Endocrinology Flashcards
What are some common causes of primary hypothyroidism and what would TFTs typically show.
TFTs show high TSH and low T4.
Common causes are:
- Autoimmune (Hashimoto’s, atrophic)
- Iodine defiency
- thyroiditis
- Iatrogenic (cytotoxics, thyroidectomy, radioiodine)
What are some common causes of secondary hypothyroidism and what would TFTs typically show.
TFTs show low TSH and low T4
Pituitary insuffiency most likely cause and so MRI of gland neccesary
What is sick euthyroid syndrome and what would TFTs typically show.
TFTs show slightly low TSH and low T4.
Associated with systemic illness during which TFTs become deranged. Test should be repeated after recovery. T3 may be particularly low.
What is Graves Disease and what would TFTs typically show.
TFTs show low TSH, increased T3 and T4.
Most common cause of hyperthyroidism accounting for ~2/3. 9 times more common in females typically presented at age 40-60yrs.
Caused by circulating IgG autoantibodies binding to and activating thyrotropin receptors leading to smooth goitre and increased hormone production.
What are some causes of thyrotoxicosis?
- Graves Disease
- Toxic multinodular goitre
- Toxic adenoma
- ectopic thyroid tissue
- exogenous (iodine excess, levothyroxine)
- Subacute de Quervain’s thyroiditis
- drugs (amiodarone, lithium)
What is subacute deQuervain’s thyroiditis?
Self-limiting post viral hyperthyroidism followed with longer hypothyroid phase, with painful goitre, febrile, and typically increased ESR. low isotope uptake on scan. Managed with NSAIDs.
Describe insulinoma its tests and treatment
This often benign (90-95%) pancreatic islet cell tumour is sporadic or seen with MEN-1. It presents as fasting hypoglycaemia, with whipple’s triad:
- Symptoms associated with fasting or exercise
- Recorded hypoglycaemia with symptoms
- Symptoms relieved with glucose
Tests: Fasting hypoglycaemia (<2.5mmol/L) with elevated insulin
Proinsulin and C-peptide test (administration of insulin does not decrease levels)
MRI,CT
Treatment:
Initial management - immediate K+ replacement and dextrose administration
Surgical excision
Unresectable - eating frequent small meals with high starch and complex carbohydrate
Describe Diabetic Ketoacidosis, precipitating conditions, presentation, investigation, and management
A medical emergency.
Ketonaemia/ketonuria (2+ standard urine sticks)
Blood glucose >11mmol/L or known DM
Bicarbonate <15mmol or venous pH <7.3
Precipitating conditions - infection, discontinuation of insulin, inadequate insulin, CV disease, drugs (steroids, thiazides, SGLT2 inhibitors), physiological stress
Presentation: abdo pain, polyuria, polydipsia, vomiting, dehydration, altered mental state, coma
Weight loss, weakness, lethargy, Kussmaul respiration, acetone smell breath (‘pear drops’)
Investigations:
- cap blood glucose
- urine dipstick
- blood: FBC, glucose, ketones, U+E, ABG, cultures
- ECG
- CXR
Management:
- ABCDE
- fluid replacement with 0.9% NaCl (add KCl after 1st bag - correct hypokalaemia)
- Continuous infusion of insulin at 0.1unit/kg/hr.
- Once blood glucose is <15mmol/l, start 5% dextrose infusion
Describe Hyperosmolar Hyperglycaemic State (HHS),its symptoms, investigations, management.
- Dehydration
- Osmolality >320mosmol/kg
- Hyperglycaemia >30 mmol/L with pH >7.3, bicarbonate >15mmolL and no significant ketonenaemia <3mmol/L
Symptoms: Generalised weakness, leg cramps, visual disturbance, nausea and vomiting, delirium, seizures, focal neurological signs
Investigations
- Urinalysis, culture
- Cap glucose
- Bloods: U+E, FBC, CRP, culture, ABG
- ECG
- CXR
Management:
- ABCDE
- IV 0.9% NaCl (fall in blood glucose should be no more than 5mmol/L/hr)
- Low dose IV insulin (0.05units/kg/hr) if blood glucose no longer falling with IV fluids
- Encourage patient to drink as soon as safe
- Identify and treat underlying precipitants
Describe Cushing’s syndrome, it’s causes, investigations, and management.
Syndrome due to chronic glucocorticoid excess.
ACTH dependent causes
- Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
- ectopic ACTH production (5-10%): e.g. small cell lung cancer
ACTH independent causes
- iatrogenic: steroids
- adrenal adenoma (5-10%)
- adrenal carcinoma (rare)
- Carney complex: syndrome including cardiac myxoma
- micronodular adrenal dysplasia (very rare)
Investigations:
Bloods: FBC, U+E
24 hour urinary free cortisol
- 9am and midnight ACTH and cortisol level (if ACTH suppressed –> non-ACTH dependent cause)
- High-dose dexamethasone suppression test
–if pituitary source then cortisol suppressed
–if ectopic/adrenal then no change in cortisol
-CRH stimulation
–if pituitary source then cortisol rises
–if ectopic/adrenal then no change in cortisol
MRI of pituitary
Chest abdo CT
Management:
- Treat cause
- Cushing’s disease: excision (transphenoidal), bilateral adrenectomy
- Adrenal adenoma or carcinoma: adrenectomy. Radiotherapy and adrenolytic drugs
- Ectopic ACTH: metyrapone, ketoconazole, fluconazole - preop or awaiting effects of radiotherapy
Describe primary adrenocortical insufficiency (addisons disease), it’s symptoms, tests and treatment
Rare but fatal
Destruction of adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency.
80% - autoimmune in UK,
TB is commonest world wide
Symptoms:
lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases), vitiligo, loss of pubic hair in women, hypotension
crisis: collapse, shock, pyrexia
Tests: U+E (hyponatreaemia, hyperkalaemia, uraemia), glucose (decrease), calcium (increased) FBC (eosinophilia, anaemia.) 9am serum cortisol ACTH stimulation test 21-hydroxylase adrenal autoantibodies
Treatment:
Hydrocortisone (in 2 or 3 divided doses; 20-30mg/day) and fludrocortisone
Education - not missing, MedicAlert bracelet and steroid cards, double glucocorticoid dose during illness
Describe secondary adrenal insufficiency
Commonest cause is iatrogenic due to long term steroid therapy leading to suppression of the pituitary adrenal axis.
Other causes: Pituitary disorders (tumours, irradiation, infiltration) Mineralocorticoid production remains intact and there is no hyperpigmentation
Describe male hypogonadism it’s features and causes
Hypogonadism is the failure of testes to produce testosterone, sperm or both.
Features: small testes, decreased libido, erectile dysfunction, loss of pubic hair, decreased muscle bulk, increased fat, gynaecomastia, osteoporosis, mood disturbance.
Primary hypogonadism causes:
•testicular failure from trauma, torsion, radiotherapy
•post-orchitis e.g mumps
•renal failure, liver failure or alcohol excess
•chromosomal abnormalities e.g. Klinefelters syndrome
Causes of secondary hypogonadism:
•hypopituitarism
•prolactinoma
•kallman’s syndrome (isolated GnRH deficiency often with anosmia and colour blindness
•systemic illness
•Laurence-moon-biedl and prader-willi syndromes
Describe the symptoms and causes of hyperprolactinaemia
Prolactin is secreted by the anterior pituitary and release is inhibited by dopamine produced in the hypothalamus.
Causes:
- excess production from the pituitary e.g. prolactinoma
- disinhibition, by compression of the pituitary stalk e.g. pituitary adenoma, or hypothalmic disease
- dopamine antagonist e.g. anti-emetics, anti-psychotics
Symptoms:
- females = amenorrhoea, oligomemorrhea, infertilty, galactorrhoea, also decreased libido, increased weight and dry vagina.
- males = erectile dysfunction, decreased facial hair, galactorrhoea.
Investigations: TFT, exclude pregnancy, basal serum prolactin (normal <400mU/L) Visual testing Pituitary imaging Assessment of pituitary function
Management
Rx underlying cause
Prolactinoma - Dopamine agonist (bromocriptine/cabergoline), surgery, radiotherapy
Prevent osteoporosis
Describe Diabetes insipidus, its symptoms, causes and tests.
This is the passage of large volumes of dilute urine due to deficiency of antidiuretic hormone, ADH, (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).
Symptoms: polyuria, polydipsia, dehydration, irritability, confusion.
Causes of cranial DI:
- Idiopathic
- congenital defects in ADH gene (DIDMOAD)
- tumour (may present with DI + hypopituitarism) - craniopharyngiomas
- Trauma
- Infiltration e.g. sarcoidosis
- vascular e.g. haemorrhage
- infection e.g. menigoencephalitis
Causes of nephrogenic DI:
- inherited
- metabolic e.g. hypokalaemia, hypercalcaemia
- drugs e.g. lithium, demeclocycline
- tubulo-interstitial disease: obstruction, sickle cell, pyelonephritis
- post-obstructive uropathy
Tests: serum and urine osmolalities and water deprivation test.
Describe acromegaly its symptoms, complications, tests and management
Due to increased secretion of GH from a pituitary tumour (99%) or hyperplasia e.g. via ectopic GHRH from a carcinoid tumour or GH.
GH stimulates bone and soft tissue growth through increased secretion of insulin-like growth factor-1 (IGF-1)
Symptoms:
- coarse facial appearance, spade-like hands, increase in shoe size
- large tongue, prognathism, interdental spaces
- excessive sweating and oily skin
- features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
- raised prolactin in 1/3 of cases → galactorrhoea
- 6% of patients have MEN-1
Complications:
- hypertension
- diabetes (>10%)
- cardiomyopathy
- colorectal cancer
Tests: Bloods: glucose, phosphate, Ca (all increase), IGF1 OGTT: serial GH measurements (normal suppress GH <2mu/L) pituitary MRI
Management
1st line: surgery (transphenoidal)
Medical: Dopamine agonist (bromocriptine), somatostatin analogue (octreotide) - can be used as adjunct to surgery, pegvisomant (GH receptor antagonist) - OD SC
External irradiation - older patients or failed medical/surgical
Describe the WHO criteria for diagnosis of Diabetes Mellitus
- Symptoms of hyperglycaemia (e.g. polyuria, polydypsia, unexplained weight loss, visual blurring, genital thrush, lethargy) and raised venous glucose detected once either fasting >7mmol/L or random >11.1mmol/L
- Raised venous glucose on 2 separate occasions
- HbA1C >48mmol/L (6.5%) but below doesnt exclude DM
Describe metabolic syndrome (syndrome X)
and treatment
A syndrome that can lead to increased risk of MI and insulin resistance.
Any 3 or more of:
- increased waist circumference: ethnicity specific e.g Caucasian men >94cm; women >80
- BMI >30kg/m2
- Raised triglycerides (>150mg/dL)
- Reduced HDL-cholesterol (<40mg/dL in men; <50 in women)
- Raised BP (>130/85)
- Raised fasting plasma glucose (>5.6mmol/L)
Management - Treat individual parameters
Describe Hypoglycaemia its symptoms and causes
plasma glucose less than 3mmol/L
Symptoms:
Autonomic: Sweating, anxiety, hunger, tremor, palpitations, dizziness
Neuroglycopenic: confusion, drowsiness, visual trouble seizures, coma, mutism, personality change, restlessness
Causes: EXPLAIN.
- EXogenous drugs e.g. insulin or oral hypoglycaemics
- Pituitary insufficiency
- Liver failure
- Addisons disease/alcohol
- Islet cell tumour (insulinoma)
- Non-pancreatic neoplasm
Describe Diabetic Neuropathy, its symptoms, and management.
A complication of diabetes, including peripheral neuropathy, autonomic neuropathy, gastroparesis.
Symptoms: numbness/burning sensation in extremities in glove and stocking distribution. May also affect Autonomic nervous system with loss of bladder control. Gastroparesis presents with erratic blood glucose control, bloating and vomting.
Management:
- amitryptilline, Duloxetine, gabapentin, or pregabalin.
- pain management clinics for resistant problems
- metoclopramide, domperidone or erythromycin may be used in gastroparesis (pro kinetic agents)
Describe Hirsutism, it’s causes, and a management.
androgen-dependent hair growth in women, with hypertrichosis being used for androgen-independent hair growth.
Causes: PCOS Cushing's syndrome CAH Androgen therapy Obesity Adrenal tumour Androgen secreting Ovarian tumour Drugs: phenytoin
Management:
- weight loss if overweight
- Cosmetic techniques
- COCP e.g. co-cyprindiol (Dianette) or Yasmin
- facial hirsutism: topical eflornithine
What are the types of hermaphroditism and some causes?
True Hermaphroditism: individual born with ovarian and testicular tissue, these may be as separate or more commonly an ovotestis.
Pseudo hermaphroditism: indictable with primary characteristics of one sex but develops secondary characteristics of another e.g. Ambiguous genitalia (cliteromegaly).
Causes: congenital adrenal hyperplasia, androgen insensitivity, 5alpha-reductase deficiency
Describe Subclinical Hypothyrodisim and the appearance of TFTs
TSH raised but T3,T4 normal. No obvious symptoms. Small risk of progressing to overt hypothyroidism risk further increased by presence of thyroid autoantibodies. Treat if TSH over 10, or antibody positive.
Describe Primary Hyperparathyroidism, symptoms, investigations, management, associations
Causes: solitary adenoma (80%) hyperplasia (15%) Multiple adenoma (4%) Carcinoma (1%)
Symptoms: Asymptomatic
- recurrent abdominal pain (peptic ulceration, pancreatitis, renal colic, constipation)
- changes to emotional or cognitive state (depression)
- polydipsia, Polyuria
- hypertension
- bone pain/fractures
Investigations: PTH elevated/normal, Calcium Elevated, Phosphate low
DEXA scan, CXR - if bone involvement
Imaging of renal tract
Management:
Mild/asymptomatic- advise increase fluid intake, avoid thiazides, check 6 monthly
Surgical - parathyroidectomy
Medical - HRT and raloxifene for post menopausal, bisphosphonate amd cinacalcet
Associations:
HTN, MEN
Describe Primary Hypoparathyroidism, its hormone profile, symptoms, and management.
Causes: AI, congenital (Di George)
Hormone profile: Decreased PTH, Low calcium, high/normal phosphate, normal ALP
Symptoms: Spasms (Trousseou's sign) Perioral paraesthesia Anxious/irritable Seizures Muscle tone increased (colic/wheeze/dysphagia) Orientation impaired (confusion) Dermatitis Impetigo herpetiformis Chovstek's, Cardiomyopathy (prolonged QT)
Management: Alfacalcidol and calcium suppplements
Describe Secondary Hyperparathyroidism, its hormone profile, symptoms, and management.
Parathyroid gland hyperplasia occurs as result of low calcium almost always in a setting of chronic renal failure.
Hormone profile: Elevated PTH, Low/normal calcium, phosphate elevated, vitamin D levels low.
Symptoms: Asymptomatic, bone disease, and soft tissue calcifications.
Management:
-Vit D and Calcium replacement
Which Diabetic medications requiring glucose fingerprick monitoring?
Those causing hypoglycaemia e.g. Sulphonylureas, insulin, glitazones.
Complications of DKA
- gastric stasis
- thromboembolism
- arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
- iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
- acute respiratory distress syndrome
- acute kidney injury
Cushing’s syndrome presentation
General: Truncal obesity, supraclavicular/interscapular fat pads, weight gain.
Facial features: Facial fullness, round face, facial plethora.
Proximal muscle wasting and weakness.
Skin: skin atrophy, purple striae, easy bruising, hirsutism, acne; pigmentation occurs with ACTH-dependent causes.
Psychological problems: depression, cognitive dysfunction and emotional lability.
Endocrine: Diabetes or impaired glucose tolerance. Gonadal dysfunction, reduced libido, irregular menses
Hypertension.
Renal: Nephrolithiasis.
Osteopenia or osteoporosis.
Oedema.
Thirst, polydipsia, polyuria.
Immune: Impaired immune function: increased infections, difficulty with wound healing.
Child: growth restriction.
ACTH-producing pituitary tumour- headaches, visual problems and galactorrhoea.
What is short synacthen test?
Normal response: increase of 420nmol/L after 30 min
Adrenal insufficiency: failure to increase
How to localise lesion in adrenal insufficiency?
ACTH measurement or long Synacthen test
Primary: no rise in cortisol in long synacthen test
secondary: chronically low levels of ACTH due to pituitary failure. prolonged simulation -> degree of recovery. peak at 24 hours
