Endocrinology Flashcards
production of which protein by the liver is stimulated by GH in order to mediate growth and anabolism in the body?
IGF-1 (insulin-like growth factor 1)
define acromegaly
a clinical condition resulting from prolonged excessive GH and hence IGF-1 secretion in ADULTS, with loss of normal pulsatile secretion of GH.
most common cause of acromegaly?
pituitary adenoma
symptoms of acromegaly?
enlargement of extremities- jaw enlargement=pronagthism, hands and feet- change in ring or shoe size? bitemporal hemianopia headaches sweating increased tiredness and lethargy joint pains
signs of acromegaly?
facial appearance- coarse features, oily skin, frontal bossing, enlarged nose. deep nasolabial furrows, prognathism, increased interdental separation
deep voice-laryngeal thickeneing
macroglossia
CTS, soft tissue swelling
MSK changes- degeneration in joints leading to OA, generalised myopathy
goitre and other organomegaly
complications of acromegaly?
HTN
IHD, CVD, CCF, possible increased prevalence of regurgitant valvular heart disease
insulin resistance and impaired glucose tolerance/DM
OSA- soft tissue swelling in NP region
increase risk of colonic polyps and colonic Ca
dynamic function test for acromegaly?
oral glucose tolerance test
what dynamic function test is used in assessing pituitary insufficiency, and what are the contraindications to this test?
insulin stress test- insulin given to pt which will reduce glucose in blood, and so normally stimulate increased ACTH and GH levels.
CI in epilepsy as can cause a seizure, and in IHD as MI risk due to stress on heart with catecholamine release.
difference between hyperthyroidism and thyrotoxicosis?
thyrotoxicosis- clinical, physiological and biochemical findings in pt with excess thyroid hormones, for any reason e.g. secondary hyperthyroidism- TSH secreting pituitary tumour and in resistance to thyroid hormones.
hyperthyroidism- thyrotoxicosis (symptoms and signs of excess thyroid hormones) due to thyroid hyperfunction.
what ADR of carbimazole must pts with thyrotoxicosis be warned about looking out for symptoms of?
agranulocytosis- neutrophils significantly reduced, can lead to dangerous sepsis, also risk of with the antipsychotic clozapine, some NSAIDs and anti-epileptic drugs
warn about develop. of fever, sore throat or mouth ulcers
2 complications to be aware of in management of a hyponatraemic patient?
heart failure
central pontine myelinolysis
how is a dehydrated hyponatraemic pt assessed to determine cause?
we want to know where fluid being lost from. if urinary Na+ more than 20mmol/L, then Na+ and water are being lost via the kidneys e.g. Addison’s disease, renal failure, diuretic excess or osmolar diuresis e.g. high glucose in DM or urea.
if urinary Na+ 20 mmol/L or less, than Na+ and water are lost other than via kidneys e.g. vomiting, diarrhoea, fistulae, burns, SBO, CF, rectal villous adenoma.
1st consideration in determining cause of hyponatraemia?
is pt dehydrated or fluid overloaded
or euvolaemic
how is non-dehydrated hyponatraemic pt assessed?
want to know if fluid overloaded or not
if oedematous, pt may have nephrotic syndrome, CCF, liver cirrhosis or renal failure.
if not oedematous, want to know urine osmolality. If >500mmol/kg, then SIADH is the cause. If 500 or less, then causes may be water overload, severe hypothyroidism or glucocorticoid insufficency.
causes of SIADH?
malignancy- lung small cell carcinoma, pancreas,prostate, thymus or lymphome
CNS- abscess, stroke, SD or SA haemorrhage, SLE, vasculitis, head injury
Endocrine disease-hypothyroidism- reduced cardiac output triggers excess ADH release from carotid sinus baroreceptors
Drugs- opiates, SSRIs, psychotropics, cytotoxics
Other- trauma, symptomatic HIV
causes of hypoglycaemia?
Fasting hypoglycaemia:
most common= insulin or sulfonylurea tment in known diabetic e.g. with increased activity, missed meal, or OD.
if non-diabetic, EXPLAIN:
EXogenous- drugs e.g. insulin, oral hypoglycaemics, beta blockers, ACEIs
Pituitary insufficiency
Liver failure
Addison’s disease
Islet cell tumours e.g. insulinoma, and immune hypoglycaemia e.g. in Hodgkin’s disease
Non-pancreatic neoplasms e.g. fibrosarcoma
post-prandial:
gastric/bariatric surgery
type 2 DM
investigation of fasting hypoglycaemia?
fingerprick glucose during attack, lab glucose if in hospital
drug history, exclude liver failure
72h fasting may be needed, take blood samples for glucose, insulin, c-peptide and plasma ketones if symptomatic
may be hypoglycaemic hyperinsulinaemia e.g. in insulinoma, sulfonylureas, insulin injection
if insulin low, and no excess ketones, think non-pancreatic neoplasm or anti-insulin receptor antibodies e.g. in Hodkin’s
if insulin reduced and ketones increased, thinck alcohol, pituitary insufficiency or addison’s disease
investigation of post-prandial hypoglycaemia?
prolonged OGTT
what is total T4 and T3 affected by in comparison to free T4 and T3?
thyroxine binding globulin (TBG)
when is thyronine binding globulin increased?
pregnancy
hepatitis
oestrogen therapy
when is TBG decreased?
nephrotic syndrome CLD acromegaly malnutrition drugs e.g. corticosteroids, phenytoin, androgens
what is sick euthyroidism?
in any systemic illness, TFTs may become deranged
typical pattern is for everything to be LOW
should rpt test after recovery
causes of a normal TSH and abnormal T4?
changes in TBG
assay interference- due to Abs in serum
amiodarone-used in AF tment
pituitary TSH tumour
pts who should be screened for abnormalities in thyroid function?
AF
hyperlipidaemia
DM-on annual r/v
women with type 1 DM during 1st trimester and post delivery
those on amiodarone or lithium-e.g. for bipolar (6 mnthly)
those with down’s, or turner’s, or Addison’s disease (yrly)
symptoms of thyrotoxicosis ( clinical effect of excess thyroid hormone)?
heat intolerance weight loss increased appetite diarrhoea sweats palpitations tremor irritability labile emotions oligomenorrhoea with or without infertility- oestrogen antagonised rarely psychosis, chorea, panic, itch, alopecia, urticaria
signs of throtoxicosis?
pulse fast or irregular-AF, SVT warm moist skin fine tremor palmar erythema thin hair lid lag and lid retraction goitre thyroid nodules bruit
signs of grave’s disease?
exophthalmos-appearance of protruding eye, proptosis-eyes protrude beyond orbit, opthalmoplegia-espec. of upward gaze
also corneal ulceration, loss of colour vision, papilloedema
pt may complain of eye discomfort, grittiness, photophobia, diplopia, reduced acuity, increased tear production ,and optic nerve can become compressed due to afferent pupillary defect-may need decompression-and be wary more likely if eye cannot protrude!
pretibial myxoedema- oedematous swellings above lateral malleoli seen over the shins due to excess glycosaminoglycan accumulation in dermis and subcutis of skin, immunological process e.g. anti-TSH receptor antibodies can bind to fibroblasts and stimulate them to increase GAG production
thyroid acropachy- clubbing, painful finger and toe swelling, periosteal reaction in limb bones.
cause of grave’s disease?
circulating IgG autoantibodies which bind to and activate thyrotropin receptors, causing smooth thyroid enlagement and increase hormone prod. espec. T3.
react with orbital autoantigens
triggered by stress, infection, childbirth
causes of thyrotoxicosis?
grace’s disease
toxic multinodular goitre- must follow symptomatic tment with radioiodine, surgery indicated for compressive symptoms e.g. dysphagia, dyspnoea
toxic adenoma- solitary nodule secreting thyroid hormones, ‘hot’ on isotope scan, rest of gland suppressed, treat with radioiodine
ectopic thyroid tissue e.g. metastatic follicular thyroid cancer, choriocarcinoma, struma ovarii-ovarian teratoma with thyroid tissue
exogenous- iodine excess e.g. contrast media-thyroid storm, levothyroxine excess-causes increased T4, decreased T3 and thyroglobulin
subacute de quervain’s thyroiditis- post viral with painful goitre, low isotope uptake on scan, treat with NSAIDs
drugs-amiodarone, lithium
post partum
TB
drug tment of thyrotoxicosis?
carbimazole- inhibitor of thyroid peroxidase required for iodination and thyroglobulin molecules. can be titrated e.g. 20-40mg/24hr PO for 4 wks, reduce according toTFTs every 1-2mnths, or block-replace- give with thyroxine.
maintain on either in grave’s for 12-18mnths, then withdraw
beta blocker e.g. propranolol 40mg/6h for rapid symptom control
50% of pts likely to relapse after stopping carbimazole tment, what else can be done?
radioiodine
surgery- thyroidectomy- but risk of recurrent laryngeal nerve damage-hoarse voice, and hypoparathyroidism, and pt can become hypo or hyperthroid
CIs to radioiodine tment in hyperthyroidism?
pregnancy
lactation
caution in active hyperthyroidism as risk of thyrotoxic storm- hyperthyroid crisis, also precipitated by recent thyroid surgery, infection, MI and trauma
signs and symptoms of thyrotoxic storm?
increased temperature confusion agitation coma tachycardia AF diarrhoea and vomiting goitre thyroid bruit acute abdomen HF CVS collapse
complications of thyrotoxicosis?
HF- thyrotoxic cardiomyopathy, increased in elderly angina AF OP ophthalmopathy gynaecomastia thyroid storm
main known RF for thyroid eye disease in Grave’s?
smoking
action of PTH?
increase osteoclasr activity to relase Ca2+ and PO43- from bones
increase Ca2+ and reduce PO43- reabsorption in kidney
increase active production of calcitriol for Ca2+ absorption by the gut
overall effect= increase Ca2+ and decrease PO43-
primary hyperparathyroidism causes?
solitary adeonoma
hyperplasia of all glands
parathyroid Ca
presentation of primary hyperparathyroidism?
often may seem asymptomatic
signs relating to raised Ca2+: weak, tired, depressed, thirsty, dehydrated but polyuric, renal stones, abdo pain, pancreatitis, ulcers
bone pain, fractures, osteopenia/OP
raised BP- so check Ca2+ in everyone with HTN
results of investigations in primary hyperparathyroidism?
Ca2+ and PTH raised, or inappropriately normal- thiazides, lithium
reduced phosphate, unless in renal failure
ALP increased from bone activity
24hr urinary Ca2+ increased
imaging: osteitis fibrosa cystica-RARE-subperiosteal erosions, cysts, DEXA-OP
management of mild primary hyperparathyroidism?
increase fluid intake to prevent renal stones
avoid thiazides and high Ca2+ and Vit D intake
see 6 mnthly
indications for surgery in primary hyperparathyroidism?
high serum or urinary Ca2+ bone disease OP renal calculi reduced renal function aged 50 or below
