Phase 2A
Endocrinology
Charlotte Allan
Joe Hardwick
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Diabetes Mellitus Type 1
• Autoimmune destruction of pancreatic beta cells in the islets
of Langerhans
• Antibodies present for several years before onset of
symptoms
• T cell mediated
• Associated with other autoimmune conditions
• Around 300,000 patients in the UK
• Usually presents in under 25s, often before puberty
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Signs and Symptoms
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Thirst (polydipsia)
Polyuria
Nocturia
Weight loss
Fatigue
Blurred vision
Nausea
Decreased concentration
• Hyperglycaemia (>11mmol/L)
• Glucosuria
• Ketonuria
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Treatment
• Insulin
• Delivered via subcutaneous injection
• Usually a basal/bolus regime – basal = long acting
bolus = short acting
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Diabetic Ketoacidosis
• Lack of insulin means glucose cannot be used as a source of
energy
• Therefore fat has to be used instead
• A by product of fat breakdown are ketone bodies, and these
build up, leading to excess ketones in the blood
• Ketones are acidic, hence leading to ketoacidosis
• Peripheral lipolysis -> ↑circulating FFA -> hepatic conversion
to ketones -> acidosis
• Hyperglycaemia leads to osmotic renal diuresis and
dehydration, which worsens the acidosis
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Causes of DKA
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Undiagnosed T1DM
Interruption of insulin therapy
Stress
Intercurrent illness – surgery/infection
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DKA Signs and Symptoms
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Very dehydrated
Vomiting – worsens dehydration
Sunken eyes
Deep rapid breathing (Kussmaul)
Acetone smell on breath (pear drops)
Altered consciousness
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DKA Investigations &
Treatment
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Blood glucose - >11mmol/L
Ketonaemia
pH <7.3 with bicarb < 15
Glucosuria/ketonuria (delayed sign)
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Find and treat any suspected infection
Replace fluid and electrolytes – Saline with potassium
Replace insulin
Restore acid/base balance over 24 hours
Monitor fluid balance
Potassium given to avoid hypokalaemia on reintroduction of
insulin
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Type 2 Diabetes
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Polygenic and environmental aetiology
Beta cell mass <50% at diagnosis
Increased insulin resistance
Decreased insulin secretion
• Risk factors: obesity, calorie and alcohol excess, lack of
exercise, male, high triglycerides
• Approximately 3 million patients in the UK
• Another 1 million undiagnosed
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Diagnosis of T2DM
• Symptoms less prominent than T1DM
Often detected on screening:
• Fasting glucose >7mmol/L
• Random glucose >11.1mmol/L
• HbA1C >48mmol/L
• OGTT: Fast overnight, give 75g glucose, measure glucose
before and 2/24 after. >11.1mmol is positive
• For diagnosis: symptoms of hyperglycaemia AND one raised
blood glucose reading, OR
• Raised blood glucose on 2 separate occasions
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Other Hyperglycaemia
• Impaired glucose tolerance = fasting glucose <7mmol/L and
OGTT 7.7-11mmol/L
• Impaired fasting glucose = fasting glucose 6-7
Gestational diabetes:
• Occurs in 4% of pregnancies
• RF: >25yr, obesity, FH, non-caucasian
• Issues: increased birth weight, neonatal hypoglycaemia
• OGTT at 6/52 post-partum
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Hyperosmolar Hyperglycaemic
State (HHS)
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History of approx. 1 wk
Often elderly patient
Common initial presentation of T2DM
Marked dehydration and glucose >35mmol/L
Acidosis absent as they have sufficient insulin to prevent
excessive fat breakdown
Treatment:
• Rehydrate with saline IVI over 48hours
• Replace potassium
• Wait 1 hour before using insulin as it may be unnecessary
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Hypoglycaemia
• Commonest endocrine emergency
• Plasma glucose <3mmol/L
• Sweating, anxiety, hunger, tremor, dizzy, confusion, irritability,
drowsiness, seizure, coma
• Most common cause is insulin treatment in T1DM combined with..
Increased activity, missed meal, accidental/non-accidental OD
Treatment:
• Oral sugar then starch
• If unable to swallow – 25-50ml IV glucose 50% or glucagon IM if no
IV access
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Diabetic Complications
MACROVASCULAR
Vascular disease – chief cause of death
• MI – 4x risk
• Stroke – 2x risk
• Address other RF – smoking/diet/HTN etc.
MICROVASCULAR
Nephropathy
• Leading cause of dialysis and kidney transplant
• High urine albumin:creatinine ratio indicates early renal
disease and increased vascular risk
• Treatment: control BP, restrict dietary protein, ARB, ACE-I,
spironolactone
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Diabetes Complications
MICROVASCULAR
Retinopathy
• Background – microaneurysms (dots), haemorrhages (blots)
and hard exudates
• Pre-proliferative – cotton wool spots (infarcts), haemorrhages,
venous beading
• Proliferative – new vessels formed
• Maculopathy – new vessels form on disc or ischaemic areas,
proliferate, bleed, fibrose, can detach retina
Laser photocoagulation is used to stop the production of
angiogenic factors. Used in proliferative
retinopathy/maculopathy
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Diabetic Feet
Ischaemia
• Absent foot pulses – may need doppler
• May need angioplasty/stents
Neuropathy
• Decreased sensation – stocking distribution
• Absent ankle jerk reflex
• Deformity
• Ulceration – painless, punched out
• Burning pain in feet at night
• Regular chiropody
• Relieve pressure with therapeutic shoes & bed rest
• Monitor for cellulitis – may need antibiotics
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Thyroid
TRH = thyrotropin releasing
hormone
TSH = thyroid stimulating
hormone (AKA thyrotropin)
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Hyperthyroidism
• Excess free T3 and T4
• Grave’s disease is the most common cause
• 5% caused by solitary toxic adenoma/nodule
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Grave’s Disease
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2/3 of cases of hyperthyroidism
F:M = 9:1
Usually presents at 40-60yrs
Circulating IgG antibodies bind to TSH receptors on the
thyroid, causing smooth thyroid enlargement and increased
hormone production – especially T3
• Triggers – stress, infection or childbirth
• RF: vitiligo, T1DM, Addison’s
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Symptoms of Hyperthyroidism
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Diarrhoea
Weight loss
Increased appetite
Increased sweating
Heat intolerance
Palpitations
Tremor
Irritability
Labile emotions
Oligomenorrhoea +/- infertility
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Signs of Hyperthyroidism
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Fast/irregular pulse – SVT/AF
Warm, moist skin
Fine tremor
Palmar erythema
Thin hair
Lid lag
Lid retraction
Goitre
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Grave’s Specific Signs
Eye signs
• Exopthalmos

• Opthalmoplegia –
weakness or paralysis of
extraocular muscles -
Pretibial myxoedema –
oedematous swellings above
lateral malleoli
Thyroid acropachy –
clubbing, painful finger and
toe swelling
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Management
• Blood Tests: TFTs – T3/4 elevated, TSH suppressed
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Block & Replace – carbimazole (anti-thyroid) & thyroxine (T4)
Titration of carbimazole only
SE of carbimazole = agranulocytosis
Radio-active Iodine
Thyroidectomy & replacement thyroxine
• Emergency treatment = Beta blockers to reduce symptoms
then carbimazole
• In pregnancy carbimazole is teratogenic so propylthiouracil is
used instead
• Wait four weeks after starting medication before re-testing
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Hypothyroidism
• Usually primary, from thyroid disease, but may be secondary
to reduced TSH from a pituitary disorder
• Autoimmune, associated with anti-thyroid antibodies leading
to lymphoid infiltration of the gland and eventual atrophy and
fibrosis.
• Reduced T3/T4 and high TSH
• Association with other autoimmune conditions
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Signs & Symptoms
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Tiredness
Weight gain
Cold intolerance
Constipation
Dry skin
Dry, thin hair
Bradycardia
Slow-relaxing reflexes
Low mood
Menorrhagia
Hoarse voice
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Treatment
• Replace with levothyroxine until TSH is within normal and
patient is asymptomatic
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Hashimoto’s Thyroiditis
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Autoimmune attack of the thyroid gland
F:M 7:1
Usually middle aged, with family history
Associated with other AI conditions
Goitre to lymphocytic infiltration and fibrosis
TPO (thyroid peroxidase) and/or thyroglobulin antibodies are
responsible
Complication: thyroid lymphoma
Diagnosis: TPO antibody detection
Symptoms of hypothyroidism, often with a hard, non-painful
goitre
Treatment: Levothyroxine
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Thyroid Cancer
• 70% papillary, 20% follicular, 5% medullary (C cells)
• F:M 3:1
• Thyroid nodules in 90%
• Commonly metastasises to lung, liver, brain & bone
• Treatment: total thyroidectomy with post-op radioactive
iodine ablation
• Lifelong levothyroxine treatment, titrated to suppress TSH –
reduces recurrence
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Adrenal Glands
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Goodness
Me
Frank
Gets
Really
Angry
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Cushing’s Syndrome
Clinical state of glucocorticoid
excess in the blood
=
Too much cortisol
Usually iatrogenic, due to steroid or
ACTH administration
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Cushing’s Syndrome
ACTH dependent:
• Pituitary dependent (Cushing’s disease)
• Ectopic ACTH-producing tumours
• ACTH administration
Non-ACTH dependent:
• Adrenal adenoma
• Adrenal carcinoma
• Glucocorticoid administration
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Cushing’s Syndrome
Symptoms:
• Weight gain – central obesity
• Thin skin
• Easy bruising
• Stretch marks
• Red puffy, round face
• Tanned skin (Cushing’s disease only)
• Muscle weakness
• Depression
• Tiredness
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Cushing’s Syndrome
Signs
• Impaired glucose tolerance
• Hypertension
• Pathological fractures – secondary to osteoporosis
• Hypokalaemia
• Striae
• Proximal myopathy
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Cushing’s Syndrome
Investigations:
48 hour low dose dexamethasone test:
• ACTH depressed: non-ACTH dependent SCAN ADRENALS
• ACTH unchanged: ACTH dependent SCAN PITUITARY
Treatment:
• Must have cortisol controlled before surgery or radiotherapy
• Transphenoidal surgery to remove pituitary tumour in
Cushing’s Disease +/- radiotherapy
• Adrenal tumour resection for non-ACTH dependent
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Conn’s Syndrome
• Excess mineralocorticoids in the blood stream – too much
aldosterone
• Usually caused by an aldosterone producing adrenal adenoma
• More common in young females
Signs & Symptoms:
• Muscle weakness
• Tiredness
• Polyuria
• Nocturia
• Hypertension
• Hypokalaemia
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Conn’s
Investigations:
Stop beta blockers, spironolatone, ACE-I, ARBs all may affect
results and should be stopped
• Aldosterone elevated
• Renin is depressed
• Adrenal CT/MRI to distinguish bilateral adrenal hyperplasia
and adenoma
Treatment:
• Laparoscopic surgery to remove adenoma
• Spironolactone for bilateral adrenal hyperplasia
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Adrenal Insufficiency
Addison’s disease:
• Destruction of entire adrenal cortex – reduced
mineralocorticoids, glucocorticoids and sex steroids all
reduced
• Autoimmune
Hypothalamic-pituitary disease:
• Inadequate ACTH – insufficient glucocorticoids, but adequate
mineralocorticoids due to RAAS
Long term steroid therapy:
• Leads to hypothalamic-pituitary-adrenal suppression if not
reduced at appropriate rate
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Addison’s Disease
• Associated with other AI diseases: Type 1 DM, pernicious
anaemia and thyroiditis
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THIN
TANNED
TIRED
TEARFUL
• Other symptoms: N/V/D, headaches, muscle pain and lightheadedness
• Very rare
• Females>Males
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Addison’s Disease
Investigations
• Short ACTH stimulation test  Impaired cortisol response
confirms hypoadrenalism
• MRI adrenals
Treatment
• In emergency (V low BP) – give hydrocortisone and fluids
• Long term – glucorticoid (hydrocortisone) and
mineralocorticoid (fludrocortisone) replacement. Titrate until
patient is asymptomatic
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Addisonian Crisis
• Severe hypotension with dehydration precipitated by
intercurrent illness, infection, surgery or trauma
• Treat with IVI and hydrocortisone
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Phaeochromocytoma
• Rare catecholamine-producing tumour
• Usually within the adrenal medulla
• Excessive catecholamines may produce life-threatening
hypertension and cardiac arrhythmias
• Associated with Multiple Endocrine Neoplasia 2 (MEN2),
Neurofibromatosis type 1 and Von-Hippel Lindau Syndrome
• Commonly present in patients aged 30-50
• Often bilateral
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Phaeochromocytoma
Symptoms
• Headache
• Profuse sweating
• Tremor
• Palpitations
Signs
• Hypertension
• Postural hypotension
• Neurofibromas
• Café au lait spots
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Phaeochromocytoma
Investigations
• 24 hour urinary catecholamines (metadrenaline &
normetadrenaline)
• Plasma catecholamines
• CT/MRI adrenals
Treatment
• Surgical resection of tumour
• Pre-surgery: Alpha blockade (mirtazapine) THEN beta blockade
(propanolol)
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Diabetes Insipidus
• Cranial DI  Deficiency of ADH
Causes: familial, idiopathic, tumour, infection, post-surgery
(most common, often transient)
• Nephrogenic DI  Failure to respond to ADH
Causes: familial, idiopathic, renal disease, hypokalaemia, drugs
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Diabetes Insipidus
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Polyuria
Nocturia
Polydipsia
Urine output = up to 15L daily
Decreased skin turgor
Signs of dehydration
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Diabetes Inspidus
Investigations
• High plasma osmolality WITH low urine osmolality
• Hypernatraemia
• High 24 hr urine volume
• Failure of urinary concentration with fluid restriction
• Fluid deprivation test: Give desmopressin:
If urine osmolality rises = cranial DI
If urinary osmolality is unchanged = nephrogenic DI
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Diabetes Insipidus
Treatment:
• Cranial DI = Intranasal desmopressin
• Nephrogenic DI = Reverse cause, polyuria may be helped by
thiazide diuretics e.g. bendroflumethiazide
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SIADH
Syndrome of Inappropriate ADH Secretion
• Important, but overdiagnosed cause of hyponatraemia
Concentrated
urine (↑ Na,
↑osmolality)
+
Hyponatraemia with
low plasma
osmolality
Without:
• Hypovolaemia
• Oedema
• Diuretics
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SIADH
Causes:
• Malignancy
• CNS disorders – stroke, SAH, SDH, post neurosurgery
• TB
• Pneumonia
• Drugs – opiates, SSRIs
Treatment:
• Treat cause and restrict fluid
• Consider salt +/- loop diuretic if severe
• Vaptans – e.g. tolvaptan – promote water excretion without
loss of electrolytes, rarely used
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Growth Hormone Regulation
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Acromegaly
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Growth hormone stimulates soft tissue and skeletal growth
Before epiphyseal fusion excess GH  Gigantism
After epiphyseal fusion excess GH  Acromegaly
Almost always due to a GH secreting pituitary tumour
(somatotroph adenoma)
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Acromegaly
Symptoms:
• Hands and feet become larger and broader (spade like)
• Unable to remove rings
• Thickened, sweaty, greasy skin, especially on the face
• Prominent jaw
• Interdental separation
• Changes can be gradual, so may go unnoticed
• Vocal cords thickened – voice deepens
• Tiredness
• Muscle weakness
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Acromegaly
Signs:
• Hypertension
• Impaired glucose tolerance
• Bitemporal hemianopia (David and Goliath)
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Acromegaly
Investigations:
• GH level – non-specific if elevated
• GTT – diagnostic if no suppression of growth hormone
(growth hormone is usually inhibited by glucose)
• IGF-1 is usually raised
• MRI – pituitary adenoma
Treatment:
• Transphenoidal surgery +/- radiotherapy
• Somatostatin receptor agonists e.g. octreotide
• Dopamine agonists e.g. bromocriptine
• GH antagonists - pegvisomant
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Disorders of Calcium Metabolism
• Serum calcium levels are mainly regulated by parathyroid
hormone (PTH) and vitamin D
• Hypercalcaemia is much more common than hypocalcaemia
Parathyroid Hormone:
• 4 parathyroid glands, situated on posterior thyroid
• PTH secreted from the chief cells of these glands
• PTH increases, as ionised calcium falls, and vice versa
• Has several major actions all of which raise serum calcium
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Parathyroid Hormone
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Hypercalcaemia
Causes:
• Most common - excess PTH, malignancy
• Other - excess vit D, excess Ca intake, drugs
Signs & symptoms:
• Mild hypercalcaemia is often asymptomatic
• General – tiredness, malaise, dehydration
• Renal – colic from stones, polyuria, haematuria
• Bone pain
• Abdominal pain
• Symptoms of underlying cause e.g. malignancy often advances
with bone metastases
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Hypercalcaemia
Investigations:
Biochemistry:
• Serum PTH
• ABG
• Renal function
• 24hr urinary calcium
• Alk Phos
Imaging:
• Abdo Xray
• DEXA bone scan
• PTH imaging
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Cause 1: Hyperparathyroidism
Primary Hyperparathyroidism:
Usually caused by parathyroid adenoma or more rarely
carcinoma or hyperplasia
PTH
Calcium
Phosphate
PTH Appropriate?
↑
↑
↓
X
Treatment:
No effective medical therapies at present, high fluid intake should
be maintained, a high calcium and vit D intake avoided and
exercise encouraged.
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Cause 1: Hyperparathyroidism
Secondary Hyperparathyroidism:
Physiological compensatory hypertrophy, secondary to
hypocalcaemia, e.g. CKD, vit D deficiency
PTH
Calcium
Phosphate
PTH Appropriate?
↑
↓
↓
✔️
Treatment:
Medical treatment is the mainstay, the underlying condition
needs treating. Treatment in CKD includes phosphate binders,
calcium supplementation, vit D and calcimimetics.
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Cause 1: Hyperparathyroidism
Tertiary Hyperparathyroidism:
Autonomous parathyroid hyperplasia after longstanding
secondary hyperparathyroidism, usually due to renal failure
PTH
Calcium
Phosphate
PTH Appropriate?
↑
↑
↑
X
Treatment:
Calcimimetics may be used. Total or subtotal parathyroidectomy
is the recommended treatment.
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Cause 2: Malignancy
Lytic bone metastases, myeloma or activation of osteoclast
activating factor by the tumour
PTH
Calcium
Phosphate
PTH Appropriate?
↓
↑
--
✔️
Raised alk phos… indicates ↑ bone turnover, probably due to
metastases
Treatment:
• Manage malignancy
• IV bisphosphonates or calcitonin
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Hypocalcaemia
Causes:
• Increased phosphate (CKD or phosphate therapy)
• Vitamin D deficiency (osteomalacia)
• Hypoparathyroidism (post surgery, DiGeorge syndrome,
severe hypomagnesiaemia)
• Pseudo hypoparathyroidism – end organ PTH resistance
• Drugs – bisphosphonates, calcitonin
• Acute pancreatitis
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Hypocalcaemia
Features:
• Paraesthesia
• Circumoral numbness
• Cramps
• Anxiety
• Tetany
If severe:
• Convulsions
• Laryngeal stridor
• Dystonia
• Psychosis
• Papilloedema
• Long QT
Chvostek’s sign
Trousseau’s sign
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Hypocalcaemia/Hypoparathyr
oidism
Investigations:
• Clinical history is usually sufficient
• Confirmed by low serum calcium
• PTH level, PTH antibodies, renal function, vit D level,
magnesium
Treatment:
• Vit D deficiency – give vit D3
• Oral calcium supplements
• Hypoparathyroidism – calcium & vit D
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Hypokalaemia
Causes:
Acute – IV fluids without potassium, as the potassium enters the
cells
Chronic – Diuretics, hyperaldosteronism, drugs
(mineralocorticoids, steroids), renal tubular acidosis, insulin
treatment, vomiting, severe diarrhoea, villous adenoma,
intestinal obstruction
Features:
Usually asymptomatic. If severe – muscle weakness and
symptoms of hyponatraemia
Increased frequency of ectopic beats in patients with heart
disease
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Hypokalaemia
Treatment:
• Identify and treat underlying cause
Dietary deficiency  increase fruit and veg intake/
supplements
Hyperaldosteronism  spirinolactone & amiloride
IV fluid replacement  add potassium to fluid
• Acute cases may resolve spontaneously
• Withdrawal of diuretics or purgatives, alongside potassium
supplements is usually all that is required
• IV replacement, only in cardiac arrhythmias, muscle weakness
or severe DKA – cardiac monitoring!
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Hyperkalaemia
Causes:
• Acute, self limiting hyperkalaemia appears after vigorous
exercise
• Decreased excretion: AKI, K sparing diuretics, ACE-I, NSAIDs,
Addison’s
• Increased cellular release: acidosis, digoxin toxicity, vigorous
exercise
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Hyperkalaemia
Features:
• Serum K >7.0 mmol/L is a medical emergency, associated with
ECG changes (tall tented T waves, wide QRS, flattened P
waves)
• Often aysmptomatic but may predispose to sudden death
from cardiac arrest
• Muscle weakness is often only symptom
• May have Kussmaul breathing if acidotic
• Hypotension/bradycardia
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Hyperkalaemia
Treatment:
• Illicit cause and treat
• Immediate treatment – calcium gluconate and IV insulin +
dextrose infusion
• Deplete body K stores through polystyrene sulphonate resins
with laxatives or an enema
• Dialysis
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MEN
MEN – Multiple endocrine neoplasia
• Rare, inherited condition causing hormone secreting tumours
• 2 types: 1 & 2
Type 1
• Diagnosis: More than 2 neuroendocrine tumours, plus the
genetic mutation
• Symptoms depend on tumour, gland involved, and hormones
secreted
• 95% have parathyroid hyperplasia/adenoma
• 70% have pancreatic endocrine tumours (gastrinoma,
insulinoma, somatostatinoma, VIPoma, glucagonoma)
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MEN
Type 2
• Medullary thyroid carcinoma seen in 100%
• Phaeochromocytoma seen in 50%
• Parathyroid hyperplasia in 80%
Treatment
• Depends on tumour type
• Can involve surgery or medications to reduce the appropriate
hormone level
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Malignant Carcinoid Syndrome
• The constellation of symptoms typically exhibited by patients
with metastases from carcinoid (neuroendocrine) tumours.
• These tumours usually secret excessive amounts of serotonin.
• They arise from neuroendocrine cells, especially in the
intestine
• Carcinoids do not produce the malignant carcinoid syndrome
until they are no longer confined to the small bowel or
mesentery. They often spread to the liver.
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Malignant Carcinoid Syndrome
Symptoms
• Tumours grow slowly and symptoms may not appear for years
• Alcohol intolerance and weight loss are common
• Diarrhoea
• Flushing of the face and neck
• Wheezing, asthma, SOB
• Palpitations, low BP, dizziness
Diagnosis
• Measure serotonin metabolite 5-HIAA in a 24 hr urine sample
• Many foods contain serotonin which complicates the diagnosis
• Imaging: Barium swallow, MIBG, CT, angiography and venous blood
sampling
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Malignant Carcinoid Syndrome
Treatment
• Interferons and octreotide may help control humorally
mediated symptoms.
• Histamine blockers may be helpful
• Serotonin antagonists can help control diarrhoea and
malabsorption
• Somatostatin may be helpful in preventing flushing
• Complete surgical removal of all tumour tissues is the best
treatment
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Quiz
Which cells in the pancreas secrete insulin? And glucagon?
Which immune cell mediates the AI response leading to T1DM?
Name 2 conditions associated with T1DM
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Quiz
2 causes of DKA
Name the type of breathing seen in DKA
Emergency treatment of DKA
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Quiz
Above what level does a random glucose need to be to diagnose
diabetes?
Why is acidosis present in DKA, but not HHS?
3 symptoms of hypoglycaemia
How would you treat hypoglycaemia in an unconscious patient
without IV access?
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Quiz
In which type of retinopathy do you have new blood vessel
formation?
Does thyroxin mostly circulate as T3 or T4?
What are the 2 specific eye signs found in graves disease?
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Quiz
What is the anti thyroid hormone medication called?
Where in the adrenals is cortisol produced?
48 hour low dose dexamethasone test, ACTH remains
unchanged, do you scan pituitary or adrenals?
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Quiz
Which hormone is produced in excess in Conn’s syndrome?
Why in adrenal insufficiency secondary to hypothalamic
pituitary disease do you have insufficient cortisol, but adequate
aldosterone?
2 drug treatments for Addison’s (long term)
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Quiz
Name 1 systemic disease that phaeochromocytoma is
associated with.
Pre-surgical treatment of phaeochromocytoma requires which 2
medications, in which order?
What is the plasma and urine osmolality in diabetes insipidus?
(high/low)?
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Quiz
Through which route do you give desmopressin for DI?
Which drug can be used in SIADH which promotes water
excretion without loss of electrolytes?
Which hormone counteracts the action of GHRH?
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Quiz
What is the commonest cause of acromegaly?
2 signs of acromegaly?
2 drugs used to treat acromegaly?
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Quiz
Which cells in the parathyroid secrete PTH?
In primary hyperPTH is phosphate high or low?
Is the PTH level appropriate in secondary hyperPTH?
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Quiz
Name 2 causes of hypocalcaemia
Which sign of hypocalcaemia is elicited by inflating a blood
pressure cuff around the upper arm?
What is the emergency treatment of acute hyperkalaemia?
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Quiz
What are the ECG changes associated with hyperkalaemia?
Which hormone is excessively secreted in malignant carcinoid
syndrome?
2 symptoms of this condition
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