Title: Endocrine

Q: What is Addison's disease?
A: Primary adrenal insufficiency with reduced cortisol and aldosterone

Q: Most common cause of Addison's worldwide?
A: TB

Q: Most common cause of Addison's in developed countries?
A: HIV

Q: Presentation of Addison's
A: Haemodynamic collapse, hyponatraemia, hyperkalaemia, lactic acidosis, hypoglycaemia, vitiligo, hyperpigmentation

Q: How does secondary adrenal insufficiency differ from primary?
A: In secondary, aldosterone production is unhindered so DO NOT get hyperkalaemia

Q: DDx of Addison's disease
A: Autoimmune
Adrenal haemorrhage (Waterhouse-Friederichsen in meningococcal)
Drugs - Ketoconazole
Infection - TB, fungal, sepsis, HIV
Infiltrative - Sarcoidosis, Amyloidosis, Haemochromatosis
Metastatic pulmonary cancer
Bilateral adrenalectomy
Hereditary - Congenital adrenal hyperplasia

Q: DDx of secondary adrenal insufficiency
A: Long-term steroid use
Post-partum pituitary necrosis (Sheehan's syndrome)
Pituitary tumor
Hypothalamic tumor
Craniopharyngioma
Pituitary irradiation/surgery

Q: Does secondary adrenal insufficiency result in hyperkalaemia?
A: No. Have intact aldosterone production

Q: Treatment of Addisonian crisis
A: IV hydrocort 250mg stat then 100mg QID
 - Can use dexamethasone is diagnostic testing is planned
Fludrocortisone 1mg IV daily if in shock
N/S resuscitation fluid
N/S + 5% dextrose maintenance
Treat hypoglycaemia, hyponatraemia, hyperkalaemia
Find and treat underlying cause

Q: Stress dosing of hydrocortisone
A: Mildly unwell - IV hydrocortisone 25mg daily
Moderate - 50mg daily then taper over 1-2 days to usual dose
Severe - 100mg daily then taper over 1-2 days once well to usual dose
Critically ill - 50mg QID then gradual taper

Q: How much more potent is prednisone than hydrocort?
A: 4x

Q: How much more potent is methylpred than hydrocort?
A: 5x

Q: How much more potent is methylpred than prednisolone?
A: 1.25x but minimal mineralocorticoid effect

Q: How much more potent is dexamethasone than prednisone?
A: 10x

Q: Does dexamethasone have mineralocorticoid effect?
A: No

Q: What did CORTICUS show?
A: Hydrocort 50mg QID in septic shock showed more rapid reversal of shock with increased risk of infection and no improvement in mortality

Q: What did ADRENAL show?
A: Hydrocortisone 200mg/day infusion showed no improvement on mortality but did show more rapid improvement in shock, ventilator free days and ICU LOS

Q: When are steroids indicated in septic shock?
A: Refractory to fluids and vasopressors/inotropes

Q: Side effects of steroid therapy
A: Cushingoid
Increased infection risk
Pancreatitis
Adrenal suppression
Myopathy
Hyperglycaemia
Leukocytosis
Impaired wound healing
Peptic ulcer disease

Q: When is alcoholic ketoacidosis seen?
A: 1-3 days after acute alcohol cessation in chronic alcoholics

Q: How does alcoholic ketoacidosis arise?
A: Alcohol metabolism in the absence of sufficient glycogen stores results in ketonaemia due to NAD depletion and counter-regulatory hormone release driving acetyl-coA to beta-hydroxybutyrate

Q: Why is early alcoholic ketoacidosis not picked up on ketosticks?
A: predominantly beta-hydroxybutyrate due to NAD depletion preventing conversion to acetoacetate

Q: Which ketones are measured on ketosticks?
A: Acetone

Q: Why does an osmolar gap arise after alcoholic ketoacidosis?
A: Beta-hydroxybutyrate eventually gets converted to acetone, which adds to osmolar gap

Q: Criteria for alcoholic ketoacidosis
A: Low, normal or slightly elevated glucose
Binge drinking ending in vomiting and reduced oral intake
Positive serum ketones
HAGMA without explanation

Q: Treatment of alcoholic ketoacidosis
A: Thiamine 300mg IV before glucose
N/S + 5% dextrose
Multivitamin
Phosphate and Mg supplementation

Q: Is insulin indicated in alcoholic ketoacidosis?
A: No proven benefit and may be dangerous in the setting of normal or low glucose levels

Q: What is Conn's syndrome?
A: Primary hyperaldosteronism

Q: How does Conn's syndrome present?
A: Triad - Hypokalaemia, HTN, metabolic alkalosis

Q: DDx of Conn's syndrome
A: Aldosterone-producing adenoma
Ectopic aldosterone-producing tumor
Bilateral adrenal hyperplasia
Aldosterone-producing adrenocortical carcinoma

Q: How do you differentiate Conn's from Cushing's?
A: Cushing's usually have morphologic features e.g. moon facies

Q: Define diabetes insipidus
A: Polyuria >3L/day, excessive thirst, polydipsia

Q: Types of diabetes insipidus
A: Nephrogenic
Central
Gestational

Q: How does ADH/vasopressin work?
A: Increases AQP-2 membrane localisation to increase water reabsorption

Q: DDx of water diuresis
A: Diabetes insipidus
Psychogenic polydipsia
Iatrogenic

Q: DDx of solute diuresis
A: Resolving sepsis/third-spacing
Iatrogenic - N/S, Hartmann's, hypertonic saline
RTA
Glomerulonephritis
Paroxysmal SVT (ANP release)
Ethanol
Methanol
Ethylene glycol
Mannitol
Loop diuretics
Thiazides
Hyperglycaemia

Q: How do you differentiate solute from water diuresis?
A: Spot urine osmolality >300 suggests solute diuresis
Spot urine osmolality <300 suggests water diuresis

Q: What does high serum osmolality >295 and low urine osmolality (<1000mOsm/kg) suggest?
A: Impaired renal concentrating ability
 - Diabetes insipidus (Uosm < 150)
 - Loop diuretics

Q: What does high plasma osmo (>295) and high urine osmo (>1000mOsm/kg) with polyuria suggest?
A: Solute diuresis
 - If osmolar gap >10: Methanol, ethanol, mannitol, sorbitol
 - osmolar gap <10: Hyperglycaemia, hyperkalaemia, hypernatraemia

Q: DDx of acquired central diabetes insipidus
A: Autoimmune
Tumors
Surgery
Base of skull fracture
Hypoxic brain death
Radiotherapy
Amiodarone
Lithium (rarely - normally nephrogenic)
Sickle cell disease
TB
Meningoencephalitis
Sheehan's
Pituitary apoplexy

Q: How does congenital nephrogenic diabetes insipidus present?
A: X-linked recessive so typically young boys with polyuria, hypernatraemia and dehydration

Q: DDx of acquired nephrogenic DI
A: Lithium
Hypercalcaemia
Hypokalaemia
Post-obstructive diuresis
Hypoproteinaemia

Q: What proportion of chronic lithium patients have DI?
A: 20% have nephrogenic DI

Q: How does lithium cause nephrogenic DI?
A: Taken up into principal cells and inhibits adenylyl cyclase to inhibit effect of ADH

Q: Treatment of nephrogenic DI
A: Stop causative agent
Correct hypokalaemia/hypercalcaemia/hypoproteinaemia
Reduce solute load (salt intake)
Thiazides causes solute loss > water loss and a drop in intravascular volume to upregulate RAS
Supplemental ADH (if not absolutely resistant)
NSAID's reduce GFR and renal flow

Q: What proportion of diabetes is type 1?
A: 5-10%

Q: Diagnosis of diabetes mellitus?
A: Fasting plasma glucose >7.0
Random plasma glucose >11.1 AND symptoms of hyperglycaemia
OGTT 2hr plasma glucose >11.1
HbA1c >6.5%

Q: DDx of Diabetes
A: Autoimmune (classic)
Chronic pancreatitis
Pancreatic carcinoma
Haemochromatosis
CF
Gestational
Cushing's
Phaeochromocytoma
Steroid-induced
COCP
Tacrolimus
Cyclosporin
HIV protease inhibitors
Acromegaly

Q: How does diabetes cause immunosuppression?
A: Phagocyte dysfunction
 - Impaired adherence, phagocytosis, bacterial killing and respiratory burst
Non-enzymatic glycation of immunoglobulins
Reduced T cell populations

Q: Classic presentation of T2DM
A: Fatigue, lethargy, polyuria, polyphagia, polydipsia

Q: Target HbA1c in diabetes?
A: <7.5% without frequent hypoglycaemic episodes
<6.5% if increased risk of arterial disease

Q: Does strict glycaemic control prevent macrovascular disease?
A: No. Prevents microvascular disease only

Q: Onset of novorapid
A: 5-15 min

Q: Peak of novorapid
A: 1-2 hours

Q: Duration of novorapid
A: 4-5 hours

Q: Onset of lantus
A: 2-4 hours

Q: Peak of lantus
A: 8-10 hrs

Q: Duration of lantus
A: 18-30hrs

Q: How does metformin work?
A: Reduces hepatic glucose production and enhances peripheral uptake of glucose

Q: How does pioglitazone work?
A: Reduces insulin resistance

Q: What are the three new generation diabetes drugs?
A: DPP-4 inhibitors e.g sitaglitpin (Januvia)
 - Prolongs action of incretins
GLP-1 inhibitors e.g. Exenatide (Byetta)
 - Reduces post-prandial hepatic glucose production and enhances peripheral glucose uptake
SGLT-2 inhibitors e.g. empaglifozin
 - Blocks renal glucose reabsorption

Q: Benefit of insulin pumps
A: Reduces hypoglycaemic episodes and HbA1c

Q: Why are T1 diabetics at increased risk of hypoglycaemia?
A: Strictly controlled, lack glucagon surge and adrenaline surge can be blunted due to autonomic dysfunction, age and neuropathy

Q: Classic triad of hypoglycaemia
A: Symptoms of hypoglycaemia
BSL <2.8
Symptoms resolve with administration of glucose

Q: Triggers of diabetic hypoglycaemia
A: Stress, infection, exercise, MI, excess insulin, renal failure, ethanol

Q: Treatment of diabetic hypoglycaemia
A: If conscious - 20g low and high GI meals
If unconscious - 50mL 50% dextrose or glucagon 0.5-1mg IM

Q: What is faster, oral glucose or glucagon IM?
A: Oral glucose

Q: How long does IM glucagon take to work?
A: 7-10min

Q: DDx of hypoglycaemia
A: Insulin overdose (accidental or intentional)
Exercise
Sulfonylureas
Beta-blockers
Valproate
Ethanol
Liver disease
Sepsis
Critical illness
Anorexia nervosa
GI dumping syndrome
Adrenal insufficiency/Addison's
Hypopituitarism
Insulinoma
Munchausen
Suicide attempt

Q: What is the Somogyi effect?
A: Excessive nocte insulin leads to overnight hypoglycaemia and rebound morning hyperglycaemia
 - Diagnosed by 0200 BSL

Q: Chronic complications of diabetes
A: Microvascular - Retinopathy, nephropathy, peripheral neuropathy
Macrovascular - CVA, MI, PVD
Non-vascular
 - Infections, sexual dysfunction, gastroparesis, cataract, dermatopathy

Q: How much higher is risk of CAD in diabetics?
A: 2-4 fold

Q: Stroke risk in diabetics?
A: 3-fold

Q: PVD risk in diabetics?
A: 2-4 fold

Q: Triad of diabetic nephropathy
A: HTN, proteinuria, renal impairment

Q: Neurological complications of diabetes
A: Subclinical neuropathy
Diffuse clinical neuropathy (glove and stocking + autonomic)
Focal neuropathy (sudden and painful)

Q: How does diabetic autonomic neuropathy present?
A: Resting tachycardia
Orthostatic hypotension
Diarrhoea
Constipation
Gastroparesis
Erectile dysfunction
Neurogenic bladder

Q: What is rhinocerebral mucormycosis?
A: Invasive fungal infection seen in diabetics of the sinuses
Black eschar on nasal mucosa or hard palate is classic

Q: Predominant bacterium in diabetic foot ulcers?
A: S. aureus but classically polymicrobial

Q: +LR for osteomyelitis with ulcer area >2cm2?
A: 7.2

Q: +LR for osteomyelitis if ESR >70
A: 11

Q: Define mild diabetic ulcer?
A: <2cm of surrounding cellulitis, not systemically unwell, negative probe to bone test

Q: Treatment of mild infected diabetic foot ulcers
A: Augmentin 875/125 BD with outpatient f/u

Q: Define complicated diabetic foot ulcers?
A: Positive probe to bone, X-ray evidence of osteomyelitis, >2cm surrounding cellulitis, systemically unwell, lymphangitis, purulent discharge, necrotic/gangreous tissue, associated limb ischaemia

Q: Treatment of complicated diabetic foot ulcers
A: PipTaz 4.5g QID + admit for consideration of debridement/MRI

Q: Signs of non-proliferative diabetic retinopathy
A: Microaneurysm
Hard exudates
Flame haemorrhages
Dot haemorrhages
Cotton wool spots
Venous tortuosity and beading

Q: Signs of proliferative diabetic retinopathy
A: Neovascularisation
Rubeosis iridis

Q: What is this?
A: Proliferative diabetic retinopathy

Q: What is this?
A: Non-proliferative diabetic retinopathy

Q: DDx of diabetic skin complications
A: Acanthosis nigricans
Necrobiosis lipoidica
Diabetic dermopathy
Scleroderma
Granuloma annulare
Diabetic bullae
Skin tags
Nec fasc
Rhinocerebral mucormycosis
Malignant otitis externa

Q: What is acanthosis nigricans?
A: Hypertrophic, hyperpigmented plaques in skin folds

Q: What is this?
A: Oval violaceous patch with red border and brown central area

Q: What is this?
A: Necrobiosis lipoidica

Q: What is diabetic dermopathy?
A: Lower extremity shin spots hyperpigmentation

Q: What is this?
A: Diabetic scleroderma

Q: What is this?
A: erythrasma due to diabetes-associated Corynebacterium minutissimum infection

Q: What is this?
A: Rhinocerebral mucormycosis

Q: How does diabetic ketoacidosis arise?
A: Insulin deficiency leads to hyperglycaemia and counter-regulatory response with subsequent ketosis

Q: Why does potassium depletion occur in diabetic ketoacidosis?
A: Osmotic diuresis leads to RAS upregulation and Na retention/K wasting

Q: DDx of DKA precipitant
A: Insulin non-compliance/pump failure
Sepsis
MI
Stroke
Pregnancy
Steroids
PE
Pancreatitis
Major trauma
Surgery

Q: Why does DKA often present with abdominal pain?
A: Prostaglandin synthesis + acidosis

Q: Definition of DKA in adults
A: pH <7.3 or bicarb <15
Ketones >3mmol/L or 2+ on urine
BSL >11

Q: Define severe DKA
A: pH <7.1, Bicarb<5, K <3.5, GCS <12, SBP <90 or SpO2 <92%

Q: Why might liver patients present with DKA atypically?
A: Lack of hepatic glycogen stores means lower glucose levels

Q: Which patients are at risk of euglycaemic DKA?
A: Ethanol abuse (impaired gluconeogenesis)
SGLT-2 inhibitors
liver failure (impaired gluconeogenesis/glycogen stores)

Q: How does severe vomiting alter presentation of DKA?
A: May not be acidaemic as have concomitant metabolic acidosis and metabolic alkalosis

Q: DDx of diabetic ketoacidosis
A: Starvation ketosis (glucose low/normal)
Alcoholic ketosis (glucose low/normal)
AKI
Lactic acidosis
Toxic alcohol ingestion
Salicylate poisoning

Q: Average free water deficit in DKA
A: 100mL/kg (5-10L)
10% BW

Q: Average sodium deficit in DKA?
A: 10mmol/kg

Q: Average K deficit in DKA?
A: 5mmol/kg

Q: Fluid regime in DKA
A: 1L over 30-60min
1L over 2 hours + K
1L over 2 hours + K
1L over 4 hours + K

Q: When is dextrose added to therapy in DKA?
A: 10% dextrose at 125mL/hr once BSL <15

Q: When is K added to fluids in DKA?
A: Once K <5 and making urine
If K 3.5 - 5: 10mmol/100mL over 1 hour
If K <3.5: 2x 10mmol/100mL over 1 hour

Q: When should insulin be started in DKA?
A: Within 60min of arrival as long as K >3.5

Q: Target drop in BSL in DKA
A: 3mmol/L/hr

Q: Insulin regime in DKA
A: 0.1U/kg/hr (max 6U/hr)

Q: Free water deficit calculation
A: 0.6 x Weight x (Current Na/140 - 1)

Q: How common is cerebral oedema in DKA?
A: 0.5-1.0%

Q: When does cerebral oedema usually occur in DKA?
A: 4-12 hours after initiation of therapy

Q: Is there any evidence of any association between volume or type of IV fluids or rate of change of glucose and cerebral oedema?
A: No

Q: Warning signs of cerebral oedema in DKA
A: Severe headache
Incontinence
ALOC
BP changes
Seizures
bradycardia
Altered temperature regulation

Q: Best indicator of improving DKA
A: Anion gap resolution NOT bicarb
Patient retains Cl- in exchange for ketones so get hyperchloraemic acidosis during recovery phase

Q: HHS mortality vs. DKA
A: 2-3x

Q: How much more common is DKA than HHS?
A: 6x

Q: Most common causes of death in DKA?
A: Pneumonia, MI, ischaemic gut

Q: What is Cushing's disease?
A: Hyperadrenalism due to pituitary adenoma

Q: DDx of Cushing's syndrome
A: Cushing's disease (adenoma)
Adrenal carcinoma
Adrenal hyperplasia
ACTH-secreting tumor
Exogenous (MOST COMMON)

Q: Presentation of Cushing's syndrome
A: Moon facies, hyperglycaemia, metabolic syndrome, truncal obesity, hirsutism, hypertension, fatigue, hypernatraemia, hypokalaemia, metabolic alkalosis, proximal myopathy, striae, easy bruising, reduced libido, amenorrhoea, depression, psychosis

Q: Total body water deficit in HHS
A: 100-220mL/kg (much higher)
10-20%

Q: Why don't HHS have ketoacidosis?
A: Remnant insulin production (at least 10%)

Q: Causes of HHS
A: Non-compliance
Pneumonia
UTI
Cocaine

Q: Predisposing drugs to HHS
A: Cocaine
Diuretics
Beta-blockers
Mannitol
Glucocorticoids
Neuroleptics
CCB

Q: What proportion of HHS present with seizures?
A: 15% and usually focal

Q: Definition of HHS
A: BSL >30
Serum osmo >320
Hypovolaemia
Ketones <3 or <2+ on dipstick
pH >7.30, bicarb >15

Q: Criteria for severe HHS
A: Osmolality >350
Na >160
Creatinine >200
UO < 0.5mL/kg/hr
GCS <12
SBP <90
SpO2 <92% on RA
pH <7.1

Q: Fluid therapy in HHS
A: Calculate deficit (0.6xbody weight x (Current Na/140 - 1) and replace 50% over first 12 hours and then rest over next 24 hours

Q: When is insulin started in HHS?
A: Once fluids started and K >3.5

Q: Initial insulin rate in HHS
A: 0.05U/kg/hr (max 3U/hr)

Q: Target drop in glucose in HHS
A: 5mmol/L/hr

Q: Complications in HHS
A: Hypoglycaemia
Hypokalaemia
APO
DVT

Q: Poor prognostic factors for HHS
A: High urea (strongest predictor)
Older age
Hypotension
Hyponatraemia
Hypernatraemia
Critical metabolic acidosis

Q: T4:T3 ratio in normal serum
A: 20:1

Q: How much more potent is T3 than T4?
A: 3-4 times

Q: DDx of primary hyperthyroidism
A: Graves (85%)
Toxic multinodular goitre
Toxic adenoma
Hashimoto's (early)
Subacute painful thyroiditis (deQuervain's)
Subacute painless thyroiditis
Radiation thyroiditis

Q: DDx of secondary hyperthyroidism
A: Thyrotropin-secreting pituitary adenoma
Exogenous thyroxine

Q: Drug-induced hyperthyroidism
A: Iodine-induced (Jod-Basedow effect)
Amiodarone
Thyroxine
Munchausen
Beef thyroid tissue ingestion

Q: How does thyroid storm arise?
A: Hyperthyroidism with subsequent stimulus for increased receptor binding or sensitivity
e.g. MI, infection, DKA, iodine, CVA, PE, delivery, eclampsia

Q: Presentation of hyperthyroidism
A: Weakness (remember thyrotoxic hypokalaemic periodic paralysis, fatigue, palpitations, hypertension, sweating, weight loss, anxiety, emotional lability, diarrhoea and hair loss

Q: Examination findings in hyperthyroidism
A: Agitated
Fever
AF
Sinus tachycardia
Fine tremor
Hyperreflexia
Lid lag
Proptosis
Ophthalmoplegia
Exophthalmos
Thyroid enlargement/bruit
Gynaecomastia
Telangiectasia
Pretibial myxoedema
Palmar erythema

Q: What is the tremor like in hyperthyroidism
A: Fine tremor

Q: What proportion of thyrotoxic individuals have AF?
A: 10-35%

Q: How does thyroid storm present?
A: Thyrotoxic symptoms + fever/CVS instability and CNS dysfunction

Q: DDx of thyroid storm
A: Sympathetic overdose
Serotonin syndrome
Malignant hyperthermia
Neuroleptic malignant syndrome
CNS meningoencephalitis
Sepsis
Phaeochromocytoma
Anticholinergic
Exposure hyperthermia

Q: Most common cause of thyroid storm
A: Untreated Graves

Q: What is apathetic hyperthyroidism
A: Paradoxical presentation of hyperthyroidism with apathy, depression, hyporeflexia

Q: TSH low, T3/4 high
A: Primary hyperthyroidism

Q: TSH high, T3/4 high
A: Secondary hyperthyroidism

Q: TSH slightly low, T3/4 normal
A: Subclinical hyperthyroidism

Q: Treatment of hyperthyroidism
A: Thiamine 300mg IV
IV N/S + 5% dextrose
Beta-blockers
 - IV propranolol 0.5mg increments to 10mg
 - PO propranolol 1mg/kg PO QID
 - Consider esmolol if underlying heart disease/asthma
Propylthiouracil 1200mg PO then 300mg q4h
Lugol's iodine 30 drops BD in divided doses
Hydrocortisone 100mg IV QID
Look for precipitant

Q: Why do beta-blockers help in thyrotoxicosis
A: Most important factor in reducing morbidity and mortality
Inhibit peripheral effects and inhibit conversion of T4 to T3

Q: What is the role of propylthiouracil in thyrotoxicosis?
A: Blocks iodination of tyrosine to inhibit synthesis and prevent peripheral conversion of T4 to T3

Q: What does Lugol's iodine do in thyrotoxicosis?
A: Prevents synthesis of new thyroid hormone

Q: What does hydrocortisone do in thyrotoxicosis?
A: Prevents peripheral conversion of T4 to T3 and treats any coincident relative adrenal insufficiency

Q: Mortality of thyroid storm
A: ~50%

Q: Which patients typically have apathetic hyperthyroidism?
A: Elderly with CCF, ALOC and absence of usual signs
Much higher mortality

Q: DDx of hypopituitarism
A: Pituitary adenoma
Tumor
Pituitary inflammation/infection
irradiation
Sheehan's
TBI
SAH

Q: How does pituitary insufficiency present?
A: Usually pale (lack of MSH secondary to lack of ACTH), hypotensive, metabolic alkalosis, hypoglycaemic, growth disturbance, loss of libido, amenorrhoea, infertility

Q: Does pituitary insufficiency result in hypoaldosteronism?
A: No. Get lack of cortisol but not aldosterone, hence not hyperkalaemic

Q: Treatment of hypopituitarism
A: Hydrocortisone 250mg IV stat then 100mg QID
IV T4 4mcg/kg stat
Correct any electrolyte disturbance
Treat underlying cause

Q: DDx of hypothyroidism
A: Primary
 - Hashimoto's
 - Thyroiditis
 - Iodine deficiency
 - Post-radiation/surgery
 - Infiltrative (lymphoma, sarcoid, amyloid)
 - Drugs (amiodarone, iodine, lithium)
 - Idiopathic
Secondary
 - Hypopituitarism
 - Hypothalamic tumors
 - Brain irradiation

Q: Symptoms of hypothyroidism
A: Lethargy, malaise, cold intolerance, irregular periods, depression, weight gain, infertility

Q: Signs of hypothyroidism
A: Periorbital oedema
Loss of outer third eyebrow
Hoarse voice
Macroglossia
Bradycardia
Reduced bowel sounds
Myxoedema (non-pitting)
Bradyreflexia
Peripheral neuropathy
Cool dry skin
Hypothermia

Q: What is myxoedema crisis?
A: Multiorgan dysfunction from hypothyroidism with triad of:
Mental status changes, hypotension and hypothermia

Q: DDx of myxoedema crisis
A: Environmental hypothermia
Addisonian crisis
Hypopituitarism
Sepsis
Depression
Sedative overdose

Q: what proportion of myxoedema crises are hypothermic?
A: 75%

Q: What does normothermic myxoedema crisis suggest?
A: Infectious precipitant

Q: Precipitants of myxoedema crisis
A: Infection
Non-compliance with thyroxine
Anaesthetic agents
Cold exposure
MI
CCF
CVA
GI haemorrhage
Surgery
Burns
Beta-blockers
Sedatives
Narcotics

Q: High TSH, low T3/4
A: Primary hypothyroidism

Q: Low TSH, low T3/4
A: Secondary hypothyroidism

Q: Treatment of myxoedema crisis
A: ABCDE
IV dextrose if hypoglycaemic
Passive rewarming (active risks vasodilation and worsening shock state)
Hydrocortisone IV 200mg (before T3/4)
IV T4 4mcg/kg stat
IV T3 20mcg stat (10mcg in elderly) then 10mcg TDS
Find and treat cause

Q: Which thyroid hormone is preferred in the elderly for treatment of myxoedema crisis?
A: T4 (less potent and less risk of arrhythmia/MI)

Q: Why is T4 alone not given in myxoedema crisis?
A: Needs to be converted to more potent T3 for action
Does not cross BBB as well as T3
Slow onset of action

Q: Mortality of myxoedema coma
A: ~50%

Q: Poor prognostic factors in myxoedema crisis
A: Elderly
Hypotensive
Bradycardia

Q: How common is hypothyroidism in pregnancy?
A: 1-2%

Q: How common is subclinical hypothyroidism in pregnancy?
A: 2.5%

Q: Does subclinical hypothyroidism need treatment?
A: Only if pregnant

Q: What proportion of hypertensive patients have phaeos?
A: 0.2%

Q: What proportion of phaeos are familial?
A: 40%

Q: What proportion of patients with phaeos are symptomatic?
A: 50%

Q: Classic triad of phaeo
A: Episodic headache, sweating and tachycardia

Q: What proportion of phaeo patients are normotensive?
A: 10%

Q: What proportion of phaeo patients have headaches?
A: 90%

Q: When do paroxysmal hypertensive episodes occur with phaeos?
A: Random
Diagnostic procedures
Surgery
Induction of anaesthesia
Tyramine intake
Beta-blockers
TCA's
Steroids
MAOi

Q: What proportion of phaeos are extra-adrenal?
A: 10%

Q: What proportion of phaeos are malignant?
A: 10%

Q: How are phaeos investigated?
A: Low clinical suspicion - 24 hr urinary fractionated catecholamines and metanephrines
High clinical suspicion - Plasma fractionated metanephrines

Q: Pre-treatment for phaeo removal?
A: Alpha blockade - Phenoxybenzamine for 1 week
Beta-blockade - Propranolol 10mg QID after 1 week of alpha blockade if BP controlled

Q: Drugs to avoid in phaeos
A: Beta-blockers, glucagon, histaminergic agents and metoclopramide

Q: Management of hypertensive crisis in phaeo
A: SNP 0.5-5mcg/kg/min

Q: How does subacute deQuervain's thyroiditis present?
A: Inflammatory hyperthyroidism followed by TSH suppression and hypothyroidism

Q: How does Hashimoto's thyroiditis present?
A: Can have early hyperthyroidism but typically hypothyroidism is the major clinical scenario

Q: Is the thyroid painful in hashimoto's?
A: No

Q: Is the thyroid painful in dequervain's thyroiditis?
A: Yes

Q: Autoantibodies in thyroid disease
A: Graves - Anti-thyroid receptor antibodies (90%), Anti-thyroid peroxidase (75%)
Hashimotos - Anti-thyroid peroxidase (90%), anti-thyroglobulin antibodies (70%)