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
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.
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
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
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
6
Q
How would hypothyroidism present?
A
- weight gain
- constipation
- fatigue
- intolerance to cold
- bradycardia
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
8
Q
How would you investigate and manage hypothyroidism?
A
- T3
- T4
- Thyroid peroxidase Antibodies
- TSH
Managment
Levothyroxine!!!
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
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
11
Q
Why is there hyperpigmentation in addisons?
A
ACTH excess due to low cortisol.
Acth stimulates melaocyte stimulating hormones which results in hyperpigmentation
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
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
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
15
Q
How would phaeochromocytomas present?
A
- panic attacks and anxiety
- headache, sweating, pallor, palpitations
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
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
How would you investigate and manage Cushings disease?
* 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
What are some symptoms of hyponatraemia?
* headache
* nausea, vomiting
* general malaise
* confusion, agitation, drowsiness later
27
How would you investigate hyponatraemia?
* 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
How would you diagnose and manage SIADH?
* 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
How would you diagnose cranial/nephrogenic diabetes insipidus?
* \>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
How would you investigate hypercalcaemia?
* 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
How would hypercalcaemia present?
* renal stones
* abdominal pain, GI upset, constipation
* Depression, fatigue, psychiatric symptoms
* Bony aches and pains
* polydypsia and polyuria
32
How would you manage hypercalcaemia?
* Surgery if Ca\>2.85
* **parathyroidectomy**
* **Calcimimetics like cinacalcet** for primary hyperparathyroidism
33
How would hypocalcaemia present?
* 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
What are some causes of hypocalcaemia?
Ca\<1.9
* Vit D deficiency = will have a low phosphate
* Hypomagnesaemia = GI loss, alcohol/drugs, PPIs
* Parathyroid gland damage from surgery etc.
35
How would you manage hypocalcaemia?
* Calcium replacement
* vitamin d supplements
* bisphospohonates
* stop offensive meds for hypomagnesaemia and give IV MgSO4 24mmol/24 hours
36
How would Conns present?
| (primary hyperaldosteronism)
* Hypernatraemia, hypokalaemia
* polyuria, polydipsia
* HTN
* metabolic alkalosis
37
How would you investigate Conns?
* **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
How would you manage Conns?
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
What is the pathophysiology of SIADH?
* 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
What is central pontine myelinolysis?
(also known as osmotic demyelination syndrome)
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
