Small muscle wasting. High arch and clawing of the toes

leading to callus formation and neuropathic ulcer.


II. Autonomic neuropathy

- Postural hypotention (faints on standing, eating, or hot bath)

- Resting tachycardia

- Urine retention

- Erectile dysfunction

- Noctural diarrhoea

- Gastroparesis (impaired gastric empting)

- Delayed or incomplete bladder empting

- Loss of cardiac pain (silent ischaemia)

- Hypoglycaemic unawareness


III. Acute painful neuropathy

• Burning pain in feet, shins, thigh.

IV. Mononeuritis multiplex

• Cranial nerves (III, IV, VI, VII).

• Foot drop. Meralgia paresthetica. Tarsal tunnel syndrome.

• V. Proximal motor neuropathy (Diabetic

amyotrophy) - painful, asymmetrical muscle wasting of

quadriceps and pelvic girdle. Pain typically worse at night.

VI. Diabetic cheiropathy

VII. Dupuytren’s contracture

VIII. Carpal tunnel syndrome

IX. Charcot joint


Courtesy: OphthoBook.com


Courtesy: Clinical Findings in Diabetes Mellitus, Romesh Khardori, MD, PhD

Facial Nerve Palsy


Courtesy: Clinical Findings in Diabetes Mellitus, Romesh Khardori, MD, PhD

Diabetic Amyotrophy


Meralgia Paresthetica


Tarsal Tunnel Syndrome


Diabetic Cheiropathy

Courtesy: Rheumatology network Limited Joint Mobility in Diabetes Mellitus: The

Clinical Implications


Dupuytren’s Disease

Courtesy: THOMAS H. TROJIAN, MD, and STEPHANIE M. CHU, DO, University of

Connecticut Health Center/Saint Francis Hospital and Medical Center, Hartford, Connecticut

Grade 1 presents as a thickened nodule and a band in the palmar aponeurosis .

Grade 2 presents as a peritendinous band that limits extension of the affected finger.

Grade 3 presents as flexion contracture.


Dupuytren’s Contracture


Carpal Tunnel Syndrome

Courtesy: Fusion Rehabilitative Medicine


Charcot joint Acute

Courtesy: Dr.Kmliau Diabetic foot


Charcot joint Chronic

Courtesy: http://www.diabetes.org.uk/Guide-to-diabetes

http://www.diabetes.org.uk/Guide-to-diabetes






• This is neuropathic arthropathy. This is bone and

joint destruction due to repeated insensate injury

to go unnoticed.


Q A 50-year-old man present with a 2 year history of

burning pains in the feet, pins and needles in the

fingers and toes and weakness and unsteadiness of

the legs. There is distal wasting and weakness in all

limbs, areflexia and glove and stocking sensory

loss to all modalities.

The most likely diagnosis is:

1. Polymyositis

2. Charcot-Marie-Tooth disease

3. Guillian-Barre syndrome

4. Diabetic amyotrophy

5. Diabetic neuropathy


Q In diabetic neuropathy you can find each of

the following except:

1. Bradicardia

2. Urine retention

3. Impotence

4. Diarrhoea it night

5. Foot ulcer


Q A 50-year-old man got into a new relationship but

has recently found out about his erectile

dysfunction problem. He casually asks you for a

prescription of Viagra.

What should you do?

1. Prescribe him

2. Ask him to reduce alcohol

3. Reduce weight

4. Check testosterone levels

5. Check blood sugar


Q Patient with thigh muscle pain and weakness,

DM, HTN, and history of DVT, loss of knee reflex.

What is dx?

1. Diabetic sensory neuropathy

2. Arterial occlusion

3. Amyotrophy


Q A 78-year-old man with Dupuytren

contracture. His random blood sugar 6.8

mmol/L. No other abnormalities.

Which investigation you would do?

1. US of the hand

2. Biopsy of hand

3. Liver function test

4. Fasting blood glucose


Q A patient presented with 3rd nerve injury.

WOF refers to diabetes?

1. Intact pupillary reflex

2. Ptosis

3. Diplopia

4. Eye deviation


• Caused by peripheral neuropathy (80%), peripheral arterial

disease (10%), deformity (Charcot foot).

• Painless, punched – out.

• Most common localisation - first metatarsal area, heel.

• Investigations:

• Blood glucose levels

• ABPI, +/- Dupplex US (to rule out arterial disease).

• Microbiology swab (if signs of infection).

• X – ray of bone (if deep ulcer based on probe to bone).

Diabetic Ulcer


Courtesy: ROBERT G. FRYKBERG, D.P.M., M.P.H.,

(Des Moines University, Des Moines, Iowa),

Diabetic Foot Ulcers: Pathogenesis and Management. -

Am Fam Physician. 2002 Nov 1;66(9):1655-1663.

http://www.aafp.org/afp/2002/1101/p1655.html


• Management:

• Good foot hygiene and appropriate footwear.

• Glycaemic control (HbA1c < 7%).

• If not infected - Surgical debridement.

• If infected but no signs of cellulitis - Amoxycillin/Clavulanate

• If signs of cellulitis - Admit, Ticarcillin/Clavulanate I/V

• If no improvement - consider osteomyelitis:

- Next step X-ray; Best step MRI.

Diabetic Ulcer


Q What is the underlying cause in diabetic foot

ulcer ?

1. Peripheral arterial disease

2. Peripheral neuropathy

3. Infection

4. Venous stasis

5. Thrombosis


• Peripheral neuropathy (seen in up to 80% of diabetic

patients with foot ulcers) reduces awareness of pain and

trauma caused by footwear and foreign bodies in shoes.

• Peripheral vascular disease (seen in up to 10% of

patients) leads to local ischemia, increase the potential

for ulcer formation and can delay wound healing when

ulceration occurs.

• Autonomic neutopathy leading to anhidrosis can dry

out the skin and cause it to crack, so allowing a portal

of entry for INFECTION.

• Venous stasis and thrombosis predispose to venous

ulcer.


Q What is the most common site of the ulcer to

occur?

1. Medial site of the leg

2. Lateral side of the leg

3. Pulps of the fingers

4. First metatarsal head


Q A 63-year-old Aboriginal Australian with

ulcer on the foot is admitted to the hospital for

one week. He has type 2 DM and hypertension.

Foot ulcer is deep and is not healing after

debridement and treatment. Wound continued to

have yellow colored discharge.

What will you do next?

1. Ask podiatrist to review

2. Oral amoxicillin/clavulanic acid

3. MRI

4. Ticarcillin/clavulanic acid

5. Continue wound dressing


Diabetic Retinopathy


Diabetic Retinopathy Symptoms

• Seeing an increasing number of floaters

• Having blurry vision

• Noticing colours appear faded or washed out

• Having vision that changes sometimes from blurry to

clear

• Seeing blank or dark areas in your field of vision

• Having poor night vision

• Losing vision


• The appearance of neovascularisation in response to

retinal hypoxia is the hallmark of proliferative diabetic

retinopathy. These newly formed vessels appear near the

optic nerve and macula and rupture easily, leading to

vitreous haemorrhage, fibrosis, and ultimately retinal

detachment.


Courtesy:

http://www.eneurosurgery.com/wpimages/wp294790

30.png

Courtesy:

http://www.medindia.net/patients/patientinfo/images/

diabetic-retinopathy.jpg

Diabetic Non-Prolipherative

Retinopathy


Courtesy:

http://www.kseyes.com/Maculardegeneration.htm

Courtesy: Theodoropoulou S, Sallam A. Current

trends in the treatment of diabetic macular edema.

Egypt retina J 2014;2:26-34.

Diabetic Macular Oedema


Diabetic Prolipherative

Retinopathy

Courtesy: http://quizlet.com/9583200/eye-

pathology-flash-cards/

Courtesy:

http://www.yamout.us/information/fundus.jpg

http://quizlet.com/9583200/eye-pathology-flash-cards/








Courtesy:


30.png

Retinal Detachment with

Haemorrhage. Cataract.


Courtesy:


30.png

Vitreous Haemorrhage


Q A 47-year-old man complains of blurring of

vision. His blood pressure is 140/80 mmHg. He is

heavy smoker and drinks 100 grams alcohol per

day. The fundus is shown.

The most likely cause is:

1. Hypertension

2. Alcohol amblyopia

3. A secondary cerebral tumour

4. Diabetes mellitus


Courtesy: Annotated Multiple Choice Questions. Australian Medical Council (AMC). –

Blackwell Publishing, 2003, 410pp., Fig.7, p.8.


Q All of the following are causes of concern for

diabetic retinopathy, except?

1. Neovascularisation

2. Cotton wool spots

3. Orbital pain

4. Dot-blot haemorrhages

5. Microaneurysms


Q What is the main reason of diabetic

ketoacidosis in Australia?

1. Undiagnosed IDDM

2. Undiagnosed NIDDM

3. Foot infection in DM

4. Omitted dose of insulin


• An insulin dose must never be omitted in type 1

diabetes, even if the illness is accompanied by

nausea, vomiting or marked anorexia, as this

could lead to diabetic ketoacidosis.


Diabetes Ketoacidosis:

Clinical features: Polydipsia, polyuria, polyphagia, weight loss, fatigue.

Dehydration.

Confusion, Drowsiness, Coma.

Abdominal pain, nausea, vomiting.

Kussmaul breathing, odor of acetone.

Investigations:

Next step – ketones in serum or urine, if glucose > 15 mmol/L Best step – ABG: metabolic acidosis with respiratory compensation.

High AG. (Na + K) – (Cl + HCO3) = 8 – 16 mEq/L

Na – (Cl + HCO3) = 10 – 14 mEq/L

Other investigations:

Electrolytes (Na, K, PO4); PO; amylase/lipase, septic screen (Chest X-ray, blood culture, urine culture), ECG.


Diabetes Ketoacidosis:

Management:

Rehydration (normal saline IV 15/20 ml/kg/hour);

If Na corrected > 145 mmol/L – give half saline IV (look for symptoms of cerebral oedema)

Insulin short acting IV:

Monitor glucose every hour: when <15 mmol/L, start glucose 5% IV

Monitor K every 2 hours: when < 5.5. mmol/L, start KCl IV

Sodium bicarbonate if pH < 7.0

Broad spectrum a/b if evidence of infection

DVT prophylaxis


Sick Day Management:

• If the acute illness is not accompanied by persistent

nausea, vomiting, ketosis or worsening

hyperglycaemia, the patient can be managed at home.

• Blood glucose and urinary ketones should be monitored

frequently (every 1 to 4 hours).

• Typically the basal insulin requirement increases, and

correction doses of short-acting insulin are required.

• Adequate fluid intake.


6 year old child presenting with

abdominal pain , vomiting , no diarrhoea

and dehydrated, glucose high, (33)

What is initial investigation?

A-blood gas analysis

B- HBA1c

C- urine ketone


A child 6 YEARS old presented with upper

respiratory tract infection, urine examination

showed very high serum glucose and

ketonuria of 2+.

What is the most appropriate test?

A-HbA1C

B-serum creatinine and electrolyte

C-FBS

D-OGTT

E-Blood gases


Q A young man presents with a diabetic

ketoacidosis. His serum potassium is 6.1

His total body potassium is most likely:

1. Increased due to acidosis

2. Increased due to lack of insulin

3. Decreased due to acidosis

4. Decreased due to renal losses


Q the most important initial treatment of

ketoacidosis is:

1. Insulin

2. Normal saline

3. Potassium

4. Bicarbonate

5. Diuretics


Hypoglycaemia (blood glucose level fall less than 3.0 mmol/l).

• Causes: Drugs: salicylates, non selective B-blockers, TCA,

MAOI, ACE inhibitors.

• Samorgyi effect, Renal failure, Addison disease, GH deficiency,

Hypopituitarism, Insulinoma, Septicaemia, Starvation, Reactive

hypoglycaemia, Hypoglycaemia of infancy and childhood.

• Classic warning symptoms:

• Adrenergic symptoms: sweating, tremor, palpitations, hunger, peri-oral paraesthesia.

• Management: give something sweet by mouth (2 barley sugars, or 6 jelly beans, glass of lemonade, teaspoon of honey), followed by a snack.


• Neuroglycopaenic symptoms:

• Poor concentration, drowsiness, double vision, violent behaviour, focal neurological signs, LOC, seizure, coma.

• Management:

• Give glucagon 1 mg intramuscular or subcutaneous if available.

• If intravenous access is obtained, glucose 50% – 20 mL IV.

• Use 10% glucose 20 – 30 ml in children (50% glucose can cause

hyperosmolality and death).

• Phone for an ambulance (dial 000) stating a ‘diabetic emergency’.

• Admit to hospital.

• When the person regains full consciousness and can swallow, they

can then be orally given a source of carbohydrate.

• Review of medications, dietary intake, driving or licensing

requirements and hypoglycaemia management is mandatory.


Q A 19-year –old with DM type 1 is taking 30

units of NPH insulin each morning and 15 units

at night. Because of persistent morning

glucosuria with some ketonuria, the evening

dose is increased to 20 units. This worsens the

morning glucosuria, and now moderate ketones

are noted in urine. The patient complains of

sweats and headaches at night.

The next step in management is:

1. Increased the evening dose of insulin

2. Increased the morning dose of insulin

3. Switch to insulin NPH to pork insulin

4. Obtain blood sugar levels between 2.00 and 3.00 am.


Somorgyi Effect


• Episodic hypoglycaemia at night is followed by

rebound hyperglycemia. This condition, called

the Samorgyi phenomenon, develops in

response to excessive insulin administration. An

adrenergic response to hypoglycaemia results in

increased glycogenolysis, gluconeogenesis, and

diminished glucose uptake by peripheral tissues.

• The insulin dosage should be slowly reduced.


Q A 55–year–old man suffering from DM

presents to your practice. He complains of

sweating and dizziness during the night time for

the last several days. He has been taking short

acting insulin (Lispro) and intermediate – acting

insulin (Protaphane) in the morning and at night.

What would you advise him?

1. Increase the short - acting insulin at night

2. Decrease the short - acting insulin at night

3. Stop intermediate – acting insulin at night

4. Decrease the intermediate – acting insulin at night.


Q A child suffering from DM type 1 collapsed at

the school in the playground.

The most appropriate first action should be:

1. Assess his neurological status

2. Do a blood sugar test

3. Test the urine for ketones

4. 50% glucose IV

5. Insulin injection

6. Glucagon IM


Q A 59-year-old woman presents to your practise complaining of hypoglycaemia which occurs more often then usually during day and night time. She has been suffering from DM type 2 for almost 20 years. She has been taking intermediate - acting insulin for the last 5 years (in the morning before breakfast and in the evening before dinner). Her diet has not been changes for a long time.

What causes this symptoms:

1. Hepatic failure 2. Overdose of insulin 3. Renal failure 4. Undiagnosed infection


Q A 28-year-old woman with diabetes type1 suffers

from frequent episodes of hypoglycaemia over the

last few months. Her diet has not been changes for a

long time. She has reduced her insulin dose twice.

She also complains of lack of energy, muscle

weakness, dizziness on standing, weight loss,

vague abdominal pain and diarrhoea. O/E: BP 115/70

mmHg on sitting and 90/60 mmHg on standing.

What is the most appropriate investigation?

1. Check tissue transglutaminase antibody

2. Check thyroxin level

3. Check C-peptide

4. Immediate CT scan of the head

5. Check cortisol level


Q A man after peptic ulcer operation felt

nausea, vomiting, sweating, palpitations.

Symptoms appeared １ – ３ hours after meal.

What should be done to get the diagnosis?

1. US

2. Abdominal CT

3. Blood glucose

4. Endoscopy


• The diagnosis is ‘Late dumping’ due to rebound

hypoglycaemia and occurs 1 – 3 h after meals.

• Rapid delivery of a meal to the small intestine

results in a high concentration of carbohydrates in

the proximal small bowel and rapid absorption of

glucose causing hyperinsulinemic response.

• Intrajejunal glucose induces a higher insulin

release than does the intravenous infusion of

glucose. So inappropriate insulin response leads

to late hypoglycemia (reactive hypoglycemia).

• To get the diagnosis OGTT can be done and

gastric emptying scintigraphy.


Q A middle aged woman who is known HT and DM

type 2 on Perindopril, Amlodipin, Atorvastatin and

Amiloride. She was also on warfarin for AF. Her BP

was well controlled. HbA1C was 7.9%. Recently she

has been put on Gliclazide. After that she

developed three attacks of hypoglycemia.

What is the reason?

1. Perindopril

2. Amiloride

3. Amlodipine

4. Atorvastatine

3. Warfarin


• Perindopril belongs to ACE inhibitors. ACE

inhibitors potentiate hypoglycemic effect of other

drugs:

• They incease insulin sensitivity of peripheral

tissues;

• Block angiotensiogen II as one of the counter-

regulatory hormones.

• Other drugs: Aspirin, BB (non-selective), TCA,

MAOI.


Q Male patient brought to the ED in coma. He has

been drinking. He has a bracelet that says diabetic.

What could be the likely diagnosis?

1. DKA

2. Hypoglycaemic coma

3. Non-ketotic hyperosmolar coma

4. Alcoholic KA


Q A 2-year-old child brought by parents after a

party. Child is lethargic, irritable. Child has taken

sips from the drinks of adults.

What is the most appropriate initial investigation?

1. Blood gas analysis

2. Drug screen

3. Blood glucose

4. Electrolytes


Q A 4-year-old child wandering at 5 a.m. in

house. He did not remember anything. Urine

test shows +++ ketones.

What is the reason?

1. Ketotic hypoglycaemia

2. Hyperglycemic ketoacidosis

3. Epilepsy


Hyperglycaemia hyperosmolar non-ketonic coma.

• Only those with type 2 diabetes are at risk of hyperosmplar coma,

especially elderly.

• Clinical Features:

• The trigger usually is the concurrent condition causing

decompensation of diabetes (infection).

• The onset may be insidious over a period of weeks.

• Fatigue, polyuria, polydipsia.

• Marked dehydration (hyperosmolarity, marked

hyperglycaemia and hypernataremia).


• Management:

• Rehydration with 0.45% saline.

• Insulin with cautions to avoid rapid changes.

• Heparin to reduce the risk of DVT.

• Treat any concurrent condition.

• Prognosis: mortality is higher than in DKA.


Q A 50-year-old obese female is taking oral hypoglycemic agents. While being treated for URTI she develops lethargy and is brought to the emergency room. On physical exam, there is no focal neurologic findings or neck rigidity. She has marked dehydration (BP 120/80 sitting, 105/65 lying down) and very high level of hyperglycaemia (55 mmol/l), increased lever of sodium (149 mmol/L), osmolarity of plasma 356 mosm/kg (high). Acidosis is absent.

The most likely cause of this patient’s condition?

1. Diabetic ketoacidosis 2. Hyperosmolar coma 3. Inappropriate ADH 4. Bacterial meningitis


• Lactic Acidosis:

• Patient with lactic acidosis present with marked

hyperventilation ‘air hunger’ and confusion. It may occur in

patient taking metformin, especially if kidney function is

impaired.

• The investigations reveal blood acidosis with low pH, low

bicarbonate, high serum lactate, absent serum ketones and a

large anion gap.

• Management: Remove the cause. Bicarbonate therapy.


Q A patient suffering from DM type 2 and

hypertension on multiple drugs therapy

(gliclazide, metformine, diuretics, enalapril and

warfarin). ABG has been done for some reason:

CO2 low, pH 7.16, base excess low.

What was the case for this ABG?

1. Enalapril

2. Warfarin

3. Metformin

4. Gliclazide


MAIN REFERENCES:


• John Murtagh.

General Practice. McGraw Hill, 6th edition,

2015. – 1508pp.

• J.Larry Jameson.

Harrison’s Endocrinology. McGraw Hill

Medical, 2nd edition, 2010. – 549pp.

• Endocrinology Expert Group.

Therapeutic Guidelines. Version 5.

Therapeutic Guidelines Limited, Melbourne.

2014. – 420pp.


• Henry M.Kronenberg, Sholmo Melmed, Kenneth S.Polonsky, P.Reed Larsen.

Textbook of Endocrinology. 11th edition. Saunders Elsevier. 2008. – 1911pp.

• Australian Medical Council.

Handbook of Multiple Choice Questions. 2009. – 805pp.

• Murray Longmore, Ian Wilkinson, Tom Turmzei, Chee Kay Cheung.

Oxford Handbook of Clinical Medicine. 7th edition. Oxford University Press. 2007. – 841pp.


• Steven L.Berk, William R.Davis, Robert S.Urban.

Pre-Test Medicine. Pre-Test Self-Assessment

and Review. – 10th edition. McGraw-Hill,

Medical Publishing Division. 2004.

• RACGP guideline.

Best practice guidelines 2016 - 2018.

mcq bridging course: endocrinology

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