Module 3D Endocrine and ENT - OSCEs Flashcards
Anterior triangle of neck borders
- Superior = inferior border of mandible
- Medial = midline of neck
- Lateral = anterior border of sternocleidomastoid
Posterior triangle of neck borders
- Anterior = posterior margin of sternocleidomastoid
- Posterior = anterior margin of trapezius
- Inferior = middle 1/3 of clavicle
What type of tuning fork is used for Rinne’s and Weber’s test and why?
512Hz
- best balance between time of deceay and tactile vibration
Describe Rinne’s test + results for:
- normal
- conductive hearing loss
- sensorineural hearing loss
- Place a vibrating 512 Hz tuning fork firmly on the mastoid process - this tests bone conduction
- Confirm pt can hear sound of tuning fork and ask them to tell you when they can no longer hear it
- Then move tuning fork in front of external auditory meatus to test air conduction
- Ask pt if they can now hear sound again - if they can then suggests air conduction > bone conduction, which is a normal result (Rinne’s positive)
.
- Normal: air conduction > bone condition (Rinne’s +ve)
- Conductive hearing loss: bone conduction > air conduction (Rinne’s -ve)
- Sensorineural hearing loss: air conduction > bone conduction (Rinne’s +ve)
Describe Weber’s test + results for:
- normal
- conductive hearing loss
- sensorineural hearing loss
- Tap a 512Hz tuning fork and place in the midline of the forehead
- Ask the patient“Where do you hear the sound?”
.
- Normal: sound hear equally in both ears
- Conductive: sound heard louder in affected ear
- Sensorineural: sound heard louder in normal ear
What are the Dix-Hallpike test and Epley manoeuvre used for?
- Dix-Hallpike test = diagnostic manoeuvre used to identify BPPV and confirm the affected side (if pt experiences vertigo in brief episodes (< 1 min) with changes of head position)
- Epley manoeuvre = used to treat BPPV (usually of the posterior canal)
Contraindications for Dix-Hallpike test and Epley manoeuvre (absolute and relative)
What is a positive result for the Dix-Hallpike test?
- what does rotatory nystagmus suggest?
- what does horizontal nystagmus suggest?
If test is positive, (patient claims vertigo and nystagmus is observed) characteristics of the nystagmus should be observed and consider performing Epley’s manoeuvre.
.
- Rotatory nystagmus (most common) - suggests involvement of the posterior semicircular canal
- Horizontal nystagmus - suggests involvement of lateral semicircular canal
What are some complications of otitis media?
- mastoiditis, tympanic membrane perforation, facial nerve palsy
- meningitis (most common itnracranial complication)
Otosclerosis management
- Conservative: hearing aids
- Surgical: stapedectomy or stapedotomy
.
(Stapedectomy = removing entire stapes bone and replacing with prosthesis)
(Stapedotomy = removing part of the stapes bone and leaving the base of the stapes (the footplate) attached to the oval window)
What is the HINTS exam used for?
HINTS - head impulse, nystagmus, and test of skew
- used to distinguish between a peripheral and central cause of vertigo
(must be done in a currently symptomatic patient with a normal full neurological exam)
HINTS exam - What does a +ve result of the head impulse test indicate?
- disruption to the vestibulocochlear-ocular reflex so eyes move with the head and saccade rapidly back
- this indicates there is a problem with the vestibulocochlear nerve on the ipsilateral side, so the cause is peripheral not central which is reassuring
HINTS exam
- What does an unidirectional nystagmus indicate?
- What does a nystagmus that changes direction or is vertical indicate?
- What does a bidirectional nystagmus indicate?
- unidirectional nystagmus - indicates peripheral origin (reassuring)
- if nystagmus changes direction or is vertical - indicates central pathology
- bidirectional nystagmus —> specific for stroke
HINTS exam - what does any abnormal movement (eg. vertical diplopia) indicate?
any abnormal movement (vertical diplopia) is specific for a central cause of vertigo
Radioactive iodine uptake scan - condition seen in
Grave’s disease
- the autoimmune condition causes the entire thyroid gland to be stimulated to actively take up iodine, resulting in a widespread increase in iodine uptake throughout the gland
Radioactive iodine uptake scan - condition seen in
Toxic multinodular goitre
- because these are regions of hyperfunctioning thyroid tissue within the gland, meaning only specific nodules or areas are actively producing excess thyroid hormone
- NOTE: can also be seen in hyperfunctioning adenomas (toxic adenoma)
Radioactive iodine uptake scan - condition seen in
Thyroid cancers (abnormally low uptake)
- cancerous cells do not actively take up iodine like normal thyroid tissue does
Graves disease
- diffuse uptake
Normal thyroid gland
Thyroiditis
- inflamed thyroid gland is not actively taking up iodine, resulting in a low uptake across the entire gland because the inflammatory process disrupts the normal function of thyroid cells needed to absorb iodine
Cold nodule
- differentials: adenomas, cancer
(most adenomas do not actively produce thyroid hormone and therefore do not readily absorb the radioactive iodine so appear as cold spots)
Hot nodule
- differentials: toxic adenoma
Toxic multinodular goitre
TFTs - which hormones are measured to assess thyroid function?
- TSH and free T4 (fT4)
(fT3 is also measured but is less relevant as the thyroid releases T4 and T3 at a ratio of about 20:1 respectively, with T3 mainly being produced by peripheral conversion of T4)
How long would you have to wait to repeat TFTs if you are monitoring the impact of an intervention (eg. increasing a pt’s levothyroxine dose)?
several weeks
- T4 has a half-life of about one week
What is primary hypothyroidism (location of pathology)?
reduced secretion of thyroid hormone from the thyroid gland itself
- Pathology which decreases the thyroid’s ability to release T4 and T3 or respond to TSH can, therefore, cause primary hypothyroidism
Primary hypothyroidism TFTs and why
- TSH:
- T4:
- TSH: High
- T4: Low
.
1. Less T4 and T3 are produced due to thyroid’s reduced capacity to produce hormone or respond to TSH
2. As a result, there is reduced negative feedback on the pituitary and hypothalamus
3. The reduction in negative feedback results in increased production of TRH (which we don’t typically measure) and TSH
4. The end result is low T4 and T3, and a raised TSH
What is subclinical hypothyroidism?
a condition where thyroid-stimulating hormone (TSH) levels are slightly elevated, but levels of free thyroxine (FT4) are normal
- causes mild symptoms
Causes of primary hypothyroidism
- Hashimoto’s thyroiditis (autoimmune thyroiditis) - 50%
(anti-TPO and anti-Tg antibodies) - Iodine deficiency (developing world)
- Treatments of hyperthyroidism - carbimazole, propylthiouracil, radioactive iodine, thyroidectomy
Management of hypothyroidism (primary and secondary)
Oral levothyroxine
- levothyroxine is a synthetic version of T4 and metabolises to T3 in the body
Secondary hypothyroidism TFTs and why
- TSH:
- T4:
- TSH: Low
- T4: Low
.
1. Decreased production or secretion of TSH results in decreased stimulation of the thyroid gland.
2. The thyroid gland, therefore, produces less T3 and T4.
3. The low T3 and T4 would normally stimulate the pituitary gland to increase TSH production, however, they are unable to increase production.
4. The end result is low T4 and T3 and a normal/low TSH.
Causes of secondary hypothyroidism
- Pituitary adenoma: the most common cause.
- Pituitary surgery or radiotherapy which damages the pituitary tissue
- Sheehan’s syndrome (post-partum haemorrhage causes avascular necrosis of the pituitary gland)
Primary VS Secondary hyperthyroidism - location of pathology
- Primary - excessive production of T3 and T4 by thyroid gland itself
- Secondary - excessive production of TSH by pituitary gland (or ectopic cause)
Primary hyperthyroidism TFTs and why?
- TSH
- T4
- TSH: Low
- T4: High
.
1. The thyroid produces excessive amounts of T4 and T3
2. The excessive T4 and T3 cause negative feedback on the pituitary and hypothalamus, resulting in decreased production of TRH and TSH
3. The end result is a raised T3 and T4 and a low TSH
Causes of primary hyperthyroidism
- Graves’ disease (75% of cases) - TSH receptor antibodies, produced by the immune system, stimulateTSH receptorson the thyroid
- Toxic multinodular goitre
- Toxic adenoma
Management of primary hyperthyroidism
- Carbimazole (or propylthiouracil in pregnancy)
- Propranolol (symptomatic relief)
- Radioactive iodine (definitive)
- Thyroidectomy
What is subclinical hyperthyroidism?
When TSH is low, but T4 (and T3) are normal
- causes mild symptoms
Secondary hyperthyroidism TFTs and why?
- TSH
- T4/T3
- TSH: High
- T4/T3: High
.
1. TSH production is increased by either the pituitary/hypothalamus or another source (known as ectopic production).
2. The excess TSH causes overstimulation of the thyroid gland, resulting in high levels of T3 and T4 production.
3. Normally a raised T3 and T4 level would cause negative feedback, decreasing TSH production, however, in this instance, the TSH production is not responsive to any negative feedback, resulting in continued excess production.
Main cause of secondary hyperthyroidism
TSH-secreting pituitary adenoma
Management of secondary hyperthyroidism (think about the main cause and how that would be treated)
Pituitary surgery often required to remove the TSH-secreting adenoma
note: Primary adrenal insufficiency is Addison’s disease
Why is a morning serum cortisol taken?
cortisol is at its highest in the morning 8/9am)
Explain how the ACTH stimulation test (Synacthen test) works and how it can diagnose Addison’s disease
ACTH stimulation test (Synacthen test) - exogenous ACTH is given to pt before measuring their cortisol lvls
- if cortisol lvls remain low - indicates that adrenal cortex is unresponsive to stimulation (diagnosis of Addison’s disease)
- if cortisol lvls increase to above normal range - this excludes diagnosis of Addison’s disease
.
(take baseline cortisol, then 30 mins after, then 60 mins after - should double)
Management of adrenal insufficiency
Oral hydrocortisone and fludrocortisone- to replace glucocorticoids and mineralocorticoids respectively
Adrenal insufficiency - sick day rules + steroid card
- Mild stress (illness) - double hydrocortisone (glucocorticoid dose) until recovery
(continue fludrocortisone (mineralocorticoid dose) at usual dose)
. - Severe stressors (acute illness or major trauma) - IV hydrocortisone +/- IV fluids, followed by continuous hydrocortisone treatment for 24hrs
(pts must carry a steroid card and keep an emergency supply of IM hydrocortisone)
Management of an Addisonian crisis (acute, severe presentation of Addison’s disease)
IV hydrocortisone + IV fluids
Main complication of treatment for adrenal insufficiency (eg. Addison’s disease)?
Cushing’s syndrome secondary to exogenous steroids
Causes of Cushing’s syndrome
- Exogenous glucocorticoids (eg. prednisolone, hydrocortisone) - most common
.
Endogenous- Pituitary adenomas (Cushing’s disease) - corticotropin-dependent
- Ectopic production of corticotropin (eg. small cell lung cancer) - corticotropin-dependent
- Adrenal adenomas and adrenal carcinomas - corticotropin-independent
Cushing’s syndrome VS Cushing’s disease
- Cushing’s syndrome is a general condition that results from too much cortisol in the body
- Cushing’s disease is a specific type of Cushing’s syndrome, caused by a tumour in the pituitary gland
- Cushing’s disease (pituitary adenoma) shows suppression on high-dose dexamethasone, as the pituitary still has some feedback sensitivity
(Plasma ACTH is slightly high due to the same reason of feedback sensitivity) - Adrenal causes (adenoma/carcinoma) and exogenous steroid use both have low ACTH due to negative feedback inhibition
Explain the low-dose dexamethasone suppression test
- Give 1 mg oral dexamethasone at 11 pm, then measure serum cortisol at 9am the following morning
- Normal result - cortisol suppression (< 50)
- Failure to suppress - suggests Cushing’s syndrome (need to do further tests)
Explain the high-dose dexamethasone suppression test
- Give 8mg oral dexamethasone at 11pm, then measure serum cortisol and plasma ACTH at 9am the following morning
. - < 50% suppression - Cushing’s disease (pituitary adenoma producing ACTH)
(pituitary adenomas retain some feedback sensitivity to glucocorticoids, so high-dose dexamethasone suppresses ACTH production) - No suppression (cortisol still high) - suggests ectopic ACTH syndrome (eg. small cell lung cancer) or adrenal Cushing’s
(ectopic ACTH-producing tumours lack feedback inhibition, so cortisol remains high)
Management of Cushing’s syndrome
- Exogenous Cushing’s - review pt’s current glucocorticoid treatments and reduce doses where possible (often with steroid-sparing immunosuppressive agents)
- Pituitary tumours - trans-sphenoidal surgery +/- radiotherapy
- Adrenal tumours - surgical removal (laparoscopic excision)
(Note: if you remove both adrenal glands you have to give replacement steroid hormones for life)
What test is used as a screening test for primary hyperaldosteronism?
aldosterone-to-renin ratio(ARR) - blood test
Management of hyperaldosteronism
Management:
- Eplerenone
- Spironolactone
.
Treatment of underlying cause:
- Surgical removalof theadrenaladenoma
- Percutaneous renal artery angioplastyvia the femoral artery to treatrenal artery stenosis
What is a phaeochromocytoma + what is it associated with?
Adrenal tumour causing excessive amounts of catecholamines (adrenaline)
- associated with MEN 2
Investigations for a phaeochromocytoma
- Plasma-free metanephrines (breakdown product of adrenaline) - longer half-life therefore more stable lvls —> more reliable
- 24-hour urine catecholamines - gives idea of how much adrenaline is being secreted by the tumour over 24hrs
.
(measuring serum catecholamine (adrenaline) level is unreliable as lvls fluctuate and have very short half-life - 1 minute)
Management of a phaeochromocytoma
- Alpha-blockers (eg. phenoxybenzamine or doxazosin)
(Beta-blockers - once established on alpha-blockers) - Surgical removal of tumour - adrenalectomy
Causes of acromegaly
- excessive GH produced in theanterior pituitary gland (most commonly occurs secondary to apituitary adenoma)
.
(rare cause of acromegaly - secondary to cancer (paraneoplastic) that secretes ectopic GNRH or GH)
Visual field defect seen in pituitary gland tumours
bitemporal hemianopia (sits close to optic chiasm)
Investigations in acromegaly
- Serum IGF-1: raised because GH increases glucose lvls
.
Growth hormone suppression test (OGTT): - pt consumes a 75g glucose drink with GH tested at baseline and 2hrs following the drink
- the glucose should suppress the GH lvl - failure to suppress GH indicates acromegaly
.
(further investigations - visual fields, MRI of pituitary)
Management of acromegaly
Surgical:
- Pituitary tumour - trans-sphenoidal surgery
- Other tumour (ectopic) - surgical removal
.
Medical:
- Pegvisomant - GH receptor antagonist
- octreotide - somatostatin analogue (blocks GH release)
- bromocriptine - dopamine agonists (blocks GH release)
Young women with fertility issues or irregular menstruation, what condition should you suspect
hyperprolactinaemia
Where is prolactin secreted?
Prolactin is secreted by lactotroph cells in theanterior pituitary gland
Causes of hyperprolactinaemia
- Physiological - stress, pregnancy, lactation, exercise
- Drug-related - antipsychotics, antidepressants, and certain antiemetics (domperidone, metoclopramide)
- Pathological - prolactinomas are tumours originating from lactotroph cells of the ant. pituitary gland
(microprolactinomas: <10mm, macroprolactinomas: >10mm)
Investigations in hyperprolactinaemia
- Serum prolactin: raised (diagnostic)
- Pregnancy test: to exclude pregnancy (common cause of hyperprolactinaemia)
Management of hyperprolactinaemia
- address underlying cause
- Prolactinomas - dopamine agonists 1st-line (cabergoline, bromocriptine)
Secondary:
- reduced calcium absorption form the intestines, kidneys, and bones —> resulting in hypocalcemia (low blood calcium)
- parathyroid glandsreact to thelow serum calciumby excretingmore PTH
- serum calcium levelwill below or normal,but theparathyroid hormonewill behigh
Explain tertiary hyperparathyroidism
occurs when secondary hyperparathyroidism continues for an extended time, leads to hyperplasia of the parathyroid glands as they adapt to producing a higher lvl of PTH
- Then, when underlying cause of secondary hyperparathyroidism is treated, the baseline PTH production remains inappropriately high
- This high PTH lvl leads to inappropriately high absorption fo calcium in the intestines, kidneys, and bones - causing hypercalcaemia
Type 1 diabetes VS Type 2 diabetes - pathophysiology
T1DM:
- Chronic autoimmune disease, causes immune-mediated destruction of insulin-producing pancreatic beta cells
- Results in an absolute insulin deficiency and subsequent hyperglycaemia
.
T2DM:
- Chronic metabolic disorder characterised by insulin resistance and impaired insulin secretion, leading to hyperglycaemia
- Multifactorial aetiology - genetic, environmental (obesity, sedentary lifestyle, and poor diet), and other factors like age, ethnicity, and smoking
- Progressive pancreatic beta-cell dysfunction and insulin resistance in target tissues
T1DM symptoms
Presents in childhood/adolescence
- Polyuria / Polydipsia / Weight loss
- OR critically unwell with DKA
Investigations done for type 1 diabetes
Blood glucose testing (capillary blood glucose):
- Fasting plasma glucose: > 7.0 mmol/L
- Random plasma glucose: > 11.1 mmol/L
.
Glycated Hb (HbA1c) - overview of blood sugar lvls over past 2-3 months
- HbA1c ≥ 48 mmol/mol (6.5%) on two separate tests indicates diabetes
.
Urine dipstick - glucosuria and ketonuria are common findings
.
Autoantibody testing - can confirm diagnosis
- GAD antibodies
- Islet antibodies
.
C-peptide - co-released with insulin from beta cells in pancreas (direct measure of endogenous insulin production)
- low lvls + hyperglycaemia suggest T1DM - due to beta-cell destruction
Criteria for diagnosis of diabetes mellitus (WHO)
- Random plasma glucose
- Fasting plasma glucose
- OGTT (plasma glucose after 75g glucose oral load)
- HbA1c
- Random plasma glucose ≥ 11.1 mmol/L + symptoms of hyperglycaemia
OR - Fasting plasma glucose ≥ 7.0 mmol/L
OR - Plasma glucose lvl ≥ 11 mmol/L 2 hours after a 75g oral load (OGTT)
OR - HbA1c ≥ 48 mmol/mol (≥ 6.5%) - note HbA1c can be unreliable if pt has condition affecting RBC survival
Once diabetes mellitus has been diagnosed, how can we identify T1DM as the cause?
- Clinical history is important - age, symptoms, ketosis
- Autoantibodies - supports diagnosis
- C-peptide: low/undetectable
Management options for type 1 diabetes mellitus
- Monitor HbA1c every 3-6 months - aiming for ≤ 48 mmol/mol (≤ 6.5%)
.
Regular self-monitoring of blood glucose (eg. 4 times a day) - 5-7 mmol/l on waking
- 4-7 mmol/l rest of day
.
MDIs (basal-bolus) regimens - Basal (long-acting) - Determir BD OR Glargine OD
- Bolus (short-acting) - NovoRapid, Humalog, Apidra
. - Insulin pump therapy (continuous subcutaneous insulin infusion)
.
Hybrid closed-loop system (eg. artificial pancreas) - adjusts insulin delivery on real-time glucose levels
How is T2DM usually diagnosed?
Usually asymptomatic (”silent disease”) and is picked up on routine screening
note: if pt asymptomatic, then criteria must be met on 2 separate occasions
T2DM - impaired fasting glucose (IFG) VS impaired glucose tolerance (IGT)
- Impaired fasting glucose (IFG): fasting glucose ≥ 6.1 but < 7.0 mmol/l (ie. 6.1-6.9 mmol/l)
- Impaired glucose tolerance (IFT): fasting plasma glucose < 7.0 mmol/l and OGTT 2-hour value ≥ 7.8 mmol/l but less than 11.1 mmol/l
.
Diabetes UK say: ‘People with IFG should then be offered an oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn’t have diabetes but does have IGT.’
Management of type 2 diabetes mellitus
- Lifestyle advice - lose weight (5-10% initially), healthy diet (high fibre, low glycaemic index carbs, low fat (saturated fats esp.)
In a patient with T2DM, when should a statin be offered?
only patients with a 10-year cardiovascular risk > 10% (using QRISK2)
What is gestational diabetes?
Glucose intolerance fist diagnosed in pregnancy (typically 2nd/3rd trimester), due to insulin resistance
Investigations for gestational diabetes
(note: HbA1c not used!)
.
OGTT at 24-28 weeks
- 2-hour post-75g glucose ≥7.8 mmol/L
OR
- fasting glucose ≥5.6 mmol/L
Management of gestational diabetes
- Lifestyle - diet, exercise
- Metformin (1st-line)
- (Insulin if metformin ineffective or fasting glucose ≥ 7.0 mmol/l)
- screen for T2DM postpartum
What is the diagnosis?
- Brief: Pt has T1DM, blurred vision, headache, and lethargy, rapid breathing (Kussmaul), sweet/fruity/acetone breath.
- (confusion, reduced consciousness, tachycardia, hypotension, abdominal pain and or vomiting)
Diabetic ketoacidosis
SIMMAN - investigations for DKA
- Blood glucose: > 11.1 mmol/l
- Ketones: urine (2+ or more on dipstick), blood (> 3 mmol/l)
- VBG: metabolic acidosis (low bicarbonate and low pH)
- U&Es: assess renal function + monitor for any electrolyte imbalances (particularly potassium)
- Urinalysis: to look for UTI (can be precipitating factor for DKA)
SIMMAN - Acute management of DKA
- Fluid replacement - 0.9% sodium chloride 1L over 1hr
(If hypotensive then give fluid bolus)
- IV insulin fixed rate infusion - e.g 50 units ACTRAPID in 50ml 0.9% NaCl (0.1 unit/kg/hour)
(continue long-acting insulin (eg. Lantus, Tresiba), stop short-acting insulin)
- Once blood glucose < 14 mmol/L, ADD 10% DEXTROSE AS A SEPARATE IV INFUSION
- Potassium replacement - unless K+ > 5.5 mmol/l
SIMMAN - DKA
Why is there a risk of cardiac arrhythmias in a pt with DKA?
due to significant electrolyte imbalances (particularly hypokalemia)
SIMMAN - DKA
How would blood glucose lvls be measured in this scenario?
point of care testing using a finger prick sample
SIMMAN - DKA
Urine dipstick for ketones or blood testing?
blood ketone testing preferred due to greater sensitivity and specificity
SIMMAN - DKA
Triggers for DKA
- non-compliance with insulin treatment
- acute infections (increases insulin requirements)
- new-onset diabetes
SIMMAN - DKA
Why is fluid replacement first priority in a DKA patient?
dehydration drives hyperglycaemia, worsening ketosis and acidosis
SIMMAN - DKA
Why is insulin given as an infusion and not a bolus?
if insulin given too quickly —> rapid glucose drop —> cerebral oedema risk
SIMMAN - DKA
Why is potassium replacement required?
insulin drives K+ into cells —> risk of hypokalemia and arrhythmias
SIMMAN - DKA
Why is dextrose 10% given once blood glucose < 14 mmol/l?
allows continued insulin administration without causing hypoglycaemia (need to continue insulin infusion to clear ketones and correct acidosis)
SIMMAN - DKA
DKA resolution criteria
- pH > 7.3
- blood ketones < 0.6 mmol/L
- bicarbonate > 15.0 mmol/L
.
(if this criteria met and pt is eating/drinking again then switch them back to subcutaneous insulin)
What is the diagnosis?
Brief: most likely a diabetic patient, sweating, tachycardia, pallor, tremors, hunger, confused, dizziness
Blood glucose: < 3.3 mmol/l
Hypoglycaemia
Acute management of hypoglycaemia
- If pt is alert: oral glucose 10-20g should be given in liquid form or sugar lumps
- If pt is confused, but conscious: Glucogel or Dextrogel (buccal absorption) - quick-acting carbs
- If pt is unconscious or unable to swallow: subcut or IM glucagon (1mg)
- Further management: IV 20% glucose solution
(note: if pt on IV insulin infusion —> STOP)
SIMMAN - hypoglycaemia
Causes of hypoglycaemia in a diabetic patient
- too much insulin
- sulfonylureas (eg. gliclazide)
- missed meals/fasting
- excessive exercise, alcohol, infection
SIMMAN - hypoglycaemia
Why do sulfonylureas increase the risk of hypoglycaemia in diabetic patients?
they act by increasing the secretion of insulin from beta-cells
SIMMAN - hypoglycaemia
Why can alcohol cause hypoglycaemia?
due to its inhibitory effect on gluconeogenesis and glycogenolysis
SIMMAN - hypoglycaemia
Diagnosis of hypoglycaemia (Whipple’s triad)
- symptoms/signs of hypoglycaemia
- low blood glucose
- resolution of symptoms with correction of blood glucose
SIMMAN - hypoglycaemia
What is a ‘HypoKit’?
often prescribed to diabetic patients, contains a syringe and vial of glucagon for IM or subcut injection at home
SIMMAN - hypoglycaemia
Once hypoglycaemia has been acutely managed, what are your next steps in management?
once blood glucose > 4.0 mmol/l, give a long-acting carbohydrate (eg. toast, biscuits) + monitor closely + identify the cause and educate patient on hypoglycaemia
SIMMAN - hypoglycaemia
Contraindications for IM glucagon
glycogen depletion (eg. liver disease) - glucagon requires liver glycogen to raise blood glucose, if stores are depleted it will be ineffective —> use IV glucose instead
What is the diagnosis?
- Brief: fatigue, lack of energy, weight loss, low blood pressure, abdominal pain, vomiting, cramps, skin pigmentation
- PMH: adrenal insufficiency receiving exogenous steroids and type 1 diabetics
Addisonian crisis
Investigations in an Addisonian crisis
- electrolytes
- blood glucose
- ABG/VBG
- BP
- GCS
- Hyponatraemia and hyperkalaemia
- Hypoglycaemia
- metabolic acidosis
- Hypotension
- Reduced GCS
Acute management of an Addisonian crisis
- IM or IV hydrocortisone - 100mg STAT, followed by 200mg infusion over 24hrs (need to admit)
- IV fluids - fluid resuscitation first if needed
- IV 10% dextrose - if hypoglycaemic
- Correct underlying cause - eg. infection (antibx for sepsis), supportive care
(monitoring of electrolytes (esp. Na+ and K+) and fluid balance)
SIMMAN - Addisonian crisis
What causes an Addisonian crisis?
severe adrenal insufficiency, where the absence of steroid hormones leads to a life-threatening emergency
- abrupt withdrawal of steroids (eg. pt on long-term steroids and stops/reduces dose by too much)
- acute illness/infection (particularly in pts with existing adrenal insufficiency)
SIMMAN - Addisonian crisis
Why is there hyponatraemia, hyperkalemia, and hypoglycaemia in an Addisonian crisis?
due to deficiency in aldosterone, it promotes Na+ reabsorption, K+ excretion, and water retention (via Na+ reabsorption)
SIMMAN - Addisonian crisis
Why do you get a metabolic acidosis in an Addisonian crisis?
ack of aldosterone also reduces H+ excretion, leading to acidosis
SIMMAN - Addisonian crisis
Why do you get hypoglycaemia in an Addisonian crisis?
due to cortisol deficiency (impaired gluconeogenesis)
Acute management of a thyroid storm (thyrotoxicosis)
- Carbimazole - to treat high thyroid function (or propylthiouracil 2nd-line)
(Iodine given 1hr after antithyroid medication to inhibit thyroid hormone release) - Propranolol - to control symptoms (HR and palpitations)
- IV paracetamol - for fever
(supportive care where needed)
SIMMAN - Thyroid storm
Causes of thyroid storm
infection, trauma, surgery
Management of epistaxis (nosebleeds)
- First aid measures: sit down, pinch soft part of nose, lean forward
(note: spit out any blood in the mouth, rather than swallowing)
.
If bleeding does not stop after 10-15 mins, then it is severe:
- If anterior bleed and can see bleed point —> nasal cautery using silver nitrate
- If low-volume bleeding, but no obvious bleed point —> nasal packing (tranexamic acid soaked nasopore pack)
(note: remove pack after 24hrs and reassess —> nasal examination +/- cautery)
- If high-volume bleeding —> Rapid Rhino pack
- If bleeding not controlled with these measures —> Surgery (sphenopalatine artery ligation)
. - DISCHARGE with Naseptin nasal cream (or vaseline)
Where does anterior epistaxis arise from
Kiesselbach’s plexus in Little’s area (a vascular network in the anterior part of the nasal septum)
Where does posterior epistaxis arise from?
branches of the sphenopalatine artery (tends to be more severe)
What is the main risk we are worried about in posterior nosebleeds
higher risk of aspiration of blood
Contraindications for Naseptin
peanut or soya allergy
Hypercalcaemia symptoms + acute signs
Bones, Stones, Groans, and Moans
- acute signs: reduced GCS, muscle weakness, hyporeflexia, nausea/vomiting
Management of acute hypercalcaemia
- IV fluids (0.9% NaCl)
- IV bisphosphonates (Zolendronic acid) - inhibits osteoclast activity –> reduces bone resorption
