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Phase 2a > MSK and rheumatology + second half of liver > Flashcards

MSK and rheumatology + second half of liver Flashcards

1
Q

What is the function of articular cartilage?

A
  • reduce friction
    -shock absorption
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2
Q

What is the function of synovial membrane?

A
  • highly vascularised
    -secretes and absorbs synovial fluid
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3
Q

What is the function of synovial fluid?

A
  • lubrication
    -shock absorption
  • nutrient distribution ; hyaline cartilage is avascular and relies on diffusion from SF
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4
Q

What are the inflammatory markers?

A
  • ESR
    -CRP
    -Auto-antibodies
    -RF
    -ANA
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5
Q

What is ESR?

A

Erythrocyte sedimentation rate
-rises with inflammation/infection
-rises and falls slowly

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6
Q

What is CRP?

A

C-reactive protein
-acute phase protein
-released in inflammation/ infection
-produced by liver in response to IL-6 (pro- inflammatory cytokine)
-rises and falls rapidly

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7
Q

What are auto-antibodies?

A

Immunoglobulins that bind to self antigens

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8
Q

What is rheumatoid factor?

A

An auto-antibody found in people with rheumatoid arthritis

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9
Q

What is anti - ccp?

A

Anti-citrullinated protein antibodies are autoantibodies that are directed against peptides and proteins that are citrullinated. They are present in the majority of patients with rheumatoid arthritis.

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10
Q

What is ANA?

A

Anti-nuclear antibody - binds to antigens within cell nuclear

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11
Q

What is osteoarthritis?

A

-most common type of arthritis
-Non inflammatory degenerative joint disease
where the cartilage within a joint begins to break down and the underlying bone begins to change.

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12
Q

What are the risk factors of osteoarthritis?

A
  • 50+
  • affects women 50+ more
    -obesity
    -occupation/sports
    -genetic (COL2A1 - genetic predisposition)
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13
Q

What is the pathology of osteoarthritis?

A

-Imbalance between cartilage breakdown and repair
-Increase in chondrocytes metalloproteinase secretion
-Degrades T2 collagen and causes cysts
-Bone attempts to overcome this with type 1 collagen -abnormal bony growth (osteophytes) +remodelling

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14
Q

What is the presentation of osteoarthritis?

A

-Transient (little <30min) morning pain –> worse as day goes on
-Bouchard + Hebderen nodes on fingers
-assymetrical, hard non inflamed joint
-typically most stressed joints in body - hip/knee/base of toe/thumb
-no extra articular Sx

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15
Q

Where are the hebderen nodes?

A

distal interphalangeal joint

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16
Q

Where are the Bouchard nodes?

A

Proximal interphalangeal joint

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17
Q

What is the diagnosis for osteoarthritis?

A

XR - LOSS
-loss of joint space
-osteophytes
-subchondral sclerosis
-sunchondral cysts
- normal bloods

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18
Q

What is the treatment of osteoarthritis?

A
  • lifestyle change - weight bearing , physio
    -NSAID pain relief
    -Last resort -consider surgery (arthroplasty - for knee+hip replacement)
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19
Q

What is rheumatoid arthritis ?

A

Autoimmune inflammatory polyarthritis
- symmetrical

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20
Q

What are the risk factors of rheumatoid arthritis?

A
  • women 30-50
    (3x more likely than M premenopausally )
  • smoking
    -HLADR4/HLADRB1 - genetic link
  • after menopause M=F
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21
Q

What is the pathology of RA?

A
  • arginine -> citrulline mutation in T2 collagen; anti-ccp formation
    -IFN-a cause further pro inflammatory recruitment to synovial
  • synovial lining expands and tumour like mass (pannus) grows past joint margins
    -pannus destroys subchondral bone + articular cartilage
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22
Q

What is the presentation of RA?

A
  • often worse in the morning >30min, eases as day goes on
    -Hand; swan neck, z thumb, ulnar finger deviation
    -bakers cyst - popliteal synovial sac bulge
  • symmetrical hot inflamed joints
    -mc in wrist/hand and feet
    -extra articular - lungs (PE), heart (increased IHD), eyes(dry eyes), spinal cord compression, CKD, rheumatoid skin nodules
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23
Q

What is the diagnosis of RA?

A

Bloods = Increased ECR +CRP
normocytic normochromic anaemia - mc from chronic disease, also can cause - microcytic (NSAID use->PUD->FE def anaemia) and macrocytic from methotrexate use -inhibits folate
Serology = positive anti-ccp, positive RF
XR-LESS
-loss of joint space
-erosions
-soft tissue swelling
-soft bones

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24
Q

What is the treatment for rheumatoid arthritis?

A

DMARD- Methotrexate - GS treatment
NSAID - analgesia
-Intra articular steroid injection if very painful
-Biologics (good but expensive)
1st line- TNF -d-inhibitor - infliximab
2nd line- B cell inhibitor- rituximab

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25
Q

What is a DMARD?

A

Disease modifying anti rheumatic drugs

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26
Q

When is methotrexate contraindicated ?

A
  • Pregnant as folate inhibitor therefore DNA synthesis affected
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27
Q

What are crystalline arthropathies?

A

a group of joint disorders caused by deposits of crystals in joints and the soft tissues around them.

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28
Q

What are the two main types of crystals that account for the majority of crystal induced arthritis?

A
  • sodium urate crystals
    -calcium pyrophosphate crystals
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29
Q

What are sodium urate crystals?

A
  • needle shaped (long and thin) crate crystals
    -negatively birefringent under polarised light
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30
Q

What are calcium pyrophosphate crystals?

A
  • small rhomboid brick shaped pyrophosphate crystals
    -positively birefringent under polarised light
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31
Q

What is Gout?

A

Inflammatory arthritis associated with high levels of uric acid and intra -articular monosodium rate crystals deposited in joints

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32
Q

What is the epidemiology of gout?

A
  • middle aged overweight men
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33
Q

What are the risk factors of gout?

A
  • purine rich foods (meat, seafood, beer)
    -CKD + diuretics
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34
Q

What is the pathology of gout?

A

purines break down into uric acid by xanthate oxidase - uric acid either excreted by kidneys or –> monosodium urate by binding with sodium ions
- increase in uric acid/CKD = impaired excretion therefore increase in monosodium rate

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35
Q

What is the presentation of gout?

A

Monoarticular; usually big toe (metatarsophalangeal joint) - sudden onset, severe swollen red toe, can’t put weight on it

DDX= septic arthritis

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36
Q

\What is the diagnosis of gout?

A

Joint aspirate + polarised light microscopy; negatively birefringent needle shaped crystals -GS

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37
Q

What is the treatment of Gout?

A

Diet = low purines and high dairy
NSAIDs, then consider colchicine, then steroid injection - acute gout
Prevention = allopurinol (xanthine oxidase inhibitor to decrease uric acid production)

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38
Q

What is pseudo gout?

A

Calcium pyrophosphate crystals deposit along joint capsule

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39
Q

What is the epidemiology of pseudo gout?

A

elderly females / 70+

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40
Q

What are the risk factors for pseudo gout?

A

diabetes, metabolic disease , osteoarthritis

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41
Q

What is the presentation of pseudo gout?

A

often poly-articular with knee commonly involved - swollen hot red joint

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42
Q

What is the diagnosis of pseudo gout?

A

joint aspiration and polarised light microscopy –> positively birefringent, rhomboid shaped crystals

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43
Q

What is the treatment for pseudo gout?

A

only acute management:
-NSAIDs then colchicine, then steroid injection
- no prevention drug

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44
Q

What is osteoporosis?

A

A systemic skeletal disease characterised by low bone density by 2.5+ standard deviations below young adult mean volume (T<2.5)

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45
Q

What is the epidemiology of osteoporosis?

A

50+ postmenopausal caucasian women

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46
Q

What are the risk factors of osteoporosis ?

A

SHATTERED
S-teroids
h-yperthyroid/ parathyroid
a-lcohol+ smoking
t-hin
t-estosterone low
e-arly menopause - low oestrogen
r-enal/liver failure
e-rosive+ inflammatory disease
d-MT1 or malabsorption

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47
Q

What is the presentation of osteoporosis?

A

only fractures -
-proximal femur
-colle’s -fractured wrist
-compression vertebral crush

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48
Q

What is the diagnosis of osteoporosis?

A

DEXA scan - GS
- dual energy XR absorptiometry
- yields T-score - compares patient BMD to reference
-FRAX score - fracture risk assessment tool - assess fracture risk in osteoporotic patients

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49
Q

What is T score?

A

Young adult bone density :
0<T<1 = normal , within 1SD
1<T<2.5 = Low BMD; osteopenia
T<2.5 =BMD 2.5+ SDs below normal young adult - osteoporotic

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50
Q

What is osteopenia?

A
  • precursor to osteoporosis
  • defined as bone density 1-2.5 standard deviations below normal young adult mean value
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51
Q

What is the treatment for osteoporosis?

A

1- Bisphosphonates (alendronate inhibit RANK-L signal therefore osteoclastic inhibitors)
2- mAB Denosumab (inhibits RANKL)
HRT - oestrogen /testosterone
Oestrogen receptor modulated - raloxifene
Recombinant PTH

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52
Q

What is systemic lupus erythematous?

A

Hypersensitivity T3 reaction (Antigen-antibody complex deposition)
-Autoimmune systemic inflammation

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53
Q

What is the epidemiology of SLE?

A
  • females
    -african carribean
    -20-40
    -premenopause
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54
Q

What are the risk factors for SLE?

A
  • female - 12x more than men
    -HLAB8/DR2/DR3
    -Drugs -isoniazid
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55
Q

What is the pathology of SLE?

A

impaired apoptotic debris presented to TH2–> B cell activation –> antigen-antibody complexes

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56
Q

What is the presentation of SLE?

A
  • butterfly rash+photosensitivity
    -glomerulonephritis(nephritic syndrome)
    –seizures
    -mouth ulcers
    -joint pain
    -raynaud’s
    -serositis
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57
Q

What is the diagnosis of SLE?

A

Bloods - anaemia, high ESR + normal CRP
Urine dipstick - hameaturia + proteinuria
Serology : ANA Ab’s - 99% cases
Anti ds DNA Ab’s - used to monitor progression
-Low c3 + c4

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58
Q

What is the treatment for SLE?

A

Lifestyle (low sunlight, stop triggering drugs)
-corticosteroids
-hydroxychloroquine
-NSAIDs

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59
Q

What is antiphospholipid syndrome?

A

Associated with antiphospholipid antibodies where blood becomes prone to clotting. Can be primary, idiopathic or secondary to other disease, like SLE.
Characterised by thrombosis, recurrent miscarriages and apl Ab’s

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60
Q

Who does Antiphospholipid syndrome effect more?

A

females

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61
Q

What is the presentation of antiphospholipid syndrome?

A

CLOTS:
Coagulopathy
lived reticular - purple discolouration of skin
obstetric issues - miscarriage
thrombocytopenia

-high risk of stroke, MI, DVT

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62
Q

What is the diagnosis of aPL syndrome?

A
  • lupus anticoagulant
    -anticardiolipin antibodies
    -anti B2 glycoprotein-1 antibodies
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63
Q

What is the treatment of aPL syndrome?

A

1st line - warfarin long term if have had a thrombosis
- if pregnant give aspirin +heparin
prophylaxis = not had thrombosis = aspirin

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64
Q

What is sjorgen syndrome?

A

Autoimmune destruction of exocrine glands, especially the lacrimal and salivary glands

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65
Q

What is the epidemiology of sjorgen’s?

A

-females 40-50
-FHx
-HLAB8/DR3
-can be primary or secondary to other autoimmune diseases - SLE

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66
Q

What is the presentation of sjorgen’s?

A

Dry eyes
-Xerstomia - mouth/ vaginal dryness

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67
Q

What is the diagnosis of sjorgen’s?

A

serology = Anti-Ro / Anti LA Ab’s - ANA often positive
Schirmer test- induce tears + place filter paper under eyes. Tears travel <10mm (should be 20mm+)

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68
Q

What is the treatment of sjorgen’s?

A

Artificial tears, saliva + lubricant for sexual activity
- sometimes hydroxychloroquine given

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69
Q

What is a complication of sjorgen’s?

A

increase risk of lymphomas

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70
Q

What is scleroderma?

A

is a group of rare autoimmune diseases that involve the hardening and tightening of the skin. It may also cause problems in the blood vessels, internal organs and digestive tract.

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71
Q

What are the subtypes of scleroderma?

A

Limited - crest
Diffuse

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72
Q

What is limited scleroderma?

A

most common type of scleroderma, limited cutaneous scleroderma

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73
Q

What is diffuse scleroderma?

A

subtype of scleroderma where excess collagen production causes skin thickening over large areas of the body.
-can be significant associated organ damage

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74
Q

What is the presentation of CREST?

A

C- calcinosis (Ca deposits in SC tissue) -> renal failure
R- raynaud’s - digit ischemia due to sudden vasospasm in response to cold
E- oesophageal dysfunction/strictures -> GI Sx
S-sclerodactyly - thickening and tightening of skin on fingers/ toes - > movement restriction
T- telangiectasia (spider veins) –> risk of pulmonary hypertension

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75
Q

What is the diagnosis of crest scleroderma?

A

Anti centromere antibodies
ANA often positive

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76
Q

What is the treatment of scleroderma?

A

No cure
Treat Sx

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77
Q

What is polymyositis/dermatomyositis?

A

Inflammation + necrosis of skeletal muscle

  • when skin is involved = dermatomyositis
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78
Q

What is the epidemiology of polymyositis?

A
  • female
    -HLAB8/DR£ genetic link
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79
Q

What is the presentation of polymyositis?

A
  • symmetrical wasting of muscles of shoulders and pelvic girdle
  • hard to stand from sitting, to squat, to put hands on top of head
    -Dermatomyositis - skin change (gottron’s papules -scales on knuckles, heliotrope - purple eyelid)
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80
Q

What is the diagnosis of polymyositis?

A

muscle fibre biopsy necrosis - diagnostic
Lactate dehydrogenase +creatinine Kinase raised
Anti Jo1 +
Anti Mi2 Ab’s - but only in dermatomyositis

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81
Q

What is the treatment for polymyositis?

A

Bed rest
Prednisolone

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82
Q

What is fibromyalgia?

A

Chronic widespread pain (ask) for 3+ months with all other. causes ruled out

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83
Q

What is the epidemiology/RF of fibromyalgia?

A

females
depression
stress
poor
60+

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84
Q

What is the presentation of fibromyalgia?

A

stressed depressed female, 60+, fatigue, sleep disturbance, morning stiffness, pain

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85
Q

What pain pathway is affected in fibromyalgia?

A

non nociceptive pathway is affected - neuropathic pain + CNS processing of pain

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86
Q

What is the diagnosis of fibromyalgia?

A
  • NO serological markers (ANA,aPL, anti-ccp/RF)
    -NO high ESR/CRP
    -PAIN in 11/18 palpation sites therefore clinical diagnosis
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87
Q

What is the treatment of fibromyalgia?

A

-educate patient + physiotherapy
-antidepressants for severe neuropathies - amitriptyline + CBT

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88
Q

What is Ddx of fibromyalgia?

A

polymyalgia rheumatica

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89
Q

What is Polymyalgia rheumatica (PMR)?

A

Large cell vasculitis presenting as chronic pain syndromes (affects muscles and joints)
- females , always 50+
-association with GCA

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90
Q

What is the diagnosis for PMR?

A

-High ESR + CRP -diagnostic
-temporal artery biopsy may show GCA, and may have anaemia of chronic disease

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91
Q

What is the treatment of PMR?

A

oral prednisolone

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92
Q

What is vasculitis?

A

Inflammatory disorder of the blood vessel walls, which can affect any organ by causing destruction or stenosis of a vessel

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93
Q

What are the types of vasculitis?

A

Large, medium and small vessel

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94
Q

What is the general treatment for vasculitis?

A

Corticosteroids- when given long term consider GI and bone protection -PPI, bisphosphonates

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95
Q

What are the types of large vessel vasculitis?

A

-GCA
-Takayatsu

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96
Q

What is takayatsu?

A

Asian/ Japanese women mainly affects aortic arch
-otherwise same as GCA

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97
Q

What is GCA?

A

Giant cell arteritis - inflammatory granulomatous arteries of large cerebral arteries, and affects the aorta and its main branches

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98
Q

What is the presentation of GCA?

A

-50+
-caucasian female
-unilateral temple headache, jaw claudication, +/- vision loss
-Temporal scalp tenderness

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99
Q

What is the pathology of GCA?

A

Affects branches of external carotid - scalp tenderness = temporal branch
Vison =opthalmic branch
Jaw= facial branch

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100
Q

What is the diagnosis of GCA?

A

-High ESR +/- CRP -1st line
-Temporal artery biopsy diagnostic = granulomatous inflammation of media + intima - Kathy skip lesions therefore take big chunk

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101
Q

What is the treatment of GCA?

A

Corticosteroids - prednisolone

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102
Q

What is the complication with GCA?

A

sudden painless vision loss in one eye
- temporary = amaurosis fugax
-may be permanent if not dealt with
TREAT- High dose IV methylprednisolone

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103
Q

What are the types of medium vessel vasculitis?

A

-Polyarteritis nodosa
-Buerger’s disease
-Kawaski disease

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104
Q

What is polyarteritis nodosa?

A

Necrotosing vasculitis that causes aneurysms + thrombosis in medium sized vessels, leading to infarction in affected organs.
-males, associated with Hep B

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105
Q

What is the presentation of polyarteritis nodosa?

A

Severe systemic Sx:
-mononeuritis multiplex (ischemia of vasa nervorum)
-GI bleeds (mesenteric artery)
-CKD/AKI (renal arter)
-skin sc nodules + haemorrhage
-abdo pain+ anorexia
-hypertension

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106
Q

What is the diagnosis of polyarteritis nodosa?

A

CT angiogram - micro aneurysms - ‘Beads on a string”
Biopsy (Kidney) - necrotising vasculitis due to htn

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107
Q

What is the treatment of polyarteritis nodosa?

A

Corticosteroids
Control HTN - ACE-i
Hep B treatment after corticosteroids -antiviral agent +plasma exchange

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108
Q

What is Buerger’s disease?

A

-Male smokers 20-40
-peripheral skin necrosis
-Thromboangiitis obliterans (Buerger disease) is caused by small and medium blood vessels that become inflamed and swollen

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109
Q

What is Kawasaki disease?

A

-Children
-causes coronary artery aneurysms

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110
Q

What are the types of small vessel vasculitis?

A
  • Eosinphillic granulomatosis with polyangitis (churg strauss disease)
    -Granulomatosis with polyangitis (Wegener’s disease)
    -Henloch schonlein purpura
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111
Q

What is Eosinphillic granulomatosis with polyangitis (EGPA)?

A
  • small and medium vasculitis
    -associated with lung and skin problems
    -severe asthma
    -pANCA positive
    -Corticosteroids
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112
Q

What is pANCA?

A

perinuclear anti-neutrophil cytoplasmic antibodies

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113
Q

What is granulomatosis with polyangitis (GPA)?

A
  • small vessel vasculitis
    -affcets respiratory tract +Kidney
    -saddle shaped nose/epistaxis/cough
    -cause of glomerulonephritis
    -cANCA positive
    -corticosteroids
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114
Q

What is cANCA?

A

cytoplasmic anti–neutrophil cytoplasmic antibodies

115
Q

What is Henloch Schonlein Purpura?

A

-IgA vasculitis , IgA deposits in small blood vessels in GBM on kidney
-DDx for IgA nephropathy but HSP has purpuric rash on lower limbs + affects other organs - joints/abdo /renal
-rest+analgesia

116
Q

What are spondylarthropathies?

A

Assymetrical seronegative (RF negative) arthritis, associated with HLAB27

117
Q

What is HLAB27?

A

Human leukocyte antigens B27
Class 1 surface antigen, encoded by major histocompatibility complex

118
Q

What are the types of spondylarthropathies?

A

-ankylosing spondylitis
-psoriatic arthritis
-reactive arthritis
-IBD associated arthritis

119
Q

What are the general features of spondylarthropathies?

A

SPINEACHE
-sausage fingers (Dactylitis)
-psoriasis
-inflammatory back pain
-NSAIDs good response
-Enthesitis - inflamed heel tendon
-Arthritis
-chrons or collitis
-HLAB27
-Eyes-uveitis

120
Q

What is ankylosing spondylitis?

A

Abnormal stiffening of joints (sacroiliac + vertebral) due to new bony formation

121
Q

What is the epidemiology go ankylosing pondylitis?

A
  • more common in young males
    -HLAB27 positive
122
Q

What is the presentation of ankylosing spondylitis?

A

young male with progressively worsening back stiffness; worst in morning and at night, better with exercise
-anterior uveitis
-enthesitis
-dactylitis
- can be kyphosis - abnormal rounding of upper back
-Schober test - shows low lumbar flexion

123
Q

What is the pathology of ankylosing spondylitis?

A

syndesmophytes (vertical abnormal bony growths) replace spinal bone damage by inflammation+ make spine less mobile
- causes inflamed tendons eyes, fingers

124
Q

What is the diagnosis for ankylosing spondylitis?

A

XR =show bamboo spine + sacroilitis + squared vertebral bodies +syndesmophytes
MRI- can show sacroilitpis before XR therefore better screening tool
-ESR/CRP raised
HLAB27 positive

125
Q

What is sacroilitis?

A

an inflammation of the sacroiliac joint (SI), usually resulting in pain

126
Q

What are syndesmophytes?

A

bony outgrowths from the spinal ligaments as they attach to adjacent vertebral bodies

127
Q

What is the treatment for ankylosing spondylitis?

A

symptoms = exercise +NSAID
DMARD - TNF alpha blockers - influximab

128
Q

What is psoriatic arthritis?

A

Autoimmune arthritis characterised by red scaly patches - associated with psoriasis

129
Q

What is the epidemiology of psoriatic arthritis?

A

-10-40% with psoriasis develop within 10years

130
Q

What is the presentation of moderate psoriatic arthritis?

A

Inflamed DIPJ +
-nail dystrophy(onycholysis)
-Dactylitis
-Enthesitis
-psoriatic rash on skin - hidden sites (behind ears, scalp , under nails , penile

131
Q

What is the presentation of severe psoriatic arthritis?

A

Arthritis mutilans (5%0 = pencil in cup deformity- osteolysis of bone = progressive shortening ; fingers telescope in on themselves

132
Q

What is the treatment for psoriatic arthritis?

A

Symptoms - NSAIDs (steroid injection if severe)
DMARD- methotrexate if fails anti TNF- influximab
If fails - IL 12+23 inhibits -ustekinumab

133
Q

What is reactive arthritis?

A

Sterile inflammation of synovial membranes + tendons, reacting to distant infection(usually GI,STI)

134
Q

What is the aetiology of reactive arthritis?

A

Gastrointestinal= C.jejuni, salmonella, shigella

STI= C.trachomatis -mc
N.gonorrhoea

135
Q

What is the presentation of reactive arthritis?

A

Reiter’s triad:
- can’t see, pee, climb a tree
- uveitis, urethritis , arthritis, enthesitis
-keratoderma blenorrhagica

136
Q

What is the main Ddx to reactive arthritis?

A

septic arthritis - hot red swollen joints +Hx of infection

137
Q

What is the diagnosis for reactive arthritis?

A

Joint aspirate MC+S = shows no organism
Plane polarised light microscopy = negative for crystal arthropathy
-ESR/CRP raised, HLAB27 positive
-sexual health review +stool culture

138
Q

What is the treatment fo reactive arthritis?

A

Symptoms = NSAIDs + steroid injection
- mostly single attack - if happens 6+ months of recurrence it is chronic - methotrexate

139
Q

What is a type of infective arthritis?

A

septic arthritis

140
Q

What is septic arthritis?

A

Direct bacterial infection of joint (either direct access or haematogenous spread)

141
Q

What is a septic arthritis medical emergency?

A
  • acutely inflamed joint with fever, typically knee
  • extremely painful
  • can destroy knee <25hr
142
Q

What organisms cause infective arthritis ?

A

S.aureus-mc
H.influenza (children)
N.gonorrhoea
E.coli/pseudomonas (IVDU)

143
Q

What are the RF of septic arthritis ?

A
  • IVDU
    -Immunosupression
    -recent surgery
    -trauma
    -prosthetic joints
    -inflammatory joint disease
144
Q

What is the diagnosis of septic arthritis?

A

urgent joint aspirate with MC+s and polarised light microscopy
septic = ID causative organism
-Raised ESR/CRP, consider blood culture + sexual health review

145
Q

Want is the treatment for septic arthritis?

A

Joint aspirate (drainage) then empirical Abx
- if on methotrexate, ant-TNF stop these
-if on steroids - double prednisolone dose(increase stress response)
-NSAIDs for analgesia

146
Q

What Abx would be given for Gram negatives ; E.coli, P.aeruginosa ?

A

Flucoxacillin

147
Q

What Abx would you give S.aureus?

A

Vancomycin

148
Q

What Abx is used to treat N. gonorrhoea?

A

IM ceftriaxone + azithromycin

149
Q

What is osteomyelitis?

A

Acutely inflamed infected bone marrow, haematogenous or local spread

150
Q

What spread is most common in children for osteomyelitis?

A

haemogenous spread

151
Q

What spread is the most common in adults for osteomyelitis?

A

local

152
Q

What organisms cause osteomyelitis ?

A

S.aureus (90%)
Salmonella in sickle cell patients

153
Q

What are the RF of osteomyelitis?

A
  • IVDU
    -immunosuppression
    -PVD
    -DM
    -sickle cell anemia
    -inflam.arthrtiid
    -trauma
154
Q

What is the pathology of osteomyelitis?

A

Direct inoculation/ local spread/ haematogenous spread–> acute bone change to inflammation and bone oedema

Chronic bone change to Sequestra (necrotic bone embedded in pus)
Involucrum (thick sclerotic bone packed around sequestra to compensate for support)

155
Q

What is the presentation of osteomyelitis?

A

Acutely -dull bony pain +hot swollen/ worse with movement
Chronic - deep ulcers

156
Q

What is a Ddx of osteomyelitis?

A

Charcot joint

157
Q

What is Charcot joint?

A

Damage to sensory nerves due to diabetic neuropathy
- causes progressive degeneration of weight bearing joint + bony destruction.
-often affects foot, presents with diabetic feet

158
Q

What is the diagnosis of osteomyelitis?

A

BM biopsy + culture +blood+MC/s = ID causative agent
XR - osteopenia then MRI- bone marrow oedema
Raises ESR/CRP

159
Q

What is the treatment of osteomyelitis?

A

Immobilise + Abx
MRSA+S.aureus = vancomycin or teicoplannin
Fusidic acid = treats S.aureus
Flucoxacillin = Salmonella

160
Q

Why would you use Teicoplannin rather than Vancomycin to treat S.aureus?

A

longer lasting than vancomycin but more side effects - AF upset/ pruritus

161
Q

What would a positive BM biopsy of caseating granulomas suggest?

A

Tuberculosis osteomyelitis

162
Q

What are the primary bone tumours?

A
  • osteosarcoma
    -Ewing sarcoma
    -Fibrosarcoma
    -Chondrosarcoma
  • rarely seen, mostly in children
163
Q

What are the secondary causes of bone tumours?

A

Breast
Lung ——–Both osteolytic

Prostate
Thyroid
RCC ——-> all osteosclerotic

Myeloma- can cause bone pain- old crab

164
Q

What is osteosarcoma?

A

-Most common primary bone malignancy
-associated with Pagets
-Px 15-19
-Mets to lung
-XR - ‘sunburst’ appearing bone

165
Q

What is Ewing sarcoma?

A

-From mesenchymal steam cells
-15 years
-rare

166
Q

What is chondrosarcoma?

A

Cartilage cancer

167
Q

What are the general symptoms of bone tumours?

A

-Local (depend on tumour) - severe pain worst at night
-low range of motion of long bone, vertebrae
-Systemic = weight loss, fever, fatigue, malaise

168
Q

What is the diagnosis of bone tumours?

A

Skeletal isotope scan - shows change before XR
XR- osteolysis (osteosclerosis -> prostatic mets)
-High ALP,ESR/CRP
-hypercalcemia of malignancy

169
Q

What is the general treatment for bone tumours?

A

Chemo/ radiotherapy
Bisphosphonates

170
Q

What is osteomalacia?

A

Defective bone mineralisation
Before epiphyseal fusion = rickets
After- osteomalacia

171
Q

What is the pathology of osteomalacia ?

A

Due to VIT D deficiency therefore low calcium and phosphate (hydroxyapatite mineral of bone)

172
Q

What are the causes of osteomalacia?

A

-HyperPTH (increase Ca release from bone therefore less available for formation)
-Vit D deficiency - malabsorption / reduced intake/ poor sunlight
-CKD/Renal failure - low active vit D production
-Liver failure = low reaction in vit D pathway
-Anticonvulsant drugs - increase CYP450 metabolism of Vit D

173
Q

What is the Vitamin D pathway?

A

7-Dehdrocholesterol -> Cholecalciferol (inactive vit D) –> 25-hydroxyvitD –>!,25-DihydroxyvitD (activated D3) -bone, GIT,Renal DCT

174
Q

What is the presentation of osteomalacia?

A

osteomalacia- fractures, proximal weakness + difficulty weight bearing

175
Q

What is the presentation of rickets?

A

-skeletal deformities
-Knocked knees + bowed legs
-Wide epiphysis

176
Q

What is the diagnosis of osteomalacia?

A

BM biopsy = incomplete mineralisation (diagnostic)
- bloods =hypocalcemia, raised PTH, low serum calcium, low 25dihydroxyvitD
-XR = looser’s zones (defective mineralisation )

177
Q

What is the treatment for osteomalacia?

A

Vitamin D replacement (calcitriol)
-Increase dietary intake - D3 tablets ,eggs

178
Q

What is Paget’s disease?

A

Focal disorder of bone remodelling (areas of patchy bone due to improper osteoblast/ class function therefore areas of sclerosis + lysis

179
Q

What is the epidemiology of Paget disease?

A

Idiopathic
Females - 40+

180
Q

What is the presentation of Paget’s disease?

A

-Bone pain
-Bone change/ skull change
-Neurological Sx = Nerve compression of CN8 (Deafness)
-Hydrocephalus = Sylvian aqueduct blockage

181
Q

What is the diagnosis of Paget’s disease?

A

XR - osteoporosis circumscripta
-cotton wool skull - Skull change areas of lysis and sclerosis

Urinary hydroxyproline = protein constituent of bone collagen , good marker of disease progression
-high ALP

182
Q

What is the treatment for Paget’s disease?

A

Bisphosphonates
NSAIDs - for pain relief

183
Q

What are two connective tissue disorders?

A

-MARFAN’s
-Ehlers Danlos

184
Q

What is Marfan’s disease?

A

Autosomal dominnat FBN1 mutation
Low connective tissue tensile strength due to FBN1 mutation which is involved in making fibrillin

185
Q

What is fibrillin?

A

An important component of connective tissue

186
Q

What is the presentation of marfan’s syndrome?

A

Marfan’s body habitus - tall and thin, long fingers , pectus excavatum/carinatum,Arachnodactyly

187
Q

What are the aortic complications of Marfan’s?

A
  • aortic regurgitation murmur
    -AA,Aortic dissection
188
Q

What is the diagnosis of Marfan’s?

A

Clinical presentation
FBN-1 mutation

189
Q

What is Ehlers Danlos?

A

Autosomal dominant mutation affecting collagen proteins
13 subtypes

190
Q

What is the presentation of Ehlers Danlos?

A

Joint hyper mobility + CV complications - mitral regurgitation and AAA,AD

191
Q

What is the diagnosis of Ehlers Danlos?

A

Clinical presentation
Collagen mutation

192
Q

What are complications of connective tissue disorders?

A

Weak valves and weak vessels
- need to monitor regurgitation murmurs
-AA ruptures/ Aortic dissection

193
Q

What is mechanical backpain?

A

Common patient complaint in community
- Common, often self limiting
-may be normal especially people 20-55, trauma/ work related
-signs for serous pathology= elderly, neuropathic pain

194
Q

What is lumbar spondylosis?

A

Degenration of IV disc, loses its compliance + thins over time
- older patients
-initially aSx, progressively worsens
-L4/5 or L5/S1- mc
-XR if serious pathology affected
-Analgesia +physiotherpay

195
Q

What is the mechanism of methotrexate?

A

It is a DMARD = they completely inhibit dihydrofolate reductase therefore inhibits folate synthesis

196
Q

What are the side effects/ risk of methotrexate?

A

At risk of folate deficiency so they need to the 5mg once weekly folate supplements but not on the same day as methotrexate taken

197
Q

What is monitored when a patient is on methotrexate?

A

FBC,LFT,U+E
- before treatment
every 1-2 weeks until therapy stabilised
-every 2-3 months after

198
Q

What is acute pancreatitis ?

A

Acute inflammation of pancreatic gland
- reversible

199
Q

What are the causes of pancreatitis?

A

I get smashed
Idiopathic
gall stones
ethanol
trauma
steroids
mumps
autoimmune
spider bite
hypercalcemia
ERCP
Drugs

200
Q

What is the most common cause of acute pancreatitis?

A

Gall stones

201
Q

What is the pathology of acute pancreatitis?

A

-Gall stones obstruct pancreatic secretions therefore accumulated digestive enzymes in pancreas
- Host defences (A1AT, pancreatic secretory transport inhibition) soon overwhelmed - autodigetsions –> inflammation and enzymes leak in blood
-increase intracellular calcium causing activation of trypsinogen which digests pancreas

202
Q

What is the presentation of acute pancreatitis?

A

Sudden severe epigastric pain radiating to back
+ jaundice, pyrexic, stearrhoea, grey turner signs (flank bleeding) and Cullen sign (periumbilical bleeding)

203
Q

What is the diagnosis of acute pancreatitis?

A

Bloods: high serum anylase/ lipase - GS - lipase more specific
Erect CXR to exclude gastroduodenal perforation
AUSS - diagnostic for gall stones - CT/MRI extent of damage

204
Q

For a diagnosis of acute pancreatitis to be made what characteristics should the patient have?

A
  • characteristic signs/symtpoms
    -raised amylase/lipase
    -Radiological evidence
205
Q

What are the pancreas scoring symptoms?

A

APACHE2 = assess severity within 24hr
Glasgow + ransen’s score- prediction of severe attack, only after 48hr

206
Q

What is the treatment for acute pancreatitis?

A

Acute emergency Px= assess severity with scoring is key
- NG tube if feeding
-IV fluid
-Analgesia -IV fluid
-catheterise
-Abx prophylaxis

207
Q

What are the complications of acute pancreatitis?

A

SIRS - systemic inflammatory response syndrome
2< of:
- tachycardia
-tachypnoea
-pyrexia
-raised WCC

208
Q

What is chronic pancreatitis?

A

3+ months of pancreatic deterioration ; irreversible pancreatic inflammation and fibrosis

209
Q

What is the most common cause of chronic pancreatitis?

A

most common = alcohol
- CKD/CF/Trauma/ recurrent acute pancreatitis

210
Q

What is the presentation of chronic pancreatitis?

A

Epigastric pain radiating to the back
-exacerbated by alcohol
-exocrine (steatorrhoea) and endocrine (T2DM) dysfunction

211
Q

What is the diagnosis of chronic pancreatitis?

A

Bloods: lipase and amylase unlikely to be raised in severe cases as there’s none left to leak out
-fecal elastase = high - indicator of exocrine function
Abdo USS + CCT= detects pancreas calcification and dilated pancreatic duct -diagnostic

212
Q

What is the treatment for chronic pancreatitis ?

A

-alcohol cessation
-NSAIDs for Sx pain
-Pancreatic supplements - insulin/ enzymes

213
Q

What is a Ddx for chronic pancreatitis?

A

Pancreatic cancer

214
Q

What is a ddx fro acute pancreatitis ?

A

AAA

215
Q

What is autoimmune pancreatitis?

A

similar presentation to chronic - as a result os autoimmune process
- high in Japan
-High serum IgG4
-oral prednisolone

216
Q

What is the pathology of chronic pancreatitis?

A
  • obstruction of bicarbonate secretion in the pancreatic lumen causes early activation of trypsinogen and auto digestion –> replaced by fibrosis
217
Q

What is portal hypertension?

A

A complication of cirrhosis; pathologically it is an increase in pressure in portal vein

218
Q

What are the pre-hepatic causes of portal hypertension?

A

Portal vein thrombosis

219
Q

What is the intrahepatic cause of portal HTN?

A

Cirrhosis - mc in UK
Schistomiasis - common worldwide

220
Q

What are the post hepatic causes of portal HTN?

A

Budd Chiari - hepatic vein obstruction
RHS herat failure
Constrictive pericarditis

221
Q

What is the pathology of portal hypertension?

A
  • normal pressure 5-8mmHg in portal vein
    -Cirrhosis = increased resistance to flow therefore splanchnic dilation and compensatory increased cardiac output - results in fluid overload in portal vein (pressure 10+=bad 12+=severe)

Results in collateral blood shunting to gastroesophogeal veins - becoming oesophageal varices

222
Q

What is the presentation of portal HTN?

A
  • mostly aSx
  • present when oesophageal varices rupture
223
Q

What are oesophageal varices?

A

dilated esophageal veins connecting the portal and systemic circulations
If varices haemorrhage = Px with haematemesis
-from long Hx of alcoholism/ cirrhosis

224
Q

What is the diagnosis of oesophageal varices?

A

OGD - oesophagogastroduodenoscopy
Upper GI

225
Q

What is the acute treatment for oesophageal varices?

A

Acutely : resus until haemodynamically stable - consider blood transfusion

226
Q

What is the treatment for oesophageal varices to stop the bleed?

A
  1. IV terupressin
  2. Variceal banding
  3. TIPPS (transjugular intraheptic portosytsgemic shunt - decrease portal pressure by diverting blood to other large veins)
227
Q

What is the treatment of oesophageal varices to prevent the bleed?

A

Bb - non selective - propanolol + nitrates
Repeat vatical banding
- liver transplant

228
Q

What is a Ddx of oesophageal varices?

A

mallory weiss tear (tear of oesophageal mucosa) - increased abdo pressure- retching

229
Q

What are ascites?

A

Accumulated free fluid in abdo cavity, a complication of cirrhosis

230
Q

What are the causes of ascites?

A

local inflammation - peritonitis, TB , abdo cancer

Low protein - nephrotic syndrome , liver failure - hypoalbuminemia

Flow stasis - cirrhosis, Budd chiari, constrictive pericarditis

231
Q

What is the presentation of ascites?

A

Abdo distention
Shifting dullness- tap on central abdo= resonant , tap on flank = fluid
Patient will lay on side and tap on flank = resonant as fluid has shifted
May have jaundice + pruritus

232
Q

What is the diagnosis of ascites?

A

Shifting dullness on exam
Ascitic tap -
1. cytology (WCC counts ) +MC+S
2. Protein measurement

233
Q

What is transudate?

A

<30g/L protein - Serum albumin -ascitic gradient <11g/L

  • clear fluid
    -fluid due to high hydrostatic pressure = portal hypertension, Budd Chiari, constrictive pericarditis, Nephrotic syndromes
234
Q

What is exudate?

A

> 30g/L protein - serum albumin - ascites gradient >11g/L

  • cloudy fluid
    -fluid due to inflammatory mediated exudation or low oncotic pressure = malignancy, peritonitis, pancreatitis
235
Q

What is the treatment of ascites?

A
  • treat underlying cause
    -Diuretic (increase Na+ excretion therefore more fluid pushed out –> spironolactone
    -paracentesis
    -liver transplant
236
Q

What is peritonitis?

A

Inflamed peritoneal cavity

237
Q

What are the sensations in the abdomen?

A

T5-9 = epigastric = greater splanchnic , foregut

T10-11 = umbilical = lesser splanchnic =midgut

T12 = hypogastric = least splanchnic = hind gut

238
Q

What are primary types of peritonitis?

A
  • ascites
    -spontaneous bacterial peritonitis -mc
239
Q

What are the secondary types of peritonitis ?

A

underlying cause = bile/ chemical cause or malignancy

240
Q

What are the bacterial causes of peritonitis ?

A

Gram neg = E.coli + Klebsiella - colliform rods

Gram pos = Staph Aureus (cocci)

241
Q

What are the chemical causes of peritonitis?

A

-bile
-old clotted blood
-ruptured ectopic pregnancy

242
Q

What is the presentation of peritonitis?

A
  • sudden onset severe abdomen pain , then collapse + septic shock + fever
    Rigidity helps pain - guarding, holding on to abdomen to stop it moving
    -poorly localised - poorer sensation of pain
    -Well localised - more inflamed - better localised sensation
    +/- ascites
243
Q

What is the diagnosis of peritonitis?

A

Ascitic tap shows neutrophilia, cultures MC+s shows causative agent
Raised ESR +CRP
Exclude pregnancy + bowel obstruction
Erect CXR shows air under diaphragm

244
Q

What is the treatment for peritonitis?

A

ABCDE
Treat underlying cause - IV fluid + IV Abx
Surgery - peritoneal lavage

245
Q

What are the complications of peritonitis?

A

Septicema if not TX early
Subphrenic, pelvic abscesses, paralytic ulcers

246
Q

What are the metabolic diseases?

A

Haemochromatosis
Wilson’s disease
A1AT deficiency

247
Q

What is haemoochromatosis ?

A

Auto recessive mutation of HFE gene on chromosome 6 result in excess body Fe/

248
Q

What are the risk factors of hameochromatosis?

A

Males - 50
FHx
- less likely in women as they lose iron via mantra cycle

249
Q

What is the pathology of haemochromatosis?

A

Excess Fe uptake by transferrin-1 and low hepcidin synthesis (protein that regulates Fe homeostasis)
Fe accumulation (normally total body Fe 3-4g, here 20-30g) +fibrosis of organs ; Liver (+pancreas, kidney , heart , akin)

250
Q

What is the presentation of haemochromatosis?

A

Fatigue, joint pain,Hypogonadism, slate grey skin, liver cirrhosis, osteoporosis, heart failure

Gross Fe overload triad:
-Bronze statue skin
-Hepatomegaly
-T2DM

251
Q

What is the diagnosis of haemochromatosis?

A

Fe studies; Raised serum Fe/ ferritin/ transferrin saturation
Low Total iron binding capacity - don’t want to bind more iron

Genetic test - HFE mutation
Liver biopsy - assess degree of liver damage with Prussian blue stain

252
Q

What is the treatment for haemochromatosis?

A

1st line - Venesection - regular removing blood
If CI= desfernoxamine (chelation therapy)
Lifestyle changes - low iron diet, avoid fruits

253
Q

What is Wilson’s disease?

A

Auto recessive mutation of ATP7B gene on chromosome 13; Excess body Cu

254
Q

What are the risk factors of Wilson disease?

A

FHx - young patient around 20

255
Q

What is the pathology of Wilson’s disease?

A

Impaired Cu biliary excretion + normal transport bound to ceruloplasmin ; increased copper accumulated in liver and CNS(basal ganglia)

256
Q

What is the presentation of Wilson’s disease?

A

hepatic = liver disease / jaundice
Neurological = Parkinsonism , memory issues
Opthalmogical = Kayser Fleischer Rings (Cu deposits in cornea) - PATHOGNAMONIC

257
Q

What is the diagnosis of Wilson’s disease?

A

Cu tests; low serum copper + low ceruloplasmin - more Cu deposited in tissue rather than in bloodstream mainly due to the fact there’s low ceruloplasmin

Liver biopsy - high copper / hepatitis - GS
MRI brain - cerebellar + BG degeneration

258
Q

What is the treatment of Wilson’s?

A

1st line - Penicillamine ( Cu chelation, lifelong)
-Change diet , avoid high copper food
Liver transplant -last resort

259
Q

What is A1AT deficiency?

A

Autosomal recessive mutation of protease inhibitor gene (serpina-1 gene) on chromosome 14 causing a deficiency of alpha 1 antitrypsin enzyme

260
Q

What is the pathology of A1AT deficiency?

A

A1AT normally inhibits neutrophil elastase which degrades elastic tissue
Deficient A1AT= causes an increase in NE:
-Lungs - degrades elastic tissue causing alveolar duct collapse, air trapping, and characteristic panacinar emphysema
-Liver - unprotected - soon becomes fibrotic ; Cirrhosis +HCC risk (A1AT made by liver - liver fibrosis will make synthetic function worse)

261
Q

What is the presentation of A1AT deficiency disease?

A

-young, middle aged male, no smoking Hx
-dyspnoea, chronic cough, sputum production, barrel chest
-Jaundice

262
Q

What is the diagnosis of A1AT deficiency?

A

Serum A1AT low <20mmol/L
Barrel chest on exam , CXR shows hyperinflate lungs
CT- panacinar emphysema
LFT- obstruction FEV1;FVC <0.7
Genetic - PI mutation

263
Q

What is the treatment of A1AT deficiency?

A
  • no cure
    -stop smoking
    -manage emphysema - inhalers
  • consider hepatic decompensation patients for transplant
264
Q

What is a paracetamol overdose?

A

Paracetamol ingestion >75mg/Kg
- 50% all fulminant liver failure in UK

265
Q

What is the presentation of paracetamol overdose?

A

acute severe RUQ pain, Severe n+v

266
Q

How is paracetamol normally metabolised?

A

paracetamol (90%) metabolised in the liver by Phase 2 conjugation/glucuronidtaion then excreted by urine
Phase 1 (10% of paracetamol) metabolised via CYP450 pathway and forms NAPQI which is toxic , conjugated with glutathione to become non toxic and can be excreted

267
Q

What happens to paracetamol metabolism if there is an overdose?

A

Phase 2 pathway is saturated, so phase 1 pathway is used, glutathione is depleted therefore a build up of NAPQI in liver

268
Q

What is the treatment of paracetamol overdose?

A

Activated charcoal (within 1hr paracetamol ingestion) + N-acetyl- cysteine

269
Q

What is a hernia?

A

protrusion of an organ through defect in its containing cavity

270
Q

What are the types of hernia?

A

Reducible - manually push back into place

Irreducible - obstructed (intestinal obstruction)
-strangulated (intestinal ischemia)
-Incarcerated

271
Q

What is a hiatal hernia?

A

stomach hernia through diaphragm aperture

272
Q

What is a rolling hiatal hernia?

A

20%
LES stays in abdo, part of funds rolls into thorax

273
Q

What is a sliding hiatal hernia?

A

80%
LES slides into abdo

274
Q

What are the Sx of hiatal hernia?

A

Gord
Dysphagia
- obese women , 50+

275
Q

What is the diagnosis of hiatal hernia?

A

CXR
Barium swallow - diagnostic
OGD

276
Q

What is an Inguinal hernia?

A

Protrusion of abdo contents through inguinal canal

277
Q

What is direct inguinal hernia?

A

20%
In hesselbach’s triangle , medial to inferior epigastric artery

278
Q

What is indirect inguinal hernia?

A

90%
Lateral to inferior epigastric artery

279
Q

What are the risk factors of inguinal hernia?

A

male
Hx of heavy lifting / abdo pressure

280
Q

What is the presentation of inguinal hernia?

A

Painful swelling groin , points along groin margin

281
Q

What is the diagnosis of inguinal hernia?

A

usually clinical
AUSS/CT/MTI if unsure

282
Q

What is a femoral hernia?

A

bowel through femoral canal

283
Q

What are the RF and complications of femoral hernia?

A

Female - middle age
- likely to strangulate due to rigid femoral canal borders

284
Q

What is the presentation of femoral after?

A

Swelling in upper thigh pointing down

Phase 2a (9 decks)

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