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5th Year Revision > Y3 - Endo > Flashcards

Y3 - Endo Flashcards

1
Q

Describe the anatomy of the thyroid gland!

A
  • left and right lobe joined by a central isthmus
  • moves on swallowing
  • supplied by the inferior and superior thyroid arteries
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2
Q

What do the thyroid hormones do?

A
  • T4 is the main circulating hormone and gets converted peripherally to T3 too
  • thyroid hormones basically increase basal metabolic rate, affecting growth in kids too.
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3
Q

How would hyperthyroidism present?

A
  • AF/ tachycardia/ palpitations
  • increased and loose bowel movements
  • menorrhagia
  • intolerance to heat
  • Insomnia/ irritability
  • weight loss, increased appetite
  • anxious/ sweating/ resting tremor
  • Graves = lid retraction, proptosis, pre-tibial myxoedema, thyroid acropachy on nails
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4
Q

What are some causes of hyperthyroidism? also known as thyrotoxicosis

A
  • Graves = autoimmune most common
  • singular toxic nodule
  • toxic multinodular goitre
  • thyroiditis (inflammatino of thyroid) caused by viral infection/ meds (amiodarone)/ post partum
    • typically followed by a hypothyroid phase
    • this is because inflammation causes follicular cell breakdown so thyroid hormones are released
    • but obviously once the store is released, the breakdown of cells means there is then underproduction
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5
Q

How would you investigate and manage hyperthyroidism?

A
  • T3
  • T4
  • TSH
  • TSH receptor stimulating antibodies = Graves
  • Thyroid peroxidase antibodies (not that specific but indicative of autoimmune)
  • US of thyroid shows nodules
  • Iodine uptake isotope scan shows either localised increased uptake (nodule) or uniform increased uptake (Graves) or absent uptake (thyroiditis)

Management

  • BBlockers for symptoms
  • Carbimozole
    • ​se = _generalised ras_h. also agranulocytosis so do urgent fbc if unexplained fever/sore throat and stop if neutrophils are low
  • definitive = Radioactive Iodine + Thyroidectomy
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6
Q

How would hypothyroidism present?

A
  • weight gain
  • constipation
  • fatigue
  • intolerance to cold
  • bradycardia
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7
Q

What are some causes of hypothyroidism?

A
  • damage from intentional treatment of thyroid disease eg surgical
  • inadvertant damage from eg radiation to head and neck
  • Hashimotos thyroiditis
  • Iodine insufficiency
  • Post partum
  • Medications like amiodarone and lithium
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8
Q

How would you investigate and manage hypothyroidism?

A
  • T3
  • T4
  • Thyroid peroxidase Antibodies
  • TSH

Managment

Levothyroxine!!!

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9
Q

What hormones are produced by the adrenal glands? What do they do

A

Cortex

  • Glucocorticoids = cortisol
  • Mineralcorticoids = aldosterone
    • distal convoluted tubule to cause K+ loss and Na+ retention
    • is regulated by Renin Angiotensin System (activated by low blood vol, low Na+ or high K+)
  • Androgens

Medulla produces adrenaline and dopamine and their metabolites

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10
Q

How would Primary Adrenal Insufficiency (Addisons disease) present?

A
  • Low Cortisol = fatigue, weight loss, nausea, abdo pain, anorexia, hypoglycaemia, hyperpigmentation from ACTH upregulation
  • Low Aldosterone = postural hypotension, dizziness, Hyponatraemia, Hyperkalaemia
  • Low androgens = loss of axillary and pubic hair, low libido
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11
Q

Why is there hyperpigmentation in addisons?

A

ACTH excess due to low cortisol.

Acth stimulates melaocyte stimulating hormones which results in hyperpigmentation

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12
Q

How would you investigate and manage Addisons?

A
  • low 9am Cortisol while ACTH is raised
  • Synacthen test for confirmation
  • Hyperkalaemia, Hyponatraemia, Hypoglycaemia, Mild anaemia, Raised urea

Management

  • Hydrocortisone for glucocorticoid replacement
  • Fludrocortisone for mineralcorticoid replacement
  • educate about steroid rules (double glucocorticoid during illness, ensure it is given in surgery/ nausea or vomiting)
  • give steroid emergency card, medical alert jewellry, details of their endo team
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13
Q

How would you manage secondary adrenal insufficiency (ACTH deficiency)

A
  • only replace Glucocorticoid = Hydrocortisone
  • steroid card etc
  • education etc inform them not to stop steroids suddenly = adrenal crisis
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14
Q

What is phaeochromocytoma and paragangliomas?

A

Phaeochromocytomas are catecholamine secreting tumours of the adrenal medulla.

Paraganglionomas are tumours of the extra adrenal chromaffin tissue

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15
Q

How would phaeochromocytomas present?

A
  • panic attacks and anxiety
  • headache, sweating, pallor, palpitations
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16
Q

How would you investigate and manage phaeochromocytomas?

A
  • 24 hour urinary catecholamines and plasma metanephrines
  • CT/MRI abdo for tumour

Management

  • surgical excision
  • alpha blockade first (as unregulated alpha = hypertensive crisis)
  • then beta blockade to control reflex tachycardia
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17
Q

What are the 5 axes produced in the pituitary and what do they do?

A

Growth hormone (GH)

  • secreted pulsatile
  • acts on liver to produce IGF-1
  • -ve feedback from somatostatin

ACTH

  • secreted circadian rhythm
  • stimulates cortisol release

Gonadal (FSH/LH)

  • FSH and LH are inhibited by prolactin

Thyroid (TSH)

  • stimulates T4 and T3

Prolactin

  • causes lactation
  • inhibits gonadal hormones
  • itself is inhibited by dopamine
18
Q

How would you assess the pituitary gland?

A
  • MRI of pituitary for microadenomas (<1cm) or macroadenomas
  • Synacthen test
  • Insulin Tolerance Test for GH and ACTH reserve (not in ischaemic heart disease or epilepsy)
  • Prolactin and TSH can be measured at any time
  • FSH and LH in women measured in first 5 days of menstrual cycle
  • FSH and LH and Testosterone in men measured at fasting 0900
  • Measure GH and IGF-1
  • Basal Cortisol at 0900
19
Q

How would you investigate hyperprolactinaemia?

A
  • MRI for microadenoma (<1cm) or macroadenoma
  • rule out pregnancy
  • medications review (dopamine antagonists like antipsychotics or antiemetics)
  • prolactin levels typically >5000 in secreting prolactinoma

Microadenoma

  • menstrual disturbance, galactorrhoea, infertility
  • unlikely to be PCOS if no pituitary lesions on MRI, also prolactin is usually <1000

Macroadenoma

  • prolactin typically >5000miU
20
Q

How would you manage hyperprolactinaemia?

A
  • give dopamine agonists like bromocriptine or cabergoline
  • SE = nausea, postural hypotension, psychiatric disturbance
  • They can cause the tumour to shrink really fast and cause CSF leak = meningitis risk
21
Q

How would acromegaly present?

A
  • large hands and feet
  • puffy hands = carpal tunnel syndrome
  • coarse facial features
  • frontal bossing of forehead
  • protrusion of chin
  • wide spaced teeth
  • Enlarged soft tissue = large soft palate and tongue
  • Snoring and sleep apnoea
  • Sweating, headaches, HTN
  • Risk of CVS, bowel cancer, DM
22
Q

How would you investigate and manage acromegaly?

A
  • GH and IGF-1
  • Oral Glucose Tolerance Test
  • Pituitary MRI to show tumour

Management

  • Surgical excision
    • repeat OGTT and follow up with GH/IGF-1 monitoring
  • Stereotactic radiotherapy if it is away from optic chiasm
  • somatostatin analogues can help
  • Monitor for sleep apnoea, bowel cancer, CVS, DM
23
Q

How would you manage hypopituitarism?

A

ACTH = hydrocortisone

GH = daily growth hormone subcut injections

FSH/LH = COCP/HRT in females or testosterone injections for males

Thyroid = levothyroxine

24
Q

How would Cushings disease present?

A

Pituitary adenoma resulting in excess cortisol.

  • dorso cervical fat pad
  • facial roundness and plethora
  • thin skin, striae, easy bruising
  • osteoporosis of limbs
  • central obesity
  • HTN, DM
25
Q

How would you investigate and manage Cushings disease?

A
  • Screen for alcoholism and depression
  • Elevated 24 hour urinary Cortisol
  • Overnight dexamethasone suppression test
    • failure to suppress cortisol <50nmol/L after overnight Dexamethasone Suppression test
  • Elevated late night salivary cortisol levels
  • Hypokalaemic, Metabolic alkalosis
  • MRI of pituitary

Management

  • Metyrapone and ketoconazole
  • Radiotherapy
  • Transphenoidal removal of pituitary adenoma
  • If it is adrenal = lap adrenalectomy
26
Q

What are some symptoms of hyponatraemia?

A
  • headache
  • nausea, vomiting
  • general malaise
  • confusion, agitation, drowsiness later
27
Q

How would you investigate hyponatraemia?

A
  • Urine Osmolality
  • Urine Sodium
    • <30mmol/L = low effective arterial vol
    • >30mmol/L and euvolaemic = SIADH once ACTH def is excluded
    • >30mmol/L and dehdyrated = Addisons/ vomiting/ DI
28
Q

How would you diagnose and manage SIADH?

A
  • Diagnosis of exclusion as there isn’t really a test…
  • Rule out other causes eg. adrenal insufficiency*** (-ve short synacthen), rule out diuretics, excess fluid intake, ckd, aki, etc.
  • clinical examination shows euvolaemia
  • low serum osmolality <275momol/kg
  • high urine osmolality >100mosmol/kg
  • urine Na >30mmol/l

Ensure to rule out ACTH deficiency as it also causes excretion of free water (cortisol deficiency causes increased vasopressin activity).***

Also look for any underlying malignancy eg. small cell lung cancer.

Management

(the goal is to correct sodium slowly to prevent central pontine myelinolysis)

  • fluid restriction
  • tolvaptan (adh receptor blocker)
    • monitor as it can cause rapid sodium increase
  • demeclocycline (tetracycline antibiotic that inhibits adh)
29
Q

How would you diagnose cranial/nephrogenic diabetes insipidus?

A
  • >3L urine in 24 hours
  • high serum osmolality >295mosmol/kg
  • low urine osmolality <300mosmol/kg
  • do water deprivation test (they should have unacceptable thirst and significant weight loss due to water loss. stop if symptoms get too severe!)
  • then give a synthetic vasopressin like desmopressin.
    • Cranial will get better, Nephrogenic no response

Management

  • Desmopressin for cranial DI
  • Nephrogenic = less salt, protein, nsaids, diuretics
30
Q

How would you investigate hypercalcaemia?

A
  • high PTH
    • high PTH is usually primary hyperPTH due to a single parathyroid adenoma
    • Parathyroid hyperplasia in more than one gland = Multiple Endocrine Neoplasia
    • Very high calcium >3.5 could be parathyroid cancer (associated with jaw tumours)
  • suppressed PTH
    • malignancy unless proven otherwise!!!
    • usually squamous cell carcinoma
    • also could be benign granulomatous disease like tb/ sarcoidosis
  • Parathyroid ultrasound for adenoma
31
Q

How would hypercalcaemia present?

A
  • renal stones
  • abdominal pain, GI upset, constipation
  • Depression, fatigue, psychiatric symptoms
  • Bony aches and pains
  • polydypsia and polyuria
32
Q

How would you manage hypercalcaemia?

A
  • Surgery if Ca>2.85
    • parathyroidectomy
  • Calcimimetics like cinacalcet for primary hyperparathyroidism
33
Q

How would hypocalcaemia present?

A
  • seizures
  • tetany
  • qt prolongation on ecg
  • Chvosteks sign +ve = facial spasm when cheek is tapped gently with finger
  • Trousseaus sign = carpo-pedal spasm induced after inflation of sphygmomanoometer
34
Q

What are some causes of hypocalcaemia?

Ca<1.9

A
  • Vit D deficiency = will have a low phosphate
  • Hypomagnesaemia = GI loss, alcohol/drugs, PPIs
  • Parathyroid gland damage from surgery etc.
35
Q

How would you manage hypocalcaemia?

A
  • Calcium replacement
  • vitamin d supplements
  • bisphospohonates
  • stop offensive meds for hypomagnesaemia and give IV MgSO4 24mmol/24 hours
36
Q

How would Conns present?

(primary hyperaldosteronism)

A
  • Hypernatraemia, hypokalaemia
  • polyuria, polydipsia
  • HTN
  • metabolic alkalosis
37
Q

How would you investigate Conns?

A
  • Aldosterone:Renin ratio >800 confirms diagnosis
    • false +ve with BBlockers
    • False -ves with ACEI, ARBs, CCB
  • ECG = hypokalaemia
  • CT/MRI for adrenal mass/hyperplasia
  • Lying and standing aldosterone:renin
    • adrenal hyperplasia = aldosterone >30% after standing over 4 hours
    • adrenal adenoma = no change
38
Q

How would you manage Conns?

A

adrenal adenoma (Conns)

  • surgial removal of adenoma
  • Spironolactone (aldosterone antagonist)

Bilateral adrenal hyperplasia

  • spironolactone
    • SE = gynaecomastia and ED as also blocks testosterone receptors
  • Amiloride
    • K+ sparing diuretic weaker than spironolactone
  • Eplerenone
    • aldosterone antagonist that does not block testosterone receptors
39
Q

What is the pathophysiology of SIADH?

A
  • ADH is produced in the hypothalamus and secreted by the posterior pituitary
  • ADH stimulates water reabsorption from collecting ducts in kidneys
  • SIADH is when ADH is secreted excessively
    • either due to posterior pituitary secreting too much
    • or ADH coming from somewhere else like a Small cell lung cancer
  • Results in excessive water, diluting sodium in the blood = hyponatraemia
  • but the water is not significant enough to cause fluid overload = euvolaemic hyponatraemia
  • Urine becomes more concentrated as water is retained = high urine osmolality and high urine sodium
40
Q

What is central pontine myelinolysis?

(also known as osmotic demyelination syndrome)

A

a complication of rapidly correcting severe hyponatraemia (>10mmol/L increase in over 24 hours)

  • as blood sodium falls, water moves from the level of low solute conc (blood) to high solute conc (brain)
  • this causes the brain to swell
  • the brain reduces its solutes so that water moves back down through the blood brain barrier and reduces oedema in the brain
  • this adaptation takes a few days and so in people who have a chronically low sodium, their brain cells will have adapted to have a low osmolality.
  • Therefore when we correct that low sodium rapidly, water rapidly shifts out of the brain cells into the blood.

Early First phase Presentation

  • electrolyte imbalance = encephalopathic and confusion
  • nausea, vomiting, headache

Second phase presentation

  • Later on the demyelination of neurones starts, particularly in the pons
  • spastic quadriparesis
  • pseudobulbar palsy
  • cognitive and behavioural changes

Management = supportive

5th Year Revision (14 decks)

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