Endocrine/ rheum Flashcards
What skin changes do you get in dermatomyosis?
Get weakness + skin changes:
photosensitive
macular rash over back and shoulder
heliotrope rash in the periorbital region
Gottron’s papules - roughened red papules over extensor surfaces of fingers
‘mechanic’s hands’: extremely dry and scaly hands with linear ‘cracks’ on the palmar and lateral aspects of the fingers
nail fold capillary dilatation
In a patient on long term hydrocortisone and fludrocortisone who has N+V what should you do re their medications
A person with Addisons’ who vomits should take IM hydrocortisone until vomiting stops
Fludrocortisone is a mineralocorticoid that is used to manage Addison’s. However, it is extra glucocorticoid (hydrocortisone) that is required in this situation
If not vomiting but unwell double hydrocortisone, keep fludrocortisone dose the same
Cushings syndrome causes?
ACTH dependent causes
Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
ectopic ACTH production (5-10%): paraneoplastic
ACTH independent causes
iatrogenic: steroids - most common overall cause
adrenal adenoma (5-10%)
adrenal carcinoma (rare)
What is limited vs diffuse cutaneous systemic sclerosis?
Limited cutaneous systemic sclerosis
scleroderma - face + distal limbs
anti-centromere antibodies
a subtype of limited systemic sclerosis is CREST syndrome: Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia
Diffuse cutaneous systemic sclerosis:
scleroderma affects trunk + proximal limbs
most common: anti scl-70 antibodies (AKA anti-topoisomerase-1 antibodies); less common: anti-RNA polymerase
commonly die from resp complications - ILD + pulmonary hypertension
other complications: renal disease + HTN
poor prognosis
What is hyperaldosteronism? How do you ix? How do you mx?
Primary hyperaldosteronism AKA conns syndrome
Causes
bilateral idiopathic adrenal hyperplasia: 60-70%
adrenal adenoma: 20-30%
familial etc
Features
hypertension, hypokalaemia, metabolic alkalosis
Investigations
plasma aldosterone/renin ratio -
should show high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone)
high resolution CT Abdo and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess
if the CT is normal adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia
Management
adrenal adenoma: surgery
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
What is Pagets disease of the bone? Sx? management and ix (and blds)?
Paget’s disease is a disease of osteoclasts -> increased + uncontrolled bone turnover.
Presentation: typically older male with bone pain and an isolated raised ALP, (e.g. pelvis, lumbar spine, femur)
untreated features: Bowing of tibia, Bossing of skull
Can rarely cause high-output HF
Investigations: Raised ALP, normal Ca and Phosphate.
x-rays- osteolysis in early disease → mixed lytic/sclerotic lesions later
skull x-ray: thickened vault, osteoporosis circumscripta
Management: only treat if sx/ fracture/ deformity.
bisphosphonate (either oral risedronate or IV zoledronate)
What raises ALP in relation to bones?
When bones have increased remodelling ALP rises as it is realeased by ostoblasts eg in osteomalacia, hyperparathyrdoisism, bones mets, pagets, bone fracture
What is blood test for sjogrens Vs polymyo/dermatomyositis?
Sjogrens - Anti Ro (more common) and anti La (less common)
anti-mI2 (more common), Anti-Jo1 (less common)- Polymyo/Dermatomyositis
What can you test for to differentiate type 1 vs type 2 diabetiics? What will these levels be like?
c-peptide is low in t1DM as no insulin is being made
What is MODY (mature onset diabetes of young)?
Maturity-onset diabetes of the young is an autosomal-dominant disease, and it is characterised by the development of type 2 diabetes mellitus in patients younger than 25 years old. In this condition, C-peptide remains in the normal range and beta-cell antibodies are negative.
How do you diagnose diabetes?
If the patient is symptomatic:
fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.
What is the most common cause of hyperthryoidism
graves disease
When are topical NSAIDs particularly useful for OA?
Topical NSAIDs may be particualrly beneficial for patients with OA of the knee or hand
What is T score on BMD indicates need for treatment?
Less than -1.5
The first-line treatment is alendronate. Patients should also be calcium and vitamin D replete.
Osteomalacia vs pagets vs primary/ secondary/ teriatry parathyroid?
Osteomalacia- low vit d, low calcium, low phos. High ALP, high PTH
(the bone is trying but has poor supplies)
Pagets - Isolated ALP rise
(bone is just doing its own thing)
Primary hyperparathyroid- high ca, low phos, high ALP, PTH can be high or normal
(the parathyroid is demanding calcium to the blood, so bones have to break down)
Secondary hyperparathyroidism - chronic disease, usually CKD. Calcium low due to disease, and phosphate raised –> PTH raised in response. ALP also raised.Low Vit D as kidneys cant make.
Tertiary hyperparathyroidism - hyperplasia of the parathyroid glands after the cause of secondary hyperparathyroidism has been corrected. Calcium remains high, but PTH would be elevated, rather than normal.
When should bisphosphonates be started without a DEXA scan?
fragility fracture (vertebral, NOF, wrist) + >= 75 years of age are presumed to have underlying osteoporosis and should be started on first-line therapy (an oral bisphosphonate), without the need for a DEXA scan.
treatment for PHaeochromocytoma
- give (alpha blocker)PHenoxybenzamine before beta-blockers
- Needs medication before eventual surgery
What steroid use (dose and length) puts you at risk of osteoporosis and requires bisphos?
7.5mg a day for 3 or more months.
Describe subacute thyroiditis?
Subacute thyroiditis AKA De Quervain’s thyroiditis, will have tender thyroid
Post viral. 4 phases.
phase 1 (lasts 3-6 weeks): hyperthyroidism,painful goitre,raised ESR
phase 2 (1-3 weeks): euthyroid
phase 3 (weeks - months): hypothyroidism
phase 4: normal
Ix: thyroid scintigraphy:globally reduced uptake of iodine-131
Mx: self-limiting, analgesia, steroids if severe - particularly in hypothyroid
How do you mx Gastrointestinal autonomic neuropathy?
management options include metoclopramide, domperidone or erythromycin (prokinetic agents)
Mx of prolactinoma
1st line medical - dopamine agonist (e.g. cabergoline, bromocriptine)
2ns line - surgery- if medication fails
Diagnosis of a DKA?
glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick
How to Mx DKA?
fluid replacement - around 5-8L
IV insulin 0.1 unit/ kg/hr
once blood glucose is < 14 mmol/l IV 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
Monitor for hypokalaemia - replace with fluids if needed. If >20mmol /hr cardiac monitor
long-acting insulin should be continued, short-acting insulin should be stopped
what would you find on an ABG in cushings syndrome?
hypokalaemic metabolic alkalos
What are the blood sugar targets for diabetics?
you can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of48 mmol/mol(6.5%), but should only add a second drug if the HbA1c rises to58 mmol/mol(7.5%)
WHat will you find on blood tests for sick euthyroid syndrome?
TSH low
T4 low
Summarise diabetes insipidus
ADH isnt working either because brain ins’t making it or kidneys aren’t responding to it causing polyuria and polydipsia
cranial DI: head injury/ surgery; sarcoidosis; haemochromotosis
Causes nephrogenic DI: genetic; hypercalcaemia; hypokalaemia; lithium; sickle-cell, pyelonephritis
Ix: high plasma osmolality (very diluted), low urine osmolality (very consentrated)
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test - depive of water and then give demopressin to see if nephrogenic vs central
Mx: thiazides + low salt diet if nephrogenic
central diabetes insipidus can be treated with desmopressin (synthetic ADH)
Drug used to treat acromegaly?
ocreotide
Drug used to treat hyperprolactin?
Bromocriptine is a dopamine agonist and it works by inhibiting prolactin secretion
What results are seen on radioactive iodine tests?
Graves - increased homogenous uptake (whole gland overactive)
toxic nodular goitre- areas of increased uptake interspersed with reduced activity
No uptake/ faint uptake at allwould be seen in inflammatory conditions such as subacute thyroiditis.
Asingle hot nodule with the rest of the gland suppressedwould be consistent with a toxic adenoma (a single hyperfunctioning area of thyroid tissue).
What is Behcets syndrome?
Vasculitis associated with HLA B51
Cause PO and genital ulcers + anterior uveitis
can cause DVT
associated with japanese + meditarranean
What is a phaechromocytoma? sx? ix?
catecholamine secreting tumour.
sx: HTN, headaches, sweating, anxiety, palpitations
ix: 24 hr urinary collection of metanephrines
What antibodies are associated with drug induced lupus?
Antihistone antibodies are associated with drug-induced lupus
mx of thyroid storm?
IV propranolol
When is exophalmos seen?
graves disease ONLY
Findings on x-ray for RA?
Early x-ray findings
loss of joint space
juxta-articular osteoporosis
soft-tissue swelling
periarticular erosions
subluxation
cushing disease vs syndrome
cushing disease = pituitary adenoma (exess ACTH) causeing cushing syndrome
Excess ACTH causes increased skin pigmentation as stimulated melanin
Ix for cushings? How does it work?
Dexamethasone suppression test and testing for ACTH
In a normal person - Dexamethasone is given —> less ACTH —> less cortisol production normally
Low dose given of dexamethasone and then a high dose.
Will not suppress cortisol in adrenal cause or paraneoplastic. However high dose will suppress cortisol in a pituitary adenoma (cushings disease)
Ix for adrenal insufficiency? How does it work?
short synacthen test
ACTH blood results
Measure cortisol at baseline –> synacthin (AKA ACTH) —> 30 mins –> 60 mins measure cortisol
Normally would double cortisol
Primary adrenal insufficiency AKA Addisons (adrenal gland not producing cortisol) - wont increase cortisol in response to synacthen - abnormal response
secondary adrenal insufficiency - lack of ACTH (central cause) - low ACTH on bloods
What is a CI to radioactive iodine treatment?
contraindications include pregnancy (should be avoided for 4-6 months following treatment) and age < 16 years. Thyroid eye disease is a relative contraindication, as it may worsen the condition
What can be used alternatively to alendronate in osteoporosis?
risedronate trial if issues with oesophagitis
IV zoledronate is the first-line treatment following a hip fracture
denosumab is generally used as a second-line treatment if bisphosphonates in appropriate eg egfr <30
diagnosis of Impaired fasting glucose and impaired glucose tolerance on OGTT?
A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)
Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l
Granulomatosis with polyangiitis AKA Wegener’s
vs
churg-strauss syndrome AKA Eosinophilic granulomatosis with polyangiitis ?
Both: dyspnoea, sinusitis, vasculitis
Granulomatosis with polyangitis: renal failure, epistaxis, haemoptysis, saddle shape deformity, c-anca
churg-strauss: asthma, eosinophilia, p-anca
what drugs can cause drug induced lupus?
Methyldopa
Hydralazine
Minocycline
Isoniazide
Sulfonamides
Etanercept
Procainamide
Phenytoin
penicillilamine
RA joints commonly affected?
MCP
PIP
What is zollinger-elliston syndrome?
A gastrin-secreting neuroendocrine tumor that is most often localized to the duodenum and pancreas –> seceretes gastrin —> ulcers
associated with parathyroid adenoma –> hypercalcaemia
Part of MEN syndrome
what infectious disease is addisons associated with?
TB
Mx of graves eye disease?
steroids
orbital decompression second line
joint hypermobility vs EDS?
joint hypermobility is assessed via the Beighton score, can get dislocations + joint pain
can get subtype of EDS (hypermobility type) which causes hypermobility + other sx eg skin that easily bruises, digestive issues, urinary incontinence, organ prolapses/ fhx
What is felty’s syndrome?
RA + spleenomegaly + neutropenia
What is caplans syndrome?
RA + pneumoconiosis (caused by mining dust) that manifests as intrapulmonary nodules
Features of microscopic polyangitis vs churg strayss?
Microscopic polyangitis features =
joint pain
renal failure - haematuria and proteinuria
purpura on skin
haemoptysis
p=ANCA positive
eosinophilia and raised eSR
NO renal failure or haemoptysis in churg strauss
What is the most common primary bone tumour in adults?
osteosarcoma
What is the most specific marker for RA?
anti-CCP is most specific for RA
How can insulinoma present?
If getting lots of episodes of hypos, not diabetic, may be insulinoma
What is Waterhouse friderichsen
disease adrenal glands due to N. meningitis, causes DIC, shock and adrenocortical insufficiency
How is hyperthyroidism managed in pregnancy?
Hyperthyroidism in pregnancy is treated in 1st trimester with propylthiouracil and 2nd and 3rd with carbimazole
Primary vs secondary hypoparathyroidism?
Primary hypoparathyroid = low PTH causing low calcium, due to surgery/ autoimmune/ di george syndrome/ secondary hypoparathyroid = low PTH due to high calcium
Medullary vs papillary thyroid cancer?
Medullary thyroid cancer releases carcinoid → leads to face flushing and carcinoid sx. Papillary cancer = most common type thyroid ca
What are the features of RA on x-ray?
RA x-ray: soft tissue swelling, juxta-articular demineralisation, erosions, joint space narrowing
What is the 1st line mx of RA
a DMARD, do not use just NSAID first, can be used for analgesia but need to be on a DMARD no matter what
Consequences of untreated HYPO vs HYPER thyroidism
Consequences of untreated HYPOthyroidism = metabolic syndrome and insulin resistance. Consequences of untreated HYPERthyroidism = AF, OP, graves orbitopathy, thyrotoxic periodic paralysis
Blood results of addisons?
Often get hypothyroidism picture with addisons, so if other things fit clinical picture of addisons eg low sodium, high potassium, low cortisol, sx, need to do short synacthen test
