Endocrine Flashcards
What is an endocrine hormone?
blood borne and acts at distant sites
What is a paracrine hormone?
acting on adjacent cells
What is an autocrine hormone?
feedback on the same cell that secreted the hormone
What is an endocrine gland?
secretes into the blood stream (thyroid, adrenal, beta cells of the pancreas)
What is an exocrine gland?
secretes through a duct (pancreas amylase and lipase)
Do fat soluble of water soluble hormones have a longer half life?
fat soluble
Are fat soluble of water soluble hormones protein bound or unbound?
fat - protein bound
water - unbound
Where do peptides store hormones?
in secretary granules
What are the different classes of hormones?
peptides, amines, idothyronines, cholesterol derivatives and steroids
Synthesis of T3 and T4?
thyroglobulin released into colloid and acts as a base for thyroid hormone sysnthesis, the incorporation of iodine forms idothyrosines, it is conjugated and then forms T3 and T4 and stored in colloid bound to thyroglobulinm TSH stimulates the movement of colloid unto secretory cell, T4 and T3 cleaved from thyroglobulin
How do adrenocortical and gonadal steroids work?
enter call and pass to nucleus by diffusing through plasma membrane, altered to an active metabolite and bind to a cytoplasmic receptor, receptor hormone complex binds to GRE, initiating transcription of gene to mRNA, and this directs protein synthesis
How is hormone secretion controlled?
continuous basal secretion, superadded rhythms (day night cycle), release inhibiting factors, releasing factors
What is synergism?
combined effects of two hormones amplified
What is permissiveness?
a hormone needed for another’s full potential effect
Function of the thyroid hormone?
accelerates food metabolism, increases protein synthesis, stimulation of carbohydrate metabolism, enhances fat metabolism, increase in ventilation rate, increase in cardiac output and heart rate, brain development during foetal life and postnatal development, growth rate accelerated
Function of growth hormone?
stimulates production of IGF-1 to induce metabolic changes
decreases adipose, increase liver function and increase muscle, increase protein synthesis, increase lipolysis
What hormone stimulates GH?
GHRH (grehlin increased GH secretion)
What hormone inhibits GH?
somatostatin
What is acromegaly?
an overgrowth of all organ systems, bones, joints, soft tissues from excessive GH secretion after fusion of the epiphyseal plates
What is giantism?
an overgrowth of all organ systems, bones, joints, soft tissues from excessive GH secretion before fusion of the epiphyseal plates
What causes acromegaly?
benign pituitary GH producing adenoma or GHRH producing bronchial carcinoid
Symptoms of acromegaly?
ABCDEF
arthralgia, arthritis, bp raised, carpal tunnel syndrome, diabetes, enlarged organs, field defect
prognathism, interdental separation, macro glossia, spade like hands and feet, increased jaw and hand size, lower pitch of voice, headaches
Investigations for acromegaly?
monitor visual fields, raised glucose, serum phosphate, urinary calcium and serum triglycerides, MRI and CT, IGFBP-3 increased, ECG, ECHO, serum prolcatin, raised IGF-1
What is the diagnostic test for acromegaly?
glucose tolerance test
GH is inhibited by glucose so should be suppressed 2 hours after oral glucose load, if not
What is IGFBP-3?
the main binding protein for circulating IGF, and is increased in acromegaly due to increased IGF-1
Management of acromegaly?
control symptoms, normalise hormones levels and correc tumour compression
trans-sphenoidal surgery of endoscopic trans sphenoidal treatment in pituitary adenomas if non invasive macroadenoma
pegvisomant
somatostatin nalogues
dopamine agonists
radiotherapy/sterotactic radiotherapy
follow ups
How does pegvisomant treat acromegaly?
for those who don’t respond to somatostatin, suppressed IGF-1 levels - does not affect tumour size
How does somatostatin analogues treat acromegaly?
inhibit GH secretion
side effect of long term dopamine agonists for acromegaly?
cardiac fibrosis - need regualr ECHO
Why is stereotactic radiotherapy better than radiotherapy in acromegaly?
more accurate for tumour location and irradiation and is less radiation to normal brin tissue
Complications of acromegaly?
hypertension, cardiac faiure, diabetes, obsturctive sleep apnoea, increased colonic polyp risk, post surgery hypopituitarism, DI, CSF rhinorrhoea, infection, hyperprolactinaemia, hormone deficiencies, gestational diabetes, gravid hypertension
Prognosis of acromegaly?
2-3x increased mortality, prediction of survival is based of the post treatment GH conc, untreated lead to death by CV disease or cancer
What are carcinoid tumours?
slow growing tumours that originate in cells of the diffuse neuroendocrine system (enterochromaffin cells)
Where do carcinoid tumours usually occur?
gastro entero pancreatic tumours, in the appendix, ileum, rectum, bronchi of lung
What condition is carcinoid tumours related to?
carcinoid syndrome
Symptoms of carcinoid tumours?
pain, weight loss, appendicitis, intussception, obstruction, RUQ pain, bradykinin, tachykinin, subsatnce P, VIP, gastrin, insuline, glucagon, ACTH, parathyroid and thyroid hormone secretion
What is carcinoid syndrome?
increased release of 5-hydroxytryptamine, prostagladins, kinins, substance P, somatostatin, corticotropin and neuron specific enolase into the peripheral circulation, secretion depends on tumour location and metastases
Presentation of carcinoid syndrome?
bronchoconstriction, paroxysmal flushing in upper body and post alcohol, coffee, food or drugs, diarrhea, abdo pain, palpitations, increased peptic ulcer risk, changes in mental state
What is the common size of a carcinoid syndrome?
1-2cm, the bigger the more likely for metastases
Investigations of carcinoid syndrome?
plasma chromogranin reflects tumour mass
24hr urinary 5-hydroxyindoleacetic acid, >25mg is diagnostic (but can be changed by other drugs and food)
pentagastrin test
gastric US and endoscopy, CT, MRI, laparotomy, scintigraphic imagaing with labelled somatostatin to find site
somatostatin SPECT
Complications of carcinoid tumours?
MEN1, appendicitus, intussception, bowel obstruction, metastatic spread
Management of carcinoid tumour and syndrome?
avoid precipitating factors, chemo e.g. doxorubicin, external beam radiotherapy, chemoembolisation, liver transplant, octreotide (somatostatin analogue) to block release of tumour mediators, loperamide for diarrhea, IFN-a, resect tumours, bebulking, radiofrequency ablation, PPI do prevent ulceration
What is carcinoid crisis?
when tumour outgrows its riction, altered mental state, hyperglyaemiablood supply or handled too much during surgery so that vasoactive mediators flow out, causing life threatening vasodilations, hypotension, tachycardia, bronchoconst
Treatment for carcinoid crisis?
octrotidem supportive measure, fluid balance managment
Prognosis of carcinoid crisis?
5-8years survival, 3 if metasatases, prognosis depends on site
What is hypothyroidism?
decreased thyroid hormone production, causing a slow down in body’s functions
Symptoms of hypothyroidism?
bradycardia, reflexes relax slowly/mentally slowing, aches, ataxia, dry skin and hair, fatigues, drowsy, cold intolerance, ascities, round puffy face, defeated demeanour, irregular/heavy periods, hoarse voice, carpal tunnel syndrome, weight gain, constripation, fluid retention, infetility, loss of libido, memory loss, confusion, goitre
What are the complications of hypothyroidism in pregnancy?
pre eclampsia, anaemia, premature labour, low birth weight, still birth, serious blleding post birth, hypothryoid coma (myxoedema coma)
How common is hypothyroidism?
0.1-0.2% of pop., increased risk with age and in women
Causes of hypothyroidism?
AUTOIMMUNE - attack thyroid gland, block binding of TSH to receptor (hashimotos if a goitre is formed)
surgery, radioactive treatment iron deficiency, medicine side effects, thyroiditis, pituitary gland problem, congenital (thyroid aplasia/dysplasia)
Risk factors for autoimmune hypothyroidism?
FH, downs, turner syndrome, enlarged thyroid, Graves disease, thyroiditis post birth, autoimmune conditions
Diagnosis of hypothyroidism?`
raised TSH, low thyroxine, thyroid antibodies, anaemia, hyperlipidaemia, hyponatraemia, incresed serum creatinine kinase levels, associated myopathy
What is subclinical hypothyroidism?
raised TSH, normal thyroxine, but thyroid glands need extra stimulation to make the required thyroxine needed, this increases hypothyroidism risk
Treatment of hypothyroidism?
lifelong levothyroxine, start low dose (esppecially in elderly) and increase dose
check TSH once a year for adjustment, which is also needed in weight gain and pregnancy
Complications of levothryoxine?
angina pain worsens, hyperthyroidism
How dose levothyroxine treat hypothyroidism?
replaces thyroxine production and normalises serum TSH concentrations
What is myxoedema coma?
severe hypothyroidism with confusion, coma, hypothermia, cardiac failure, hypoventilation, hypoglycaemia and hyponatraemia, common in elderly
Treatment of myxoedema coma?
oral T3, o2, gradual rewarming, hydrocortisone, glucose in fusion, supportive managment, thyroid diet by changing iodine in food into thyroid hormones
What is borderline hypothyroidism?
slight increased serum TSH, normal T4, due to early phase chronic autoimmune thyroiditis so 2-4% will develop overt hypothyroidism, treat with levothyroxine
What is Hashimoto’s disease?
autoimmune hypothyroidism with a goitre
Examples of thyroid diet foods?
protein, green leafy vegetables, fish, iodized salt, eggs, seaweed, avoid alcohol
Cause of Hashimoto’s disease?
iodine, medications, infection, smoking, stress
goitre associated with HLA-DR5 causing lymphatic and plasma cell infiltration, formation of lymphoid molecules from follicular hyperplasia, and damage to follicular basement membrane
In who is Hashimoto’s disease most common?
women aged 60-70
Symptoms of Hashimoto’s disease?
rapidly enlarged thyroid gland, dyspnoea, dysphagia, mild neck pain and tenderness, increase in size, thyrotoxicosis, hyperlipidaemia, fatigue, forgetfullness, myxoedema, feeling cold, weight gain, depression, poor memory
Investigations of Hashimoto’s disease?
low T3 and T4, high thyroid antibodies (anti-TPO and anti-Tg) and TSH, damaged thyroid cells, increase lymphocytes and plasma cells, thyroid parenchyma atrophy, follicular hyperplasia, lymphoid follicles, radioactive iodine uptake for hot or cold classification
Whats the difference between a hot and cold thyroid nodule?
cold has higher malignancy risk and needs a fine needle aspiration biopsy
Treatment of Hashimoto’s disease?
levothyroxine sodium to restore clinically and biochemically euthyroid state, surgery if large goitre or cosmetic reasons
Complications of Hashimoto’s disease?
over replacement can cuase bone loss and increased heart rate, hyperlipidaemia if untreatment, Hashimoto’s encephalopathy, myxoedema coma
Prognosis of Hashimoto’s disease?
good and most achieve normal thyroid levels
What is hyperthyroidism?
raised thyroid level from overactive thyroid gland
Causes of hyperthyroidism?
grave’s disease (most common), thyroid nodules, De Quervains thyroiditis, postpartum thyroiditis
What is De Quervains thyroiditis?
acute inflammation of the gland from viral infection, presenting with fever, maliase, goitre and neck pain, treated with aspirin
Symptoms of hyperthyroidism?
restless, nervous, emotional, irritable, poor sleeping, hand tremor, losing weight, increased appetite, palpitations, sweating, heat intolerance, increased thirst, diarrhoea, sob, hair thinning, irregular and light periods, tiredness, muscle weakess, neck goitree, exophthalmos, graves dermopathy
Complications of hyperthyroidism?
atrial fibrillation, cardio myopathy angina, heart failure, pregnancy complications, osteoporiosis
How common is hyperthyroidism?
10x more common in women, 20-40years
What does hyperthyroidism show in investigations?
high T4, high T3 in graves, suppressed TSH, thyroid ultrasound, positive microsomal and thyroglobulin antibodies, isotope scan to classify thyroid nodules, fine needle aspiration to exclude malignancy
Treatment of hyperthyroidism?
anti thyroid medications e.g. carbimazole to reduce thyroxine production, high dose then reduce
radioactive iodine drink to destroy thyroid tissue
regular bloods for thyroxine level check
remove part of thyroid gland
treat eye problems: artificial tears, sunglasses, eye protectors during sleep, surgery, radiation treatment, steroid tablets, stop smoking
BBs for first few weeks of treatment and reduces symptoms of tremor, palpitations, sweating, angitation and anxiety
Side effect of carbimazole?
agranulocytosis with fever, sore throat and mouth ulcers (propylthiouracil is better if pregnant)
Precautions during radioactive iodine treatment?
do not get pregnant for 6 months after, no breastfeeding, limit close contact with babies, children, pregnant women and pets, sleep alone, stay more than an arms length away from other people, avoid going places in close proximity to people, take time off work
Symptoms of ophthalmic Grave’s disease?
bilateral eye involvement, pressure and pain in one eye, a gritty sensation, reduced vision, photophobia, exophthalmos and opthalmoplegia, MRI shows enlarged muscle and oedema
What is exophthalmos and opthalmoplegia?
retro orbital inflammation, causing eye popping, worse in smokers
Treatment of ophthalmic Grave’s disease?
correct thyroid dysfunction, hyperthryoidism, smoking cessation, artificial tears, high dose systemic steroids to reduce inflammation, surgery to partially sew eyelids together to protect cornea, corrective eye muscle surgery
Triggers of ophthalmic Grave’s disease?
stress, infection, childbirth, hyperthyroid
Pathophysiology of ophthalmic Grave’s disease?
IgG autoantibodies bind to and activate G protein coupled thyrotropin receptors cyasing smooth thyroid enlargement, increased hormone production and react with orbital autoantigen, leading to catecholamine sensitivity of the levator palpebrae superioris causing lid retraction and lid lag. T lymphocytes react with antigens and cause retro orbital inflammation. Swelling and oedema of the extraocular muscles leading to movement limitation and proptosis, increasing pressure on optic nerve, leading to atrophy
How common is thyroid cancer?
1% of all malignancies, incidence is increasing, most common malignancy of endocrine system
Symptoms of thyroid cancer?
lymph node metastases, increased thyroid nodule size which is hard and irregular, enlarged lymph node
What are different types of thyroid cancer?
papillary, follicular, medullary, thyroid lymphoma, Hurthle cell, anaplastic thyroid
What is the most common thyroid cancer and in who is it most common?
papillary - women aged 35-40
What is the spread and prognosis of papillary and follicular thyroid cancer like?
spreads locally to neck, compressing trachea and recurrent laryngeal nerve, metastases most often in lung and bone
What causes follicular thyroid cancer?
areas of low iodine
In who is follicular thyroid cancer most common?
women 30-30years
Where does medullary thyroid cancer arise from?
parafollicular cells due to their malignancy making them produce carcinoembryonic antigen and calcitonin
mainly autosomal dominant inherited
Who gets thyroid lymphomas?
women aged 50 with Hashimoto’s
Symptoms of thyroid lymphoma?
dyspnoea, dysphagia, non Hodgkin’s,
Treatment of hurthle cell carcinoma?
surgery, postoperative radioative iodine 131, levotyroxine, external radiotherapy
What kind of thyroid cancers are more aggressive ?
medullar and anaplastic
Where do anaplastic thyroid cancers arise from?
follicular cells - normally from a pre existing, well differentiated thyroid tumour which has undergone additional mutational events
Risk factors of thyroid cancer?
exposure to ionising radiation, history/family history of thyroid problems, mutation in RET proto oncogenes which causes MEN2 as well, MEN1/2, Cowden’s syndrome, familial adenomatous polyposis, obesity
TNM staging?
1 - no lymph node spread or metastases, 45
3 - >4cm but contained in thyroid, or localised tumour with spread to lymphs
4a - spread to nearby structure, or localised with distant lymph node spread
4b - spread beyond nearby structures
4c - metastases
Presentation of thyroid cancer?
thyroid nodule, hard and fixed nodules suggest malignancy more, usually non tender on palpitation, firm cervical masses suggest regional node mestastases, vocal cord paralysis suggests recurrent laryngeal nerve involvement
Investigations of thyroid cancer?
TFTs, serum thyroglobin, serum calcitonin, thyroid US, fine needle aspiration cytology if >1cm or suspected malignancy (distinguishes between benign and malignant), radionuclide imaging with 123 iodine uptake studies, Gallium 67 Ga for thyroid lymphoma diagnosis, Ct and MRI for metastatic spread
Treatment of thyroid cancer?
total thyroidectomy, may need intraoperative nerve monitoring for the laryngeal nerves, radioiodine remnant ablation and therapy, adjuvant external beam radiotherapy, targeted multikinase inhibitor (sorafenib), surgery, iodine 131 for microscopic residuals, effective thyroid ablation with TSH stimulation so need extra administration
Complications of thyroid cancer?
laryngeal nerve palsy, hypoparathyroidism, nerve damage
What is Cushing’s syndrome?
increased glucocorticoid in the body
How common is Cushing’s syndrome?
5/1 million a year develop ot, main women 20-50
Functions of cortisol?
regulate BP, regulate immune system, balance insulin effect, help stress response, bone formation inhibition, decreases immune function, increase gluconeogenesis, lipolysis and proteolysis
Causes of Cushing’s syndrome?
long term steroid medication e.g. prednisolone, pituitary adenoma (Cushing’s disease) which increases ACTH, adrenal hyperplasia, ectopic ACTH production (lung cancers, MEN1), alcohol, depression
Cushing’s syndrome symptoms?
obesity, PLETHORIC complexion, moon face, facial puffiness and REDNESS, diabtes, facial hair in women, hypertension, thin EASILY BRUISED skin, STRIAE, tiredness, ache and pains, mood swings, loss of libuido, irregular periods, osteoporosis, ankle oedema, excess thirst, increased susceptibility of infections (children tend to be obese and short), PROXIMAL MUSCLE WEAKNESS
Investigations for Cushing’s syndrome?
48hr low dose dexamethasone suppression test, suppressed in normal individuals
high dose dexamethasone suppression test in suppressed in pituitary dependent Cushing’s syndrome and normal suggests ectopic source of ACTH
24hr urine cortisol (normal
Treatment of Cushing’s syndrome?
trans-sphenoidal surgery to remove adenoma
hydrocortisone for several months post surgery to normalise cortisol levels
remove both adrenal glands - but will lead to lifelong replacement therapy
external beam radio therapy
drugs to inhibit cortisol synthesis e.g. metyrapone, ketoconazole, etomidate
remove ectopic tumours
immunosuppressants with steroids
intubation and mifepristone to compete with cortisol at receptors
stop steroids
What is Conn’s syndrome?
hyperaldosterone, excessive levels of aldosterone, causing increase in sodium retention in distal convoluted tubule, increasing water retention, volume expansion with hypertension and excretion of potassium, leading to hypokalaemia
What is the most common cause of secondary hypertenision?
primary hyperaldosterone
What is primary hyperaldosterone?
excessive aldosterone independent of the RAAS, can be an adrenal adenoma (Conn’s), familial hyperaldosterone, adrenal carcinoma
What are the 2 forms of familial hyperaldosterone?
1 - glucocorticoid remediable aldosterone (GRA) - regulatory portion of the 11b-OH gene binds to the aldosterone synthase gene, meaning ACTH releases stimulates this abnormal chimera and excessive aldosterone production from the zona fasciculata not zona glomerulosa, autosomal dominant
2 - inherited aldosterone producing adenoma or inherited bilateral adrenal hyperplasia, increasing aldosterone production, can also be unilateral
What can type 1 familial hyperaldosteronism lead to?
causes early age hypertension, leading to haemorrhagic strokes, so need regular aneurysm sceening, and can become hypokalaemic
Symptoms of hyperaldosteronism?
hypertension, hypokalaemia, metabolic alkalosis, slight increased sodium, polyuria, polydipsia as can’t concentrate urine, weakness from hypokaelaemia, headaches, lethargy
What can Conn’s syndrome lead to?
periodic cramps and occasional lower limb paralysis, the adenomas are usually unilateral
What will investigations show in hyperaldosteronism?
hypokalaemia, hypernatraemia, renal impairment, raised aldosterone and low renin, arrhythmias from electrlyte imblance, CT/MRI show adenomas and hyperplasia, selective adrenal venous sampling to localise cause, genetic testing, salt loading,
When should tests for hyperaldosteronism be done?
when the patient is off diuretics for 4 weeks and off BBs and CCBs for 2 weeks as can lead to false positives and false negatives, should also stop steroids, potassium suppplements and laxatives
How should aldosterone and renin levels be measured?
lying and standing as they are affected by the upright position, aldosterone should increases after being upright for a few hours
How is the salt loading done for hyperaldosteronism diagnosis?
loading with salt for 2 weeks, then take samples to suppress aldosterone, failure to suppress confirms primary hyperaldosteronism, if renin is high this excludes primary hyperaldosteronism
DD for hyperaldosteronism?
congenital adrenal hyperplasia, renal artery stenosis, coarctation of aorta, fibromuscular dysplasia, renin secreting tumors, congestive cardiac failure, nephortic syndrome, Gitelmans syndrome, Bartter’s syndrome
Treatment of Conn’s?
aldosterone anatgonists e.g. spironolactone or eplerenone before adrenalectomy, could be long term hypertension though, CT quided acetic acid injections into small functioning adenomas
Treatment of BAH?
aldosterone antangonists e.g. amiloride, spironolactone, eplerenone
Treatment of GRA?
steroids to reduce aldosterone productioon drive, dexamethasone
spironolactone if hypertension persists after
Treatment of adreanl carcinoma?
surgery with post operative adrenolytic therapy with mitotane
What is secondary hyperaldosteronism?
excessive renin due to reduced renal perfusion, stimulating the normal adrenals to produce more aldosterone
Causes of secondary hyperaldosteronism?
diuretics, congestive cardiac failure, hepatic failure, nephrotic syndrome, renal artery stenosis, malignant hypertension
Complications of secondary hyperaldosteronism?
causes myocardial fibrosis, reducin cardiac function and can lead to long term hypertension
Treatment of secondary hyperaldosteronism?
lifelong antihypertensive therapy, aldosterone antagonists
side effects of spironolactone?
gynaecomastia, menstural problems and erectile dysfunction
Which aldosterone antagonists is best to prevent hypokalaemia?
amiloride as it is potassium sparing and counteracts hypokalaemia (but lacks mineralcorticoid inhibition and is only a week antihypertensive)
Which aldosterone antagonist is selctive?
eplerenone
What is Addison’s disease?
lack of steroid hormone rlease form the adrenal glands
How common is Addison’s disease?
8000 people in the UK, age 30-50 normally
What makes steroid hormones?
adrenal cortex
What controls steroid release?
ACTH from the pituitary gland which is stimulated by CRH from the hypothalamus
What makes adrenaline and noradrenaline?
adrenal medulla
Causes of adrenal insufficiency?
autoimmune (80%), TB, meningitis, HIV, cancer, adrenoleukodystrophy, congenital adrenal hyperplasia, critical illness, trauma to adrenal gland, radiotherapy, medicine e.g. ketoconazole
Symptoms of Addison’s disease?
general weakness, easily fatigued, pigmentation on sun exposed areas and pressure points from excess ACTH, vitiligo, loss of body hair in women, postural hypotension, dizziness, loss of appetite, weight loss, food cravings, abdominal pains, diarrhea, constipation, cramps, muscle pain, decreased or irregular menstural cycle, depression, psychosis
What sudden symptoms occur in Addison’s crisis of sudden low cortisol?
severe vomiting and diarrhea, pain andback and abdomen, dehydration, hypotension, collapse, severe illness
When would Addison’s crisis occur?
triggered by other illnesses when more cortisol is needed of after a period of less severe symptoms
Tests for Addison’s disease?
decreased sodium and glucose, increased postassium and calcium, morning cortisol levels, tetracosactide stimulation test, x-rays to find cause, ACTH levels are high or low depending on cause, 21-hydroxylase adrenal autoantibodies if autoimmune, plasma renin and aldosterone levels
How is a short tetracosactide stimulation test from ACTH used for Addison’s disease diagnosis?
there is no cortisol rise in blood post injection in Addison’s disease - Synacthen test
What does high ACTH and low cortisol in the morning suggest?
primary adrenal insufficiency
What does low ACTH and low cotrisol in the morning suggest?
secondary or tertiary adrenal insufficiency
Treatment of Addison’s disease?
hydrocortisone for cortisol replacement, 2 or 3 doses a day to mimic cortisol changes in the day, dose based on weight, height, age, gender, activity levels, ill, surgery, trauma, shift work etc, reduce dose gradually
fludrocortisone regular BP and blood salt levels
need steroid card
Treatment of Addison’s crisis?
hydrocortisone injections and fluids to increase BP, may need ICU
When are cortisol level highest?
in the morning
Complications of Addison’s disease?
other autoimmune disease, adrenal crisis, osteoporosis
What is secondary adrenal insufficiency?
inadequate pituitary of hypothalamic stimulation of the adrenal glands, from hypothalamic-pituitary disease or long term steroid therapy
What is critical illness related corticosteroid insufficiency (CIRCI)?
patients who are critically ill and at increased risk of adrenal dysfunction e.g. in sepsis, severe pneumonia, ARDS, trauma, HIV infection
How do renin levels differ in primary and secondary adrena insufficiency?
renin high and aldosterone low in primary, and unaffected in secondary
How is secondary adrenal insufficiency diagnosed?
insulin tolerance test, hypoglycaemia is induced by an insulin infusion and cortisol response is monitored
test other hormones from the hypotahalmus/pituitary
screen for adrenoleukodystrophy (x linked condition) by measuring very long chain fatty acids in serum sample
CRH stimulation test
Management of secondary adrenal insufficiency?
hydrocortisonem fludrocortisone, regular examinations, educate, steroid card, emergency self injection kit,
Prognosis of adrenal insufficiency?
can be fatal in untreated, prognosis is based on the underlying cause
What diabetes insipidus?
hyposecretion of or insensitivity to the effects of ADH, leading to the inability to concentrate urine in the distal renal tubules, so increased passage of dilute urine, usually >3L/24hrs of low osmolality
Where is ADH made?
in the hypothalamus, transported as neurosecretory vesicles to posterior pituitary and released into the circulation
What is gestational diabetes insipidus?
results from degradation of ADH by a placental vasopressinase
What is dipsogenic diabetes insipidus?
primary polydipsia, caused by primary defect in osmoregulation of thirst, seen in TB meningitis, MS and neurosarcoidosis
What are the two types of diabetes insipidus?
cranial - decreased ADH secretion
nephrogenic - resistance to ADH in kidney
Causes of cranial diabetes insipidus?
idiopathic, tumours, head injury, TB, sarcoidosis, Wegeners granulomatosis, encephalitis, meningitis, cerebral abscess, haemorrhage, thrombosis, sickle cell disease, auto immune hypophysitis, hypophysectomy, post radiotherapy, Woldrams syndrome, mutations in ADH gene
Causes of nephrogenic diabetes insipidus?
idiopathic, hypokalaemia, hypercalcaemia, CKD, drugs, renal tubular acidosis, pregnancy, post obstructive uropaathy, X linked mutation in V2 ADH receptor gene, defect in AQP2 gene, sporadic
Symptoms of diabetes insipidus?
polyuria, >3L or urine a day, polydispsia, dehydration, chronic thirst, hypernatraemia, nocturia/bed wetting, failure to thrive in infants with irritability fever and feeding problems, chronic overdistention, urinary incontinenece, enlarged bladder
DD of diabetes insipidus?
psychogenic or primary polydipsia, DM, Cushings syndrome, hypercalcaemia, hyperkalaemia, diuretic abuse
Investigations in diabetes insipidus?
24 hour urine collection, water deprivation test, MRI to find cause, US, IV peylogram to assess obstruction, increased plasma osmolality, decreased urine osmolality, increased sodium, increased urine output
What is the water deprivation test for diabetes insipidus?
deprive patient of fluids for 8 hours, if patient has >600, it is primary polydipsia, then use desmopressin 2mg IM, if >600 it is cranial, if less it is nephrogenic
Management of cranial diabetes insipidus?
oral/nasal/parenteral desmopressin increased AQP-2 channels in distal convoluted tubule and collecting ducts, miss dose once a week to prevent overdosing, increase water intake
Management of nephrogenic diabetes insipidus?
treat cause, high dose desmopressin with thiazide diuretic, NSAIDs reduce urine volume and plasma sodium by inhibiting PG synthase which can inhibit ASH action, surgery, intermittent catheterisation to reduce urinary tract back pressure complications
Complications of nephrogenic diabetes insipidus treatment?
desmopressin can worsen MI
prognosis of diabetes insipidus?
rare death form dehydration, hypernatraemia, fever, CV etc
annual review of symptoms and 24 hour urinary measurement if lithium use
good prognosis
What is hyponatraemia?
excess of water in relation to serum sodium which is
What is SIADH?
syndrome of inappropriate ADH secretion from posterior pituitary/ectopic source despite low serum osmolarity
Who is most at risk of hyponatraemia?
infants and elderly as less likely to express their thirst and control their own fluid intake , infants with diarrhea and given tap water not fluids as treatment, or given watered down milk formula
Presentation of hyponatraemia?
mild - asymptomatic, anorexia, headache, nausea, vomiting, lethargy
moderate - personality change, muscle cramps, weakness, confusion, ataxia
severe - drowsiness, decreased consciousness, cognitive impairment, seizures, brainstem herniation, can be no symptoms due to cerebral adaption
signs of hypovalaemia - dry mucous membranes, tahycardia, diminished skin turgor
signs of hypervolaemia - pulmonary rales, s3 gallop, JV distention, peripheral oedema, ascites
Diagnostic features of SIADH?
hyponatraemia, plasma hypo-osmolality proportional to hyponataemia, inappropriately elevated urine osmolality (>100mOsmol/kg) commonly >plasma osmolarity, persistent urine Na>30mmol/L with normal salt intake, euvolaemia, normal thyroid and adrenal function , elevated ADH level and low blood uric acid levels
Causes of SIADH?
thiazide diuretics, SSRIs, ACE-I, PPIs, llop diuretics, opiates, idiopathic, hereditary, stress, endurance exercise, marathon runners, herpses zoster, trauma, tumours, infection, MS, GBS, SLE
What will investigations show in SIADH?
low sodium, and low or high serum hypo osmolality, absence of hypervolaemia, adrenal or thyroids dysfunction and use of diuretics, continued urine sodium level (if >20mmol/L, a renal cause should be looked for), serum TSH and thyroxine normal, imaging, will not respond to slaine, radom serum cortisol levels of ACTH stimulation test
Management of SIADH?
correct underlying cause
severe - hypertonic saline with furosemide to prevent circulatory overload and gradually correct hyponatraemia, not rapid as that can cause osmotic demyelination syndrome
hypovolaemic - IV saline replacement, may need desmopressin
normovolaemic - fluid restriction, demeclocycline blocks ADH and induces partial nephrogenic DI, vaptans (vasopressin receptor antagonists)
hypervolaemia - treat hypervalemia, usually HF, AKI, liver cirrhosis
Complications of vaptans?
used in hyponatraemia secondary to SIADH, can induce thirst, expensive, limited availability and can increase sodium levels too rapidly
Complications of hyponatraemia?
gait disturbance in elderly leading to falls, reduces bone mass, increased fractures, severe cerebral oedema with cerebral herniation and death if the fall in sodium is too quick, permanent neurological sequelae, seizures, respiratory arrest, pontine myelinolysis from too rapid a correction
Symptoms of pontine myelinolysis?
quadriplegia, pseudobulbar palasy, locked in syndrome (risk factors: females, hypokalaemia, alcoholism, liver transplant)
What is hypokalaemia?
mild = 3.1-3.5mmol/L
moderate = 2.3-3mmol/L
severe =
What are the classifications of hypokalaemia causes?
increased excretion via kidney, skin or Gi tract, trans-cellular shift, decreased intake (other include chronic alcoholism, chronic peritoneal dialysis and plasmapheresis)
Causes of hypokalaemia from increased loss in kidney, skin and GI?
kidney - diuretics, renal tubular acidosis, hypomagnesaemia, hyperalsosteronism, tubulointerstitial renal disease, liquorice, RAAS activation
GI - diarrhea, vomiting (causing increased Cl, increased aldosterone, inhibiting potassium reabsorption), intestinal fistula, villous adenoma, pyloric stenosis, laxative abuse
skin - burns, erythroderma, increased sweating or increased loss in sweat
Causes of hypokalaemia from transcellular shift
alkalosis, insuline and glucose administration, catecholamines and B2 sympathomimetics, toluene intoxication, CCB, hypothermia
Causes of hypokalaemia from decreased intake?
inadequate fluid replacement during nil by mouth, parenteral nutrition, malnutrition, anorexia, hypocaloric protein diets
Presentation of hypokalaemia?
asymptomatic then lassitudem general weakness and muscle pain and constipation, thread pulse, shallow respirations, confusion, alkalosis
if more severe: severe muscle weakness and paralysis, starts in lower extremities and ascends, resp failure, paraesthesia, tetany, hyporeflexia, arrhythmias, light headedness
What is the most common cause of hypokalaemia?
Gitelman’s syndrome - with impaired renal tubular ion transport from mutation in Na/Cl transporter gene, presents with hypotension, alkalosis, salt wasting, hypomagnesaemia, hypocalciuria, hypermagnesuria, salt cravings, cramps, muscle weakness, aches, fatigue, general weakness, dizziness, nocturia and polydipsia
Investigations in hypokalaemia?
low sodium suggests thiazide use of marked volume depletion, serum bicarbonate is high on long term diuretics, serum glucose, chloride, low serum magnesium, spurious potassium, ECG, low urinary potassium, urinary sodium, urinary osmolality, serum digoxin, ABGs, urine calcium, 24 hour uruine matanhephrines, sodium and potassium, sweat chloride test, low dose dexamethasone suppression test, renal angiogram
What do ECGs show in hypokalaemia?
ST depression, prominent U wave, shallow T wave, slightly prolonged PR interval
premature ventricular contractions, torsades de pointes, ventricular tachycardia and ventricular fibrillation may occur
Treatment of hypokalaemia?
oral (IV if severe) potassium supplements/replacement (KCl), regular potassium monitoring, take potassium sparing diuretic if on diuretic, no potassium if oliguric or as fast stat bolus, normalize serum magnesium, never more IV potassium than 20mmol/hr unless ECG monitoring and hourly serum potassium measurement, treat underlying cause , potassium rich foods, avoid glucose solutions, ampoules of potassium mixed with saline to prevent hypoglycaemia
Complications of hypokalaemia?
cardiac arrhythmias, sudden cardiac death, muscle weakness, flaccid paaralysism rhadomylysis, abnormal renal function (DI, metabolic alkalosis), iatrogenic hyperkalaemia, digoxin toxicity, hepatic encephalopathy in cirrhosis
Prevention of hypokalaemia?
potassium supplements, loss dose diuretics in hypertension, potassium sparing diuretics, needs careful monitoring
What is hyperkalaemia?
mild = 5.5-5.9mmol/L moderate = 6-6.6mmol/L severe = >6.5mmol/L
How much of potassium is intracellular?
98%
Who is most at risk of hyperkalaemia?
young and elderly, hopsital, men
What is artefactual hyperkalaemia and what causes it?
lysis of RBC during vigorous phlebotomy or in vitro release from red cells in some blood disorders (leukaemia) or thrombocytoenia or contaminated with potassium EDTA anticoagulant in FBC bottles
What classifications of hyperkalaemia are there?
renal cause, increased circulation (endogenous or exogenous), shift from transcellular to extracellular space, psuedohyperkalaemia, dehydration, diabetics
What are renal causes of hyperkalaemia?
AKI, CKD as most potassium is excreted renally, renal tubular acidosis, Addison’s, hypereninaemic hyperaldosteronism, drugs that interfere with poassium excretion
What can cause an increase of potassium in the circulation?
potassium supplementation, tumour lysis syndrome, trauma, burns, massive tissue damage, fresh water drowning which causes lysis or erythrocytes, releasing potassium suddenly
What causes a shift of potassium from intracellular to extracelullar?
acidosis (diabetic ketoacidosis), digoxin toxicity, beta blockade, theophylline, hyperkalaemic periodic paralysis, metabolic acidosis, tissue necrosis or lysis
What can give unexpectedly high results of potassium?
prolonged tourniquet time, clenched fist, difficulty collecting sample, test tube haemolysis, wrong anticoagulant, excessive cooling of a specimen, length of storage of specimen, marked leucocytosis, thrombocytosis, sample from a limb that is receiving IV fluids with potassium
Why can diabetic patients get hyperkalaemia?
they are on ACE-I and low in sodium and high in potassium, insulin pushes glucose and potassium into cells and glucagon impairs the intracellular shift of potassium
Symptoms of hyperkalaemia?
MURDER
muscle cramps and parakysis, urine abnormalities, respiratory distress, decreased cardiac contractility with bradycarida, ECG changes, reflexes depressed or absent
palipitations, chest pain, fast irregular pulse
What will and ECG show in hyperkalaemia?
peaked T waves, prolonged PR interval, widened QRS complex, reduced/loss p wave, AV dissociation, sine wave pattern, asystole
What will blood show in hyperkalaemia?
normocytic normochromic anaemia, thrombocytosis, leukocytosis
Management of hyperkalaemia?
ABCDE and early warning score and start escalating
determine severity, ECG, find cause and treat, reduce potassium diet
10ml 10% calcium gluconate to protect cardiac membrane and improve ECG, give 10ml every 10 minutes till ECG normalises
the use insulin glucose IV to shift potassium into cells, give nebulised salbutamol to reduce potassium
add bicarbonate is added until pH is normalised but there are many risks, then use calcium resonium with regular lactulose to remove potassium via GI tract
plan dialysis if necessary
Treatment of resistant hyperkalaemia?
further glucose and IV insuin/iv calcium, IV diuretics, sodium bicarbonate, haemodialysis
Prognosis of hyperkalaemia?
an independent risk factorr for death, most fatal cases are complicated by AKI
Prevention of hyperkalaemia?
reduced potassium retaining drugs, reduce potassium diet, potassium excreting diuretics
What is crush syndrome?
severe systemic manifestation of trauma and ischemia from prolonged severe crushing, increased permeability of the cell membrane and postassium, enzyme and myoglobin release from within cells, results in acute tubular necrosis and uraemia
Cause of crush syndrome?
continuous pressure on muscle tissue due to ischemic reperfusion causing muscle injury, common after earthquakes, during war, after explosions and industrial accidents. It is in 2-15% of all trauma patients.
Pathophysiology of crush syndrome?
the muscle injury causes potassium and other substance leakage into circulation causing renal tubular obstruction and renal damage (mainly from increased myoglobin levels as it is nephrotoxic), also causes intravascular volume depletion and renal hypoperfusion, causing renal dysfunction
How is crush syndrome characterised?
hypovolaemic shock from sequestrain of water in the injured muscle cells and hyperkalaemia
Complications of crush syndrome?
metabolic acidosis from release of cellular phosphate and sulphate by the injury muscle cells, AKI, DIC, compartment syndrome, peaked creatinine kinase levels, infection, hyperkalaemia
Symptoms of crush syndrome?
crushing injury into a large mass of skeletal muscle, sensory and motor disturbances in the compressed limbs which then become tense and swollen, body parts may be pulseless, myoglobinuria, haemoblobinuria, oliguria, hypovolaemic shock, nausea, confusion, vomiting, agitation, hypocalcaemia
Initial management of crush syndrome?
ABC, monitor vital signs, O2, assess limbs using the 5 ps to estimate ischemic injury, venous access, preserve body heat, arterial tourniquet if compression was more than 30 mins, saline infusion, hydration, catheter to monitor urine output, analgesics
What is rhabdomyolysis?
total creatine kinase levels 5-10x above normal, with other symptoms/risk factors
Investigations for crush syndrome?
bloods, electrolyte measurements, LFTs show hepatic dysfunction, ECG shows hyperkalaemia, x-ray, assess compartment pressures, urine dipstick for myoglobin, clotting studies to look for DIC
Further management in crush syndrome?
maintain urine output until myoglobinuria has ceased
forced mannitol alkaline diuresis for increased renal perfusion and reduce muscle injury to prevent against myoglobin damage and reduce risk of hyperkalaemia
urinary alkalinisation with sodium bicarbonate to prevent AKI
treat hyperkalaemia, renal dialysis, treat DIC and may need to amputate crushed limbs
Prevention of crush syndrome?
adequate rehydration and fluid support reduce AKI and improves prognosis, identify those who need urgent attention
What is hyperparathyroidism?
increased parathyroid hormone release leading to increased calcium levels in the blood
Effects of parathyroid hormone?
causes bone to release calcium, calcium absorption in the gut, reduces kidney calcium excretion, increases phosphate excretion
Effects of calcium?
combines with phosphate to make calcium phosphate to make bones and teeth hard and strong, helps to clot blood after injury, for muscle function (phosphate works alongside and is also used for energy production)
What is primary hyperparathyroidism and the causes?
enlarged and overactive parathyroid gland, increasing parathyroid hormone caused by parathyroid benign adenoma, parathyroid gland hyperplasia, parathyroid carcinoma and familial isolated hyperparathyroidism or multiple endocrine neoplasia (MEN)
What is secondary hyperparathyroidism and the causes?
caused by diseases that causes hypocalaemia so the parathyroid glands are continually being stimulated to increase calcium levels so it becomes enlarged caused by CKD, vit D deficiency (rickets/osteomalacia) and gut malabsorption
What is tertiary hyperparathyroidism and the causes?
caused by longstanding secondary hyperparathyroidism so the parathyroid glands are no longer sensitive to blood calcium levels, seen in CKD or after kidney transplant
Symptoms of primary and tertiary hyperparathyroidism?
tiredness, weak and fatigued muscles, nausea, vomiting, loss of appetite, constipation, abdominal pain, thirsty, depression
if extreme: confusion, loss of consciousness, heart rhythm disturbances, hypertension
no symptoms in seconday as low calcium - but can develop osteoporosis
Complications of hyperparathyroidism?
kidney stones, haematuria, corneal calcification, pancreatitis, peptic ulceration, kidney damage, osteoporosis
hyperparathyroidism investigations?
high calcium (low in 2) and parathyroid hormone, low blood phosphate (high in CKD), 24h urine calcium, DEXA for osteoporosis, x-rays show changes in bones from calcium release, kidney US for kidney stones, US/CT to show enlarged parathyroid gland, biopsy to exclude cancer
Treatment of primary hyperparathyroidism?
regular monitoring, stay hydrated, avoid diuretics, avoid vomiting and diarrhea, parathyroidectomy if severe (try and leave a little to have some hormone), bisphosphonate medication if severe but no surgery to improve bone density and correct calcium, cinacalcet reduces calcium and parathyroid hormone levels and increase phosphate levels, HRT if post menopause
Treatment of secondary hyperparathyroidism?
treat underlying cause, reduce phosphate in diet, calcium carbonate medication to bind to phosphate and prevent its absorption, vit d supplements, calcimimetic cinacalet to reduce parathyroid hormone release, parathyroidectomy
Treatment of tertiary hyperparathyroidism?
parathyroidectomy, put a small amount of one of the glands into forearms, so the body has some calcium control but it is then easier to get to if further surgery is needed
Complications of parathyroidectomy?
hypocalcaemia, hypoparathyroidism, never damage in neck, bleeding infecton, persistant hyperparathyroidism
Prognosis of hyperparathyroidism?
primary is good, but secondary and tertiary are worse as they are associated with CKD
How common is hypercalcaemia?
uncommon, 30/100,000, but is the most frequently encountered endocrine/electrolyte disorder in malignancy associated hospital patients
Presentation of hypercalcaemia?
3.5mmol/L - abdominal pain, vomiting, dehydration, lethargy, cardiac arrhythmias, shortened QT, coma, pancreatitis
Causes of hypercalcaemia?
hyperparathyroidism, malignancy of squamous cell lung, breast, renal cell, sarcoidosis, TB, thyrotoxicosis, phaeochromocytoma, primary adrenal insufficiency, thiazide diuretics, vit d and vit supplements, familial hypocalciuric hypercalcaemia, prolonged immbolisation, calcium alkali syndrome, AIDS
Investigations of hypercalcaemia?
x rays show bone abnormalities like demineralisation, bone cysts, pathological fractures, bony metastases, US/CT, 24 urine calcium, protein electrophoresis for myeloma, TSH to exclude hyperthyroidism
serum phosphate, serum alk pho, urine calcium, urine phophate and PTH depend on cause
What is the cause of hypercalcaemia if urine calcium, phosphate, PTH and serum alk phos are high but serum phosphate low?
hyperparathyroidism
What is the cause of hypercalcaemia if urine phosphate is high, serum phosphate low and alk phos, calcium and pTH are variable?
malignancy
What is the causes of hypercalcaemia if serum phosphate, urine phosphate and urine calcium are high but PTH and alk phos low?
vitmain D excess
Management of hypercalcaemia?
increase circulating volume with saline to increase urine output of calcium, loop diuretics for fluid overload, rehydrate, bisphosphonates e.g. oamidronate, salmon calcitonin, UV gallium if malignant cause, cinacalcet HCl reduces parathyroid levels, block RANK-L to prevent calcium release from bones,dialysis
What does a raised calcitonin level in hypercalcaemia suggest?
B cell lymphoma
What does a raised alk phos with hypercalcaemia suggest?
bony metastases, sarcoidosis, thyrotoxicosis
What is hypoparathyroidism?
characterised as hypocalcaemia, hyperphosphateaemia, low or inappropriately normal PTH
What 3 things are involved in calcium regulation?
calcitrol, PTH, 1,25-dihydroxyvitamin D3
What causes calcium absorption?
1,25 dihydroxyvitamin D3
What stimulated calcium release from bone?
1,25-dihydroxyvitamin D3 and PTH
What is transient hypoparathyroidism in the neonatal period?
when neonates reduce calcium levels in first 24-48 hours of age, but can develop hypocalcaemia at 72 hours
What causes hypocalcaemia in neonates?
mothers with diabetes, delay in PTH surge, maternal hyperparathyroidism, premature birth
Causes of hypoparathyroidism?
Di George’s syndrome, defects in PTH gene, defects in calcium sensing receptor gene, pseudohypoparathyroidism, autoimmune polyglandular syndrome type 1 or 2, isolated hypoparathyroidism, HDR, HRD, neck surgery, radiotherapy, magnesium deficiency/excess
Presentation of hypoparathyroidism?
muscle pains, bone pain, abdominal pain, paraesthesiae of face fingers and toes, facial twitching, carpopedal spasm, convulsions, syncope, emotional lability, anxiety, depression, memory impairment, lethargy, headahces, brittle nails, dry gair and skin, painful menstruation, Chvostek’s sign, Trousseaus sign, raised ICP, papilloedema, cataracts, dental abnormalities, enamel dysplasia, hyperreflexia
Typical blood result in hypoparathyroidism?
low serum calcium, high serum phosphate, low PTH, normal alkaline phosphatase
Typical blood results in pseudohypoparathyroidism?
low serum calcium and normal or high PTH
What is pseudohypoparathyroidism?
defects in PTH action - can be hypo or normocalcaemia and associated with somatic anomalies, short staurs, round face, short neck, shorteing of metacarpals and metatarsals
Treatment of hypoparathyroidism?
IV calcium, rich calcium diet with vit D and calcitrol, wear bracelet, recombinant PTH or post menopausal osteoporosis and prevent hypercalcuria, monitoring, parathyroid autotransplantation and allotransplantation
Complications of hypoparathyroidism?
laryngospasm, stridor, airway obsturction, neuromuscular irritability, muscle cramps, tetany, seizures, arrhythmias, death, calcium deposition in kidneys, stunted growth, malformed teeth, mental impairement, dental problems, hypercalcaemia, renal impairment, cataracts
How common is hypocalcaemia?
very common, in up to 88% of ICU patients
Symptoms of hypocalcaemia?
SPASMODIC
spasms (Trousseau’s sign), paraesthesia, anxious, seizures, muscle cramps, orientation impaired, dermatitis, impetigo herptiformis, tetany, Chvostek’s sign
prolonged QT, laryngospasm, bronchospasm, subcapsular cataract, papilloedema, abnomral teeth, ectopic calcification
What is Trousseau’s sign?
occlude arterial circulation of the forearm using a blood pressure cuff inflated to the systolic blood pressure for 3 minutes
capopedal spasm involving flexion at the wrist, metacarpophalangeal joint, extension of the interphalangeal joints, adduction of the thumbs and fingers
Causes of hypocalcaemia?
CKD, pseudohypoparathyroidism, acute rhabdomyolysis, vit D deficiency, hypomagnesaemia, osteomalacia, acute pancreatitis, over hydration, respiratory alkalosis, hyperventilation, calcium chelators, bone resorption inhibitors, tumour lysis, osteoblstic metastases, toxic shock syndrome
DD of hypocalcaemia?
CKD, hypoparathyroidism, pseydohypoparathyroidism, vit D deficiency
Management of hypocalcaemia?
correct magnesium level, oral calcitrol
mild - calcium 5mmol/6h and daily plasma calcium levels, vit d and calcium supplements if persistent
severe - 10ml calcium gluconate with IV
CKD - alfacalcidol to maintain serum calcium
What is Chvostek’s sign?
detects latent tetany, tap 5th facial nerve in front of ear with patients mouth slightly open to cause contraction of facial muscles
Prevention of hypocalcaemia?
ensure adequate dietary intake, avoid total parenteral nutrition, ensure magnesium and calcium levels check twice a week (more if ill), 1,25-dihydroxyvitmainD and calcium before parathyroidectomy
What is classed as mild and severe hypocalcaemia?
mild = 2-2.12mmol/L
severe =
Investigations in hypoparathyroidism?
ECG - prolonged QT interval renal US to look for renal calculi imaging - shortened metacarpals brain MRI - basal ganglia calcification 24 hour urinary calcium is low TSH and ACTH levels 25-hydroxyvitamine D3 and 1,25-dihydroxyvitamin D3 to look for vitamin D deficiency
What is DiGeorge’s syndrome?
abnormal parathyroid gland development from third and fourth pouches
