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Year 4/5 Revision > Rheum > Flashcards

Rheum Flashcards

1
Q

Three main categories of Rheum?

A

Arthropathy, vasculitides and connective tissue disorders

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2
Q

Osteoarthritis: epidemiology and presentation

A

F>M, 10% of >65s. Genetic factors + overuse + injury. Presents with painful joints (knee, hip, DIP/PIP/carpal/thumb MCP) after use, swelling, deformity and loss of function/ROM. Antalgic gait (in hip OA or knee OA if extensive). Can be symmetrical/asymmetrical and poly/oligo/monoarthritis. Can have referred pain. No systemic sx; and little to no morning stiffness.

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3
Q

Osteoarthritis is generally a clinical diagnosis, but a plain XR can be done if uncertain. What are the typical findings? (4)

A

LOSS
Loss of joint space (reduced cartilage in localised area)
Osteophyte formation (new bone)
Sclerosis (subarticular) - whiter part on XR (bone thickening under the cartilage)
Syst (subchondral cyst) - fluid filled cyst within the bone

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4
Q

Management of OA: conservative (4) medical (1-4th line) surgical (1)

A

Conservative-
- Lifestyle (weight loss, exercise)
- Orthotics
- Physio
- OT
Medical
- 1st line = topical NSAID e.g Diclofenac
- 2. Oral NSAID + PPI
- 3. Pct/weak opiod if other options not effective, or for short-term pain relief
- 4. If standard treatment not effective –>steroid injection (short term, 2-10weeks)
Surgical
- joint replacement/lavage & debridement if locking

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5
Q

How to screen for rheumatological conditions affecting mobility?

A

GALS; Asess Gait (L) Arms (LFM) Legs (LMF) Spine (LFM).

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6
Q

Define rheumatoid athritis and its typical serology.
Which type is present in 80% and which in 70%?

A

An autoimmune condition (genetic susceptibility + trigger) characterised by symmetrical periperhal polyarthritis and systemic inflammtory symptoms.
Anti-CCF (in 80%) and RF (IgM antibody targeting Fc domain of altered igG antibodies, in 70%)

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7
Q

Presentation of RA (joints, systemic & extra-articular)

A

Joints - typically smaller joints, pain, early morning stiffness and “bogginess” (fluid).
Systemic symptoms - fatigue, muscle ache, flu-y.
Extra-articular - affects eyes, lungs, heart, skin, nerves etc.

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8
Q

Hand examintion findings of RA (5)
+ which test is positive?

A
  1. Ulnar deviation (of fingers and wrist)
  2. Volar subluxation (finger ligament weakness)
  3. Boutonniere deformity (DIP hyperextension, PIP flexion)
  4. Swan neck deformity (DIP fleion, PIP hyperextension)
  5. Z thumb

+ positive MCP/MTP joint squeeze test

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9
Q

Susceptibility genes - RA? (2)
Triggers include

A

HLA- DR1 and 4 linked
Smoking, pathogens

CLue- Dr Szebenyi - person 1 and 4 please

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10
Q

Investigations (if uncertain)
Bloods (FBC- anaemia, U&E, LFT - baseline. Inflammatory markers - CRP and ESR. Serology - RF and anti-CCF).
Plain XR
What are the typical x-ray findings (4)

A

Soft tissue swelling
Juxtaarticular osteopenia
Decreased joint space
Erosions

Some Joints Degrade Easily

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11
Q

The American College of Rheum classification takes into account the number of joints involved, the presence of RA/anti-CCP, presence of inflammatory markers and duration >6 weeks. A score of what indicates likely RA?

A

> =6

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12
Q

After referring to rheum, what is the likely medical management for inducing remission (4)

A
  1. DMARD Monotherapy
  2. DMARD Duotherapy
  3. DMARD (Methotrexate) + TNF-a inhibitor (Infliximab, Adalimumab, Etanercept)
  4. DMARD (Methotrexate) + CD-20 inhibitor (Rituximab)
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13
Q

What can be used for short term flare-ups in RA?

A

Steroids.
NSAIDs + PPI in primary care whilst awaiting specialist management.

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14
Q

What type of arthritis is psoriatic?
What percentage of peoople with psoriasis develop it, and after how many years does it present following onset of skin symptoms?

A

A seronegative spondylarthropathy associated with psoriasis (skin & nail changes).
Occurs in <10% of patients with psoriasis - usually developed within 10 years after skin symptoms (but also possible to not have skin changes with ot)

Spondylarthropathy = inflammatory type of arthritis

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15
Q

Characteristic features of the following RA-associated syndromes:
1. Sicca
2. Felty
3. Caplan

A
  1. Secondary Sjorgen’s (got sicker)
  2. Splenomegaly & neutropenia (have you felt my spleen)
  3. Pulmonary fibrosis & pulmonary nodules (scarred captain)
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16
Q

Patterns of psoriatic arthropathy.
Which is most severe/rare?

A

Symmetrical poly
Asymmetrical pauci
Spondylitis
Arthritis multilans

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17
Q

Characteristic feature of arthritis multilans

A

telescope finger

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18
Q

Other features of psoriatic arthritis (affecting fingers, nails, heart, liver & other organs)

A

Dactylitis
Nail changes - pitting, oncholysis, sublingual hyperkeratosis
Aortitis
Amyloidosis

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19
Q

X-ray findings for psoriatic arthritis

A

Pencil in cup
“periarticular erosisons and joint resorption”
Also other erosions, periostitis, dactylitis

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20
Q

How is psoriatic arthritis managed?

A

Similarly to RA: DMARDS (Methotrexate) +/- biologic agents e.g. mabs. +/-Apremilast (PDE4n inhibitor)
If mild may only require NSAIDs for pain

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21
Q

What is the most common cause of reactive arthritis and how does it present?

A

Chlamydia, or another GU infection
Anterior uveitis & conjunctivitis, urethritis/balantitis, monoarticular joint LL pain/swelling (e.g. knee).

Can’t see, can’t pee, can’t bend the knee.

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22
Q

What skin condition can reactive arthritis can present with - brown papules on palms and soles?

A

Keratoderma blenorrhagica

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23
Q

Investigations
How is reactive arthritis assessed and managed?
What would be the finding on aspirate?

A

Ix
- MSU for MC&S
- Bloods - raised CRP and ESR
- XR: shows enthesitis
* Treat as per “hot joint” policy - with abx until septic arthritis has been ruled out
* Aspirate –> for 4 things - culture, sensitivies, gram staining and crystal examination
* Findings - organism cannot be cultured from the gram staining
* Once septic arthritis excluded –> NSAIDS or local steroid injections + splint
* Systemic steroids if multiarticular

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24
Q

Name the 4 main spondyloarthropathies
- typical blood findings (2)
- typical associations

A
  1. Psoriatic arthritis
  2. Reactive arthritis
  3. Ankylosing spondylitis
  4. Enteric arthritis (note IBD)

All are
- seronegative (RF -ve)
- associated with HLA B27
- associated with tendon damage e.g. achilles tenodinitis and plantar fascitis
- extra-articular manifestations - uveitis, PF, amyloidosis, aortic regurg

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25
Q

Define ankylosing spondylitis:

A

An inflammatory condition, associated with HLA-B27 affecting the spine and sacro-iliac joints, causing progressive back pain & stiffness.

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26
Q

Clinical features: ank spond
- Describe pain
- Describe systemic features (7 As)
- Describe extra-articular features (eyes, tendons, heart, lungs, GI)

A

Back pain - progressively worsening (>3 mo), stiffness worse in morning and at rest, relieved by exercise.
Associated features:
1. Achilles tendinopathy; enthesitis, plantar fascitis
2. Anterior uveitis
3. Apical fibrosis
4. Aortic regurgitation
5. Amyloidosis
6. Apical fibrosis
7. And cauda equina
systemic (fatigue, weight loss), chest pain (intercostal joint stiffness), anterior uveitis (HLA-B27), enthesiits (Achilles tendon rupture & plantar fascitis), IBD, heart block, restrictive lung disease (restricted lung movements).

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27
Q

What is Schober’s test positive?

A

Lumbar restriction
(indicated by <20cm during lumbar flexion)
Supports diagnosis of ank spond.

Procedure - locate the iliac crest line. Measure 5cm below and 10cm above. On flexion the distance between the two points should be >20. In ank spond it is <20; reduced flexion due to fusion.

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28
Q

What typical finding would ank spond have on plain XR spine?
If no visible signs but suspicion remains high what is the next test?
Other tests for extra-articular manifestiations?

A
  1. Sacroilitis: subchondral erosions and sclerosis
  2. Squaring of lumbar vertebrae
  3. Bamboo sign (late & uncommon)
  4. Dagger sign - single entral radiodense line (ossification of supra/intraspinous ligaments)

AKA
1. Ossificiation
2. Fusion
3. Sclerosis
4. Erosions
5. Sydesmophytes (ossification of annulus fibrosus - the disc)

E,S,S.

  • Then - MRI - can show sacroiliac joint inflammation.
  • Other tests - Spirometry
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29
Q

How is ank spond managed? (conservative and medical)
And if severe?
Are DMARDs useful?

A

**Conservative: **
exercise (NOT REST) e.g. swimming physiotherapy,
smoking cessation.
Medical:
NSAIDs for pain
**If severe: **
TNF-a inhibitors (e.g. Etanercerpt, Adalimumab) +/- surgery for deformities
- DMARDs only if peripheral joint involvement

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30
Q

M;S ratio for ank spond.
How does this vary when men are >30?

A

<30s: Men, 16:1
>30s, Men, 2:1

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31
Q

List 5 differentials for acute red and swollen joint (e.g. knee)

A

Septic arthritis
Reactive arthritis (e.g. SARA)
Gout
Pseudo-gout
Haemarthrosis

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32
Q

Inv & Management for suspected septic arthritis (presents with acutely hot swollen knee and reduced movement, raised CRP, WCC)
+ name of guideline to follow
+ typical causative organism (young adults sexually acrtive or otherwise)

A

Hot joint policy
Urgent ortho review
Inv
* joint aspiration for MC&S, gram-staining and crystal assessment.
* Bloods- FBC (inf), U&E, LFT, bone profile.
* Blood cultures - most commonly caused by haematagenous spread
Mng
* start empirical IV abx then switch once sensitivities known
* if severe pt may require debridement surgery

typical causative organism is staph aureus
but in young sexually active adult could be gonoccus

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33
Q

Function of Koch’s criteria

A

To distinguish between septic arthritis and transient synovitis in paeds

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34
Q

Septic arthritis 1st line management

A

Flucloxacillin + Rifampicin
(or Vancomycin if penicillin allergic)
aka empirical abx until sensitivites known

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35
Q

Risk factors for gout (6) - causing increased production or reduced clearance of urate

A

Alcoholism
High purine diet - meat
CVD, CKD
Obesity
Diuretics - lost fluid –> dehydration –> higher conc. of urate crystals
FHx

36
Q

Define gout
Whis joints does it affect most commonly?
Defined by UA levels greater than what?

A

Crystal monoarthropathy associated with high blood levels of uric acid. Results in deposition of urate crystals in joints and tissues. Disorder of purine metabolism.
Joints affected - base of big toe, wrist, thumb, knee, ankle.
Raised uric acid greater than 450mmol/l

37
Q

Tophi = firm white nodules under translucent skin
What are the steps leading to tophaceous gout?

A

Long period asymptomatic hyperuricaemia –> once urate levels are persistently above 380 —> acute episodes of pain following by sx-free intervals –> chronic tophaceous gout. Tophi develop normally 10 yrs after an attack.
tophi is subcutaenous uric acid deposition

38
Q

X-ray findings for gout

A
  • Joint effusion
  • Erosions - punched out, “rat-bite” with overhanging edges
  • +/- tophi
  • soft tissue swelling

note maintained joint space

39
Q

Inv for gout - firstly exclude septic arthritis.
Bloods (FBC, U&E, serum urate levels) Imaging - plain XR
Special tests - What is the gold standard test and what is the typical finding?

A

Joint aspiration:
Negatively birefringed
Needle shaped
Monosodium urate crystals

40
Q

What are the typical joint aspiration findings for pseudogout?

A

Rhomboid crystals
Positively befringed
Calcium pyrophosphate

41
Q

Gout: management
- Acute

Gout: prophylaxis of attacks
- Conservative
- Medical:
- Agent of choice (1st, 2nd, 3rd line)
- Important points
- Aim for uric acid level of what?

A

Acute:
* rest, cool environment, limb elevation.
* Colchicine or NSAID+PPI

Prophylactic
Conservative: weight loss, low purine diet, increase vitamin C, reduce alcohol, ?stop offending meds e.g. thiazides
Medical: urate lowering therapy - 1st to 3rd line
1. *Allopurinol *(xanthine oxidase inhibitor; start low and titrate upwards until urate <300) with Colchicine/NSAID (adjunct).
2. Febuxostat if renal impairment prevents dose increase increase for Allopurinol.
3. Uricase

A delay in ULTis advised at least until not in pain
Need colcicine coprescribed at same time during start of ULT
Caution in renal impairment
Aim for uric acid level less than 360 or less than 300 if severe/tophaceous gout

42
Q

Gout is caused by monosodium urate crystal build up. What is different about pseudogout?
- build up of?
- severity compaired to gout/SA?
- management

A

Caused by calcium pyrophosphate buildup.
Milder presentation.
MAnaged similarly with NSAIDs/Colchicine & conservative measures but NOT with Allopurinol.

43
Q

Xray findings for gout vs psuedogout

A

Gout - punched out erosions, maintained joint space, lytic lesions.
Psuedogout - chondrocalcinosis.

44
Q

Pseudogout is associated with older age and underlying risk factor - such as electrolyte imbalance (low Mg, low PO4) but what other conditions?(4) WAHH (wailing in pain)

A
  1. Haemochromatosis (loss of libido, fatigue, bronze skin etc)
  2. Wilson’s (copper deposition - neuropsychiatric and liver sx)
  3. Acromegaly
  4. Hyperparathyroidism
45
Q

Describe a typical patient with PMR - including systemic/extra-articular symptoms.

A

A 50 yr old white lady with less than 1 month onset of pain/stiffness in proximal limb muscles - shoulders, neck and pelvic girdle, that worsens with movement. Associated with lethargy, fever and nightsweats. May have depression.
Associated with GCA.
Note prolonged morning stiffness - >45 mins
NOTE - MUSCLE WEAKNESS (EG REDUCED MRC GRADING) is not a typical feature of PMR

46
Q

What bloods are typically raised in PMR?

A

CRP, ESR & plasma viscosity.

47
Q

Define SLE. What are the main 4 presenting symptoms?

A

An auto-immune inflammatory connective tissue disease, cuasing chronic inflammation and multi-system tissue damage.
Non specific sx - joint/muscle pain, fever, fatigue, weight changes.

caused by antibodies targeted against cell nucleus proteins
has multisystemic effects - cardioresp, skin, neuropsychiatric, renal, vascular…

48
Q

Investigation results for SLE - what would you expect?
* FBC
* Inflammatory markers
* Complement (C3 AND C4)
* ANA and anti-ds DNA
* Biospy - renal
* Urinalysis/urine PCR

Which antibody is most specific to SLE?
Name for test to look for antibodies to distinguish between types of CTDs?

A
  • Normocytic anaemia (of chronic disease)
  • ESR and CRP raised
  • C3 and C4 low in active disease (sign of complement activation)
  • Raised (ANA in 80%, anti-ds DNA in 70% - antidsDNA most specific whereas ANA can be found in other conditions like AIH)
  • Lupus nephritis
  • Proteinuria (raised PCR)

Test - extractable nuclear antigen - antibodies like Anti-SM (also SLE) and others for other conditions

49
Q

Explain the sensitivity and specificity of the following tests for SLE (ANA, anti-dsDNA)

A
  1. ANA - high sensitivity, low specificity. Present in 80% of cases.
  2. Anti-ds DNA - low sensitivity, high specificity. Present in 70%.

E.g. ANA also present in hepatitis.

50
Q

Name 2-3 subtypes of anti-nuclear antibodies - which is most specific to SLE?

A

Anti:
* Smith
* Ro/La
* Scl-70
* Jo-1
* centromere

51
Q

Management for SLE (1st, 2nd, 3rd line)

A
  1. NSAIDs/Pred/Hydroxychloroquine
  2. Immunosuppression - DMARD e.g. Methotrexate
  3. Biologic agent - e.g. Rituximab (CD20 inhibitor) or Belimumab (B-cell activating factor)
52
Q

Complications of SLE
due to long term inflammation of multiple organs, and confounded by immunsuppression

A
  • CVD - inflammation of arteries
  • Lupus nephritis and CKD
  • Pneumonitis and pulmonary fibrosis
  • Anaemia, increased infection risk
  • Recurrent miscarriage
  • Secondary APLS
  • Neuropsychiatric lupus - optic neuritis, transverse myelitis and psychosis
53
Q

Drug induced SLE
- Px
- Causative drugs (2 most common)
- Antibodies

A
  • Fatigue, dry cough, pleuritic chest pain & facial
  • Procainamaide (antidysrythmic), hydralazine (vasodilator/HF)
  • rash - malar rash
  • ANA positive (100%), dsDNA negative, anti-histone antibodies (80%)
54
Q

Define systemic sclerosis and the two main types?

A

An autoimmune inflammatory and fibrotic connective tissue disease.
- Limited cutaneous (CREST) - mainly skin changes
- Diffuse cutaneous- multi-organ involvement (lungs, heart, kidneys) - e.g. PF, HTN/CAD, glomerulonephritis

55
Q

Define CREST

A
  1. Calcinosis
  2. Raynaud’s phenomenon
  3. Eosophageal motility
  4. Sclerodactyly - stiffening of fingers in skin, causing reduced ROM and blistering
  5. Telangectasia
56
Q

ANA is a non-specific antibody assoicated with conditions such as SLE, autoimmune hepatitis and systemic sclerosis. Which antibodies are most associated with
1. - limited cutaneous systemic sclerosis (CREST)
2. - diffuse cutaneous systemic sclerosis

A
  1. Anti-Centromere (Crestromere)
  2. Anti-Scl-70
57
Q

general management systemic sclerosis

A

Conservative:
- manage symptoms
- smoking cessation
- skin stretching, emollients, physiotherapy, occupational therapy
Medical:
- DMARDs/Steroids/Biologics
- Symptom relief

58
Q

What is Sjorgren’s syndrome?
What is it often secondary to?
What are sicca symptoms?
How does this compare to sarcoidosis?

A

An autoimmune condition affecting exocrine glands, causing dry mucous membranes (eyes, mouth, vagina); parotid gland enlargement. Typically affects salivary and tear glands.
Associated with other autoimmune conditions such as vitiligo/DM/RA
Sicca symptoms - dry eyes and mouth.
General signs - arthralgia and dry skin
Rarely can affect other organs - pneumonia, non-HL lymphoma, peripheral neuropathy.
Secondary to RA or SLE.
Sarcoidosis - granulomatous formation in lymph nodes throughout body (rather than localised in face/neck); no sicca symptoms

59
Q

Antibodies specific for Sjorgen’s

A

Anti-Ro
Anti-La
Also RF and ANA if RA/SLE associated.

60
Q

What is Schrimer’s test used for?

A

Diagnosing Sjorgren’s. Measures tear production onto blotting paper (test of <10mm in 5 mins is positive).

61
Q

Management for dry mucous membranes in Sjorgens (3)

A
  1. Artificial tears; Pilocarpine
  2. Artificial saliva
  3. Vaginal lubrication
62
Q

What rare rheumatological condition could be a presentation of an underlying malignancy?

A

Dermatomyositis / polymyositis
A pareneoplastic syndrome
Could be underlying breast/ovarian/lung/gastric cancer

63
Q

What is the typical blood test (and result) for polymyositis/dermatomyositis

A

CK
>1000

64
Q

How does polymyositis present?
What does dermatomyosits have additionally?

A

Progressive proximal muscle weakness (e.g. shoulder, pelvic girdle), myalgia and arthralgia.
Skin changes - rashes (Gottron lesions, purple facial rash, photosensitive neck rash, calcinosis deposits)

65
Q

List 3 investigations (2x blood tests, 1 other) for myositis/dermato”

A
  1. CK
  2. Auto-antibodies (Jo-1, Mi-2, ANA)
  3. Electromyography

Anti Jo-1 = both
Anti-Mi-1=dermatomyositis
ANA = dermatomyositis

66
Q

1st line treatment for polymyositis or dermatomyositis

A

corticosteroids

also may require physio and occupational therapy for strength and function

67
Q

Still’s disease (adult onset juvenile idiopathic arthritis) is an inflammatory conditioning presenting with….(3)

A
  1. Fever
  2. Polyarthritis
  3. Rash - maculopapular, salmon-pink

Others - leucocytosis, raised ferritin, negative ANA/RF

68
Q

Three screening questions for musculoskeletal disease

A
  1. Pain/stiffness in joints, muscles, or back
  2. Ability to dress without difficulty
  3. Ability to walk up and down stairs?
69
Q

What is the Beighton score?

A

Assessment of hypermobility, max 9 points

Palms flat on floor with legs straight
Thumb to forearm
little finger hyperextends to 90 degrees
knee hyperextension
elbow hyperextention

70
Q

4 subtypes of Ehlos-Danlos - which is most common & also least severe?

A
  1. Classical (autosomal dominant)
    2.Hypermobile - most common and least severe
  2. Kyphoscolotic
  3. Vascular
71
Q

What syndrome can occur with hypermobile Ehlos-Danlos, as a result of autonomic dysfunction?

A

**POTS : postural orthostatic tachycardia syndrome **
- inappropriate tachycardia when sitting/standing –> headache, nausea, syncope etec

72
Q

Marfan’s is an autosomal dominant condition resulting in fibrillin dysfunction - list 5 physical features this can present with:

A
  1. Tall stature, long neck, long limbs
  2. High arch palate
  3. Upwards lens dislocation, myopia
  4. Arachnodactyly
  5. Hypermobility
  6. Pectus carinatum/excavatum
  7. Scoliosis
73
Q

Examination for Marfan’s - what 3 tests are particuarly important?

A
  1. Hypermobility - Beighton Score
  2. Arachnodactyly (thumb tip past edge of hand, overlapping thumb and fingers on other hand)
  3. Aortic/mitral regurg - auscultate heart
74
Q

CVS effects of Marfan’s

A

Aortic aneurysm/dissection and valve prolapse (mitral)

75
Q

Classification of small vessel vasculitis

A
  1. ANCA associated: *granulomatosis with polyangitis (Wegner’s), microscopic polyangitis, eosinophilic polyangitis
    2.     Immune complex associated:** HSP, Goodpasture’s
76
Q

Polyarteritis nodasa is associated with which infection?

A

Hep B
note flu like sx, N+V, and pruritus

77
Q

Types of medium and large vessel vasculitis

A

Medium - polyartertitis nodusa, Kawasaki
Large - GCA, Takayasu

78
Q

Small vessel vasculitis - ANCA associated
Eosinophilic granulomatosis with polyangitis & microscopic polyangitis are associated with which antibody?

A

p-ANCA
* both make you pant
* both are small vessel vasculitides
* Eosnophilic - affects lungs mainly - severe late onset sthma, sinusitis, rhinitis
* Microscopic - affects lungs and kidneys: alveolar haemorrhage (haemopytsis)

79
Q

Small vessel vasculitis- ANCA associated
what antibody is wegner’s (granulomatous with polyangitis) associated with?

A

c-ANCA
* small vessel vasculitis
* affects URT, LRT & kidneys

80
Q

Takayasu’s arteritis
- phases
- symptoms
- vessels show changes of

A
  • Large vessel vasculitis
  • Acute phase + chronic pulseless
  • upper limb claudication type pain
  • proflieration, fibrosis of intima and media
    increasing pain in forearms whilst working, with reduced upper limb pulses and raised ESR
81
Q

Polyarteritis nodosa
- symptoms associated with hep b

A
  • medium vessel disease
  • flu-type symptoms - fevers, myalgia
  • systemic signs- anorexia and weight loss
82
Q

Osteoporosis - DEXA score cut off and first line treatment?
The T score is based against what?
What does the Z score account for?

A

<-2.5
Bisphosphonates (alnendronic acid) but correct hypocalcaemia first
T score - no. of SDs your score is above or below the average bone mass of a young healthy adult
z score - adjusted for age, sex and ethnicity

83
Q

Presentation of methotrexate-induced pneumonitis?

A

SoB
Cough
Fever

84
Q

Anti-phospholipid syndrome

A

Recurrent miscarriage
Arterial and veinous thrombosis
Raised APPT
Autoantibodies: anti-cardiolipin and anit-B2 glycoprotein and lupus anticoagulant
Can be secondary to SLE

85
Q

Define “marble bone disease”

A
  • Dense joints prone to fracture
  • Osteopetrosis -
  • bones more susceptbile to osteomyleitis
86
Q

Methotrexate
adverse effects (5)

A
  1. Pneumonitis (non-productive cough, fever, SOB, crackles)
  2. Pulmonary fibrosis (fine end inspiratory crackles)
  3. Liver fibrosis
  4. Mucositis
  5. Myelosuppression (note other antifolates e.g. trimethoprim shouldn not be co-prescribed)

Year 4/5 Revision (21 decks)

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