Rheumatology Flashcards
How to classify causes of chronic polyarthopathies
Rheumatoid like:
symmetrical and proximal-stiffness of 30 mins +
Psoriatic
RA
Osteroarthritis (worse at evening)
Spondyloarthropathy: asymmetric oligoarthritis + spine
Gout
Connective tissue- SLE, Sjögrens
Causes of acute polyarthropathies
Infective:
Viral- migratory joint arthritis (rheum fever)
Gonococcal
Non-infective:
Reactive + Reiter’s
Acute causes of a monoarthropathy:
Gout Haemoarthropathy Osteoarthritis Septic joint Trauma
Common sites of psoriasis to check:
Elbows Hair line/ scalp Umbilicus Natal cleft Genitalia
Cause of monoarthritis:
vITAMin Infective- septic arthritis T- haemarthrosis, OA Autoimmune- early RA Metabolic- gout/pseudogout
Causes of oligoarthritis (<5 joints)
Seronegative arthropathies- psoriatic, reactive, ank spond
OA
Crystal arthropathies
Symmetrical vs Asymmetrical polyarthropathy causes?
Symmetrical- vITAmin:
Infection- Hep A, B, C, mumps (athralgia)
Trauma- OA
Autoimmune- RA
Asymmetric-
Seronegative arthropathies
What is Schober’s test?
Mark on back at level of posterior iliac spine
Measure 5cm below to 10cm above
Bend forward
Should increase by 5cm
How do neutrophil levels help to determine cause of swollen joint, once aspirated?
< 50% osteoarthritis or haemoarthrosis
~ 80% crystal arthropathies
> 90% septic arthritis
Radiological features of RA vs OA vs Gout:
OA: LOSS
Loss of joint space, osteophytes, subchondral cysts, subchondral sclerosis
RA: LOSED
Loss of joint space, osteopenia, soft tissue swelling, erosions, deformities
Gout: NOSE
No loss of joint space, soft tissue swelling, erosions
Back pain red flags:
Under 20, over 55, acute in the elderly
PC: SOCRATES S- thoracic O- pain at night C- constant R- bilateral/alternating sciatica A- fever, night sweats, weight loss, abdo mass, neuro disturbance, sphincter disturbance, leg claudication, morning stiffness T- progressive E- worse when supine, exercise-related (spinal stenosis)
3 clinical tests for sacroiliitis:
- Direct pressure
- Lateral compression
- Sacroiliac stretch test- hip + knee flexed + adduction = pain
Cauda equina compression signs:
Pain: alternating or bilateral leg pain
Sensation: saddle anaesthesia
Power: loss of anal tone on PR
Functional: bladder + bowel incontience
How is cauda equina compression differentiated from acute cord compression?
Spinal level in cord compression with UMN and LMN signs
In cauda equina there’s only LMN signs
How does OA differ from RA in symptom presentation?
OA:
S- distal hand joints, knees; monoarthritis, oligoarthritis, polyarthritis
O- evening;
E- exercise, stiffness after rest
RA:
S- proximal joints of hands feet; symmetric polyarthitis
O- worse in morning, stiffness >30 mins
A- extra-articular + systemic features
Management of osteoarthritis:
Conservative: exercise- aerobics, weight loss, PT, OT, walking aids, heat/cold packs, TENS machines
Medical: PO Paracetamol ± NSAIDs topical
2. Short term NSAIDs (+PPI), codeine, capsaicin, intra-articular steroids
Surgical: joint replacement
Patient has a red hot joint, what risk factors of septic arthritis should be asked about:
Over 80
PMH: joint disease-RA, diabetes, CKD, immunosupression
PSH: recent joint surgery, prosthetic joint
SHx: IVDU
Things to tell patients about NSAIDs:
Take lowest dose for shortest time, may not need every day
Don’t take additional over the counter NSAIDs
Look out for: malaena (GI bleeding), oliguria (renal impairment)
DHx: Avoid if already taking Aspirin
PMH CI: severe heart failure
SEs: increased risk of MI + stroke
How do the following drugs work?
A. NSAIDs
B. Aspirin
C. Paracetamol
A. Cyclooxygenase competitive inhibitor- preventing formation of prostaglandins and thromboxane from arachidonic acid
(COX1 in stomach makes prostaglandins that are protective)
Prevents fever by reduction of PGE2 signalling (acts on CNS)
B. Cyclooxygenase irreversible inhibitor
C. COX2 inhibitor ?Central actions + ?acting on endocannabinoid pathways
Hand signs of RA
Hands:
Swollen or red proximal small joints of hand (MCP, PIP, wrist)
Swan necking, Boutoniére’s, Z thumb deformity
Ulnar deviation, dorsal wrist subluxation
Elbow:
Bursitis, rheumatoid nodules
Tenosynovitis
Extra-articular features of RA:
Hands- Raynaud’s, carpal tunnel syndrome
Neck- lymphadenopathy
Face- episcleritis, scleritis, scleromalacia (conjuctiva degeneration) or keratoconjunctivitis sicca (dry eye)
Amyloidosis (glossitis)
Chest- bronchiectasis, basal fibrosis, obliterative bronchiolitis
Pleural + pericardial effusion
Abdominal- splenomegaly
Osteoporosis
Tests for rheumatoid arthritis?
Bloods: Anticyclic-citrullinated peptide, rheumatoid factor (70%)
Platelets, ESR, CRP
X rays: late disease
MRI or USS: synovitis
What 4 things make up the diagnostic criteria for diagnosing RA?
J-ASS score of 6/10 is diagnostic
- Joint involvement (swelling or tenderness) max score 5
- Acute phase reactants (abnormal CRP or ESR) max score 1
- Serology (anti-CCP or RF, high or low titres) max score 3
- Symptoms duration (>6 weeks) max score 1
Management of rheumatoid arthritis:
Conservative: PT, OT, help to stop smoking (increases symptoms), NSAID analgesia
Medical: Methotrexate + 1 DMARD (sulfasalazine, hydroxychloroquine)
Short term steroids (oral or intra-articular)
Surgical: to prevent pain or deformity, or improve function
After 6 months, DAS28 score >5.1
What is the DAS28 score?
An assessment of tenderness and swelling at 28 joints:
MCPs, PIPs, wrists, elbows, shoulders, knees
ESR and patient’s self-reported symptom severity
Main SEs of the rheumatoid arthritis DMARDS
A. Methotrexate
B. Sulfasalazine
C. Hydroxychloroquine
A. Pneumonitis, liver cirrhosis, myelosupression
B. S for skin rash, U for ulcers (oral), L for low sperm count
C. Irreversible retinopathy
What are the 4 ways biological agents may act to help treat rheumatoid arthritis?
- TNFa inhibitors (infliximab, etanercept, adalimumab)
- B cell depletion (Rituximab)
- IL-1 and IL-6 inhibition (Toclizumab = IL 6)
- Disrupted T cell function (Abatacept)
SE of biological agents:
Serious infection
TB reactivation and Hep B
Hypersensitivity
Heart failure worsening
Aside from the typical presentation of RA, name 6 other ways it can present:
- Sudden onset widespread arthritis
- Palindromic RA- recurrent arthritis, lasts days to hours, visiting and revisiting different joints (precedes RA, SLA, Whipple’s, Beçet’s)
- Persistent mononeuritis- knee, shoulder, hip
- Systemic illness with initially few joint problems, fever, fatigue, weight loss, pericarditis
- Polymyalgic onset, vague limb girdle aches
- Recurrent soft tissue problems- frozen shoulder, carpal tunnel, tenosynovitis
Causes of gout:
What goes in: alcohol, purines, diuretics (from blood, enter tubular cell, excreted into tubular lumen in exchange from urate)
What happens inside: leukaemia, cytotoxics- tumour lysis
Hereditary
Rx of acute attack of gout
Include options for renal impairment
- NSAIDs
- Colchicine
- Steroids (PO, IM, intraarticular) if AKI/CKD
Long term Rx of gout and it’s indications:
Conservative: lose weight
avoid fasts + EtoH + red meats + low dose aspirin
Medical:
allopurinol if 2 attacks in one year, tophi, or urate stones
Start 3 weeks after acute attack, give NSAID cover for 6 months
What are the 3 patterns of calcium pyrophosphate joint disease?
- Acute calcium pyrophosphate crystal arthritis- large joints often
- Chronic calcium pyrophosphate deposition- symmetrical RA like polyarthritis
- Osteoarthritis with calcium pyrophosphate deposition- OA with acute pseudogout attacks superimposed
Rx of calcium pyrophosphate deposition in joints?
Acute: NSAIDs, intra-articular steroids ± colchicine
Chronic: methotrexate might have a role
7 features of seronegative arthropathies:
Who:
- Seronegativity (RF -ve)
- HLA B27 associated
What joint:
- Axial arthritis- spine + sarcoiliitis
- Asymmetric large joint oligoarthritis or monoarthritis
What other stuff:
- Enthesitis- inflammation of insertion site of tendon/ligament (plantar fasciitis, Achilles tendonitis, costochondritis)
- Dactylitis- sausage digit from oedema, tenosynovial + joint inflammation
- Extra-articular manifestations: psoriaform rashes, uveitis, oral ulcers, aortic valve incompetence, IBD
How do joint problems present in ankylosing spondylitis?
15-30 year old man
Gradual lower back pain
Worse at night, stiff in the morning, better with exercise
Best imaging for ankylosing spondylitis?
- MRI (most sensitive and better for detecting early disease)
- Xray- sacroiliitis with irregularities, erosions, sclerosis
syndesmophytes (bone forming from enthesitis of ligament)
bamboo spine- calcification of ligaments
Bloods: FBC, ESR, CRP, HLA-B27 (non-diagnostic)
Management of ankylosing spondylitis:
Conservative: Exercise with PT guidance, NSAIDs
Medical: TNFa-blockers, temporary steroids
Surgical: hip replacement if involved
Which conditions affecting the gut are associated with enteric arthropathy (seronegative arthritis)?
IBD
GI bypass
Coeliac disease
Whipple’s disease (trophema whippleii)
Nail features of psoriasis?
Pitting
Oncholysis (separation from nail bed)
Subungal hyperkeratosis
Thickening
What are the forms of psoriasis?
- Plaque psoriasis
- Small plaque psoriasis (guttate- drop like papules on trunk)
- Palmoplantar psoriasis (yellow pustules on a brown base)
- Erythrodermic psoriasis (desquamation of 90% of skin)
Management of psoriatic arthritis:
NSAIDs
DMARDs: methotrexate, sulphasalazine, ciclosporin
Anti-TNFa biologics
Patient has aysmmetric painful swollen elbow, back and MCP points. What features in the history would suggest a reactive arthritis is the cause?
Is it a seronegative arthritis?
Enthesitis- plantar fasciitis, achilles tendonitis, costochondritis
Dactylitis, uveitis, oral ulcers, rashes
Is it secondary to recent:
Urethritis- chlamydia or ureaplasma (may have circinate balanitis = chlamydial painless ulcers)
Dysentery- campylobacter, shigella, salmonella, yersinia
± Keratoderma blenorrhagia (brown raised plaques on soles and palms)
What is the different between diffuse and limited cutaneous systemic sclerosis?
Both are due to increased fibroblast activity increasing deposition of connective tissue
Limited cutaneous (CREST)
Slow progression of calcinosis, Raynaud’s, esophageal + gut motility, sclerodactyly, telangiectasia
Anti-centromere (less central organ involvement)
Diffuse cutaneous- organ fibrosis
Rapid progression of lung, cardiac, renal, GI fibrosis
Anti-Scl70 and Anti-RNA polymerase
What is relapsing polychondritis?
Chondritis- inflammation of cartilage Affects pinna (floppy ears), nasal septum, larynx (stridor) and joints
Features of dermatomyositis:
Symmetrical proximal muscle weakness- dysphonia, dysphagia, resp weakness
Shawl sign- macular rash over shoulders and back
Helitrope rash ± eyelid oedema
Gottron’s papules- hands, elbows + knees
Nailfold erythema (redness at base of nail)
SC calcifications
Also: fever, arthralgia, Raynaud’s, lung fibrosis, myocarditis
Tests for dermatomyositis:
Muscle enzymes (ALT, AST, CK, LDH, aldolase)
Electromyography- fibrillation potetnials
Anti-Mi2, Anti-Jo (mijositis? No, myositis)
Which autoimmune conditions are often positive for ANA antibodies?
(ANA Seager is noisy so SLEep = SHh)
SLE
Srögren’s
Autoimmune hepatitis
Which antibodies are associated with SLE?
Specific: Anti-dsDNA
Most specific: Anti-Smith
Others: Rheumatoid factor, ANA, Anti-Ro, Anti-La, Anti-RNP
Drug induced: antihistone (better take a good HISTory)
Don’t Stop agent SMITH, R-AN, RoLa-ed and RuNPast
Srögren’s is associated with which antibodies:
Rheumatoid factor
ANA
Ro
La
(How they’d love to ROw ANA LAke of tears)
Liver antibodies to check for?
Antimiiiiitochondrial Abs- priiiimary biiiiilary ciiiiirhosis, autoimmune hepatitis
Smoooooth muscle Abs- Autoooooooimmune hepatitis, PBC
Antibodies often +ve in diabetes mellitus type 1:
Anti-Islet cell Ab
Glutamic acid decarboxylase Ab
Antibody associated with thyroid disease?
Thyroid peroxidase Ab- Hashimoto’s thyroiditis + Graves
What vasculitidies are associated with c-ANCA vs p-ANCA?
Most are c-ANCA
imagine a C connecting your node and kidneys (= Wegener’s)
All C have polyangiitis in them-
Granulomatosis Polyangiitis
Microscopic Polyangiitis
Polyangitis nodosum
Main P-ANCA is Churg-Strauss (p for pulmonary as asthma occurs)
Pulmonary-renal aka Goodpasture’s
What vasculitidies are C-ANCA +ve?
Like a C connecting your nose and kidney (Wegener’s)
All have polyarteriitis in them:
Granulomatous polyarteriitis
Microscopic polyarteriitis
Polyarteritis nodosum
What vasculities are P-ANCA positive?
P for pulmonary:
Churg Strauss (asthma involvement) Pulonary-renal vasculitidies (Goodpasture's)
What is limbic encephalitis and what antibodies is it associated with?
Autoimmune-mediated inflammation of the brain parenchyma
Anti-voltage gated K+ channel Abs
10 diagnostic criteria for SLE:
3 skin, 3 blood, 2 surfaces, 3 miscellaneous
Skin:
1 malar rash
2 discoid rash
3 photosensitivity
Blood:
1 haem (HAMA, low Plts, 2x low WCC, 2x low lymphocytes)
2 Abs (ds-DNA, Smith, phospholipid)
3 ANA+ve
Surfaces:
1 oral ulcers
2 serositis
Miscellaneous 1 CNS (seizures or psychosis) 2 Bone (proteinuria or cell casts) 3 Non-erosive arthritis x 2 joints
What is the pathophysiology of SLE?
Polyclonal B cell’s secrete pathological autoantibodies which:
Form immune complexes
Activate complement
Have direct Ab-effects
Tests for SLE:
Bloods: Coombs +ve haemolytic anaemia FBC- low WCC,lymphocytes, platelets ESR, CRP (often normal) C3, C4 (low) Antibodies: dsDNA, Smith, RhF, ANA, Ro, La, RNP
BP
Urine microscopy- protein + casts
Causes of drug-induced lupus:
Drug Induced Problem
Diltiazem (non-hydropyridine for HTN + angina)
Isoniazid (TB)
Phenytoin (epilepsy)
Rx of SLE:
Acute induction of remission: IV cyclophosphamide + pred
-haemolytic anaemia, severe pericarditis, nephritis
Maintenance: DMARDS- azathioprine, methotrexate, low dose steroids
Skin: topical steroids, sunblock
Kidneys: careful BP control
Biologics- disappointing outcomes so far
Features of antiphospholipid syndrome:
CLOTS: Clots- may cause arterial thrombosis under age 50, or recurrent VTE, or unusual sites (mesenteric, portal vein thrombosis) Livedo reticularis Obstetric- 3 miscarriages Thrombocytopenia
What are the different vasculitidies according to vessel size?
Large- giant cell arteritis + Takayasu’s arteritis
Median- polyarteritis nodosum + Kawasaki disease
Small- ANCA negative: Henoch Schönlein, ?Goodpasture’s
C ANCA: Granulomatosis polyangiitis (Wegener’s), microscopic polyangiitis
P ANCA: Churg Strauss
What are the subtle differences in management if a patient has a large vessel vasculitis vs medium or small vessel?
Acute vasculitic attack- everyone gets steroids
Medium or small vessel- add IV cyclophosphamide
Symptoms to ask about that suggest giant cell arteritis?
Headache
Jaw claudication
Amaurosis fugax
Scalp tenderness
PMR in 50%- bilateral aching, tenderness,morning stiffness
In Takayasu’s arteritis, granulomatous inflammation causes which 3 abnormalities in vessels?
Stenosis, thrombosis and aneurysms
40 year old woman is suspected to have renal artery stenosis, you notice her arm pulses are weak and she has been getting fever, fatigue + feeling dizzy.
What may be the unifying diagnosis + tests to do?
Takayasu’s arteritis
HTN from renal artery stenosis + weak pulses
ESR + CRP
MRI or PET
Which type of vasculitidies do you get glomerulonephritidies in?
ANCA+ve like granulomatous polyangiitis (Wegener’s)
Or Churg Strauss
Features of Granulomatosis Polyangiitis (Wegener’s):
Eyes- conjunctivitis, scleritis, episcleritis, uveitis
Nose- nasal obstruction, epistaxis, destruction of nasal septum, saddle shaped, sinusitis
Mouth- ulcers
Lungs- cough, haemoptysis, pleuritis
Skin- purpura or nodules
Patient age 46 has recently been diagnosed with asthma, recently her creatinine has been increasing and her urine dipstick shows haematuria. What is the diagnosis?
Churg Strauss syndrome
Adult onset asthma, eosinophilia and vasculitis
Septic shock picture may occur with glomerulonephritis/renal failure if ANCA +ve
65 year old woman comes to her GP surgery with 2 weeks of bilateral aching, tenderness and morning stiffness in shoulders and proximal limb muscles. Feels fatigued, denies weakness or sensation changes.
Differential?
Polymyalgia rheumatica (CRP up, CK normal)
Vascular- spinal stenosis
Infection- occult infection
Trauma- osteoarthritis (Cervical spine or shoulder), bilateral impingement
Autoimmune- Recent onset RA, polymyositis
Metabolic- hypothyroidism
Idiopathic- PMR
Neoplasm- occult malignancy
How can polymyalgia rheumatica be distinguished from myositis with blood tests?
Creatinine Kinase is normal
Rx of Polymyalgia Rheumatica?
Prednisolone 15mg OD
Consider PPI + bone protection (Vit D/Calcium) as steroids for long ter
If not responding to steroids, revisit diagnosis
Diagnostic features of fibromyalgia:
Chronic pain >3 months
Widespread- left, right, above and below waist, axial skeleton
Absence of inflammation
11/18 tender points
± morning stiffness, fatigue, poor concentration, low mood, sleep disturbance
Where are the 18 ‘tender’ points in fibromyalgia?
On the back: 2 base of skull 4 base of neck 2 natal cleft 2 posterior to hip trochanter
On the front: 2 base of neck 2 at 2nd rib (midline) 2 lateral elbow in anterior cubital fossa 2 medial knee
Management of fibromyalgia:
CBT, long term graded exercise programmes
Low dose TCAs + SNRIs which act through noradrenergic system?
Not SSRIs
What is chronic fatigue syndrome?
Disabling fatigue >6 months Affecting physical and mental function Present 50% of time And 4 of: Unrefreshing sleep Reduced memory
Fatigue after exercise for more than 24 hours
Myalgia
Polyarthralgia
Persistent sore throat
Tender cervical/axillary lymph nodes
Difference in diagnostic criteria of fibromyalgia and chronic fatigue?
Fibromyalgia >3 months
Chronic fatigue >6 months
Fibromyalgia- physical symptoms for diagnosis: 11/18 tender points
Chronic fatigue- criteria included mental symptoms of reduced memory, unrefreshing sleep, physical criteria include polyarthralgia, myalgia, fatigue
Which inflammatory disorders are associated with scleritis and episcleritis?
RA
SLE
Vasculitis
How are dry eyes tested for?
Schirmer filter paper test (<5mm of tear formation in 5 minutes)
= Keratoconjunctivitis sicca
Shiny ‘silver wiring’ arteries are seen on fundoscopy of the eye, what is this a sign of?
Hardening of the arteries, occurs with atherosclerosis secondary to hypertension.
May also get AV nipping or cotton wool spots if narrowed arteries become blocked
Fundoscopy signs of hypertensive retinopathy
Think of a hyper tense sheep caught on barbed wire fence, trying to nip it’s way free- might get eaten (flames)
Silver wiring (shiny looking arteries)
AV nipping
Cotton wool spots
Leaks from oedema leave behind hard exudates
Flame haemorrhages = accelerated hypertension
What causes amaurosis fugax?
Emboli in retinal vasculature causing retinal artery occlusion
Retina may appear pale as reduced blood supply
Which rheumatological diseases cause anterior uveitis and which cause scleritis?
Anterior uveitis- Ank Spond + Reiter’s (seronegative arthropathies)
Scleritis- RA, SLE, Vasculitis (Wegener’s- GPA)
Causes of erythema nodosum?
Painful red blue lesions on shins ± arms, thighs
NODOSUM: No cause- 50% Drugs- sulphonamides, Dapsone Oral contraceptives Strep infections + Sarcoid UC, Crohns, Beçhet's Microbiology- viruses, fungi, TB
Causes of erythema multiforme?
Symmetrical target lesions on palmes, soles, limbs
Forms a spectrum with Stephen-Johnson syndrome (fever + mucosal involvement)
DRUG HIM
Herpes
Idiopathic 50%
Mycoplasma
Drugs- NSAIDs, sulfonamides, allopurinol
Which rash is Lyme disease associated with?
Erythema marginatum
Small papules at tick site, spreading into erythematous ring with central fading
What is the difference between erythema multiforme, migricans and marginatum?
Multiforme- occurs on soles, palms and limbs more = DRUG HIM aka drugs (allopurinol, sulphonamides) herpes, idiopathic, mycoplasma
Migrans- centre has a small papule (tick bite site) and centre fades = Lyme
Marginatum- on trunk more, rings come and go = rheum fever associated
Pyoderma gangrenosum is associated with:
Autoimmune- IBD, Vasculitis (Wegener’s GPA), Autoimmune hepatitis
Neoplastic- myeloma + others
Derm manifestations associated with Crohns?
Erythema nodosum (the U in NODOSUM is UC, Crohns, Bechet’s)
Pyoderma gangrenosum
What is diabetes insipidis?
Impaired resorption of water due to lack of ADH (cranial DI) or failure of the kidney to respond to ADH (nephrogenic DI)
ADH is like a bath plug, without it mass amounts of water are lost
Causes hypovolaemic hypernatraemia
Causes of cranial diabetes insipidis?
Cranial: Vascular- Sheehan's syndrome Infection- meningioencephalitis Trauma- may be temporary Autoimmune- autoimmune hypophysitis Metabolic- iron deposition in pituitary Idiopathic- 50% Neoplastic- pituitary tumour, craniopharyngeoma, mets
Congenital- DIDMOAD (diabetes insipidis, diabetes mellitus, optic atrophy, deafness)
Causes of nephrogenic diabetes inspidis?
No ADH response (no bath plug):
Drugs- lithium
Metabolic- low K+, high Ca+
CKD
Post-obstructive uropathy
How is serum osmolality measured?
2 x (Na + K) + urea + glucose = 285-295mOsmol/kg
Patient is polyuric, dehydrated and polydipsic, their sodium is high. What tests should be done to elucidate endocrinological causes?
Glucose- diabetes mellitus
U+E- safety
Ca- a cause of nephrogenic diabetes inspidis
Serum + urine osmolality- osmolality should be 2:1 in urine compared to serum if salt is high, so if urine is more dilute than it should be in light of hypernatraemia suggests diabetes insipidis
Test for diagnosing diabetes inspidis?
Preliminary: check that daily urine volume >3L (if plasma Na+ plasma osmolality are normal) otherwise not diabetes inspidis
8 hour water deprivation test:
Stage 1- Empty bladder, deprive of fluids for 8 hours
1 hourly weight, ordering serum osmolality if 3% weight loss
2 hourly urine osmolality
4 hourly serum osmolality
If urine is concentrated (>600) not diabetes inspidis
Stage 2- give desmopressin (ADH analogue)
Water can be drunk
See if urine osmolality becomes more concentrated = cranial diabetes inspidis
Management of diabetes inspidis, depending on broad type?
Cranial DI (on water deprivation test Stage 2, giving desmopressin concentrates urine)
Head MRI
Anterior pituitary function
Rx: Desmopressin
Nephrogenic DI:
Rx: cause
if persistent bendroflumethiazide (inhibits sodium chloride channel)
± NSAIDs (lower urine volume)
How is emergency hypernatraemia managed?
Lower Na+ very gradually, no more than 12mmol a day to prevent cerebral oedema
0.9% sodium IV to keep up with urine output (where diabetes insipidis is the cause)
Complications of acromegaly:
Impaired glucose tolerance or insulin resistance (GH phosphorylate insulin R) > DM or ketoacidosis
Hypertension, LVH ± CCF, cardiomyopathy (±arrhythmias)
Colon cancer risk increase
Causes of acromegaly:
Pituitary adenoma (5% MEN1) Ectopic carcinoid tumour
Features of acromegaly:
Growth of bone- hands, jaw, coarsening face, widened nose
Growth of soft tissue- macroglossia, carpal tunnel, wide spaced teeth, puffy lips/eyelids, snoring
Endo related- low libido, subfertility, goitre, acanthosis nigricans (DM), hypertension
Tests for acromegaly:
Oral glucose tolerance test: measuring GH levels every 30 minutes during the test
(GH should normally be suppressed by glucose)
What causes a false +ve on oral glucose tolerance testing for acromegaly?
Pregnancy Puberty Problems with kidneys or liver Purging- Anorexia nervosa DM
Rx of acromegaly:
- Transphenoidal surgery
- Somatostatin analogues (octreotide) ± radiotherapy
- GH antagonist (pegvisomat)
Symptoms of hyperprolactinaemia:
Women:
Menstrual disturbance- oligomenorrhoea, amenorrhoea
Low libido, dry vagina, infertility (prolactin inhibits GnRH + oestrogen therefore)
Galactorrhea
Men:
Erectile dysfunction (prolactin inhibits GnRH)
Galactorrhea
3 causes of hyperprolactinaemia:
- Excess production by pituitary (levels >5000)
- Reduced dopamine inhibition from pituitary stalk, from compression
- Use of a dopamine antagonist (antipsychotics)
Tests to do in suspected hyperprolactinaemia?
Basal prolactin level
Pregnancy test (high normally)
TFTs (hypothyroidism)
U+Es
MRI head if can’t find cause
Rx of hyperprolactinaemia?
- Bromocriptine (DA agonist) to cause inhibition of secretion
- Transphenoidal surgery (if Rx resistant)
Definition of a macroprolactinoma and how it may be identified from blood tests?
Tumour >1mm on MRI
Can cause prolactin levels 10000-100000
Whereas microprolactinomas give levels ~5000
Features of Ank Spond
All the A's: Apical fibrosis Anterior uveitis Aortic regurgitation Achilles tendonitis AV node block Amyloidosis and cauda equina syndrome peripheral arthritis (25%, more common if female)
