Endocrinology

Question 1

Criteria for diagnosis of DM?

Answer 1

Random fasting glucose of 11.1
OGTT 2 hr glucose of 11.1
Random plasma glucose of 7
HBA1C of 6.5%

Question 2

Name 3 antibodies associated with T1DM.

Answer 2

anti-insulin AB
anti-GAD
islet auto-antigen 2 (IA2)

Question 3

What clinical features might DM present with?

Answer 3

URINE: polyuria, nocturia
THIRST: polydipsia
BLURRED VISION
WEIGHT LOSS, FATIGUE
DKA:
- GIT: nausea and vomiting, abdominal pain
- NEURO: lethargy, drowsiness, decreased LOC, coma
- RESP: tachypnoea, Kussmaul breathing, fruity breath

Question 4

What HBA1C should you aim for in DM?

Answer 4

<7%

Question 5

How might you monitor a patient with DM?

Answer 5

Self-monitoring of BGL

HBA1C every 3-6 months

Question 6

What is the treatment of hypoglycemia in an adult?

Answer 6

DRSABCD
Assess LOC
If oral intake safe, 15g PO carbohydrates - e.g. glucose tablet, juice.
Measure BGL again in 15 min - repeat above is <3.9.
If oral intake unsafe, establish IV access:
- IV bolus 50% dextrose
If no IV access:
- IM glucagon
- Establish IV access.
Close monitoring.
Endocrine consult - optimize insulin regime, education e.g. re food intake, exercise, sick day planning.

Question 7

How would you treat DKA?`

Answer 7

DRSABCD, LOC, Vital signs

Assess volume status and begin rehydration - start 0.9% saline infusion starting at 1L/hr.

Insulin: start with SC insulin, followed by insulin infusion in normal saline.
When blood glucose falls to <15 mmol/L - continue insulin infusion, switching from normal saline to 5% dextrose.

K:
Initial K < 3.5 –> give K, don’t start insulin until with K < 3.5
Initial K 3.5-5.5 –> start K replacement
Initial K >5.5 –> delay K replacement until <5.3.
Aim to maintain K at 4-5 mmol/L.

Close monitoring: esp. BGL, ABG and EUCs.

Question 8

What is Addison’s disease? What are the common causes?

Answer 8

Addison’s disease is primary adrenal insufficiency - caused by dysfunction of the adrenal cortex –> insufficient cortisol and insufficient aldosterone.
Caused by:
- Autoimmune (most common)
- Infection: TB, HIV

Question 9

What are the clinical features of Addison’s disease?

Answer 9

Non-specific clinical fx:
VITALS: orthostatic hypotension, fever
SYSTEMIC: fatigue, weakness, anorexia, weight loss
GENERAL INSPECTION: skin and gum pigmentation
CNS: headache, psychiatric (anxiety, irritability, depression)
ABDO: pain, N&V, diarrhoea
MSK: pain - myalgia, arthralgia

Question 10

What lab findings would you expect in Addison’s disease?

Answer 10

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

Question 11

How would you treat Addison’s disease?

Answer 11

1. Education + sick day plan + medic alert bracelet
2. Replace corticosteroid
   - hydrocortisone PO BD or TDS - mimic the normal circadian rhythm or cortisol release (higher dose in morning)
   - increase the dose if stress (e.g. infection, surgery, trauma)
3. Replace mineralocorticoid (may not be necessary if disease is mild).
   - fludrocortisone
4. Consider need for DHEA replacement
5. Watch for acute adrenal crisis and treat if occurs –>
   - IX: if suspect acute adrenal crisis order urinalysis, FBC, EUC, BGL, serum cortisol, plasma ACTH, blood cultures
   - WITHOUT waiting for results, begin immediately: hydrocortisone, IV fluids, empirical broad spectrum ABX (often occurs due to infection) plus treat any hypoglycaemia or electrolyte abnormalities.

Question 12

What are the causes of Cushing’s syndrome?

Answer 12

EXOGENOUS
- corticosteroid treatment (most common cause)
ENDOGENOUS
- Cushing disease - i.e. ACTH-secreting pituitary adenoma
- Ectopic ACTH-secreting tumour - commonly SCLC
- Adrenal disease - hyperplasia, adenoma, carcinoma

Question 13

List clinical features of Cushing’s syndrome.

Answer 13

VITALS: hypertension
GENERAL INSPECTION:
acne, plethora, moon face, buffalo hump, central obesity, abdominal striae, thin extremities
skin: thin skin, bruising, possibly hyperpigmentation (if ACTH increased)
NEUROPSYCH:
- decreased concentration, executive dysfunction, labile mood, irritability, depression, anxiety, psychosis
MSK: proximal muscle atrophy –> weakness; osteoporosis –> fragility fracture –> loss of height, back pain etc.
ENDOCRINE: hyperglycaemia, diabetes mellitus
IMMUNO: poor wound healing, immunosuppression –> infections
GYN/URO:
Oligomenorrhoea, amenorrhoea, infertility, female virilization
Erectile dysfunction, decreased libido

Question 14

How would you diagnose suspected Cushing’s syndrome?

Answer 14

SCREENING:
1. Late night salivary cortisol or
2. Low dose (1mg) overnight dexamethasone suppression test
CONFIRMATORY:
If abnormal screening test -->
1. 24 hour urinary free cortisol
2. 48hr dexamethasone suppression test
FURTHER INVESTIGATION OF CAUSE:
Consider:
- plasma ACTH
- Imaging: CT chest & abdomen, MRI pituitary

Question 15

Primary hyperaldosteronism -
COMMON CAUSES
CLINICAL FX

Answer 15

Primary hyperaldosteronism is caused by:
1. Bilateral adrenal cortical hyperplasia
2. Adrenal cortical adenoma
Clinical features:
- Treatment-resistant hypertension!!
- May cause hypokalaemia –> muscle weakness

Question 16

Outline how you would diagnose suspected Addison’s disease.

Answer 16

ACTH stimulation test –> will show failure of expected rise in cortisol level

Question 17

Explain the aetiopathogenesis and clinical features of hyperglycaemic hyperosmolar syndrome.

Answer 17

Relative insulin deficiency in setting of stressor (e.g. infection, ischemia, dehydration) –> enough insulin to prevent ketogenesis, but insufficient to stop hepatic gluconeogenesis/glycogenolysis and peripheral glucose uptake –> hyperglycaemia

Hyperglycaemia leads to:

(1) Hyperosmolality –> fluid shifts out of cells in brain –> mental status change, focal neurologic signs, seizures, coma
(2) Polyuria, polydipsia –> dehydration

Question 18

Explain how you would treat HHS.

Answer 18

DRSABCD.
Admit.

Rehydration: IV cannula + aggressive IV fluids (1L NS in first hr, then titrate down)

Do NOT begin insulin infusion initially –> causes too rapid a drop in osmolality. Once glucose is no longer improving with IV fluids alone, then administer IV insulin bolus followed by infusion. As patient improves (normal osmolality and mental status achieved) –> switch to SC insulin.

Correct electrolyte disturbance
- insulin shifts K into cells - frequently causes hypokalaemia.
Do not give insulin if K < 3.3.
Do not give K if K >5.2.
If K 3.3-5.2 administer 30mmol/L K with every 1 L fluids.

Close monitoring of hydration status, BGL and EUCs.

Referral to endocrinology.
Seen by diabetes educator.
Plan for discharge - with appropriate insulin/oral diabetes medications arranged.