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M E D > r h e m concise > Flashcards

r h e m concise Flashcards

1
Q

what is OA

A

degenerative joint disorder where there is progressive loss of hyaline cartilage

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2
Q

what are the rx associated with OA

A

increasing age
obesity
joint abnormality or trauma

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3
Q

what are the sx seen in OA

A

pain worse after movement, worse at the end of the day

stiffness - after rest, lasts 30 mins

deformity

reduced ROM around the joint

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4
Q

which joints are affected by OA

A 
knee
hip
DIPS
PIPS
CMC of thumb
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5
Q

what are the signs seen in OA

A

bouchards - PIPs
Herbedens nodules DIPS
thumb CMC squaring
fixed flexion deformity

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6
Q

what are ddx for OA

A

septic
crystal - gout and pseudo gout
trauma

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7
Q

what are the x ray features of oA

A

LOSS

loss of joint space/ narrowing
osteophytes
subcondral cysts
subcentral sclerosis

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8
Q

how is OA managed

A

conservative = weight loss, physio muscle strengthening, walking aids, supportive footwear

medical - analgesia = paracetamol, NSAID’s - diclofenac
joint injections - methyl pred

surgery - arthroscopic washout, athroplasty, osteotomy

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9
Q

what is septic arthritis

A

acutely red, hot, infected joint

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10
Q

what are the source of infection or SA

A

haematogenous

local

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11
Q

what organisms cause SA

A

staph most common - staph aureus

gonococcus most common in young sexually active pts

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12
Q

what are the risk factors for SA

A

joint disease e.g RA
immuosupression e.g DM
prosthetic joints

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13
Q

what are the sx associated with SA

A

acutely tender, swollen joint

reduced range of movement

systemically unwell

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14
Q

what Lx are required in SA

A

joint aspiration for MCS raised acc

raised ESR/CRP, raised WCC, blood cultures

x-ray

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15
Q

how is SA managed

A

IV abx - vancomycin and cefotaxime
consider joint washout under GA
physiotherapy after infection

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16
Q

what are the ddx for SA

A

reactive arthritis

crystal arthropathy

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17
Q

what are the complications associated with SA

A

osteomyelitis
arthritis
ankylosis - fusion

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18
Q

what is RA

A

chronic, autoimmune inflammatory disease characterised by symmetrical deforming peripheral polyarthritis

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19
Q

describe the pathophysiology behind RA

A

self antigens are recognised by b and t cells
leading to production of RF and anti CCP antibodies
macrohages and fibroblasts produce TNF a, cascade of inflammation

and proliferation of synoviocytes on cartilage as well as differentiate of osteoclasts which contributes to bone damage

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20
Q

what are the risk factors associated with RA

A

smoking
female gender
increasing age (5th -6th decade)
genetics - HLA DR4/DR1 linked

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21
Q

what are the features of RA

A

ANTI CCP Or RF

  1. arthritis
  2. nodules
  3. tenosynovitis
  4. immune
  5. cardiac
  6. carpal tunnel
  7. pulmonary
  8. opthalamic
  9. raynaud’s
  10. felty’s syndrome
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22
Q

describe the arthritic features seen in RA

A

symmetrical polyarthris of MCPs. PIPs of hands and feet = pain, swelling and deformity

  1. swan neck
  2. boutonniere
  3. z thumb
  4. ulnar deviation of the fingers
  5. dorsal subluxation of ulnar styloid

morning stiffness more than an hour
improves with exercise

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23
Q

what is a swan neck deformity

A

PIPs hyperextension

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24
Q

what is boutonniere’s deformity

A

DIPs in hyperextension and PIP’s in flexion

seen in RA

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25
Q

where are nodules in RA seen?

A

seen in elbows and fingers - firm, non tender mobile or fixed

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26
Q

what cardiac features are seen in RA, which pulmonary features

A

pericarditis, pericardial effusion

fibrosing alveolitis, exudative pleural effusions

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27
Q

what ophthalmic features are seen in RA

A

episcleritis

secondary sjogren’s syndrome

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28
Q

what is Felty’s syndrome

A

RA with splenomegaly and neutropenania

Thrombocytopenia
anaemia

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29
Q

how is the diagnosis of RA made

A

4/7 of

  1. Morning stiffness >1h (lasting >6wks)
  2. Arthritis ≥3 joints
  3. Arthritis of hand joints
  4. Symmetrical
  5. RA nodules
  6. positive RF
  7. radiographic changes
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30
Q

what x-ray features are seen in RA

A

LESS

loss of joint space or narrowing
boney erosions
soft bones - osteopenia
soft tissue swelling

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31
Q

what investigations are requird in RA

A

bloods =FBC - feltys syndrome - anaemia, thrombocytopenia, neutropenia

CRP/ESR

RF, anti CCP = specific, ANA

X-ray

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32
Q

what ddx for RA

A

psoariatic arthritis = nail changes and plaques

chronic crystal arthritis

jaccoud’s arthritis

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33
Q

describe the management for RA

A

conservative = regalar exercise, PT, OT = aids, splints

medical = DAS28 assessment to monitor disease activity, DMARDS and biologicals early

steroids IM PO or intra articular for exacerbations

NSAIDs for sx relied

manage CVS risk = RA accelerates atheresclosis

prevent osteoporosis and gastric ulcers

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34
Q

what are the main DMARD’s used and their SE

A

cause myelosuppression = pancytopenia

methotrexate = hepatotoxic, pulmonary fibrosis

sulfalazine = hepatotoxic, reduced sperm count

hydrochloroquine = retinopathy, seizures

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35
Q

what is the pathophysiology of gout

A

deposition of monosodium rate crystals in and around joints

36
Q

describe the presentation of gout

A

acute monoarthrits with severe joint inflammation

greater toe MTP = podagra

can also present as asymmetric oligoathrits, deposition of rate in pinna and tendons = tophi

renal disease = radiolucent stones and interstitial nephritis

37
Q

ddx for gout

A

SA
pseudogout
haemoarthritis

38
Q

what are the causes of gout

A
  1. hereditary
  2. drugs = diuretics, NSAIDs
  3. reduced renal excretion = renal impairment
39
Q

what investigation are required in gout

A

polarised light microscopy = negatively birefringent needle shaped crystals

increased serum rate

40
Q

describe acute rx of gout

A

NSAID’s - diclofenac
colchicine
use steroids if NSAID’s are contraindicated

41
Q

describe prevention of gout

A

conservative = weight loss, avoid EtOH excess

allopurinol = xanthine oxidase inhibitors

42
Q

what are seronegative sponyloarthropathies

A

group of inflammatory conditions affecting spine and peripheral joints without production of RFs, associated with HLA B27 allele

AS
psoriatic arhtris
reactive arthritis

43
Q

what is AS and its sx

A

chronic disease characterised by stiffening and inflammation of spine and sacroiliac joints

gradual onset back pain
progressive loss of all spinal movements
costocondritis

44
Q

what test is done for AS, what is the question marker posture

A

Schober’s test , less than 5cm

some pt with question mark posture = thoracic kyphosis and neck hyperextension

45
Q

what are the extra articular manifestations of as

A

osteoporosis
acute iritis or anterior uveitis
apical pulmonary fibrosis

46
Q

what Lx are required in AS

A

clinical dx

sacroiliitis - ireegularitis, sclerosis, erosions
bamboo spine - calcification of ligaments and periostea bone calcification

FBC anemia, increased ESR/CRP, HLA B27

DEXA scan and CXR

47
Q

how is AS managed

A

conservative - exercise, physio
medical - NSAID’s, anti TNF if severe, local steroid injections, bisphosphonates

hip replacement to reduce pain and increase mobility

48
Q

what is an x ray features of psoriatic arthritis

A

pencil in cup deformity = erosion

49
Q

management for psoriatic arthritis

A

NSAIDs, sulfasalazine, methotrexate, ciclosporin, anti TNF

50
Q

what is reactive arthritis

A

sterile arhtris 1=4 weeks after urethritis or dysentry

Urethritis: chlamydia, ureaplasma
 Dysentery: campy, salmonella, shigella, yersinia

51
Q

what lx are required in reactive arthritis

A

increased cap, ESR
stool culture if diarrhoea
urine chlamydia PCR

52
Q

how is reactive arthritis managed

A

NSAID’s and local steroids

53
Q

what is GCA/ temporal arteritis

A

inflammation of medium to large sized vessels, arteries

associated with PMR

54
Q

what are the features of GCA

A 
systemic = fever, malaise, fatigue 
headache - unilateral
temporal artery and scalp tenderness 
jaw claudication 
amarosis fugax
prominent temporal arteries, pulsation
55
Q

management and lx in GCA

A 
do ESR and starrt red 40-69mg/d PO
increase ESR, CRP
increased ALP
reduced Hb, increased Plts
temporal artery biopsy

PPI and alendronate cover = steroids risk

56
Q

what is PMR, how does it present

A

severe pain and stiffness i shoulders, neck and hips, symmetrical, worse in morning, no weakness

carpal tunnel
systemic sx = fever. fatigue, weight loss

GCA association

57
Q

what are the Lx and management of PMR

A

increased ESR, CRP, increased ALP
normal CK

rx = pred tapering course add PPI and alendronate cover

58
Q

what is fibromyalgia and its associations

A

condition of central pain processing characterized by chronic widespread pain in all 4 quadrants of the body

sleep deprivation

59
Q

what are the rx for FM

A

neurosis = depression, anxiety, stress
low income
divorce

60
Q

what are the features of FM and Lx

A

chronic widespread MSK and tenderness

morning stiffness 
fatigue 
poor concentration 
sleep disturbance 
low mood

Lx all normal

61
Q

how is FM managed

A

educate pt
CBT
graded exercise programs
amitriptyline or pregabalin

62
Q

what is SLE

A

multi systemic autoimmune inflammatory disease

which autoAbs to a variety of autoantigens result in the formation and deposition of immune complexe

63
Q

features of SLE

A

relapsing and remitting history
constitutional sx = fatigue, weight loss, fever and myalgia
SOAP BRAIN

64
Q

soap brain in SLE

A

S erositis - Pleurisy, pericarditis
 O ral ulcers - usually painless; palate is most
specific
 A rthritis – small joints nonerosive
 P hotosensitivity – or malar or discoid rash
 B lood disorders – low WCC, lymphopenia,
thrombocytopenia, hemolytic anemia
 R enal involvement -glomerulonephritis
 A utoantibodies (ANA positive in >90%
cases)
 I mmunologic tests e.g. low complements
 N eurologic disorder - Seizures or psychosis

65
Q

what lx required in SLE, what results are seen

A

ANA

Anti Ro, Anti La

Anti dsDNA

Antiphospholipid - increase risk of pregnancy loss and thrombosis

66
Q

what is the management of SLE

A

sun protection - SPF
reduce CVS risk
hydrochloroquine = rash and arthralgia
short courses of prednisolone for flares
mycophenolate mofetil, azathioprine commonly used

67
Q

what is SS

A

multisystem autoimmune disease

increased fibroblast activity result in abnormal growth of connective tissue leading to vascular damage and fibrosis

limited SS (70%) vs diffuse SS

68
Q

what syndrome and features are seen in SSc

A

limited SSc

CREST

calconosis cutis  
raynaud's
oesophageal and gut dismotility 
scelrodactyly
telangiectasia 
skin involvelemt = beak nose, microstomia 
pulmonary HTN
69
Q

How is SSc managed

A

no cure
pre for acute attacks
 Raynaud’s: CCBs, ACEi, IV prostacyclin
 Renal: intensive BP control – ACEi 1st line
 Oesophageal: PPIs, prokinetics (metoclopramide)  PHT: sildenafil,

70
Q

what lx are required for SSc

A

FBC - anaemia, UE renal impairment

ANA positive

Abs - centromere in limited,

Scl 70 and RNA polymerase III in diffus
e 
X-ray hands- calcinosis
CXR, HRCT, PFT- pulmonary disease
ECG & ECHO - PA hypertension, heart failure, myocraditis and arrhythmias,
71
Q

what is sjogrens syndrome, how does it present

A 
mnemonic –madfred!
Myalgia
Arthralgia
Dry Mouth
Fatigue
Raynaud’s phenomenon Enlarged parotids
Dry eyes
72
Q

what lx are required in sjogren’s and management

A

Anti Ro and Anti La Antibodies – 90% of patients RF & anti ds-DNA
salivary gland biopsy may be needed

treatment is symptomatic
Avoid dry or smoky atmospheres
Dry eyes–artificial tears
Dry mouth -artificial saliva, sugar free gum/pastilles Skin emollients, vaginal lubricants

73
Q

what is Osteoporosis

A

A skeletal condition characterized by low bone mass, deterioration of bone tissue, and disruption of bone architecture that leads to compromised bone strength and an increased risk of fractur

74
Q

what are the rx factors modifiable and non

A

Non-modifiable
- Advanced age (>65 years)
- Female gender
- Caucasian or south Asians
- Family history of osteoporosis-genetic
- History of low trauma fracture (fall from
standing height or less, at walking speed or less.

Modifiable
- Low body weight (58 kg or body mass index
[BMI] <21)
- Premature menopause (age<45)
- Calcium/vitamin D deficiency
- Inadequate physical activity
- Cigarette smoking
- Excessive alcohol intake (>3 drinks/day)
- Iatrogenic: e.g. corticosteroids, aromatase
inhibitors

75
Q

how is a diagnosis of OP made

A

DEXA) of the lumbar spine and hip

76
Q

what is T score and its interpretation

A
  • T-score is the number of SDs from the mean bone density of persons of same gender at age of peak density (25 years)
  • T-score minus 2.5 or less = osteoporosis
  • Normal BMD = T-score ≥ −1
  • Osteopenia = T-score between −1 and −2.
77
Q

what is a Z score

A

The Z-score is a comparison of the patient’s BMD with an age- & gender-matched population

-A Z-score

78
Q

what is the treatment for osteopenia and osteoporosis

A

osteopenia = weight-bearing exercise, vitamin D3 supplementation (800-2000 IU/day), limiting alcohol, and smoking cessation. Dietary advice regarding calcium intake; supplements if needed.

osteoporosis = Vitamin D ± calcium supplementation plus:
1st line: Oral bisphosphonates, or IV if oral not tolerated.
2nd line: Denosumab or teriparatide

79
Q

what is raynauds phenomenon, puts and color changes

A

due to vasospasm of the digits. It is painful and is characterized by a typical sequence of colour changes in response to a cold stimulus. It is often also precipitated by stress.

white- inadequate blood flow blue -venous stasis
red -re-warming hyperaemia.

80
Q

diseases and causes associated with raynauds

A

SSc
SLE
Sjogrens syndrome

use of heavy vibrating tools
cervical rib
beta blockers

81
Q

treatment of raynauds

A

keep warm
avoid smoking.

Calcium-channel blockers are the first-line. Phosphodiesterase-5 inhibitors, and prostacyclins are usually effective.

82
Q

complications of raynauds

A

digital ulcers, severe digital ischaemia and infection.

83
Q

what is OM

A

steomalacia describes softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content.

rickets in children

84
Q

causes of OM

A 
vitamin D deficiency
malabsorption
lack of sunlight
diet
chronic kidney disease
drug induced e.g. anticonvulsants
inherited: hypophosphatemic rickets (previously called vitamin D-resistant rickets)
liver disease: e.g. cirrhosis
85
Q

features of OM

A

bone pain
bone/muscle tenderness
fractures: especially femoral neck
proximal myopathy: may lead to a waddling gait

86
Q

lX IN OM

A

bloods
low vitamin D levels
low calcium, phosphate (in around 30%)
raised alkaline phosphatase (in 95-100% of patients)
x-ray
translucent bands (Looser’s zones or pseudofractures)

87
Q

TREATMENT IN OM

A

vitamin D supplmentation
a loading dose is often needed initially
calcium supplementation if dietary calcium is inadequate

M E D (18 decks)

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