Endocrine Flashcards
myxoedema coma treatemnt
thyroxine and hydrocortisone
hypothyroidism features
General
Weight gain
Lethargy
Cold intolerance
Skin
Dry (anhydrosis), cold, yellowish skin
Non-pitting oedema (e.g. hands, face)
Dry, coarse scalp hair, loss of lateral aspect of eyebrows
Gastrointestinal
Constipation
Gynaecological
Menorrhagia
Neurological
Decreased deep tendon reflexes
Carpal tunnel syndrome
A hoarse voice is also occasionally noted.
SGLT-2 inhibitor mechanism
reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.
side effects SGLT-2 inhibitors
urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored
Patients taking SGLT-2 drugs often lose weight, which can be beneficial in type 2 diabetes mellitus.
-agliflozin
mild hyponatraemia management
130-134 mmol/l
Non-specific symptoms such headache, lethargy, nausea, vomiting, dizziness, confusion, and muscle cramps
Fluid restriction (less than 800 mL/day) Loop diuretics
moderate hyponatraemia Mx
20-129 mmol/l
Hypertonic saline in first 3-4 hours to increase Na+ >120 mmol/l
Rest is the same as mild
severe hyponatraemia Mx
Less than 120 mmol/l
Seizures, coma, and respiratory arrest
Bolus of hypertonic saline until symptom resolution
With or without conivaptan
what is conivaptan?
Vasopressin/ADH receptor antagonists (conivaptan):
These act on V1 and V2 receptors. The V1 receptors cause vasoconstriction while the V2 receptors results in selective water diuresis, sparing the electrolytes.
They should be avoided in patients who have hypovolemic hyponatremia.
Vasopression/ADH receptor antagonists can stimulate the thirst receptors leading to the desire to drink free water. They can be hepatotoxic in patients with underlying liver disease.
hyponatraemia Mx complications
Osmotic demyelination syndrome (central pontine myelinolysis)
can occur due to over-correction of severe hyponatremia
to avoid this, Na+ levels are only raised by 4 to 6 mmol/l in a 24-hour period
symptoms usually occur after 2 days and are usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma
patients are awake but are unable to move or verbally communicate, also called ‘Locked-in syndrome’
causes of hypertonic hyponatraemia
hyperglycaemia
mannitol
causes of isotonic hyponatraemia
hyperproteinaemia
hyperlipidaemia
hypotonic hyponatraemia need to look at…
fluid status
Low serum osmolality with dehydration
suggests salt and water loss from the kidneys or elsewhere. Low urinary sodium (<20 mEq/L) in these patients is suggestive of GI or sequestrational loss, such as due to vomiting, diarrhoea or third spacing. Normal urinary sodium (>20 mEq/L) is suggestive of renal loss, such as due to diuretics, mineralocorticoid deficiency, renal tubular acidosis, cerebral salt wasting or salt wasting nephropathy.
Low serum osmolality with euvolaemia
suggestive of redistribution. Urine osmolality <100 mOsm/kg may be due to primary polydipsia or beer potomania syndrome; urine osmolality >100mOsm/kg suggest SIADH, hypothyroidism or glucocorticoid deficiency.
Low serum osmolality with hypervolaemia
suggestive of water retention. Low urinary sodium (<20 mEq/L) in this case is suggestive of renal failure as a cause, while normal urinary sodium (>20 mEq/L) suggests other causes of fluid overload such as heart failure, liver cirrhosis, nephrotic syndrome or hypoalbuminaemia.
SIADH causes
Malignancy
small cell lung cancer
also: pancreas, prostate
Neurological stroke subarachnoid haemorrhage subdural haemorrhage meningitis/encephalitis/abscess
Infections
tuberculosis
pneumonia
Drugs sulfonylureas* SSRIs, tricyclics carbamazepine vincristine cyclophosphamide
Other causes
positive end-expiratory pressure (PEEP)
porphyrias
SIADH Mx
correction must be done slowly to avoid precipitating central pontine myelinolysis
fluid restriction
demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH
ADH (vasopressin) receptor antagonists have been developed
gynaecomastia causes
physiological: normal in puberty syndromes with androgen deficiency: Kallman's, Klinefelter's testicular failure: e.g. mumps liver disease testicular cancer e.g. seminoma secreting hCG ectopic tumour secretion hyperthyroidism haemodialysis drugs: see below
Drug causes of gynaecomastia spironolactone (most common drug cause) cimetidine digoxin cannabis finasteride GnRH agonists e.g. goserelin, buserelin oestrogens, anabolic steroids
renal tubular acidosis type 1
(distal)
inability to generate acid urine (secrete H+) in distal tubule
causes hypokalaemia
complications include nephrocalcinosis and renal stones
causes include idiopathic, rheumatoid arthritis, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy
renal tubular acidosis type 2
(proximal)
decreased HCO3- reabsorption in proximal tubule
causes hypokalaemia
complications include osteomalacia
causes include idiopathic, as part of Fanconi syndrome, Wilson’s disease, cystinosis, outdated tetracyclines, carbonic anhydrase inhibitors (acetazolamide, topiramate)
rental tubular acidosis type 3
(mixed)
extremely rare
caused by carbonic anhydrase II deficiency
results in hypokalaemia
renal tubular acidosis type 4
(hyperkalaemic)
reduction in aldosterone leads in turn to a reduction in proximal tubular ammonium excretion
causes hyperkalaemia
causes include hypoaldosteronism, diabetes
stess urinary incontinance Mx
pelvic floor muscle training: NICE recommend at least 8 contractions performed 3 times per day for a minimum of 3 months
surgical procedures: e.g. retropubic mid-urethral tape procedures
duloxetine may be offered to women if they decline surgical procedures
a combined noradrenaline and serotonin reuptake inhibitor
mechanism of action: increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced
contraction
urge incontinance management
bladder retraining (lasts for a minimum of 6 weeks, the idea is to gradually increase the intervals between voiding) bladder stabilising drugs: antimuscarinics are first-line. NICE recommend oxybutynin (immediate release), tolterodine (immediate release) or darifenacin (once daily preparation). Immediate release oxybutynin should, however, be avoided in 'frail older women' mirabegron (a beta-3 agonist) may be useful if there is concern about anticholinergic side-effects in frail elderly patients
causes of hypocalcaemia
vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis
Contamination of blood samples with EDTA may also give falsely low calcium levels.
Hypocalcaemia Mx
acute management of severe hypocalcaemia is with intravenous replacement. The preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended
further management depends on the underlying cause
osteomalacia bloods
hypocalcaemia associated with a low serum phosphate
phaeochromocytoma
rare catecholamine secreting tumour. About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome
Basics
bilateral in 10%
malignant in 10%
extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)
1,2,3
NF-1, MEN 2, VHL (chromosome 3)
phaeochromocytoma features
hypertension (around 90% of cases, may be sustained) headaches palpitations sweating anxiety
phaeochromocytoma Ix
24 hr urinary collection of metanephrines (sensitivity 97%*)
this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)
phaeochromocytoma Mx
Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)
thyroid function in pregnancy
In pregnancy, there is an increase in the levels of thyroxine-binding globulin (TBG). This causes an increase in the levels of total thyroxine but does not affect the free thyroxine level.
causes of lower than expected HBA1c
reduced lifespan of RBCs
Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis
causes of higher than expected HBA1c
increased RBC lifespan
Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy
gliptin MoA
DPP-4 inhibitors increase levels of incretins (GLP-1 and GIP)
oral preparation
trials to date show that the drugs are relatively well tolerated with no increased incidence of hypoglycaemia
do not cause weight gain
hypercalcaemia management
The initial management of hypercalcaemia is rehydration with normal saline, typically 3-4 litres/day. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days
Other options include:
calcitonin - quicker effect than bisphosphonates
steroids in sarcoidosis
Loop diuretics such as furosemide are sometimes used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration. However, they should be used with caution as they may worsen electrolyte derangement and volume depletion.
primary prevention statins
NICE recommend we use the QRISK2 CVD risk assessment tool for patients aged <= 84 years. Patients >= 85 years are at high risk of CVD due to their age. QRISK2 should not be used in the following situations as there are more specific guidelines for these patient groups:
type 1 diabetics
patients with an estimated glomerular filtration rate (eGFR) less than 60 ml/min and/or albuminuria
patients with a history of familial hyperlipidaemia
> 10% = treat
QRISK 2 underestimates in who?
people treated for HIV
people with serious mental health problems
people taking medicines that can cause dyslipidaemia such as antipsychotics, corticosteroids or immunosuppressant drugs
people with autoimmune disorders/systemic inflammatory disorders such as systemic lupus erythematosus
criteria for starting statin in T1 diabetes
older than 40 years, or
have had diabetes for more than 10 years or
have established nephropathy or
have other CVD risk factors
statin monitoring
NICE recommend we follow-up patients at 3 months
repeat a full lipid profile
if the non-HDL cholesterol has not fallen by at least 40% concordance and lifestyle changes should be discussed with the patient
NICE recommend we consider increasing the dose of atorvastatin up to 80mg
neuropathic pain Mx
BPH/or any cause of urinary retention … exclude amitryp
Renal impairment make pregab prefered over gaba
narrow-angle glaucoma exclude dulox and ami.
addisons features
lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia
causes of hypoadrenalism
Primary causes tuberculosis metastases (e.g. bronchial carcinoma) meningococcal septicaemia (Waterhouse-Friderichsen syndrome) HIV antiphospholipid syndrome
Secondary causes pituitary disorders (e.g. tumours, irradiation, infiltration)
Exogenous glucocorticoid therapy
*Primary Addison’s is associated with hyperpigmentation whereas secondary adrenal insufficiency is not
options for treating Graves
titration of anti-thyroid drugs (ATDs, for example carbimazole), block-and-replace regimes, radioiodine treatment and surgery. Propranolol is often given initially to block adrenergic effects
