ENDOCRINE Flashcards
HYPERPARATHYROIDISM
What blood results would you see in the 3 types of hyperparathyroidism?
PRIMARY =
- PTH = high
- calcium = high
- phosphate = low
- alk phos = high
SECONDARY =
- PTH = high
- calcium = low
- phosphate = high
- alk phos = high
TERTIARY -
- PTH = high
- calcium = high
- phosphate = high
- alk phos = high
HYPERPARATHYROIDISM
Describe the treatment for hyperparathyroidism
PRIMARY
- parathyroidectomy
- calcimimetics (cinacalet)
- bisphosphonates
- HRT
SECONDARY
- vitamin D supplementation
- renal transplant
- calcium supplementation
- phosphate binding agent
TERTIARY
- parathyroidectomy
- cinacalet
HYPOPARATHYROIDISM
what are the causes of hypoparathyroidism?
- iatrogenic (neck surgery)
- autoimmune (isolated autoimmune hypothyroidism)
- metabolic (hyper/hypomagnesaemia)
- congenital (DiGeorge syndrome)
HYPOPARATHYROIDISM
What is the treatment for hypoparathyroidism?
ACUTE
- IV 10% calcium gluconate
LONG TERM
- increased dietary calcium + vitamin D
- calcium supplements
- Vitamin D supplements
- thiazide diuretics
HYPERCALCAEMIA
Give 2 ECG changes that you might see in someone with hypercalcaemia
- Tall T waves
- Shortened QT interval
HYPOCALCAEMIA
Name 3 causes of hypocalcaemia
Hypoparathyroidism
Vitamin D deficiency
Hyperventilation
Drugs
Malignancy
Toxic shock
HYPOCALCAEMIA
what is the treatment for hypocalcaemia?
10ml calcium gluconate/chloride 10% slow IV,
oral calcium and Vit D
HYPOCALCAEMIA
Give 2 ECG changes that you might see in hypocalcaemia?
- Small T waves
- Long QT interval
T2DM
What class of drugs can cause diabetes?
Steroids
Thiazides
Anti-psychotics
T2DM
Describe the treatment pathway for T2DM
MEDICATIONS
1st line = metformin
if patient has HF offer metformin + SGLT2i (-gliflozin)
if HbA1c >58, commence dual therapy
1. DPP4i (linagliptin, sitagliptin)
2. Sulfonylurea (gliclazide)
3. Pioglitazone
4. SGLT2i (dapagliflozin, empagliflozin)
if HbA1c > 58 despite dual therapy, commence intermediate acting insulin or triple therapy
triple therapy = metformin + sulfonylurea + GLP-1 mimetic (liraglutide)
T2DM
what are the side effects of Sulfonylurea?
Hypoglycaemia
weight gain
hyponatraemia
HYPOGLYCAEMIA
Briefly describe the treatment of hypoglycaemia
CONSCIOUS + CAN SWALLOW:
- fast acting carbohydrate (glucose tablets, glucose 40% gels, glucose liquid, fruit juice), repeat blood glucose after 10-15 mins
- long acting carbohydrate once blood gluucose >4mmol/L (biscuit, bread)
- IM glucagon or IV glucose 10% if patient does not respond to fast acting carb
REDUCED CONSCIOUSNESS/EMERGENCY
- IM glucagon
- IV 10% glucose 150-200ml
- long acting carbohydrate, once blood glucose is >4mmol/L (biscuit, bread, milk or normal carb containing meal)
in malnourished/alcoholic patients, IV glucose should be given alonside thiamine to prevent wernicke’s encephalopathy
ACROMEGALY
what are the clinical features of acromegaly?
SYMPTOMS:
visual disturbance
headaches
rings and shoes are tight
polyuria + polydipsia due to T2DM
tingling in hands
galactorrhoea
menstrual irregularity/erectile dysfunction
SIGNS:
hypertension,
bitemporal hemiopia
prominent jaw + supraorbital ridge
coarse facial appearance
Prognathism (protrusion of lower jaw)
Macroglossia (large tongue)
Spade-like hands
Sweaty palms + oily skin
ACROMEGALY
What are the investigations for acromegaly?
1st line = IGF-1 (high)
2nd line = oral glucose tolerance test (gold standard)
3rd line = pituitary function tests
4th line = MRI
also investigate for complications
ACROMEGALY
what is the management for acromegaly?
1st line = trans sphenoidal surgery
2nd line
- medical = CABERGOLINE (dopamine agonist), bromocriptine is alternative
- OCTEOTIDE (somatostatin analogue) used in moderate/severe disease
3rd line = PEGVISOMANT (GH receptor antagonist)
4th line = radiotherapy
PROLACTINOMA
what are the causes of prolactinoma?
- Pituitary adenoma
- Anti-dopaminergic drugs
- Head injury - compression of the pituitary stalk
PROLACTINOMA
what are the clinical features of prolactinoma
SYMPTOMS:
amenorrhea,
galactorrhoea,
gynaecomastia,
low libido,
erectile dysfunction
SIGNS:
low testosterone,
infertility
visual field defects
headache
PROLACTINOMA
What is the treatment for prolactinoma?
Dopamine agonists - cabergoline - inhibits prolactin release
Occasionally transsphenoidal pituitary resection
CUSHINGS
what are the causes of excess cortisol? And are they ACTH dependent or independent?
ACTH dependent (ACTH raised):
- Cushing’s disease
- Ectopic ACTH production
- ACTH treatment
ACTH independent (ACTH not raised)
- adrenal adenoma
- iatrogenic
CUSHINGS
what are the investigations for Cushing’s syndrome?
CONFIRM HYPERCORTISOLISM
- 1st line = overnight dexamethasone suppression test (shows failure of cortisol suppression)
- 24hr urinary free cortisol (2 measurements required)
SOURCE LOCALISATION
- 9am ACTH (elevated = ACTH-dependant cause)
if positive then perform
- high dose dexamethasone suppression test
CUSHINGS
What is the treatment for Cushing’s syndrome?
ACTH-dependent
- cushings disease - 1st line = trans-sphenoidal resection
- ectopic ACTH source - treat underlying cause of cancer
ACTH-independent
- iatrogenic = review need for medication + try weaning
- adrenal tumour = tumour resection/adrenalectomy
ADDISONS DISEASE
what are the causes of Addison’s disease?
- autoimmune destruction (21-hydroxylase present in 60-90%) - most common in developed countries
- TB - most common in developing countries
- adrenal metastases- long term steroid use
ADDISONS DISEASE
what are the clinical features of Addison’s disease?
SYMPTOMS
Lethargy + weakness
N+V
weight loss
‘salt cravings’
collapse + shock (addisonian crisis)
SIGNS
Hyperpigmentation (particularly in palmar creases)
loss of pubic hair
hypotension + postural drop
ADDISONS DISEASE
What is the pathophysiology of Addison’s disease?
Destruction of the adrenal cortex results in decreased production of the hormones
All steroids reduced
Reduced cortisol levels = increased CRH and ACTH production through feedback
ADDISONS DISEASE
What are the investigations for Addison’s disease?
1st line = 8-9am cortisol (<100nmol/L = highly suggestive, 100-500nmol/L = refer for ACTH stimulation test)
Gold standard = ACTH stimulation test (short syntacthen test) - failure of rise in cortisol = addisions
Other tests
- 8am ACTH
- adrenal antibodies (anti-21-hydroxylase)
- U&Es (hyponatraemia + hyperkalaemia)
- aldosterone/renin ratio (decreased)
- CT adrenal (atrophied glands)
ADDISONIAN CRISIS
What is the management of adrenal crisis (addisonian crisis)?
ACUTE
- IV fluids - normal saline
- Corticosteroids = HYDROCORTISONE 100mg IV stat followed by 200mg over 24hrs. Oral replacement after 24 hrs with reduction to maintenance level over 3-4 days
- treat underlying cause
CHRONIC
- long term hydrocortisone + fludrocortisone
Fluid resuscitation - saline (IV)
ADDISONS DISEASE
What would sodium and potassium levels be in someone with adrenal insufficiency?
Hyponatraemia = low sodium
Hyperkalaemia = high potassium
Lack of aldosterone and so less sodium reabsorbed and less potassium excreted
GRAVES DISEASE
Name 5 risk factors for Graves disease
- Female
- Genetic association
- E.coli
- Smoking
- Stress
- High iodine intake
- Autoimmune diseases
GRAVES DISEASE
Name 5 autoimmune diseases associated with thyroid autoimmunity
- T1DM
- Addison’s disease
- Pernicious anaemia
- Vitiligo
- Alopecia areata
- Rheumatoid arthritis
THYROID GOITRE
Name 4 types of sporadic non toxic goitre
- Diffuse –> physiological –> Graves
- Multi nodular
- Solitary nodule
- Dominant nodule
HYPERTHYROIDISM
what are the causes of hyperthyroidism?
PRIMARY
- graves disease
- toxic multinodular goitre (iodine deficiency)
- toxic adenoma
- subclinical hyperthyroidism
- drugs (amiodarone)
SECONDARY
- pituitary adenoma
- ectopic tumour
- hypothalamic tumour
HYPERTHYROIDISM
What are the thyroid function test results in primary hyperthyroidism?
high T4
high T3
low TSH
HYPERTHYROIDISM
What are the thyroid function rests in secondary hyperthyroidism?
high T4
high T3
high TSH
HYPERTHYROIDISM
What is a complication of hyperthyroidism?
- Thyroid crisis/storm
- osteoporosis
- proximal myopathy
- thyrotoxic crisis
- iatrogenic (agranulocytosis from carbimazole, congenital malformations, foetal goitre)
HYPERTHYROIDISM
What is the treatment for a thyroid crisis?
symptomatic treatment e.g. paracetamol
treatment of precipitating event
beta blockers e.g. IV propranolol
anti-thyroid drugs - methimazole/propylthiouracil
lugols iodine
dexamethasone 4mg IV QDS to stop conversion of T4 to T3
HYPOTHYROIDISM
Briefly describe the pathophysiology of secondary hypothyroidism
Reduced release or production of TSH so reduced thyroid hormone release
HYPOTHYROIDISM
Briefly describe the pathophysiology of tertiary hypothyroidism
Thyroid gland overcompensates until it can reestablish correct concentration fo thyroid hormone
HYPOTHYROIDISM
what are the causes of primary hypothyroidism
- autoimmune thyroiditis (hashimotos thyroiditis)
- De Quervains thyroiditis (follows viral prodrome)
- post-partum thyroiditis
- iodine deficiency
- post-thyroidectomy or post-radioiodine
- drugs (amiodarone, lithium, anti-thyroid drugs e.g. carbimazole)
HYPOTHYROIDISM
Name 3 causes of secondary hypothyroidism
- compression from a pituitary tumour
- hypothalamic tumours
- drugs (cocaine, steroids + dopamine)
HYPOTHYROIDISM
What are the TFT results for primary hypothyroidism?
- High TSH
- low T4
HYPOTHYROIDISM
What are the TFT results for secondary hypothyroidism?
- normal/low TSH
- low T4
HYPOTHYROIDISM
what are the complications of hypothyroidism?
- hypercholesterolaemia
- carpal tunnel
- peripheral neuropathy
- myoxedema coma
- thyroid lymphoma
DIABETES INSIPIDUS
what are the causes of cranial(central) DI?
CONGENITAL
- malformations of hypothalamus
- wolfram syndrome
ACQUIRED
- pituitary surgery
- tumours (craniopharyngiomas + metastasis, NOT pituitary adenomas)
- traumatic brain injury
- subarachnoid haemorrhage
- CNS infections (meningitis + encephalitis)
- pituitary stalk disease (sarcoidosis)
- drugs (phenytoin)
DIABETES INSIPIDUS
what are the causes of nephrogenic DI?
CONGENITAL
- mutations in vasopressin or aquaporin receptors
ACQUIRED
- drugs (lithium, gentamicin, cisplatin)
- renal disease (renal amyloid, obstructive uropathy)
- electrolyte disturbance (hypokalaemia, hypercalcaemia)
DIABETES INSIPIDUS
what are the investigations for diabetes insipidus?
- Urine + serum osmolality = low urine osmolality + high serum osmolality
- U&Es = normal/raised Na
- serum glucose (to rule out DM)
- 24hr urine output (if <3L, DI is unlikely)
- Water deprivation test = low urine + high serum osmolality
- desmopressin suppression test = in cDI, urine volume decrease + osmolality increases, in nDI no response
To consider
- MRI pituitary
- anterior pituitary function tests
- genetic testing
DIABETES INSIPIDUS
What is the treatment for cranial DI?
- desmopressin
- manage fluid balance (water readily available in patients able to manage own fluids, IV fluids for those not able to)
- low sodium diet
DIABETES INSIPIDUS
What is the treatment for nephrogenic DI?
- manage fluid balance
- treat underlying cause
- sodium restriction
- thiazide diuretics (BENDROFLUMETHIAZIDE)
SIADH
what are the clinical features of SIADH?
MILD
- N+V
- headache
- lethargy
MODERATE
- weakness
- muscle aches
- confusion
- ataxia
SEVERE
- reduced consciousness
- seizures
- respiratory arrest
All patients are EUVOLAEMIC (no features of hyper/hypovolaemia)
SIADH
what are the causes of SIADH?
NEURO
- meningitis
- encephalitis
- intracranial haemorrhage
- stroke
MALIGNANCY
- small cell lung cancer
INFFECTION
- pneumonia
- TB
ENDOCRINE
- hypothyroidism
DRUGS
- SSRIs + TCAs
- PPIs
- Carbamazepine
- Cyclophosphamide
- Sulfonylureas
OTHER
- porphyria
- PEEP
SIADH
what are the investigations for SIADH?
- urine osmolality = inappropriately high in relation to serum osmolality
- urine sodium concentration = high
- ADH levels
- U and Es (low sodium normal potassium),
- fluid status
distinguish SIADH from salt & water depletion - test with 1-2L of
0.9% saline:
* Sodium depletion will respond
* SIADH will NOT RESPOND
SIADH
Describe the treatment for SIADH
ACUTE (<48hrs)
- hypertonic 3% NaCl
CHRONIC (>48hrs)
- Na correction maximum 10mmol/L per day
- mild-moderate asymptomatic cases = fluid restriction (750-1000ml per day)
- severe or symptomatic = demeclocycline or tolvaptan
SIADH
How do you treat very symptomatic SIADH?
Give 3% saline (hypertonic)
demeclocycline or tolvaptan
PITUITARY ADENOMA
Give 4 local effects a pituitary adenoma
- Headaches
- Visual field defects - bitemporal hemianopia
- Cranial nerve palsy and temporal lobe epilepsy
- CSF rhinorrhoea
DIABETES MELLITUS
Name 3 exocrine causes of Diabetes
- Inflammatory - actue/chronic pancreatitis
- Hereditary haemochromatosis
- Pancreatic neoplasia
- Cystic fibrosis
PHEOCHROMOCYTOMA
What is Pheochromocytoma?
A rare catecholamine secreting tumour in the adrenal medulla (chromatin cells)
PHEOCHROMOCYTOMA
what are the clinical features of pheochromocytoma?
SYMPTOMS
Headache
Profuse Sweating
Palpitations
Tremor
SIGNS
Hypertension
Postural hypotension
Tremor
hypertensive retinopathy
Pallor
PHEOCHROMOCYTOMA
What are the investigations for pheochromocytoma?
- Plasma metanephrines and normetanephrines
- 24 hour urinary total catecholamines
- CT – look for tumour
PHEOCHROMOCYTOMA
What is the treatment for pheochromocytoma?
Without HTN crisis:
1st Line = Alpha blockers (PHENOXYBENZAMINE)
Most patients will eventually get the tumour removed and then managed medically.
With HTN crisis:
1st Line = Antihypertensive agents (PHENTOLAMINE)
PHEOCHROMOCYTOMA
What is the management of a phaeochromocytoma crisis?
Non-competitive alpha-blocker e.g. phenoxybenzamine
Excision of paraganglioma
Biochemistry: measure plasma and serum metanephrines
CONNS SYNDROME
What is Conn’s syndrome?
Primary hyperaldosteronism caused by an adrenal adenoma
High aldosterone levels independent of RAAS activation - H20 and sodium retention and potassium excretion
CONNS SYNDROME
What are the clinical features of Conn’s syndrome?
SYMPTOMS
- lethargy
- mood disturbance
- paraesthesia + muscle cramps
SIGNS
- refractory hypertension
- metabolic alkalosis
CONNS SYNDROME
A deficiency in which electrolyte causes the symptoms of Conn’s syndrome?
HYPOKALAEMIA
causes:
1. Muscle weakness
2. Tiredness
3. Polyuria
CONNS SYNDROME
What hormone is raised in Conn’s syndrome and what hormone is reduced? Where are these hormones synthesised?
- Aldosterone is raised - synthesised in the zone glomerulosa
- Renin is reduced - synthesised in the juxta-glomerular cells
CONNS SYNDROME
What investigations might you do in someone to confirm a diagnosis of Conn’s syndrome?
1st line = aldosterone renin ratio (high aldosterone + low renin)
serum U&Es = hypokalaemia + hypernatraemia
high resolution CT abdomen
adrenal venous sampling
CONNS SYNDROME
Give 4 ECG changes you might see in someone with Conn’s syndrome
HYPOKALAEMIC ECG
1. Increased amplitude and width of P waves
2. Flat T waves
3. ST depression
4. Prolonged QT interval
5. U waves
CONNS SYNDROME
What is the treatment for Conn’s syndrome?
1st line
- laparoscopic adrenalectomy for unilateral
- spironolactone for bilateral
2nd line
- spironolactone if surgery is inappropriate in unilateral disease
HYPERKALAEMIA
What ECG changes might you see in someone with hyperkalaemia?
GO - absent/flat P waves
GO LONG - prolonged PR
GO TALL - Tall T waves
GO WIDE - Wide QRS
HYPERKALAEMIA
What is the treatment for hyperkalaemia?
CARDIAC MEMBRANE PROTECTION
- 10ml 10% IV calcium gluconate or calcium chloride given immediately
POTASSIUM REDUCTION
- insulin/dextrose infusion
- nebulised salbutamol
- potassium binders (sodium zirconium cyclosilicate or calcium resonium)
- sodium bicarbonate
- haemodialysis
HYPOKALAEMIA
What ECG changes might you see in someone with hypokalaemia?
- Increased amplitude and width of P waves
- ST depression
- Flat T waves
- U waves
- QT prolongation
U have no Pot (potassium), no T, but a long PR and a long QT
HYPOKALAEMIA
What is the treatment for hypokalaemia?
POTASSIUM REPLACEMENT
- mild to moderate = oral supplements (Sando-K)
- severe = 20-40mmol IV KCl in 0.9% saline.
- the fastest rate of correction is 10mmol/hr so 1L bag with 40mmol KCl is run over 4hrs or more
TREAT UNDERLYING CAUSE
THYROID CANCER
Name 5 types of thyroid cancer
- Papillary - thyroid epithelium
- Follicular - thyroid epithelium
- Anaplastic - thyroid epithelium
- Lymphoma
- Medullary - calcitonin C cells
THYROID CANCER
What types of thyroid cancers are usually asymptomatic thyroid nodule (usually hard and fixed)?
Papillary
Follicular
Anaplastic
THYROID CANCER
What is the most common form of thyroid cancer?
Papillary - 70%, young people, 3x more common in women
Follicular - 20%
DE QUERVAINS THYROIDITIS
what is the treatment for de quervain’s thyroiditis?
Treat with aspirin and only give prednisolone for severely symptomatic
cases
DIABETES PHARMACOLOGY
what is the mechanism of action for SGLT-2 inhibitors?
inhibits resorption of glucose in the kidney causing urinary glucose excretion
DIABETES PHARMACOLOGY
what is the mechanism of action for pioglitazone?
PPAR gamma agoinsts reduce peripheral resistance
DIABETES PHARMACOLOGY
what are the side effects of pioglitazones?
Weight gain
Fluid retention
Hepatotoxicity
Bladder cancer
HYPEROSMOLAR HYPERGLYCAEMIC STATE
what is the pathophysiology of hyperosmolar hyperglycaemic state?
hyperglycaemia drives osmotic diuresis, resulting in fluid + electrolyte loss (hyperosmolality + hypovolaemia)
due to presence of small amounts of circulating insulin, lipolysis does not occur so ketoacidosis is not seen
HYPEROSMOLAR HYPERGLYCAEMIC STATE
what is the treatment for hyperosmolar hyperglycaemic state?
FLUID REPLACEMENT
- IV 0.9% NaCl
- aim to replace 50% fluid loss in first 12 hrs
FIXED RATE INSULIN INFUSION
- do not use insulin initially due to risks of rapid correction
- IV insulin only used if there is ketonaemia or if blood glucose is not longer falling with IV fluids alone, otherwise do NOT start insulin
POTASSIUM REPLACEMENT
- if >5.5 in first 24hrs = no replacement required
- if 3.5-5.5 in first 24hrs = 20-40mmol/L KCl
- if <3.5 in first 24hrs = require senior review
ANTICOAGULATION
- LMWH unless contraindicated
-
HYPERTHYROIDISM
what is the mechanism of action for carbimazole?
prevents thyroid peroxidase from producing T3 and T4
ACROMEGALY
what are the side effects of GH receptor antagonists e.g. pegvisomant?
- reactions at injection site
- GI disturbance
- hypoglycaemia
- chest pain
- hepatitis
PHARMACOLOGY
what is the mechanism of action for vasopressin antagonists e.g. tolvaptan?
- inhibits vasopressin-2 receptor -> increases fluid excretion
- causes aquaresis (excretion of H2O with no electrolyte loss) -> increased Na+
PHARMACOLOGY
what are the side effect of vasopressin antagonists e.g. tolvaptan?
- GI disturbance
- headache
- increased thirst
- insomnia
PHARMACOLOGY
what is the mechanism of action for vasopressin analogues e.g. desmopressin?
binds to V2 receptors -> aquaporin 2 inserted in collecting duct which increases water reabsorption
PHARMACOLOGY
what are the side effects of vasopressin analogies e.g. desmopressin?
- headache
- facial flushing
- nausea
- seizures
PHARMACOLOGY
what is the mechanism of action for metyrapone?
- blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide enzyme
PHARMACOLOGY
what are the side effects of metyrapone?
- GI disturbance
- headache
- dizziness
- drowsiness
- hirsutism
ADRENAL INSUFFICIENCY
how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?
short ACTH = no change
long ACTH = increase
CUSHINGS
what investigation can be used to differentiate between cushing’s syndrome and cushing’s disease?
dexamethasone suppression test
- overnight = cushing’s syndrome (including disease) is confirmed when there is no suppression
- 48 hours = cushing’s syndrome (not disease) = no suppression
HYPERNATRAEMIA
what is the management?
- fluid replacement = IV 5% dextrose
- treat causes
- suspend medications
HYPONATRAEMIA
what is the management?
ACUTE (<48hrs)
- mild/no symptoms = stop non-essential fluids + meds that can provoke hyponatraemia + treat cause
- moderate/severe symptoms = hypertonic 3% NaCl
CHRONIC (>48hrs)
- maximum increase 10mmol/L per day
- if hypovolaemic = 0.9% NaCl
- if hypervolaemic = fluid restriction
HYPONATRAEMIA
what are the complications?
- central pontine myelinolysis
DIABETES INSIPIDUS
What are the test results for serum osmolality, urine osmolality + post desmopressin urine osmolality in cranial + nephrogenic DI?
CRANIAL
- high serum osmolality
- low urine osmolality
- high urine osmolality post desmopressin suppression
NEPHROGENIC
- high serum osmolality
- low urine osmolality
- no response post desmopressin suppression
DIABETES PHARMACOLOGY
what is the mechanism of action for DPP-4 inhibitors?
prevent degradation of incretins _ promote insulin secretion
DIABETES PHARMACOLOGY
what are the side effects of DPP-4 inhibitors e.g. linagliptin?
pancreatitis
DIABETIC KETOACIDOSIS
what is the management?
IV FLUIDS
- if SBP<90 500ml bolus of 0.9% NaCl over 15 mins + call for senior help
- if SBP>90 1L 0.9% NaCl over 1 hour, 1 litre 0.9% NaCl with kCl over 2hrs, 2hrs, 4hrs, 4hrs and then 6hrs
INSULIN
- fixed rate insulin infusion
- 0.1U/kg/hr
- once glucose <14mmol/L add 10% glucose + consider reducing insulin
- do not stop long acting insulin
POTASSIUM REPLACEMENT
- >5.5 in first 24hrs = no replacement required
- 3.5-5.5 in first 24hrs = 40mmol/L KCl
- <3.5 in first 24hrs = consider HDU/ITU
DIABETIC KETOACIDOSIS
what are the complications?
- venous thrromboembolism
- arrhythmias
- ARDS
- AKI
- cerebral oedema
- hypokalaemia
- gastric stasis
HYPERNATRAEMIA
what are the complications?
- cerebral oedema
- coma
- death
HYPOTHYROIDISM
what is the management for mxyoedema coma?
- ITU/HDU admission
- IV thyroid replacement (levothyroxine)
- antibiotics
- IV hydrocortisone (100mg)
HYPERLIPIDAEMIA
what is the management?
1st line
- lifestyle modifications (dietary changes, increased physical activity, weight loss + smoking cessation)
- statins (atorvastatin or simvastatin)
- fibrates
2nd line
- ezetimibe
- PCSK9 inhibitors (evolocumab)
DIABETES INSIPIDUS
how do you differentiate between cranial and nephrogenic DI?
DESMOPRESSIN SUPPRESSION TEST
- cranial DI = decreased urine volume + increased urine osmolality
- nephrogenic DI = no response
DIABETES INSIPIDUS
when is the desmopressin suppression test contraindicated?
- hypernatremia
- uncontrolled diabetes mellitus
- kidney insufficiency
- pregnancy
CUSHINGS
what are the results for high dose dexamethasone suppression test for cushings syndrome, disease and ectopic ACTH syndrome?
CUSHINGS SYNDROME
- cortisol = not suppressed
- ACTH = suppressed
CUSHINGS DISEASE
- cortisol = supressed
- ACTH = suppressed
ECTOPIC ACTH SYNDROME
- cortisol = not suppressed
- ACTH = not suppressed
PRIMARY HYPERALDOSTERONISM
what are the causes?
- bilateral idiopathic adrenal hyperplasia (most common)
- adrenal adenoma = Conn’s syndrome
- unilateral hyperplasia
- familial hyperaldosteronism
- adrenal carcinoma
HYPERCALCAEMIA OF MALIGNANCY
what is the pathophysiology?
three main mechanisms:
- secretion of PTH-related protein (PTHrP) = most common
- osteolytic metastases
- secretion of 1,25-dihydroxyvitamin D (calcitriol)
HYPERCALCAEMIA OF MALIGNANCY
what is the management?
SUPPORTIVE
- stop medications that contribute to hypercalcaemia (thiazides, calcium supplements, vitamin D supplements, lithium)
- stop medications that can worsen renal function (NSAIDs, ACEis)
- medications for associated symptoms
= laxatives for constipation
= anti-emetics for nausea
= analgesia for bone pain
REHYDRATION
- IV fluids (3 litres in first 24hrs)
BISPHOSPHONATES
- 1st line = IV zoledronic acid 4mg
- 2nd line = disodium pamidronate 30-90mg
- if hypercalcaemia lasts >7 days then further bisphosphonates may be considered or denosumab
CARCINOID TUMOURS
what is the difference between carcinoid tumours and carcinoid syndrome?
carcinoid tumours = type of neuroendocrine tumour which can secrete serotonin
carcinoid syndrome = liver mets impair hepatic excretion of serotonin during 1st pass metabolism, resulting in increased serotoninergic symptons
CARCINOID TUMOURS
what are the clinical features?
SYMPTOMS
- abdominal pain
- diarrhoea
- flushing
- wheezing
- pulmonary stenosis
patients with GI carcinoid tumours will only experience symptoms if they have liver mets
CARCINOID TUMOURS
what are the investigations?
- urinary hormone levels = 5-HIAA
- plasma chromogranin A y
- CT or MRI
- tissue biopsy
CARCINOID TUMOURS
what is the management?
- somatostatin analogues = octreotide
- surgery
- cyproheptadine can help with diarrhoea
HYPERTHYROIDISM
what antibody is raised in Grave’s disease?
TSH receptor antibody
HYPERTHYROIDISM
what are the 2 methods of medical management?
- suppress with carbimazole until euthyroid
- block with carbimazole and replace with levothyroxine
HYPERTHYROID
what is the most serious side effect of carbimazole?
agranulocytosis
