LOCO Revision6 Flashcards
HLA B27 is associated with
Rheumatoid arthritis
Osteoarthritis
Osteoporosis
Ankylosing spondylitis
Ankylosing spondylitis
This picture depicts
Rheumatoid arthritis
Osteoarthritis
Osteoporosis
Ankylosing spondylitis
Osteoporosis Vertebral bone with osteoporosis demonstrates decreased bone mass with fewer and narrower bony spicules.
What is the name for this sign of dermatomyositis? [1]
Gottron sign: red, thickened, scaly skin over the knuckles
This rash is likely to be sign of:
Scleroderma
Ankylosing spondylitis
Dermatomyositis
SLE
Dermatomyositis: purple rash around eye lids and face
Describe the difference in pathology of calcinosis between scleroderma and dermatomyositis [1]
systemic sclerosis: vascular hypoxia
dermatomyositis: release of calcium from mitochondria in muscle cells damaged by myopathy
Inflammation of the middle layer of the eye is a complication of:
Scleroderma
Ankylosing spondylitis
Dermatomyositis
SLE
Ankylosing spondylitis: anterior uveitis
Describe the onset of ankylosing spondylitis [5]
Onset of back discomfort before age 40
Insidious onset
Duration longer than 3 months
Associated with morning stiffness
Improvement with exercise
95% of patients with ankylosing spondylitis have which gene? [1]
HLA B27
Why is AS referred to as a seronegative spondyloarthropathy? [2]
Lack of rheumatoid factor positivity
Abscence of specific antibodies
Describe the symptoms of SLE
90% of patients have arthritis:
* symmetrical small joint polyarticular arthiritis (most common)
* jaccoud arthropathy (rare)
* avascular necrosis
Fatigue
Weight loss
arthralgia
myalgia
fever
butterfly rash: gets worse with sunlight
shortness of breath
hair loss
Describe the pathophysiology of Scleroderma [1]
Autoimmune inflammatory and fibrotic connective tissue disease: immune mediated damage to vascular stuctures and excessive synthesis and depostion of extracellular martrix like collagen.
Cause chronic fibrosis, scarring and damage to organs
Cause of condition unknown
What are the two main patterns of disease in scleroderma? [2]
Limited cutaneous systemic sclerosis / scleroderma: aka CREST syndrome
Diffuse cutaneous systemic sclerosis / scleroderma: progressive organ dysfunction due to fibrosis
Describe skin changes seen in scleroderma [8]
Pruritus (usually early)
‘Puffy’ appearance due to oedema (often seen in digits)
‘Salt and pepper’ appearance: due to hyperpigmentation and hypopigmentation
Loss of hair
Dryness
Changes to capillaries in nail bed: may only be seen with special dermatoscope (Capillaroscopy)
Atrophy of subcutaneous tissue
Ulcerations: may be seen over joints due to tight skin or on finger tips
Telangiectasia: abnormal dilation of capillary
Calcinosis: calcium deposits in the skin
Perioral skin tightening with decreased oral opening: gives rise to a ‘pursed-string’ appearance
Describe a phenomenon associated with scleroderma [1]
Raynaud phenomenon: skin colour changes that occur in the fingers and toes from vasospasm.
Desribe the characteristic features of CREST syndrome [5]
C - calcinosis: calcium deposits in the skin
R - Raynaud phenomenon
E - oEsophageal dysmotility: swallowing difficulty
S - sclerodactyly: skin thickening and hardening affecting the fingers and toes
T - telangiectasia: dilated capillaries. Usually appear on face, palms and mucous membranes
State the clinical definition of dermatomyositis [1]
Autoimmune myopathy characterised by symmetric proximal muscle weakness and rash
What is the key investigation for diagnosing dermatomyositis? [1]
Creatine kinase blood test: inflammation in the muscle cells (myositis) leads to release of creatine kinase.
Normal creatine kinase levels are 300 U/L; in dermatomyositis is usually over 1000 U/L
What are skin features of dermatoymyositis? [5]
Gottron lesions (scaly erythematous patches) on the knuckles, elbows and knees
Photosensitive erythematous rash on the back, shoulders and neck
Purple rash on the face and eyelids
Periorbital oedema (swelling around the eyes)
Subcutaneous calcinosis (calcium deposits in the subcutaneous tissue)
Which are the key joints effected by AS? [2]
Sacroiliac joint
Joints of the vertebral column
How do you treat AS?
Conventional analgesia / NSAIDs:
* Naproxen
* Ibuprofen
* Celecoxib
Convetional DMARDs: although not much evidence for
Sulphasalazine, methotrexate
Biological DMARDs
State how a usual AS patient presents
- Lower back pain and stiffness and sacroiliac pain in the buttock region.
- The pain and stiffness is worse with rest and improves with movement
- The pain is worse at night and in the morning and may wake them from sleep.
- It takes at least 30 minutes for the stiffness to improve in the morning and it gets progressively better with activity throughout the day.
Describe extra-articular manifestations of AS [3]
Anterior uveitis: inflammation of the middle layer of the eye. Typically causes unilateral eye pain and redness
Aortitis: can lead to aortic regurg
Atrioventricular block
When does reactive arthritis occur? [2]
Seronegative asymmetric arthritis following:
Urethritis or cervicitis
Infectious diarrhea (e.g. C.diffe)
Articular features of reactive arthritis? [3]
Extra-articular associations of reactive arthritis? [3]
Articular features:
* Peripheral arthritis
* Axial arthritis: inflammatory back pain
* Enthesitis and/or dactylitis
Extra-articular associations
* Bilateral conjunctivitis (non-infective)
* Anterior uveitis
* Circinate balanitis is dermatitis of the head of the penis
* Triad: arthritis, urethritis and, conjunctivitis
Which infections are the most common cause of reactive arthritis? 2[]
Chlamydia is the most common sexually transmitted cause of reactive arthritis.
Gonorrhoea commonly causes a gonococcal septic arthritis
Describe the pathophysiology of reactive arthritis [1]
How does reactive arthritis compare to septic arthritis? [1]
Reactive arthritis is where synovitis occurs in the joints as a reaction to a recent infective trigger
In reactive arthritis (unlike septic RA) there is no infection in the joint.
Reactive arthritis has a triad of which 3 symptoms? [3]
Classic triad of urethritis, conjunctivitis and arthritis
‘Can’t see, pee or climb a tree’
Which disease is depicted?
Systemic lupus erythematosus
Dermatomyositis
Scleroderma
Tendinitis
Scleroderma: Perioral skin tightening with decreased oral opening: gives rise to a ‘pursed-string’ appearance
Name this sign of scleroderma [1]
Telangiectasia: abnormal dilation of capillary
Name this sign of scleroderma [1]
Calcinosis: calcium deposits in the skin
Raynaud phenomenon is when skin colour changes that occur in the fingers and toes from vasospasm.
Which pathology is it most likely seen in ?
Systemic lupus erythematosus
Dermatomyositis
Scleroderma
Tendinitis
Scleroderma
This lady presents with puffy eyes. What disease is she most likely to have?
Systemic lupus erythematosus
Dermatomyositis
Scleroderma
Tendinitis
Dermatomyositis: Periorbital oedema (swelling around the eyes)
This is a radiography of pelvis (AP view) of a patient with ankylosing spondylitits.
Which letter shows a dagger sign
A
B
C
D
This is a radiography of pelvis (AP view) of a patient with ankylosing spondylitits.
Which letter shows a dagger sign
A
B
C
D
This is a radiography of pelvis (AP view) of a patient with ankylosing spondylitits.
Which letter shows the bamboo spine
A
B
C
D
C: continuous lateral spinal border
This is a patient with AS. What are the arrows pointing to? [1]
dagger spine
Name this sign [1]
What is it a complication of? [1]
Circinate balanitis: due to reactive arthritis
.
.
Reactive arthritis has a triad of which 3 symptoms? [3]
Classic triad of urethritis, conjunctivitis and arthritis
‘Can’t see, pee or climb a tree’
A 54-year-old woman, who is known to have systemic sclerosis, complains that her hands change colour in the cold. This is associated with severe pain. She asks if there is any medication you can prescribe.
Which of the following is a suitable first line option?
Amlodipine
Atenolol
Amitriptyline
Bisoprolol
Nifedipine
Nifedipine is a pharmacological option for Raynaud’s phenomenon
Describe the 4 types of pain [4]
Nociceptive
Inflammatory: describes the behaviour of pain signalling and transmission in the presence of an inflammatory process.
Neuropathic: describes a specific type of pain which results from damage to the signalling and transmission of neurones both within and outside of the CNS
Nociplastic: pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain
How does pain stimulus alter between damaged and healthy tissue? [1]
(e.g. if burnt yourself & touch it)
In the presence of damaged tissue, pain is percieved greater than in healthy tissue due to
Explain the peripheral mechanism of inflammation during tissue injury [4]
Release of inflammatory mediators (K+ H+ bradykinin, histamine, 5HT, nitric oxide): make membranes more unstable
Activation of arachidonic acid pathway: production of leukotrienes and prostanoids
Activation of peripheral nociception (pain enhanced in inflammation)
Modulation of primary afferents to subsequent stimulus
Describe the pain pathways in neuropathic [4]
Pain is felt somewhere else, but pathology could be more proximal
Inflamamtion / mech. pressure causes the nerve to change behaviour: cell membrane becomes unstable and fires ectopic signals.:
* Alteration in ion channel expression
* Ectopic and spontaneous discharge
* Ephaptic conduction
* Collateral sprouting at primary afferents
* Sprouting of sympathetic neurones at DRG
Describe the pain pathways in nociplastic pain:
Central Pain Sensitastion [3]
Dysfunctional Inhibitory Pathways [34]
Central Pain Sensitisation
* Spinal reorganisation, WDR
* Wind up, glutamate and NMDA receptors
* Dysfunctional central pathway (pain loop)
Dysfunctional Inhibitory pathways: when pain is functional, these pathways modulate pain. When pain is abnormally percieved these pathways are decreased
* GABA
* Opioid
* Mono-aminergic
* Cannabinoid
Explain the basic difference between nociceptive and neuropathic pain [3]
Nociceptive pain:
* due to activation of nociceptors in tissues by a stimulus (e.g. trauma or burning for acute pain; cancer or rheumatism for chronic pain)
Neuropathic pain:
* due to damage of the nerve itself (e.g. amputation, shingles)
Both can be the underlying pathogenetic mechanism for acute or chronic pain
Both can appear together – e.g. back pain
What is duration for acute pain to be diagnosed as acute pain? [1]
< 12 weeks
How can exercise help treat chronic pain? [1]
Exercise can re-write pain pathways but need patients to believe in process
Why are benzodiazepines useful for pain medication? [1]
Anti anxiolytics
Describe the ideal timing of taking analgesics to prevent pain [1]
Drugs should be taken ‘by the clock’ at regular intervals, rather than ‘on demand’ and each patient should receive tailored pain management.
What is major side effect of overdosing paracetamol? [1]
Liver damage
State 4 side effects of naproxen [4]
GI, renal, CVS and bleeding effects
Where are the sites of action of tramadol and tapentadol? [3]
CNS, Locus Coreulus, Dorsal Raphe
State the sites of action of morphine [2]
PAG, spinal cord
