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Phase 2a Gold Standard > Rheumatology/MSK > Flashcards

Rheumatology/MSK Flashcards

1
Q

Define osteoarthritis

A

Non inflammatory, progressive synovial joint damage caused by wear and tear of most commonly used joints.

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2
Q

Joints commonly affected in osteoarthritis

A

Knees
Hips
Sarco-ileac joints
Wrist
Carpometacarpal
Interphalangeal

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3
Q

Risk factors for osteoarthritis

A

Age
Female sex
Raised BMI/obesity
Joint injury/trauma
Joint malalignment (congenital or not)

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4
Q

Pathophysiology of osteoarthritis

A

Usually, cartilage breakdown and production by chondrocytes is under balance.

In OA, chondrocytes secrete more metalloproteinases (degrading enzymes) leading to loss of Type 2 cartilage. (Type 1 has less elasticity)

IL-1 and TNF-a also stimulate metalloproteinase production and inhibit collagen production.

Causes decreased joint space, which causes damage to bones on movement. Bone attempts to repair itself with type 1 collagen but causes bony overgrowths

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5
Q

Signs/symptoms of osteoarthritis

A

Asymmetrical non inflamed joint pain, which gets worse as the day goes on

  • Herbeden’s nodes (DIP Swelling)
  • Bouchard’s nodes (PIP swelling)
  • Fixed flexion deformity of carpometacarpal
  • Joint pain worse with activity
  • Mechanical locking
  • Joint stiffess, tenderness, crepitus (crunching sensation when moving)
  • NO EXTRA ARTICULAR MANIFESTATIONS
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6
Q

Typical presentation of osteoarthritis

A

> 45 years old
Typical activity related pain
No morning stiffness (<30 mins)

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7
Q

Investigations in osteoarthritis

A

1st - X ray (LOSS)
L - Loss of joint space
O - Osteophytes (bony overgrowths)
S - Subchondral sclerosis
S - Subchondral cysts

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8
Q

Non pharmacological treatments of osteoarthritis

A
  • Weight loss
  • Low impact exercise
  • Physiotherapy
  • Occupational therapy
  • Heat/cold packs at site of pain
  • Orthotics (helps with foot issues)
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9
Q

Pharmacological treatment of osteoarthritis

A

1st - Oral paracetamol, topical capsaicin, topical NSAID

Topical NSAID first for knee

Others:
- Intra articular steroid injection
- Joint replacement

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10
Q

Define Rheumatoid arthritis with epidemiology

A

Autoimmune, systemic disease causing symmetrical deforming inflammation of small joints which progresses to larger joints and organs.

More in women aged 30-50

Type 3 hypersensitivity reaction

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11
Q

Risk factors for Rheumatoid arthritis

A
  • Female
  • Smoking
  • Family history
  • Post menopause
  • HLA-DR1, HLA-DR4
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12
Q

Pathophysiology of rheumatoid arthritis

A

Arginine -> Citrulline mutation of type 2 collagen. Immune cells cannot differentiate self and non-self, causing antibody formation. Anti-CCP (cyclic citrullinated peptide) antibodies formed. These bind to citrullinated peptides and form immune complexes, which accumulate in synovial fluid, causing inflammation.

Cytokines recruited by macrophages (TNF, IL1,6) proliferate, forming thick pannus containing cytokines, myofibroblasts and fibroblasts. These grow past joint margins, destroy subchondral bone and articular cartilage. T cells also express RANKL, which bind to osteoclasts, causing bone breakdown.

Inflammatory cytokines also escape joint space, causing systemic effects

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13
Q

Signs/symptoms of rheumatoid arthritis

A

Symmetrical polyarthritis
Signs
- Boutonniere deformity (PIP flexion, DIP hyperextension)
- Swan-neck deformity (PIP hyperextension, DIP flexion)
- Z thumb deformity (thumb IP hyperextension, MCP flexion)
- Ulnar deviation
- Popliteal cysts (synovial sac bulges posterior to knee)
- Rheumatoid nodules (lumps under skin and around organs)

Symptoms
- Morning stiffness, >30 mins, improves throughout day
- Carpometacarpal joint spared in rheumatoid but not psoriatic

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14
Q

Investigations in rheumatoid arthritis

A

ESR/CRP high

Autoantibodies:
- Anti CCP (more specific - can be detected 15 years before symptoms)
- Rheumatoid factor (present in other diseases e.g. Sjogren’s)

X ray- LBSP

Loss of joint space
Bone erosions
Soft tissue swelling
Periarticular osteopenia (punched out erosion)
Subluxation

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15
Q

Extra articular manifestations of rheumatoid arthritis
(skin, respiratory, CVD, eyes, haem, systemic)

A

Skin
- Rheumatoid nodules

Respiratory
- Pulmonary nodules
- Pleurisy
- Bronchiectasis
- Caplan’s syndrome
- Interstitial lung disease

Opthalmological
- Keratoconjunctivitis sicca
- Scleritis
- Corneal ulceration

CVD
- IHD and pericarditis

Anaemia, Amyloidosis, Felty syndrome

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16
Q

Treatment of rheumatoid arthritis

A

DMARD - Methotrexate (CI in pregnancy!)
NSAID
Intraarticular steroid injections

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17
Q

Main life threatening complication of rheumatoid arthritis

A

Felty’s syndrome
- Rheumatoid arthritis
- Splenomegaly
- Neutropenia

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18
Q

Monitoring of rheumatoid arthritis

A

Monitor FBC, LFT, U&E weekly until treatment stabilised

Check ESR/CRP monthly

  • Check disease activity score (DAS-28) annually
  • Check for comorbidities
  • Assess for surgery need
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19
Q

What type of reaction is rheumatoid arthritis

A

Type 3 hypersensitivity

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20
Q

Define gout

A

Inflammatory Arthritis caused by deposition of monosodium urate crystals in joints (Most commonly first metatarsophalangeal (MTP) joint - big toe)

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21
Q

Risk factors for gout

A
  • Elderly
  • Male
  • Purine rich foods (red meat, seafood, alcohol)
  • Obesity
  • Hypertension
  • Impaired kidney function
  • Type 2 diabetes mellitus
  • Family history
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22
Q

Causes of gout

A

Increased uric acid production
- Increased cell turnover (leukaemia, haemolytic anaemia)
- Purine rich diet (shellfish, red meat, organ meat)
- Obesity/metabolic syndrome

Decreased excretion
- CKD
- Diuretics/aspirin/pyrazinamide
- Lead toxicity

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23
Q

What type of diet would you recommend a patient with gout switch to

A

High dairy diet is protective from Gout

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24
Q

Pathophysiology of gout

A

Normally, purines are broken down into uric acid by xanthine oxidase, which is then excreted by kidney. Uric acid has limited solubility in blood, in high concentrations, can become a urate ion which binds to sodium to become monosodium urate, which deposits in areas of low blood flow (joints/ kidney tubules).

WBCs attack said crystals, causing inflammation

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25
Q

Signs/symptoms of gout

A

Generally monoarticular (can be up to 4) joint swelling, tenderness, erythema.
- Usually 1st MTP but can affect ankle, wrist, knee, small hand joints.

Gouty tophi (nodular masses of urate crystals - massive lump under skin) can appear

Flares last between 7-10 days, first 12 hours worst

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26
Q

Investigations in gout

A

Joint x ray:
- Joint effusion, preserved joint space.
- Lytic lesions
- Punched out erosions with sclerotic margins and overhanging edges
- Loss of joint space is a very late sign

Joint aspiration w/ polarised microscopy:
- Needle shaped crystals with negative birefringence

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27
Q

Management of gout
General life advice
Acute flares
Prevention

A

General life advice:
- Low purine, lose weight, avoid alcohol (especially beer)

Acute flares:
- NSAID+PPI OR colchicine OR steroid injection 2nd line

Prevention:
- Allopurinol (xanthine oxidase inhibitor)

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28
Q

Complication of gout caused by hyperuricaemia

A

Urate nephrolithiasis: Hyperuricaemia can cause urate renal stones

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29
Q

Define pseudogout

A

Pseudogout is an inflammatory arthritis caused by deposition of calcium pyrophosphatase crystals in synovium

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30
Q

Risk factors for pseudogout

A
  • Increasing age
  • Female
  • Previous joint trauma
  • Hyperparathyroidism
  • Hypomagnesaemia
  • Hypophosphataemia
  • Haemochromatosis
  • Acromegaly
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31
Q

Pathophysiology of pseudogout

A

Also known as chondrocalcinosis.

Calcium pyrophosphatase crystals trigger synovitis, most commonly in the knee, shoulder and wrist.

Acute - mainly larger joints in elderly
Chronic - Inflammatory RA-like symmetrical arthritis

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32
Q

Signs/symptoms of pseudogout

A

Usually indistinguishable from gout, except that knee, wrist, ankle are most affected
- Inflammation: warm, swelling, erythema, pain and joint stiffness

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33
Q

Investigations in pseudogout

A

X ray: Chondrocalcinosis (suggestive but not diagnostic, absence doesn’t exclude)

Joint aspiration w/ polarisation: Weakly positively birefringent rhomboid shaped crystals

Also check: Bone profile/PTH, Iron studies, serum magnesium to check cause

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34
Q

Management of pseudogout

A

Acute
- NSAID or colchicine or corticosteroid injection
- Cool packs + rest

Chronic
- DMARD (methotrexate) or joint replacement

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35
Q

Main differential of crystal arthropathies

A

Septic arthritis!

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36
Q

Gout vs pseudogout joint aspiration

A

Gout - Negative birefringent needle shaped crystals
Pseudogout - Positively birefringent rhomboid shaped crystals

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37
Q

Name the 2 types of infective arthritis

A

Septic - Infection of joints caused by either direct inoculation or haematogenous spread. Medical emergency

Osteomyelitis - Inflammatory disease of the bone marrow. Can be acute or chronic.

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38
Q

Define Septic arthritis

A

Infection of joints caused by most commonly staph aureus. occurs by direct inoculation or haematogenous spread

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39
Q

Causative microbes in septic arthritis

A

Staph Aureus - Most common
Staph epidermidis - prosthetic joints
Strep pyogenes - Children under 5
Neisseria gonorrhoeae - Sexually active

Pseudomonas aeruginosa and Ecoli in elderly, immunosuppressed or IV drugs

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40
Q

Risk factors for septic arthritis

A
  • Underlying joint disease
  • IV Drug use
  • Immunosuppression
  • Prosthetic joint
  • Recent joint surgery
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41
Q

Pathophysiology of Septic arthritis

A
  • Medical emergency due to risk of sepsis, permanent joint destruction and osteomyelitis.
  • Direct or haematogenous spread
  • 90% cases staph or strep
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42
Q

Signs/symptoms of septic arthritis

A

Mainly affects 1 joint. (Knee most common. but also hip, shoulders, wrists, elbows)
- Hot, tender, erythematous, swollen joint with very limited range of movement (weight bearing joints wont allow use its that painful/limited)
- Fever

  • Distal skin lesions if gonococcal
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43
Q

Investigations of septic arthritis

A
  • FBC - High WBC, high ESR/CRP
  • Blood culture - Check before antibiotics!
  • Urine if gonococcal

Joint aspiration GOLD
- Yellow/cloudy, high WCC, culture positive, neutrophils
- Must be sent for gram staining and culture
- Take before antibiotics!

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44
Q

What scoring criteria is used in Septic arthritis

A

Kocher criteria

(non weight bearing, temp, ESR, WCC)

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45
Q

Differential diagnoses of monoarticular arthritis

A

Gout
Pseudogout
Septic arthritis
Reactive arthritis

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46
Q

Treatment of septic arthritis

A

Empirical antibodies until cause known.
1st - Flucloxacillin and rifampicin

Joint drainage/washout

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47
Q

Drugs to stop in septic arthritis

A

Methotrexate/Anti TNF-a

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48
Q

Define osteomyelitis

A

Inflammatory condition of the bone/bone marrow, caused by infection (Staph aureus most common). Can be acute or chronic, leading to soft tissue infection, infarction and reactive new bone.

Mostly occurs in children

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49
Q

Causative organisms in osteomyelitis

A

SPSNM

Staph aureus - MC
P aeruginosa - MC (gram negative rod)
Salmonella
N gonorrhoeae
M tuberculosis

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50
Q

Risk factors for osteomyelitis

A
  • Diabetes
  • Old age
  • PVD
  • Immunocompromise
  • Malnutrition
  • IV drugs
  • Recent invasive surgery
  • Trauma
  • Sickle cell anaemia
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51
Q

Pathophysiology of osteomyelitis

A

Pathogen can get into bone through
- Haematogenous spread (E.g. through cannula)
- Contiguous spread
- Direct inoculation

Disease course can be acute or chronic

Acute
- Bacteria reaches bone and proliferates. Infection fought off by immune system, however this damages bone. Osteoclasts repair damage and form new bone

Chronic
- Acute osteomyelitis can become chronic if lesion is large or if there is not enough viable bone for repair.
- Affected bone can become necrotic and separate from the healthy part of the bone (this is a Sequestrum)
- Osteoblasts from the periosteum may form new bone that wraps the sequestrum in place (this is called an involucrum)
- Cloaca (gaps in an involucrum where necrotic bone and pus can discharge) also form.

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52
Q

Causes of osteomyelitis

A

Diabetic foot ulcer/skin infection
Open fracture
Cannula
Trauma
Insect bites
Prosthetic joints contaminated during surgery
Kidney disease
Nearby infections (Contiguous spread!!)

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53
Q

Signs and symptoms of Osteomyelitis

A
  • Dull bony pain with redness and swelling at site of infection
  • Joint pain
  • Fever
  • Reluctance to weight bear (child with limp)
  • Ulcers or skin breaks
  • Discharging sinus
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54
Q

Histopathology of Osteomyelitis

A

Acute
- Inflammation
- Oedema
- Vascular congestion
- Small vessel thrombosis

Chronic
- Necrotic bone (sequestrum)
- New thick sclerotic bone formation around sequestrum (Involucrum)
- Neutrophil exudate
- Tissue macrophages

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55
Q

Main differential of osteomyelitis

A

Charcot joint
- Damage to sensory nerves due to diabetic neuropathy
- Causes progressive degeneration of weight bearing joint and bony destruction
- Non infective, patient presents with Diabetic feet

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56
Q

Investigations in osteomyelitis

A
  • High WBC, ESR/CRP

Imaging
X ray
- Local osteopenia
- Lytic lesions
- Cortical bone loss
- Periosteal reaction (thickening)
- Involucrum/sequestrum (“fallen leaf sign” - Sequestrum falls into medullary canal)
MRI - Most definitive imaging modality, may show signs of infection in medullary canal or surrounding soft tissue and abscesses

Microbiology
- BM biopsy + Culture GOLD
- Blood culture
- Urine MSU

-HbA1c MUST BE CHECKED

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57
Q

Management of Osteomyelitis with indications for surgery

A
  • Flucloxacillin and Rifampacin empirical, give vancomycin if MRSA suspected
  • Oral fusidic acid

Surgical debridement of sequestrum and necrotic bone if:
- Failure to respond to Abx
- Abscess formation
- Vertebral osteomyelitis

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58
Q

Main functions of bone

A

Haematopoiesis
Lipid/mineral storage
Support body framework
Protection (axial skeleton around major organs)

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59
Q

What are the cellular components of bone

A

Osteoblasts - Synthesise osteoid which later is calcified/mineralised into new bone
Osteocytes - As osteoid mineralises, osteoblasts become entombed between lamellae and mature into osteocytes. Monitor minerals, proteins and regulate bone mass.
Osteoclasts - Derived from monocytes, resorb bone by releasing H+ ions. Large, multinucleated cells.

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60
Q

What is the main component of bone ECM

A

Calcium hydroxyapatite crystals, main source of mineralisation of bone. Make bone hard and strong, and are organised into thin layers called lamellae

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61
Q

What are the main parts of bone

A

Cortical bone
Spongy/trabecular bone

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62
Q

What does cortical bone consist of

A

Multiple osteons, containing Haversian canals (blood supply and innervation) and lamellae, with collagen and hydroxyapatite crystals.

Gaps between lamellae, called lacunae, contain osteocytes

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63
Q

How does bone remodelling work

A

Osteoclasts resorb bone
Osteoblasts form new bone

Cortical/compact bone replaced every 10 years
Spongy/trabecular bone replaced every 3-4 years

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64
Q

Factors that affect bone remodelling

A

PTH
Calcitonin (thyroid gland hormone released in hypercalcaemia - Essentially antiPTH)
Vitamin D

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65
Q

What is the main difference between osteoporosis and osteomalacia

A

Osteoporosis refers to thin, porous bone with decreased mass and density but proper mineralisation. Usually due to increasing age and menopause

Osteomalacia refers to normal bony tissue but improper mineralisation, causing soft, weak bones, usually due to vitamin D deficiency

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66
Q

What bone changes increase risk of fragility fracture in osteoporosis

A
  • Thinning of cortical bone
  • Fewer trabeculae
  • Widening of Haversian canals
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67
Q

Define osteoporosis

A

Skeletal disease characterised by low bone density and micro-architectural defects in bone, resulting in bone fragility and increased risk of fragility fracture.

Bone mineral density of 2.5 standard deviations below mean peak mass

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68
Q

Risk factors for osteoporosis

A

SHATTERED
S - Steroid (glucocorticoids decrease Ca2+ absorption in gut)
H - Hyperthyroid, HyperPT, hypocalcaemia/Hypercalciuria
A - Alcohol/smoking
T - Thin (low BMI)
T - Testosterone decrease
E - Early menopause
R - Renal/liver failure
E - Erosive bone disease (myeloma, RA)
D - Dietary reduced Ca2+, malabsorption, diabetes

Also, older age, female, previous fragility fracture, physical inactivity

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69
Q

Conditions that can cause osteoporosis

A
  • Turner syndrome
  • Hyperprolactinaemia
  • Cushings
  • DM
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70
Q

How does peak mass relate to osteoporosis

A

A higher peak bone mass is protective. At 25ish we have peak bone mass then begin losing bone

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71
Q

Signs and symptoms of osteoporosis, and most common fracture

A

Usually ASYMPTOMATIC TILL fracture! If symptoms likely to be something else.

  • Easy fragility fracture
    Most common:
  • Vertebral crush fracture
  • Distal radius/ Colles fracture (wrist)
  • Proximal femur/Femoral neck

In vertebral crush:
- Patient will have hunched posture (kyphosis), back pain and height loss (>4cm)

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72
Q

What are the types of osteoporosis

A

Type 1- Postmenopausal: Decreased oestrogen causes increased bone resorption

Type 2 - Senile: osteoblasts lose ability to form new bone.

Type 3 - Secondary: to coexisting condition

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73
Q

Scoring tool used in osteoporosis

A

FRAX Tool - Risk calculator for fragility fracture in next 10 years

Age, sex, weight, height, previous fracture, smoking, glucocorticoids, alcohol >3 units/day, femoral neck BMD.

If risk low, reassure
if intermediate - offer DEXA and recalculate
If high - Offer treatment

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74
Q

Investigations in osteoporosis

A

FRAX tool conducted first.

DEXA scan (Dual Energy Xray Absorptiometry) - measures bone mineral density. Usually measured at hip

Provides 2 readings;
- Z score - number of SDs patients BMD falls below mean for their age
- T score - number of SDs patients BMD falls below mean for young healthy adult

T score
>-1 - normal
-1 to -2.5 - Osteopenia
<-2.5 - Osteoporosis

Ca2+, phosphate and ALP should all be tested (and appear normal unless underlying cause)

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75
Q

Lifestyle management of osteoporosis

A

Activity/exercise
Maintain healthy weight
Stop smoking/alcohol
Adequate calcium/vit D
Avoid falls

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76
Q

Pharmacological management of osteoporosis

A

Bisphosphonates first line
- E.g. alendronate

If bisphosphonate CI
- Teriparatide (recombinant PTH)
- HRT (Testosterone/Oestrogen)
- Denosumab
- Raloxeifene

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77
Q

What are some side effects of bisphosphonates

A
  • Reflux/oesophagitis
  • Osteonecrosis of jaw
  • Osteonecrosis of external auditory canal
  • Oesophageal ulcers
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78
Q

How should bisphosphonates be taken

A

To be given on empty stomach, first thing in the morning with a full glass of water. Stay upright for 30 mins after taking and dont eat or drink for 30 mins after.

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79
Q

How is osteoporosis monitored

A

Follow up in 5 years if no treatment

On treatment, FRAX/DEXA in 3-5 years. Come off treatment if BMD improves with no fragility fracture

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80
Q

Define Osteomalacia

A

Metabolic bone disease caused by incomplete mineralisation of underlying osteoid. This causes softening of bone and results in rickets in children.

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81
Q

Risk factors for osteomalacia

A

Limited sunlight exposure
Vit D deficiency
Calcium deficiency
Phosphate deficiency
Malabsorption
CKD
Dark skin

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82
Q

Pathophysiology of osteomalacia

A

Usually due to Vit D deficiency, which can be due to reduced sunlight exposure, poor nutrition, malabsorption, liver/renal failure.

83
Q

Signs/symptoms of osteomalacia

A

Skeletal deformities
Waddling gait
Underlying hypocalcaemia/related signs
Bone pain
Muscle weakness and spasms

84
Q

Investigations in osteomalacia

A

Vit D, Calcium and phosphate - Low
ALP, PTH - High

GOLD - Iliac bone biopsy with double tetracycline labelling

85
Q

Management of osteomalacia

A

Correct vit D deficiency

Usually, large loading regime then smaller lifelong maintenance

86
Q

Define seronegative spondyloarthropathy

A

Inflammatory rheumatic conditions that cause arthritis. These conditions are:
- Rheumatoid factor negative (Seronegative)
- HLA-B27 associated
- Asymmetrical
- Often affect axial skeleton (spine/sacroiliac joints)

87
Q

What are the common spondyloarthropathies

A

Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Enteric arthritis

88
Q

What is the current theory of pathophysiology of spondyloarthropathies

A

Molecular mimicry
Infection triggers immune response against infectious agent that his peptides similar to HLA-B27 proteins. Hence, autoimmunity against HLA-B27 proteins

89
Q

Common spondyloarthropathy features (mnemonic)

A

SPINEACHE
Sausage digit (Dactylitis)
Psoriasis
Inflammatory back pain
NSAIDs work well
Enthesitis (inflammation where tendon joins bone, usually in heel - plantar fasciitis)
Arthritis
Crohns/Colitis/elevated CRP
HLA-B27
Eye (Uveitis)

90
Q

Common extra-articular manifestations of spondyloarthropathies

A

Iritis
Uveitis
Psoriaform rashes
Oral ulcers
Aortic valve incompetence
IBD

91
Q

Define ankylosing spondylitis

A

Progressive inflammation of spine, sacroiliac joints and vertebral column causing abnormal stiffening due to syndesmophyte formation

92
Q

Pathophysiology of ankylosing spondylitis

A

HLA-B27 codes for a MHC class 1 molecule which sits on outside of most cells.

Key affected joints are sacroiliac joints of vertebral column. Enthesitis occurs, which heals with new bone (syndesmophyte) formation. This can progress to fusion of the spine and sacroiliac joints, causing “bamboo spine”.

Can progress to kyphosis, neck hyperextension and spino-cranial ankylosis

93
Q

Signs/symptoms of ankylosing spondylitis

A

Typical presentation is young male with gradual onset pain and stiffening of lower back.
- Pain/stiffness is worse during night/in morning but better with exercise
- Eye irritation/photophobia/blurred vision
- Chest pain

94
Q

Extra-spinal manifestations of ankylosing spondylitis

A

Normocytic anaemia
Iritis
Uveitis
Dactylitis
Costochondritis
Aortitis
Enthesitis
Weight loss
Fatigue
Pulmonary fibrosis

95
Q

Investigations in ankylosing spondylitis

A

X ray - BFSSS
- Bamboo spine
- fusion of facet, sacroiliac and costovertebral joints
- Syndesmophytes
- Squaring of vertebral bodies
- subchondral sclerosis and erosions

MRI - May show bone marrow oedema and erosion of joint spaces

High ESR/CRP, HLA-B27 positive, normocytic anaemia may be present

96
Q

What test can be conducted on examination for ankylosing spondylitis

A

Schober’s test - Assess spine mobility

Have patient stand. Locate L5 vertebrae. Mark 10cm above and 5cm below. Ask patient to bend forward as far as possible and measure distance between 2 points. <20cm distance = reduced lumbar movement.

97
Q

Management of ankylosing spondylitis

A

1st line - NSAID (Naproxen, ibuprofen)
Steroids (Oral/IM) in flares
Anti TNF (Infliximab)

(main complication is vertebral fractures + extra articular manifestations - CBA to make new card lol)

98
Q

Define reactive arthritis

A

Reactive arthritis (Reiter’s syndrome) refers to synovitis following a infection in other part of body.

Most commonly gastroenteritis or STIs. Affects men 30-50x more than women

99
Q

Causes of reactive arthritis

A

STI
- Chlamydia
- Gonorrhoea

Gastroenteritis
- Salmonella
- Shigella
- Campylobacter
- Yersinia enterocolitica

100
Q

Signs and symptoms of reactive arthritis

A

“Cant see, pee, climb a tree” Urethritis, arthritis (of lower leg), conjunctivitis

Acute, asymmetrical monoarthritis, typically of lower leg.
- Warm swollen join
- Keratoderma blennorhagica
- Mouth ulcers

101
Q

Investigations of Reiter’s syndrome

A

“Hot joint” policy - assume warm swollen joint is septic
- Joint aspiration - Culture and gram stain. Should show no organism, excludes differential (Septic arthritis).
- ESR/CRP raised
- RF/ANA negative

Sexual health review/stool test will be diagnostic of underlying cause

X ray:
- Enthesitis
- Sacroiliitis with periosteal reaction

102
Q

Management of Reactive arthritis

A

Give antibiotics and aspirate joint
NSAID, Steroids
Methotrexate

103
Q

Define psoriatic arthritis

A

Chronic inflammatory joint disease associated with skin psoriasis

104
Q

Types of psoriatic arthritis

A

Asymmetrical Oligoarthritis - asymmetrical, less than 5 joints

Symmetrical polyarthritis (rheumatoid like) - symmetrical, more than 5 joints. Hands wrists, ankles DIP joints (RA has PIP involvement)

Spondyloarthritis - Spine and sacroiliac joints involved

Distal Interphalangeal Arthritis - Only affects DIPs of fingers and toes, causes dactylitis

Athrtitis mutilans - Most severe, osteolysis of bones around joints in digits, shortening of the digit. “telescopic finger”

105
Q

Signs/symptoms of psoriatic arthritis

A
  • Joint warmth, tenderness, reduced range of motion.
  • Typically affects DIP, as opposed to MCP/PIP in rheumatoid arthritis
  • Joint pain/stiffness
  • Psoriasis: Psoriatic lesions, scalp/nail symptoms (another card)
  • Telescopic finger in arthritis mutilans

Skin signs usually present before arthritis

106
Q

Signs/symptoms of psoriasis

A
  • Dry flaky scaly skin lesions
  • Auspitz sign (small bleeds on scratching)
  • Koebner phenomenon (psoriatic lesions to areas of trauma)

Nail signs
- Nail pitting
- Nail thickening
- Discolouration
- Ridging
- Onycholysis (Separation of nail from bed)

107
Q

Investigations in psoriatic arthritis

A

Bloods - Negative for RF and anti CCP

X ray
- Periostitis
- Pencil in cup appearance
- Ankylosis
- Dactylitis
- Osteolysis

108
Q

What criteria can be used to diagnose psoriatic arthritis

A

CASPAR - 2+ can be enough to diagnose PA

History of psoriasis +2 (rest are +1)
Rheumatoid factor negative
Psoriatic nail changes
History of dactylitis
Juxta-articular periostitis/Radiological evidence

109
Q

What screening tool is used in psoriatic arthritis and when is it used

A

PEST (Psoriasis Epidemiological Screening Tool) used to screen for psoriatic arthritis in psoriasis patients
- Joint pain
- Swelling
- Arthritis
- Nail pitting

110
Q

Management of psoriatic arthritis

A

First line: NSAIDs and physiotherapy
DMARD
Ustekinumab (treats psoriasis!)
Emollients/topical steroids

111
Q

Complications of psoriatic arthritis

A

CVD (Increased risk)
Aortitis
Amyloidosis
Conjunctivitis
Uveitis

112
Q

Patient with reactive arthritis gets dermatitis at head of penis what is this called?

A

Circinate balanitis

113
Q

Define Enteropathic arthritis

A

Arthritis in patients with IBD symptoms/Coeliacs

E.g. patient presents with IBD symptoms, rash and joint pain could indicate enteropathic arthritis

114
Q

Investigations and treatment of Enteropathic arthritis

A

Arthrocentesis
Stool culture and blood (FIT)
Colonoscopy

Treated with DMARD

115
Q

Define SLE with epidemiology

A

Systemic Lupus Erythematous

Type 3 hypersensitivity reaction (antigen-antibody complex deposition), causing systemic autoimmune inflammation

Typically affects females in reproductive years (high oestrogen), Afro-Caribbeans and Asians.

116
Q

Risk factors and environmental triggers of SLE

A
  • 15-45 year old woman
  • Afro-Caribbean descent
  • Family history
  • HLA association

Environmental triggers
- UV light
- Smoking
- Oestrogen
- EBV
- Drugs such as isonazid, hydralazine

117
Q

Pathophysiology of SLE

A

Trigger such as UV light causes cell death, creating apoptotic bodies with exposed DNA. Due to genetic factors, immune system recognises these as foreign, creating antibodies against them (anti-dsDNA). Anti-Nuclear Antibodies (ANA) also produced. These antibodies bind to their antigens, forming antigen-antibody complexes which deposit around the body. Cause inflammation through compliment system on site of deposition.

Patients can also get antibodies targeting RBCs, WBCs. These kill these cells. This is a type 2 hypersensitivity reaction

118
Q

What are the 4 types of hypersensitivity reaction

A

Type 1 - IgE antibodies, initially sensitise person to allergen before providing a quick inflammatory response on next exposure (Allergy/anaphylaxis)

Type 2 - IgG IgM antibodies bind to cell surface inducing a cascade of events leading to cell death

Type 3 - Antigen-antibody complexes are formed that deposit around body. Immunity against these causes inflammation, damaging underlying tissue. (SLE, RA)

Type 4 - T cell mediated. Delayed reactions to antigens. (chronic asthma, contact dermatitis)

119
Q

What is the classic presentation of SLE

A
  • Malar “butterfly” rash (across cheeks but not nose)
  • Fatigue
  • Fever,
  • Widespread
  • Musculoskeletal pain
  • Lymphadenopathy and splenomegaly

In a middle aged, African female.

Disease follows relapsing-remitting course

120
Q

Systemic effects of SLE

Skin
Pulmonary
GI
Kidney
+ random ones
(Probs dont need to know all of these but good to go over them every now and then)

A

Skin: Malar rash, Discoid Rash, Photosensitivity, Raynaud’s phenomenon

Pulmonary/CV: pleurisy, interstitial lung disease, pericarditis, heart block.

GI: lupus peritonitis, mesenteric artery occlusion

Kidney: Nephritis

AHA (Type 2 reaction!)
Pancytopenia
Antiphospholipid syndrome
Mouth ulcers
Sjogrens syndrome!

121
Q

Investigations in SLE

A

FBC - Anaemia (potential pancytopenia)
ESR raised but CRP usually normal
C3/C4 low as has been used up in complex formation

Urinalysis - Proteinuria + haematuria (Nephritis)
X ray for athralgia, CXR for resp symptoms

Antibodies
- ANA - Sensitive
- Anti dsDNA - Specific
- Anti Smith (targets ribonucleoproteins) - Very specific
- Anti-histone- if drug induced
Anti-Ro, Anti-La - Sjogrens

122
Q

Antibodies in SLE

A

ANA - Sensitive
Anti-dsDNA - Specific
Anti-Smith - most specific but low sensitivity
Anti histone - Drug induced
Anti-Ro, Anti-La - Sjogrens

123
Q

Treatment of SLE

A

Acute therapy then maintenance

Acute
Mild - Prednisolone + hydroxychloroquine + NSAID
Moderate/severe - Prednisolone + Hydroxychloroquine + immunosuppressant (methotrexate, azathioprine)

Maintenance:
- Reduce flare up dose
- Then switch exclusively to hydroxychloroquine

124
Q

Sjogren’s syndrome definition

A

Autoimmune condition affecting exocrine glands, leads to dry mucous membranes (dry eyes, mouth, vagina)

Can be primary or secondary to rheumatoid arthritis or SLE

HLA-B8 / HLA-DR3 association

125
Q

Symptoms of Sjogrens

A

Dry mucous membranes

Dry eyes (keratoconjunctivitis)
Dry mouth (Xerosomia)
Dry vagina
Dry skin

126
Q

Tests and examination for Sjogrens

A

Antibodies - Anti Ro, Anti La

Schirmer test - strip of filter paper left under eyelid for 6 mins, moisture distance measured. Tears should travel 15mm in healthy young adult, less than 10 significant.

127
Q

Management of Sjogrens

A

Pilocarpine - increases exocrine secretion
Hydroxychloroquine
Artificial tears saliva and lubricant

128
Q

Define vasculitis

A

Group of autoimmune conditions that cause inflammation of the blood vessel walls. Can be primary (autoimmune) or secondary to SLE, RA, hepatitis, HIV, polymyositis. Affect small, medium and large vessels.

129
Q

Types of vasculitis

A

Large vessels:
- Giant cell arteritis ☆
- Takayasu’s arteritis

Medium vessels:
- Polyarteritis nodosa ☆
- Kawasaki disease

Small vessels (capillaries/arterioles)
ANCA +ve
- Wegener’s granulomatosis (granulomatosis with polyangiitis) ☆
- Eosinophilic granulomatosis with polyangiitis
- Microscopic polyangiitis

ANCA -ve
- Henoch-Schonlein purpura

(the ones with stars are covered in more detail)

130
Q

Define Giant cell arteritis

A

Temporal arteritis, affects branches of the carotid artery. Most common vasculitis. Often associated with polymyalgia rheumatica.

131
Q

Pathophysiology of GCA

A

Granulomatous vasculitis of large/medium arteries. Arteries become inflamed, intima is thickened and vascular lumen is narrowed. Usually cerebral (temporal) arteries affected:
- Superficial temporal artery: Headache/scalp tenderness
- Mandibular artery: jaw claudication
- Ophthalmic artery: visual loss (retinal ischaemia)

132
Q

Signs/symptoms of GCA

A
  • Severe unilateral headache around temple/forehead
  • Diminished/absent temporal artery pulse
  • Reduced visual acuity
  • Optic disc pallor
  • Scalp tenderness (painful to comb)
  • Jaw claudication
  • Blurred/double vision

Fever, muscle aches, weight loss, loss of appetite

Complete loss of sight is an emergency

133
Q

GCA typical presentation

A

50+ white female with unilateral temple headache, scalp tenderness (painful to comb), jaw claudication and vision changes.

134
Q

Investigations in GCA

A

ESR/CRP high
Normocytic anaemia

Duplex ultrasound
- Halo sign of temporal artery

Temporal artery biopsy GOLD
- Presence of granuloma (multinucleated giant cells)
- Intimal thickening and narrowed lumen
- Large biopsy should be taken as lesions are skip lesions.

135
Q

Diagnostic criteria in GCA

A

3 of:
- Over 50
- New headache
- Temporal artery tenderness/diminished pulse
- ESR Raised
- Abnormal temporal artery biopsy

136
Q

Management and possible complications of GCA

A

High dose prednisolone

  • Sight loss (amaurosis fugax!)
    Should be dealt with ASAP or could lead to permanent blindness
  • Ischaemic cranial complications (Visual loss/stroke)
  • Aortic aneurysm
137
Q

In cases where long term steroids are given, what 2 systems should be protected and how is this done?

A

GI (stomach and oesophagus) and Bones
- PPI (omeprazole)
- Alendronate (bisphosphonate)
- Ca2+ and vitamin D

138
Q

Rules in patients taking steroids

A

DONT STOP
Dont - Stop taking abruptly; due to adrenal crisis risk
S - Sick day rules (Take extra when unwell - prevent adrenal crisis)
T - Treatment card given to patient (if dose above 100mcg a day)
O - Osteoporosis and oesophagitis prevention with PPI Calcium and vit D
P - PPI for gastric protection

139
Q

Define polymyalgia rheumatica

A

Condition that causes pain stiffness and inflammation in neck, shoulders and hips. Limits range of motion. Occurs alongside GCA often.

Morning pain/stiffness in shoulders etc. Leads to fatigue, fever, weight loss, anorexia and depression

Managed with prednisolone

140
Q

Define Takayasu’s arteritis

A

The other large vessel vasculitis.
- Affects branch points of aortic arch, leads to weak or no pulse. If it affects branches serving head, can cause visual and neurological symptoms.
- Asian women under 40
- Weak/absent pulse and arm claudication + systemic symptoms

141
Q

Give the types of medium vessel vasculitis

A
  • Polyarteritis Nodosa (Hep B associated, affects skin, GI tract, kidney, heart supplying vessels)
  • Kawasaki disease (Affects coronary arteries, usually boys under 5 with Japanese descent)
142
Q

Define polyarteritis nodosa

A

Hep B associated inflammation of several arteries as a result of body confusing hep B infection and fighting vessels as a result. Typically affects skin, GI tract, kidneys, heart.

  • Causes range of symptoms including skin ulcers, renal failure (haematuria, HTN, proteinuria), neurological symptoms.
  • Renal angiogram: String of beads pattern
  • Biopsy: Transmural fibrinoid necrosis and inflammation.
143
Q

Define Kawasaki disease

A

Coronary artery medium vessel vasculitis affecting japanese boys under 5.
CRASH
- Conjunctivitis
- Rash (which peels)
- Adenopathy (lymph nodes enlargened)
- Strawberry tongue
- Hands and feet (swollen and rashy)

Treated with IV immunoglobulins and aspirin

144
Q

Define Wegners granulomatosis

A

AKA Granulomatosis with polyangiitis

Necrotising granulomatous inflammation of many small and medium sized vessels at once.

Affects ears, nose, kidneys, sinuses, lungs

145
Q

Pathophysiology of Granulomatosis with polyangiitis

A

B cells release cANCA (Cytoplasmic Anti-Neutrophilic Cystoplasmic antibodies) which target the granules of the hosts own neutrophils. Causes them to release free radicals.

Affects nasopharynx, lungs and kidneys

146
Q

Signs and symptoms of Granulomatosis with polyangiitis

A

Nasopharynx
- Chronic pain from sinusitis
- Nose bleeding (epsitaxis)
- Saddle shaped nose

Lungs
- SOB, cough, wheeze
- Bloody cough

Kidneys
- Proteinuria
- Haematuria
- HTN

147
Q

Investigations in Granulomatosis with polyangiitis

A

cANCA positive
ESR CRP raised
Urinalysis to look for proteinuria and haematuria

CXR may show fluffy infiltrates of pulmonary haemorrhage and nodules.
Renal biopsy will show granulomatous inflammation on vessel walls

148
Q

Management of Granulomatosis with polyangiitis

A

Steroids and cyclophosphamide (immunosuppressant)

Methotrexate for maintenance

149
Q

Complications of Granulomatosis with polyangiitis

A

Glomerulonephritis!
Relapse as cANCA still present
Pulmonary fibrosis

150
Q

Main differentials of Granulomatosis with polyangiitis

A

Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss Syndrome)

  • High eosinophils on FBC
  • Presents as severe asthma, doesnt affect kidneys
  • p-ANCA present
  • Treated with ICS

Microscopic polyangiitis
- Doesnt affect nose, only lungs and kidney
- No granuloma, pANCA present

151
Q

Define Henoch-Schonlein purpura

A

Small vessel vasculitis in kids under 10.
No ANCA involvement
Purpuric rash on buttocks and thighs as well as joint pain, haematuria, abdominal pain.

Treated supportively

152
Q

Normal pain conduction

A

Pinprick will cause nociceptors to generate electrical signal. This goes to dorsal root ganglion, which releases substance P. This binds to 2nd order neuron.
Inhibitory neurons in dorsal horn dampen pain response by releasing serotonin and Nad.
If nociceptor signal greater than inhibition, AP fired
Mast cells release NGF which boosts growth of nociceptors, more pain.

153
Q

Define fibromyalgia

A

Syndrome characterised by widespread pain, sleep disturbances, fatigue and depression. (Essentially MSK equivalent of IBS)

154
Q

Pathophysiology of fibromyalgia

A

Hypersensitivity to pain, due to excess substance P and NGF or low serotonin.

More common in females 20-60 years, with low socioeconomic status. Associated with RA, SLE etc.

155
Q

Key presentation of fibromyalgia

A

Woman with chronic (>3 months) severe pain all over, cant sleep, depressed and stressed.
Pain aggravated by stress, cold, activity

156
Q

Investigations in fibromyalgia

A

All tests normal, done to exclude
TFT (hypothyroid), ANA/dsDNA (SLE), ESR/CRP (Inflammation), Vit D (Deficiency), RF and anti-CCP (exclude RA)

157
Q

Diagnostic criteria of fibromyalgia

A

Chronic pain >3 months
Widespread pain all over (left and right sides, above and below waist)
On digital palpation of tender points, mild pain in at least 7 areas, and severe in at least 5

158
Q

Management of fibromyalgia

A

Regular exercise, physiotherapy, CBT

Amitriptyline (increase serotonin levels)

159
Q

Define antiphospholipid syndrome

A

Disease of excess clotting associated with antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibody and anti-beta2-glycoprotein 1), as well as excess thromboses and miscarriage

Can occur on its own or secondary to autoimmune conditions such as SLE

160
Q

What do antiphospholipid antibodies cause

A

CLOT
Coagulopathy
Livedo reticularis (purple discolouration of skin)
Obstetric issues (recurrent miscarriages etc)
Thrombocytopenia (low platelet)

161
Q

Antibodies involved in antiphospholipid syndrome

A

Lupus anticoagulant antibodies
Anti-cardiolipin antibodies
Anti-beta-2 glycoprotein 1 antibodies

162
Q

Signs of antiphospholipid syndrome

A

Thrombosis
Miscarriage
Purple skin (livedo-reticularis)
Thrombocytopenia

(Ischaemic stroke TIA MI (Arteries)
DVT, PAD, Budd-Chiari syndrome (Veins))

163
Q

Management of Antiphospholipid syndrome

A

Warfarin to minimise thrombosis (CI if pregnant)

If pregnant, LMWH and Aspirin

164
Q

Define polymyositis (and Dermatomyositis)

A

Autoimmune inflammation and necrosis of skeletal muscle. Where skin is involved this becomes dermatomyositis

HLA B8
HLA DR3

165
Q

Signs and symptoms of polymyositis and dermatomyositis

A

Bilateral muscle pain, fatigue and wasting
Proximal muscles (shoulders/hips) most affected
(Difficulty squatting or raising hands above head)

Skin:
- Gottron Lesions - Scaly, red patches on backs of fingers elbows and knees. PHOTOSENSITIVE, itchy, painful, bleeds.
- Heliotrope rash
- Periorbital oedema
- Subcutaneous calcinosis

166
Q

Investigations in polymyositis and dermatomyositis

A

Antibodies:
- Anti-Jo-1: Polymyositis
- Anti-Mi-2: Dermatomyositis

Creatinine Kinase (enzyme found in muscle cells) - Raised
(aldolase and LDH also raised)

Muscle biopsy GOLD: Inflammatory cell infiltrates

167
Q

Other causes of raised creatinine kinase

A

Rhabdomyolysis
AKI
MI
Statin use
Strenuous exercise

168
Q

Management of polymyositis and dermatomyositis

A

Corticosteroid (prednisolone)
Hydroxychloroquine if skin rashes

Immunosuppressants if other treatment doesnt work

169
Q

Define scleroderma

A

Multisystem, autoimmune disease characterised by fibrosis of skin and visceral organs

  • Sclerqoderma - hardening of skin
  • Systemic sclerosis - when it affects rest of body and visceral organs as well

CREST used for symptoms

170
Q

Both types of scleroderma

A

Limited Cutaneous Systemic Sclerosis (Most common) - CREST features and Raynaud’s Phenomenon early

Diffuse Cutaneous Systemic Sclerosis - CREST and other internal organs

171
Q

Signs/symptoms of scleroderma

A

CREST
- Calcinosis (deposits in skin, esp hands) - Renal Failure!!
- Raynaud’s (fingers go white then blue in response to mild cold, due to vasoconstriction)
- oEsophageal dysmotility - Dysphagia, acid reflux, oesophagitis
- Sclerodactyly and scleroderma (skin tightening and hardening, restricts motion and causes fingers to be clawed)
- Telangiectasia - Dilated small blood vessels with thin, thready appearance.

Beaked nose, small mouth, pulmonary HTN, fibrosis and heart failure possible

172
Q

Investigations in scleroderma

A

FBC - Anaemia, high Urea/Creatinine due to AKI

Autoantibodies
- Anti-centromere: Limited (MC)
- Anti-SCL 70: Diffuse
- ANA (positive but non specific)

X Ray - Calcinosis

Barium swallow - Impaired oesophageal motility

CT chest to check for fibrotic lung

173
Q

Management of scleroderma

A

No cure, can just help symptoms

Raynauds - Hand warmers, CCB (to allow vasodilation)
Immunosuppression
PPI for oesophagus
ACEi to prevent renal crisis
Analgesia

174
Q

Complications of scleroderma

A
  • Skin ulcers
  • Hypothyroid
  • Osteomyelitis
  • Malabsorption
  • Digital amputation
175
Q

What cancers metastasise to bone

A

BLKTP

Breast
Lung
Kidney
Thyroid
Prostate

BL - Osteolytic
KTP - Osteosclerotic

176
Q

Name 4 primary bone tumours

A

Osteosarcoma - Bone cancer, associated with Pagets!
Ewing sarcoma - Mesenchymal stem cell
Fibrosarcoma
Chondrosarcoma - Cartilage cancer

(Primary less common, more common are secondary)

177
Q

General local and systemic signs and symptoms of bone cancer

A

Local
- Severe, deep pain worst at night
- Fractures
- Decreased range of motion of long bones/vertebrae

Systemic
- Weight loss
- Fatigue
- Fever
- Malaise

178
Q

Investigations in bone cancer

A

Skeletal isotope scan
X ray - Osteolysis, metastasis etc
Increased ALP alone!
Hypercalcaemia

179
Q

How does bone remodelling work

A

Osteoblasts release RANKL which binds to osteoclasts and activates them

Osteoclasts resorb bone by secreting lysosomal enzymes e.g. collagenase and HCl, digesting collagen and dissolving minerals in bone matrix

Osteoblasts secrete osteoprotegerin which stops activity of osteoclasts by binding to RANKL

Osteoblasts release osteoid seam which builds scaffold upon which calcium and phosphate can get deposited on, forming new bone

180
Q

Define Paget’s disease

A

Chronic increased bone remodelling, resulting in overgrowth of poorly organised bone.

Also known as Osteitis deformans

Associated with Osteosarcoma!

181
Q

Pathophysiology of Pagets

A

Phase 1 - lytic phase
- Osteoclasts with up to 100 nuclei aggressively demineralise bone

Phase 2 - Mixed (lytic and blastic)
- Blastic - rapid, disorganised proliferation of new bone tissue by large number of osteoblasts

Phase 3 - Sclerotic phase
- New bone formation exceeds bone resorption. Bone disorganised and weak.

182
Q

Signs/symptoms of pagets

A

Bone pain
Growth signs in skull
- Leontiasis
- Hearing loss/ deafness (bone narrows auditory foramen, impinge on auditor nerve)
- Vision loss
Kyphosis (spine curve)
Bowlegs (if tibia affected)
Bone enlargement

183
Q

Investigations in Pagets

A

LFT and bone profile
- ALP raised, others normal
- Calcium and phosphate normal

X ray
- Bone enlargement and deformity
- Osteoporosis circumscripta (lytic lesions in lytic phase)
- Cotton wool appearance of skull
- V shaped defects of long bones
- Thickened bone cortices

184
Q

Management of Pagets

A

NSAIDs, bisphosphonates, surgery to decompress nerve impingement, correct bone deformities

185
Q

Complications of pagets

A

Pagets sarcoma (osteosarcoma)
Spinal stenosis/spinal cord decompression
Fractures
Vision loss
Hearing loss
Arthritis
Cardiac failure

186
Q

Define Marfans

A

Autosomal dominant FB1 (fibrillin 1 protein) (chromosome 15) mutation causing defective connective tissue.

Causes fewer microfibrils, so less integrity and elasticity. TGF beta signalling excessive so excess growth in bones

187
Q

Signs/symptoms of Marfans

A

Tall stature, long arms, long legs
Long fingers
Scoliosis
Flexible joints
Stretch marks

188
Q

Investigations of Marfans

A

Diagnose based on features
- Lens dislocation
- Aortic dissection/dilation
- Dural ectasia
- Long arms, fingers etc
- Scoliosis
- Flat feet

189
Q

Complications of Marfans

A
  • Retinal detachment
  • Joint dislocations and pain
  • Bulla formation on lungs causing pneumothorax

CVD effects
- Aortic dilation
- Aortic dissection, aneurysm, rupture
- Mitral valve prolapse
- Aortic valve prolapse

190
Q

Define Ehlers Danlos syndrome with joint and skin effects

A

Group of 13 connective tissue disorders caused by mutations of connective tissue proteins, with collagen most affected.

Causes joint hypermobility, pain, dislocation and scoliosis.

Causes Hyper elasticity, Easy bruising, Atrophic skin

191
Q

Complications of Ehlers Danlos

A

Subarachnoid haemorrhage
Abdominal hernia
GORD
Degenerative arthritis

CVD
- Mitral valve prolapse
- Aortic dissection
- AAA
- Organ rupture

192
Q

Causes of mechanical back pain

A
  • Strain
  • Heavy manual handling
  • Pregnancy
  • Trauma
  • Lumbar disc prolapse
  • Osteoarthritis
  • Spondylolisthesis (vertebral disc slip)
  • Lumbar disc prolapse
  • Fracture
193
Q

Syndromes causing mechanical back pain

A

Lumbar spondylosis
Facet joint syndrome
Fibrositic nodulosis
Postural back pain/”swayback” of pregnancy

194
Q

Symptoms caused by mechanical back pain

A

Stiff back
Scoliosis
Muscular spasm
Pain worse in evening, worse with exertion
Relieved by stress and morning stiffness absent
Sudden onset
Usually self limiting

195
Q

What artery causes erectile dysfunction

A

Interior Pudendal Artery

196
Q

Define cellulitis

A

Bacterial infection of the dermal and sub-cutaneous tissues. Infection enters through break in skin and can occur anywhere but usually affects legs.

Usually caused by:
- Staph aureus
- Beta-haemolytic streptococcus (pyogenes, agalacticae)

197
Q

Risk factors for cellulitis

A

History of cellulitis
Cutaneous tissue break (ulcer, wound, puncture from IV drug use)
Immunocompromise (Diabetes, HIV, leukaemia)
Venous insufficiency
Eczema
Obesity
Pregnancy

198
Q

Where does cellulitis normally affect and spread to?

A

Typically affects lower leg or arm and spreads proximally. Other sites usually affected include abdomen, perianal and periorbital! areas.

199
Q

Signs/symptoms of cellulitis

A

Red hot painful area, typically shin
Macular erythema with indistinct borders
Shiny skin
Oedema

200
Q

Investigations of Cellulitis

A

Swab and gram stain to identify bacteria

Diagnosis is clinical

201
Q

Classification of Cellulitis

A

Eron’s classification used.
1 - no systemic toxicity
2 - Systemically unwell or comorbidity that may delay resolution (e.g. PAD)
3 - Significant systemic upset (confusion, tachycardia, hypotension)
4 - Sepsis or severe infection (e.g. necrotising fasciitis)

202
Q

Management of Cellulitis

A

Flucloxacillin first line

Co amoxiclav if periorbital or severe

203
Q

What are factors for hospital admission/IV antibiotics in cases of cellulitis?

A
  • Eron 3 or 4
  • Severely deteriorating cellulitis
  • Under 1 or frail
  • Immunocompromise
  • Facial cellulitis including periorbital
  • Lymphoedema
204
Q

Complications of cellulitis

A
  • Sepsis
  • Necrotising fasciitis
  • Lymphoedema (chronic swelling in tissues)
  • Abscess formation

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