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phase 2a mine > msk mid tier > Flashcards

msk mid tier Flashcards

1
Q

what do all autoimmune connective tissue disorders share

A
  • All linked by ANA antibody +(antinuclear antibody)
  • All relate to immunosuppression
  • Can affect any organ
  • All relate to inflammation
  • Scarring as a result
  • Damage is irreversible
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2
Q

sjorgens pathophysiology and symptoms

A

Lymphocytic infiltration → Exocrine glands (salivary and lacrimal) destroyed → fewer secretions

Symptoms

  • Dry eyes
  • Dry mouth
  • Arthritis
  • Vasculitis
  • Rash
  • Neurological
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3
Q

marfan’s symptoms

A 
Tall
Arm span greater than height
Long fingers
Lens dislocation
High arched palate (mouth)
Aneurysm -- Collagen in vessels
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4
Q

ehler danos symptoms

A

Genetic collagen defect
vascular/skeletal types
Joint hypermobility
Skin elasticity

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5
Q

which connective tissue disorders are NOT autoimmune

A

ehler danos

marfans

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6
Q

sjorgen’s

- investigations

A

Shermer’s test = paper dipped in eye

Raised ESR and immunoglobulins

Antibodies

  • antiRO
  • antiLA
  • ANA
  • RF
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7
Q

sjorgen’s treatment

A

Replace saliva and tears

Immunosuppression for systemic complications

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8
Q

scleroderma pathophysiology

A

Increased fibroblast activity → abnormal growth of connective tissue

systemic sclerosis

collagen depsotion, inflammation, autpimmune
vascular damage

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9
Q

scleroderma symptoms

A

CREST (limited disease)

  • Calcinosis = calcium deposition sub-cut (white lumps)
  • Raynaud’s (vasculopathy)
  • Esophageal dysmotility and strictures and dilated (reflux)
  • Sclerodactly = thickened skin
  • Telangiectasia = widened venules - spider naevi
\+ tight skin (restriction)
ulcers (esp digits)
watermelon belly
short history of raynauds
pulmonary hypertension

more diffuse disease

  • Rapid and widespread onset
  • Heartburn
  • Reflux oesophagitis
  • Delayed gastric emptying
  • Pulmonary fibrosis and hypertension
  • Skin involvement, also proximal - trunk
  • Raynaud’s history shorter
  • Increased risk of CV
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10
Q

scleroderma investigations

A
  • ACA anticentromere antibodies
  • ANA +
  • Spirometry and echo to detect pulmonary and arterial hypertension
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11
Q

scleroderma treatment

A
  • PPIs (GORD)
  • ACEi - prevent renal crisis
  • Vasodilators (raynauds) — CCB
  • Monitor for pulmonary hypertension
  • Treat skin oedema
  • UV protection
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12
Q

dermatomyotis
polymyotis

what is the symptoms and treatment for these both

A
  • skin rash - eyelids, knuckles(Derm)
  • muscle weakness (polymyo)
  • breathlessness (both)

steroids
immunosuppression

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13
Q

antiphospholipid syndrome =

  • pathophys
  • who
  • presentation
  • management
  • compli
A

autoimmune
arterial and venous thrombosis (antiphospholipid antibodies are hypercoaguable)

fertile-age women + if black

presentation = clot-y

management = heparin

compl = clot-y (MI,stroke, miscarriage, DVT etc)

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14
Q

primary bone tumours

  • commonness
  • age group
A

rare (secondary more com)

young patients

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15
Q

most common primary bone tumour in children / adults

A

children - osteosarcoma

adults - chrondrosarcoma

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16
Q

primary bone cancer types

A 
multiple myeloma
lymphoma
osteosarcoma
fibrosarcomas
chondrosarcome
ewings tumour
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17
Q

osteosarcoma

  • age
  • where
  • disease progression
A
  • 15-19
  • knees mainly (humerus, femur)
  • destroys bone and spreads to surrounding tissues + metastasises to lung rapidly
  • but relatively painless
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18
Q

what bloods might be interesting for bone tumours

A
  • Serum alkaline phosphatase (from bone) raised
  • Hypercalcemia occurs in 10-20% of those with metastatic malignancies
  • FBC (low something - bone makes stuff?)
  • u/e
  • PSA = prostate specific antigen. May be raised with prostatic metastases
19
Q

mirel’s score=

A

likelihood of fracture

  • based on site
  • pain
  • lesion nature (blastic, lytic, mixed)
  • lesion size
20
Q

enneking system for grading

A

for primary bone tumours

1A : low grade- intracompartmental
1B: low grade- extracompartmental
2A: high grade -intracompartmental
2B : high grade - extracompartmental 
3: metastases
21
Q

how much bone density must be lost before lytic areas to be seen

A

60%

22
Q

onion skinning

A

layers on edge - periosteum lifted off then bone calcifies sequentially

bone tumours

23
Q

sunburst spicules

A

calcification of capillaries supplying tumour

bone tumour

24
Q

codman’s triange

A

periosteum lifted off bone

bone tumour

25
Q

what does the periosteum reveal on a bone tumour scan

A
  • periosteum covers bone.
  • comes off with tumour, infection, trauma
  • indicates tumour speed of growth
  • slow – callus
  • fast – interputs process causing layers. may burst through periosteum. (onion skinning, sunburst spicules, codman’s triangle)
26
Q

secondary bone tumours

  • metastasise from where to bone
  • nature of these tumours
A 
Lungs, bronchus
Breast
Prostate - often osteosclerotic too
Rarer
- Thyroid
- kidney

osteolytic (bone resoprption via osteoclast activation by tumour cells (RANK-L binds to RANK…))

27
Q

chondrosarcoma

  • what
  • symptoms
  • where
A

cancer of the cartilage

dulll, deep pain
swollen
tender

pelvis
also - femur, humerus, scapula, ribs

28
Q

red flags for bone tumours

A
  • Suspected infection
  • Systemically unwell inc weight loss
  • Night pain / rest pain
  • – Non-mechanical
  • – Constant
  • Rapid deterioration
  • Structural deformity
  • Loss of movement/function
  • Lump present
  • – Tender, enlarging, deep to fascia, large
  • Neurological symptoms
29
Q

bone tumour presentation

A
  • tender at site
  • systemic - weight loss, malaise, fever,
  • aches, pains
  • ewing’s sarcoma can be associated with paralysis, numbness, incontinence
30
Q

primary/ secondary tumours sclerotic/lytic

A 
primary = lytic
secondary = i think depends on from where
31
Q

is a well/ill defined zone of transition more optimistic for bone tumours

A

well defined = more benign

ill defined = malignant, or could be infection

32
Q

fibromyalgia

  • age
  • gender
  • other risk factors
  • assocaited with what
  • triggers
A
  • 30-60
  • female
  • low household income, divorced, low education status
  • chronic fatigue, IBS, chronic headaches, depression
  • physical trauma, PTSD, infection, distress, hormone alteration
33
Q

fibromyalgia presentation

A
  • Chronic pain - Responds poorly to analgesia
  • Soft tissue tenderness - Usually at multiple sites
  • Depression , anxiety
  • Fatigue
  • Poor concentration
  • Sleep disturbance
  • Altered bowel habit
  • Headache
  • parasthesia
34
Q

fibromyalgia management

A
  • Address social stressors and depression
  • Education
    — Not “in their head”
    — Not destructive arthritis → exercise will not harm joint. Not degenerative like OA
  • Exercise/ strength programmes- may reduce pain and fatigue
  • CBT
  • physiotherapy
  • accupuncture
  • Tricyclic antidepressants eg amitriptyline
    may help pain and improve sleep
  • Anticonvulsants eg pregabalin, gabapenlin (If amitriptyline ineffective)
  • Dual reuptake inhibitors eg duloxetine– Good for anxiety/depression
  • Antiinflammatory ones have no use
  • analgesia but poor response
35
Q

fibromyalgia investigations

A

Examination of tender trigger points (need teens of them)

Exclude other diagnoses - all other investigations are normal

36
Q

mechanical lower back pain

  • age
  • common
  • where
A
  • 20-55
  • common
  • back :lumbrosacral. buttock/thigh
37
Q

mechanical back pain

A 
back pain - lumbrosacral
buttock/ thigh
varies with physica; activity and time
normally resolves in 6w
may persist/ relapse
38
Q

mechanical back pain management

A 
Conservative management 
- Education
- Exercise 
Analgesia
NSAIDs
Muscle relaxants
39
Q

osteomalacia treatment

A

Vitamin D replacement= calciferol

40
Q

osteomalacia symptoms

A
  • Rickets - bowed legs, knock knees
  • Proximal Muscle weakness + pain
  • Widespread bone pain (diffuse but esp hips) + tenderness
  • Bone weakness–Fractures, esp femoral neck
  • Muscle spasm and numbness – due to hypocalcaemia
41
Q

osteomalacia pathophysiology

A
  • Normal amount of bone but its mineral content is low
  • Defective mineralisation
  • Excess uncalcified osteoid and cartilage
  • Bone mineralisation needs adequate calcium and phosphate
  • so bones are soft and weak
42
Q

how does vit d play a part in osteomalacia

A

Vitamin d promotes calcium absorption in the intestines and promotes bone resorption (by increasing osteoclast number) - so more for bones

so vit d deficiency is common cause

43
Q

osteomalacia causes (inc epidemiology!)

A

Vitamin D def

  • Lack of sunlight
  • – Dark skin *
  • – Elderly *
  • – institutionalised
  • Poor diet (not enough oily fish /egg yolk)
  • Renal disease
  • Liver disease
  • Some drugs eg anticonvulsants breakdown vit D precursor

Calcium def

Phosphate def

  • GI malabsorption
44
Q

osteomalacia investigations

A

Blood

  • Low calcium and phosphate
  • Raised serum alkaline phosphatase
  • Elevated parathyroid hormone
  • Low 25-hydroxy vitamin D

Biopsy = gold standard
- Incomplete mineralisation in bone

X ray
- Psuedo fractures, low BMD, osteopenia

phase 2a mine (38 decks)

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