Fichas
MDEMO 2
Fichas del conjunto (200)
- 1epidemiology of sjogrens syndromeWomen:men 9:1. Mainly presents in 4th and 5th decades.
- 2Which autoantibodies are associated with sjogrensMost common associations are with anti-Ro (SSA) and anti-La (SSB) Not specific to sjogrens (also seen in SLE), correlate with earlier onset and more aggressive disease.
- 3What are the genetic factors in sjogrens?In caucasians, HLA-DR3 has been found in over 50% of sufferers, although this is less strong in other ethnic backgrounds.
- 4Describe the pathophysiology and histology of sjogrensPostulated that genetically predisposed individuals may become exposed to an environmental trigger such as a virus, which then initiates the autoimmune process. Patients with sjogrens are known to have b lymphocyte hyperreactivity and their serum often shows high levels of circulating Abs. Histologically, affected organs show a lymphocytic infiltration which leads to progressive functional disability, although molecular studies have shown that both B and T cells contribute to this.
- 5What is the initial presentation of sjogrensMay be insidious, patients complaining of dry, gritty eyes, difficulty swallowing foods and problems with teeth or dentures. As disease progresses, evidence of other organ involvement may become apparent. When secondary sjogren's occurs in the context of RA, extraglandular features are uncommon, and symptoms are usually restricted to eyes and mouth.
- 6What are the clinical manifestations of sjogren's syndrome?1) general - fever, malaise
2) glandular - xerostermia, dental caries, parotid gland enlargement, keratoconjunctivitis sicca, corneal ulceration, dry vagina, dysparuenia
3) MSK - arthralgia, arthritis, myalgia
4) skin -raynaud's, palpable purpura (cutaneous vasculitis)
5) kidney - interstitial nephritis, renal tubular acidosis and renal stones
6) lung - interstitial lung disease
7) lymphoreticular - splenomegaly, lymphadenopathy, lymphoma - 7What is schirmer's test a and what may it be used for?Strip of paper placed underneath lower eyelid and left for five mins. Less than 5mm of moisture strongly suggestive of decreased tear secretion, which may indicate sjogrens (not definitely).
- 8What special investigations may be used in sjogrens?-Schirmer test
-Rose bengal stain - placed in conjunctival sac, damaged corneal epithelium takes up the stain, visible under slit lamp.
-sialography - measuring the anatomy of major salivary gland ducts using radiographic contrast. Gold standard in minor salivary gland biopsy, which will reveal characteristic lymphoicytic infiltrates.
- - 9Which lab features are associated with sjogren's?-Anaemia of chronic disease
-raised ESR (although not normally raised CRP)
- usually raised gammaglobulin levels. -Various autoantibodies may be found - 10Treatment of sjogren's;s1) sicca - artificial tears
2) xerostomia - artificial saliva, lozenges, pilocarpine, oral hygiene
3) dyspareunia - lubricant jelly
4) major organ involvement - glucocorticoids - 11Describe the association between sjogren's and malignancyPatients with sjogrens have a 40 fold relative risk of developing a lymphoid malignancy, usually b cell.
- 12What is scleroderma?Represents a group of disorders characterised by development of hardened sclerotic skin. Multisystem, involvement of internal organs such as lungs and GI tract is common. Raynaud's is often a presenting feature.
- 13Epidemiology of sclerodermaFemale:male 3:1. Certain environmental pollutants have been implicated in the development of a scleroderma like illness, namely silica, epoxy resins, vinyl chloride.
- 14Describe the pathophysiology of sclerodermaInflammation not normally a feature. Overproduction of CT, notably collagen, with fibrosis and widespread microvascular damage. The microvascular changes are of considerable importance, as they account not only for raynaud but also for affected internal organs.
- 15Describe the histology of sclerodermaHistologically, there is a narrowign of the digital arteries with intimal hyperplasia and endothelial damage, which results in platelet activation and the release of potent vasoconstrictors such as 5-HT and thromboxane A2. The accumulation of ECM, particularly type I and type III collagen accounts for the finding of tightened skin.
- 16Describe CREST syndromeTends to be a more benign disease than its diffuse counterpart (scleroderma) with less widespread skin involvement and less rapidly progressive internal organ involvement.
1) calcinosis - subcut deposits of calcium which can be painful and ulcerate
2) Raynaud's
3) oesophageal dysmotility - GI involvement can be widespread, but generally limited to this. Pts may complain of dysphagia and heartburn due to reflux oesophagitis. Barium swallow used to diagnose.
4) sclerodactyly - thickening of the skin of the fingers, with consequent loss of finger pulp and associated flexion contractures.
5) talengectasia - 17What lab results are seen in scleroderma-normocytic, normochromic anaemia (chronic disease)
-95% will have positive ANA, often anticentromere or anti-Scl-70 antibodies.
-pulmonary function tests may show a restrictive pattern with reduced gas transfer
-echo may reveal right sided dilation consistent with pulmonary HTN.
-Barium swallow - 18Treatment of sclerodermaNo agents can slow disease progression. Given the microvascular complications, stopping smoking is extremely important.
-Accelerated HTN (scleroderma renal crisis) should be treated aggressively with ACE inhibitors, as this carries poor prognosis.
- - 19Aetiology of dermato/polymyositis-Genetic studies have shown association with HLA-DR3 and DRw52.
-Certain environmental factors have also been implicated: 1) in childhood cases, onset more common in winter and spring, and certain viruses eg influenza, coxsackie and echo have been shown. They are able to produce a myositis like syndrome. - 20Which drugs can cause myositis?-statins
-D-penicillamine
-chloroquine - 21What is the histology of myositis?1)Damage and necrosis of myocytes
2) inflammatory cell infiltrate, mainly lymphocytes and macrophages
3) atrophy of myocyte
4) replacement with fibrosis and fat - 22What autoantibodies are associated withAnti-Jo most frequently identified, correlates with high incidence of itnerstitial lung disease.
The disease is often called anti synthetase syndrome, because Jo-1 is a type of anticytoplasmic aminoacy-tRNA synthetase enzyme. - 23What is the hallmark clinical feature of poly/dermatomyositis?Painless proximal muscle weakness. Patients complain difficulty getting out of a chair. With more advanced disease, pharyngeal musculature may result in difficulty swallowing, whilst exertional dyspnoea may result from respiratory muscle weakness. d
- 24What are the clinical features of poly/dermatomyositis?1) general - fatigue
2) MSK - myositis, joint pains
3) cutaneous - heliotrope rash, gottron's papules, calcinosis (especially in childhood), raynauds
4) respiratory - muscle weakness, aspiration pneumonitis, interstitial lung disease
5) CVS - myocarditis, conduction defects
6) pharyngeal - dysphagia. - 25What do blood test show in poly/dermatomyositis?-Acute phase response, with raised ESR or PV.
-muscle enzymes will be grossly elevated. CK is the most sensitive, and best guide to inflammation, but lactate dehydrogenase and ALT and AST may also be raised. - 26Treatment of poly/dermatomyositis?Oral pred used initially to control the inflammatory process, followed by other agents such as azathioprine or MTX as maintenence drugs. Drugs to prevent glucocorticoid nduced osteoporosis such as bisphosphonates should also be considered.
- 27What is the association between poly/dermatomyositis and malignancy?-In around 10-15% of cases, found to be an underlying neoplastic lesion within first six months of presentation.
-examples include: - adenocarcinoma of the colon
-prostate carcinoma
-ovarian tumours
-breast cancers - 28What features may be seen in vasculitis?-unexplained pyrexia with normal cultures
-high inflammatory response
-unexplained weight loss
-unusual rashes (especially ulceration and palpable purpura)
-new onset renal disease (especially microscopic haematuria)
-widespread MSK problems
-mouth ulcers, abdominal pain, bloody diarrhoea
-dyspnoea, haemoptysis
-sensory or motor loss - 29Give the classification of vasculitisLarge arteries - giant cell (temporal arteritis)
-takayasu's
Medium - polyarteritis nodosa
-kawasaki disease
Small - wegener's granulomatosis
-churg strauss syndrome
-microscopic polyangiitis
-henoch schonlein purpura
-cutaneous leukocytoclastic angiitis
Ateries and veins - behcet's
-secondary vasculitis - 30What are the clinical features ofgiant cell arteritis?A granulomatous arteritis of the aorta and its major branches, with a predeliction for the extracranial branches of the carotid. Disease of the elderly, often associated with PMR.
- 31What are the clinical features of Takayasu's arteritis?Granulomatous arteritis of the aorta and its major branches. usually occurs under age 50
- 32What are the clinical features of kawaaki disease?Usually affects infants and young children. Acute vasculitis of large, medium and small sized arteries. Often affects coronary arteries. Also known as mucocutaneous lyph node syndrome - conjunctival injection, desquamination of hands and feet, cervical lymphadenopathy, oropharyngeal changes
- 33What are the clinical features of wegener's granulomatosisNecrotising granuloma of upper and lower respiratory tract, necrotising vasculitis of capillaries, venules, arterioles and arteries. Necrotising glomerulonephritis is common. Strongly associated with antineutrophil cytoplasmic Abs (ANCA)
- 34What are the clinical features of churgg strauss syndrome?Granulatomous inflammation of resp tract, with necrotising vasculitis of small and medium sized vessels. Assocaited with asthma. Eosinophilia prominent features. Strongly associated with ANCA.
- 35What are the clinical features of microscopic polyangitis?Necrotising vascilitis of capillaries, venules and arterioles. Necrotising glomerulonephitis is very common. Pulmonary cappiliaritis (with haemorrhage) often occurs. Strongly associated with ANCA.
- 36What are the clinical features of Henoch schonlein purpura?Vasculitis of small vessels with IgA dominant immune deposits. Typically involves skin (palpable purpura), gut (abdo pain, blood diarrhoea) and glomeruli (microscopic haematuria) and is assocaited with arthritis or arthralgias.
- 37What are the clinical features of cutaneous leukocytoclastic angiitis?Isolated cutaneous small vessel vascultis, associated with immune complex deposition. palpable purpura usually seen. systemic features absent. Often caused by drug hypersensitivity or malignancy.
- 38What are the clinical features ofsecondary vasculitis?Secondary to rheumatic disease eg RA and SLE,
- 39Clinical features of GCASevere headaches and scalp tenderness, with more advancing disease - visual disturbances and jaw claudication.
- 40Lab and histology results in GCA-Show an acute inflam response - very high ESR, and temporal artery biopsy shows disruption of the elastic lamina, mononuclear ell infiltrates with formation of giant cells and granulomata.
- 41What is the most important complication of GCA?Sudden irreversible blindness due to central retinal artery occlusion.
- 42Presentation of PMRPain and intractable early morning stiffness around the shoulder and hip girdles, without obvious synovitis in the joints. Malaise, weight loss and low grade fever may also occur. Mean age of onset is 70 years and it is extremely rare under 50.
- 43Treatment of PMRModerate doses of pred will result in dramatic resolution of symptoms within 48 hours. If this does not occur then diagnosis is in doubt.
- 44Aetiology of behcet'sAssociated with HLA-B51.
- 45Clinical features of behcet's-orogenital ulceration
-rashes
-arthritis
-eye involvement (may present as a panuveitis with hypopyon). Reitnal vasculitis also occurs.
-In severe cases, widespread GI ulceration may occur, with bloody diarrhoea and occasionally perforation. - 46What is the interesting feature with behcets?Pathergy reaction. Pustules form at site of simple trauma eg needle puncture, usually within 24-48 hours. This is pathognomonic.
- 47Clinical features of polyarteritis nodosaFever, weight loss, malaise along with GI upset and occasionally a vasculitic rash. Other organ involvement may also occur.
Association with previous hep B infection. Peripheral neuropathy may also occur, due to involvement of the vasa nervorum. - 48Treatment of polyarteritis nodosaHigh dose steroids, usually with pulsed cyclophosphamide therapy.
- 49Why is fundoscopy important in CT disease?To exlude microhaemorrhage, cytoid bodies, retinal infiltrates
- 50What is a heliotrope rash?Feature of dermatomyositis. Violet discolouration on the face neck shoulder upper chest elbows knees knuckles and back. The lilac, erythematous heliotrope rash generally surrounds the eyes and is highly characteristic of this condition because it is rarely observed in other disorders. Patients look like they have racoon eyes. Characterised by inflammatory infiltrate containing mostly CD8+ t cells.
- 51What is libman sacks?non bacterial endocarditis that is seen in association with SLE
- 52What are the commonest causes of a lytic lesion?-mets
-multiple myeloma
-primary bone tumour - 53Describe two common avulsion fractures. What technique can be used to correct these?1) avulsion fracture of the patella can result from unexpected rapid flexion of the knee as in falling on a felxed knee or jumping
2) avulsion fracture of the olecranon form sudden extension of the triceps following a fall on an outstretched hand
tension band wiring - 54What is a colles fracture? How are these fractures reduced?Extra articular distal radius fracture. On radiograph there is shortening and radial deviation of the distal radius and dorsal angulation.
Traction to dis impact the fracture, apply pressure dorsally to push the fragment back in place, radial deviation to correct the deformity. - 55What is a potential complication of a distal radius fracture in a child?Median nerve damage leading to paraesthesia of the radial three and a half fingers.
- 56Describe the anatomy of the hip joint capsuleat the femur end is attached anteriorly to the trochanteric line and posteriorly about 1cm above the trochanteric crest
- 57Treatment of an extra capsular NOF fractureIM nailing or DHS
- 58treatment of a non displaced intra articular neck of femur fracturecannulated screws
- 59Treatment of a displaced intra articular neck of femurdepends on patient. if patient young and mobile, total hip replacement. if patient old and immobile, hemiarthroplasty (cement).
- 60What is spondylosisTerm used to describe intervertebral disc degeneration, instability and OA of the facet joints within any part of the spine but more commonly in cervical and lumbar region.
- 61Describe the pathophysiology of intervertebral disc degenerationDisruption of the cartilaginous annulus fibrosis and inner gel like nucleus pulposus. This result in micro tears in the annulus fibrosis, escape of the nucleus pulposus and decreased disc space, reduced shock absorption and flexibility. The vertebrae and the synovial joints then develop compensatory degenerative changes typical of OA.
- 62Presentation of spondylosisProduces chronic or intermittent back pain typically following physical activity, which is progressive and is often associated with acute exacerbations and diminished spinal mobility, stiffness and muscle spasms.
- 63Complications of spondylosisIncreased risk of intervertebral disc prolapse, the development of spinal stenosis and spondylolisthesis.
- 64Presentation of simple low back pain-onset 20-55 years
-lumbosacral, buttock and thigh pain
-mechanical in nature, varying with physical activity and time
-patient otherwise well
-clinical features typically resolve within six weeks
-pain may persist or relapse over time - 65What is a traction spur?Spur of cortical and cancellous bone that has grown up from the margin of a bone under the influence of traction from an apophyseal attachment of a tendon or ligament. The ligament is pulled from its attachment and as a result lifts adjacent periosteum. Bone forms beneath this lifted periosteum in much the same way as it forms when the periosteum is lifted following fracture of the diaphysis of a long bone. Spur is not usually attached to the ligament but is adjacent to it.
- 66What is spondylolisthesisOne vertebra slips forward or backward in relation to its adjact verebrae. Can be congenital or acquired.
- 67Presentation of nerve root pain-Unilateral leg pain which is worse than low back pain
-pain which radiates to the calf, foot or toes
-numbness and paraesthesia present in the same direction
-clinical signs of nerve root irritation
-localised neurological signs - 68What are the clinical signs of nerve root irritation?-Straight leg raise reproduces leg pain below the knee
-bow string sign
-lasegues sign
-cross leg pain - 69What are the red flag symptoms with back pain?-onset less than 20 or greater than 55
-constant, progressive, unreleting non mechanical pain
-thoracic pain
-past history of carcinoma
-drug misuse, steroid therapy, HIV
-general features eg malaise, fever, fatigue, weight loss
-presence of neurological features
-structural deformity
-severe persistent restriction of lumbar flexion - 70Clinical features of disc prolapse-Sudden or insidious onset of severe low back pain
-muscle spasm
-localised tenderness
-diminished lumbar spinal movements
-visible scoliosis
Commonest between L4/L5 and L5/S1 - 71Describe the neurological signs that would be seen in various disc prolapses1) L1/L2 - compressed L2 nerve root - sensory loss over anterior thigh, weak hip flexion, adduction and knee extension
2) L2/L3 - compressed L3 nerve root - sensory loss over medial thigh and knee, weak hip flexion, adduction and knee extension. Reduced knee flexion
3) L3/L4 - compressed L4 nerve root - sensory loss over medial aspect of calf, weak knee extension, reduced knee reflex
4) L4/L5 - compressed L5 - sensory loss over dorsum of the foot, weak hallux extension
5) L5/S1 - Compressed S1 - sensory loss over posterior aspect of calf and sole of foot. Weak foot plantar flexion. Reduced ankle reflex. Calf pain. - 72Most common causes of osteomyelitis in the UKS. aureus, E. coli, Pseudomonas, proteus
- 73Describe the pathogenesis of osteomyelitisInfection with a subsequent inflammatory response, abscess formation, ischaemia and therefore bone death (sequestrum). New bone can also occur (involucrum0 as can the development of sinuses (clocae) in severe disease which then discharge pus. This can present as a swelling in the groin from a psoas abscess.
- 74What is a gibbus deformity?Form of structural kyphosis typically found in the upper lumbar and lower thoracic vertebrae, where one or more adjacent vertebrae become wedged. Gibbus deformity most often develops in young children as a result of spinal TB and is the result of collapse of vertebral bodies.
- 75What is cauda equina syndrome?How does it present and what should be askeed?Cauda equina becomes compressed. Surgical emergency. Ask the patient if they can distinguish between motion and wind.
-sphincter dysfunction leading to bladder or bowel dysfunction (either incontinence or retention
-gait disturbance
-saddle anaesthesia (loss of sensation restricted to buttock, perineum and ineer surfaces of thighs
-bilateral lower limb weakness
-sexual dysfunction
-muscular pain
-numbness
-paraesthesia - 76Where does metastatic bone disease commonly originate from and hw does it present?-Breast, bronchus, prostate, kidney, thyroid. T and L spine common sites and spread is mostly haematogenous.
-Back pain is typically persistent, severe and at night.
-Swellings, hypercalcaemia and general features. - 77What lab results are seen in a patient with metastatic bone disease?-elevated ESE
-elevated ALP
-low Hb - 78What is multiple myeloma?Disorder presenting the accumulation of malignant plasma cells in the bone marrow resulting in the over production of immunoglobulin, predominantly igA, IgG and IgD (bence jones protein a free monoclonal antibody of kappa and gamma light chains)
- 79What can multiple myeloma cause if not treated early and what other features may be present?Secondary hypocalcaemia, anaemia and renal damage. Often characterised by diffuse osteoporosis, usually in pelvis, spine, ribs and skull. Displacement of normal bone marrow causes increased risk of infection.
- 80Most common reason for revision of THR?1) aseptic loosening (50%)
2) pain (23.1%)
3) dislocation (12.9%)
4) infection (9%)
5) peri-prosthetic fracture (8.6%)
6) implant fracture (3.3%) - 81Risk factors for hip fracture1) sex - 70% occur in females
2) age - 90% in people over 65
3) chronic conditions including hyperthyroid and malabsorption can lead to osteoporosis
4) medication eg steroids
5) inactivity
6) nutritional lack of vit D and calcium
7) smoking and alcohol - 82What is the Garden classification?Classification on intra capsular hip fractures
1) incomplete stable fracture with impaction valgus
2) complete fracture but non displaced (fixed with a cannulated screw)
3) complete fracture with partial displacement (arthroplasty)
4) complete fracture with full displacement (arthroplasty) - 83How are intertrochanteric sub fractures managed?inter - DHS
sub - IM nail - 84What is the most common system to assess severity of symtoms in OA?oxford hip score
- 85Describe different approaches for hip replacement surgery1) posterior - gluteus maximus is dissected. Increases risk of post operative muscle weakness. Risk to sciatic nerve due to excessive traction. Risk of posterior dislocation.
2) anterolateal - incision made between gluteus medius and tensor fascia lata. Risk to lateral femoral cutaneous nerve. Risk to sciatic nerve due to excessive tractio.n - 86Describe the advantages and disadvantages of cementedA layer of bone cement sits in between the bone and the prosthesis
Advantages - suitable for porous (osteoporotic) bone
-antibiotic material can be added to the cement reducing risk infection
-cement dries very quickly allowing quick fixation
Disaadvantages - cement can break down causing the joint to become loose
-cement debris can irritate surrounding soft tissue
-cement can occasionally produce a systemic reaction (severe hypotension) during the operation - 87Describe the advantages and disadvantages of using uncemented arthroplastyProsthesis has a rough surface, which encourages the bone in growth
Advantages - considered to produce a more durable bond between bone and prosthesis
-no risk of cement breakdown
Disadvantages - healthy bones are required - osteoporosis is a CI
-bone ingrowth can take up to 3 months - 88What are the early complications of hip arthroplasty?-bleeding
-infection
-pain
-damage to structures during surgery (nerve injury, intra operative fracture)
-anaesthetic complications - 89What are the medium term complications of hip arthroplasty?-pain
-infection
-DVT
-PE
-dislocation - 90What are the late term complications of hip arthroplasty?-pain
-infection
-prosthetic loosening
-prosthetic wear
-joint stiffness
-peri-prosthetic fracture
-implant failure
-infection - 91What is the most sensitive test for hipOA?Pain on internal rotation of the hip
- 92What percentage of patients who suffer a hip fracture will die within 30 days?10% die within first 30 days. 30% die within the first year.
- 93Describe the GCSMotor response- 1) no response
2) extends to pain (decerebrate)
3) flexes to pain (decorticate)
4) withdraws from pain
5) localises to pain
6) obeys command
Verbal response - 1) no response
2) incomprehensible sounds
3) inappropriate words
4) confused
5) oriented
Eye opening - 1) no opening
2) opens in response to pain
3) opens in response to verbal command
4) spontaneous - 94Describe the various pupil sizes and what they mean1) unilaterally dilated with sluggish or fixed response to lights - IIIrd nerve compression due to tentorial herniation
2) bilaterally dilated with sluggish or fixed response to light - inadequate brain perfusion or bilateral IIIrd nerve palsy
3) bilateral constricted - drugs (opiates), metabolic encephalopathy, pontine lesion
4) unilaterally constricted with preserved response to light - injured sympathetic pathway - 95A 27-year-old man is recovering from a grand mal seizure, which lasted for 5 minutes and was successfully terminated by a single dose of lorazepam. He remains very drowsy with a GCS of 9. What Type of airway adjunct?Nasopharyngeal
- 962. An 82-year-old lady with longstanding chronic obstructive pulmonary disease (COPD) has a respiratory tract infection and becomes very breathless, with a respiratory rate of 26 breaths/minute. What kin do fairway adjunct?Venturi mask with 24% O2
- 973. A 50-year-old man is brought in to AE in the early hours of Saturday morning after being involved in a fight outside a nightclub. He has a serious head and facial injury, and his Glasgow Coma Scale score is 6/15. Paramedics have inserted an oropharyngeal airway. What is the next step?Endotracheal tube
- 984. A 47-year-old woman was in the train crash and the carriage she was on caught fire shortly after the collision. She has severe burns around her face with singed eyebrows and has inhaled a lot of smoke. She has stridor and a GCS of 7. The anaesthatist has tried to intubate her, but failed. What next?Surgical cricothyroidotomy airway
- 995. A 10-year-old boy with severe asthma is brought in unable to talk in sentences even after using his salbutamol inhaler. His sats are 90%. What airway adjuct?High flow oxygen with a reservoire mask
- 1001. A 66-year-old man comes in to AE complaining of central crushing chest pain and palpitations for 2 hours. An ECG shows new left bundle branch block.MI
- 101A 23-year-old male student presents to the Emergency Department after a long train journey from his family home in Edinburgh. In the last hour he has noticed non-specific chest pain and is concerned enough to want to get it checked out. He is a non-smoker, is a keen sportsman, and is normally fit and well. He has no previous medical or significant family history. The ECG is normal. Which single blood test would be useful in this situation?D -dimer. Can exclude the diagnosis of VTE in low risk patients.
- 102What is D-dimer?Product of fibrin degradation which indicates that clotting and fibrinolysis have been occurring. Not a specific test and will be raised in many different conditions. However, if normal, can exclude diagnosis of VTE in low risk patients.
- 103Describe the indications for a CT head in head injury-suspicion of non accidental injury
-post traumatic seizure
-on initial assessment, GCS less than 13
-at 2 hours after injury, GCS less than 15
-suspected open or depressed skull fracture
-any sign of basal skull fracture
-focal neurological deficit
-more than one episode of vomiting - 104What clinical signs suggests brain herniationBradycardia and pupil dilation both strongly suggestive. Changes in breathing pattern and hypertension. Raised ICP causes the temporal lobe to herniate through the tentorial hiatus, compressing the IIIrd nerve, which results in ipsilateral pupil dilation.
- 105Give examples of tetanus prone wounds-Wounds or burns that require surgical intervention that is delayed for more than 6 hours
-wounds or burns that show a significant degree of devitalised tissue or a puncture type injury, particularly where there has been contact with soil or manure
-wounds containing foreign bodies
-compound fractures
-wounds or burns in patients who have systemic sepsis - 106What are the three types of wound closure?1) primary - surgical closure either in ED or theatre, by whatever means possible, soon after injury
2) secondary closure - no intervention, allowing skin to heal by secondary intention and the formation of granulation tissue.
3) Delayed primary closure - closure 3-5 days after injury
If no underlying injury, treating with primary closure is recommended - 107When are wounds referred to surgeons?-with associated crush injury or significant devitalised tissue/skin loss
-wounds with tendon, joint or neurovascular involvement
-stab wounds to the trunk and neck
-most wounds >12 hours old (except clean facial wounds)
-heavily contaminated or infected wounds - 108When are steri strips an appropriate choice for wounds?inappropriate over joints, but useful for pre tibial lacerations, and where skin is notoriously thin and sutures are likely to disintegrate
- 109When are skin tissue glue an appropriate choice for wounds?Very useful in children with superficial wounds and scalp wounds. Can be used in areas where the skin is not under tension, and so should not be used over joints/ Eyes should also be avoided.
- 110When are staples an appropriate choice for wounds?Particularly suited for scalp wounds and although staple removers are recquired to remove them, they are a quick and easy method of closure.
- 111When would you use nylon and vicryl sutures in wound closure?Nylon - non absorbable. most traditional and common method of primary closure.
Vicryl - absobable and are appropriate for inside the mouth such as lips and tongue lacerations. - 112When would you give iV acetylcysteine?Should only be given if time of ingestion of paracetamol is unknown (given immediately) or once plasma paracetamol conc is known (at 4 hours) and compared against a paracetamol treatment graph.
- 113What is a diplegic gait and how can it be caused?-abnormal narrow gait base and dragging both legs
-adductor spasm and tip toes from lower lim extension
-upper limbs are flexed
-scissor gait is seen when legs cross midline, solved by adductor release surgery.
Can be seen in cerebral palsy. - 114A 28 year old man comes in with a twisted knee after falling awkwardly from his skateboard. The patient has McMurray test positive and has experienced locking symptoms in his affected knee. Which part of the knee anatomy is affected?Meniscus
- 115What is a myopathic gait and what is it seen in?Characterised by weak gluteus medius, trendelenburg sign. Seen in myopathies eg muscular dystrophy, spinal muscular atrophy, congenital hip dysplasia
- 116What is a neuropathic gate and what is it seen in?-lifts thigh up to attempt to counteract foot drop (also called equine gait, like a horse trot)
-gait is more pronounced in dark settings where eyes can no longer compensate and guide feet.
Unilateral - seen in peroneal nerve palsy and L5 radiculopathy
Bilateral - ALS, charcot marie tooth, other peripheral nerve diseases eg DM - 117Describe the parkinsonian gait-Rigidity, bradykinesia, difficulty initiating movement
-upper limbs in flexion, with trunk flexed partially and neck craned forward
-once walking is initiated, the steps will be short and accelerate in rate (festinating)
-may be pill rolling tremor - 118What is an ataxic gait and when is it seen?-broadening of gait base to compensate for poor balance
-unable to keep trunk stable and level
-pathological trunk/head wobbling in cerebellar disease - titubation
-gait will not follow a straight path, will deviate and look for extra support
Seen in cerebellar disease and alcoholism - 119What radiological findings are seen in RALESS
L - loss of joint space, mostly uniform
E - Erosions (juxta articular)
S - soft tissue swelling
S - soft bones (osteopaenia) - 120Non articular manifesations of ank spon-Aortic incompetence
-anterior uveitis
-achilles tendonitis
-arthritis
-amyloidosis - 121What is finkelsteins test?Test for de quervains tensosynovitis. This tensosynovitis can mimic a fractured scaphoid and is seen in overuse of the tendon, or inflammatory conditions like RA.
- 122What is the best scan to use in suspected cauda equina syndrome?Lateral spinal MRI.
- 123What are the classical symptoms of multiple myeloma?CRABI
-Calcium high
-Renal failure
-anaemia
-bony lysis
-infections - 124What are the 6 radiological signs of a fracture?-Lucency or break in the continuity of the cortex
-impaction (angulation)
-loss of trbecular pattern
-cortical bulging
-cortical angulation
-epiphyeal misalignment - 125Describe how the ACL can be injured?-stopping suddenly
-rapid change in direction
-poor landing following a jump
-collisions
-rapid decleleration after running - 126What are the signs and symptoms of an ACL injury?Classically, an injury to the ACL may present as a popping noise and the feeling of the knee giving way under load
-pain followed by swelling
-loss of full range of motion
-discomfort while walking
-tenderness and pain along joint line - 127Three tests to assess for an ACL injury?-pivot shift
-anterior draw
-lachman test (generally considered most reliable and sensitive) - 128What is the unhappy triad?Medial meniscus, ACL, MCL
- 129How can damage to menisci occur?-commonly a twisting injury
-force against knee whilst in squatting position
-simple movements eg getting out of a chair, this is due to degenerative change and is seen in the elderly. - 130Signs and symptoms of meniscal tears-popping when tear takes places
-knee pain
-swelling and stiffness, gradual (whereas cruciate is rapid)
-knee joint locking/reduced ROM
-feeling of knee giving way, unable to take weight
-Tenderness along joint line
-effusion
-incapable of full extension
-positive mcmurray test - 131What types of mensical tears are there?-bucket handle
-flap
-degenerative
-radial - 132Describe the treatment of mensical tears-tears to the outer third can heal as they have an adequate blood supply, these may be surgically repaired ie sutures
-tears to the inner third have an inadequate bloody supply so are usually surgically trimmed away - 133Blood supply of the glenohumeral (shoulder) jointAnterior and posterior circumflex humeral arteries. These originate from the axillary artery and form an anastamotic ring around the surgical neck of humerus.
Other arteries include
-thoraco acromial artery: supplies anterior axillary wall
-lateral thoracic artery - supplies medial wall of the axilla
-subscapular artery - supplies posterior part of the axilla and posterior scapula region
-suprascapular artery - arises in base of neck and supplies the supraspinatus and infraspinatus muscles - 134Describe the nerve supply of the glenohumeral joint and descrribe the clinical relevence1) Axillary nerve - teres minor and deltoid. Nerve is often damaged in anterior shoulder dislocation or fracture to surgical neck of humerus
2)Suprascapular nerve - supra and infraspinatus. Entrapment can occur as it passes through the suprascapular notch leading to loss of abduction and external rotation.
3) subscapular nerve - subscapularis - 135What is the clinical relevence of knowing the coracoid process as an anatomyical landmark?Avoidance of neurovascular damage. Major structure enter the limb medial to the coracoid process, so that surgical approaches to the shoulder region should always take place laterally to the coracoid process.
- 136Describe the epideiomology and aetiology of frozen shoulder-More common in females and those who are diabetic, tending to affect those in the 4th and 5th decade
-pain is often constant and effects sleep
-shoulder capsule is thickened and contracted resulting in loss of mobility of the shoulder joint especially in external rotation - 137What is impingement?-Rotator cuff dysfunction (due to tears, calcification or movement pattern dysfunction) means the centralising and depressing effect on the humeral head is impaired, the humeral head rides higher during movement and friction is increased under the coracoacromial arch. Bony spurs (calcium deposits) can form around the arch and lead to friction, inflammation and pain during movement. Pain is often felt during the middle range of abduction, known as a painful arc.
- 138What is calcific tendonitis?Calcium deposits in the rotator cuff tendons, leading to irritation. Also reduces the space under the coraoacromial arch contributing to impingement. pain from this pathology tends to be severe and disabling.
- 139What is the clinical implication of the AC joint?Pathology is either the result of trauma (direct fall) or arhritis. The scarf test maximally loads the AC joint and is positive if pain occurs.
- 140Presentation of adhesive capsulitis?-Often insidious onset with increasing pain and reducing range of movement
-pain often constant, disrupts sleep, difficult with overhead activities (hair washing) and rotation (putting on a jacket and doing up a bra) - 141What are the three phases of adhesive capsulitis?1) freezing (acute)- pain with loss of movement
2) frozen (adhesive) - pain subsides, movement is globally restricted with pain at limits of motion
3) thawing (resolution) - spontaneous progressive increase in movement - 142How is a rotator cuff tear tested?-pain or weakness when asked to return the arm slowly to the side from an abducted position (drop arm test)
- 143What are the risk factors for shoulder iompingement?-osteophyte formation under the acromion
-rotator cuff weakness affecting the position of the humeral head
-chronic rotator cuff irritation due to repetitive overhead activites
-poor posture and poor muscle patterning - 144Describe how the site/character of the pain in the shoulder indicates different pathologies?1) upper lateral arm "grasping sign" = subacromial impingement including rotator cuff pathology and calcific tendonitis
2) superior tip of clavicle "pointing sign" - ACJ pathology: didsruption or OA
3) diffuse shoulder pain reproduced on rotation = glenohumeral origin - adhesive capsulitis/OA
4) shoulder pain, interscapular pain and radiation to occiput - neck pain, can refer down arm to hand indicating nerve root pain - 145What is a capsular pattern of of stiffness?external rotation and abduction affected first indicates adhesive capsulitis
- 146What is true and apparent winging of the scapula? Wha are the rare causes of winged scapula?True - serratus anterior palsy due to long thoracic nerve injury
Apparent - can occur with disruption of the ACJ, dysrhythmia of scapula due to instability or glenohumeral joint pathology.
Rarer causes - fascioscapulahumeral dystrophy or brachial plexus injury - 147This patient has globally restricted painful movement, on both active and passive assessment. External rotation and abduction are most limited.Glenohuemral joint pathology. OA or adhesive capsulitis will display a capsular restrictive pattern.
- 148This patient has pain localising to the lateral end of the clavicle with horizontal adduction (90degree's of shoulder flexion with the arm brought across the body).ACJ patholoy.
- 149The patient has pain when abducting the arm, and with passive internal and external rotation with the arm at 90degree's of abduction. Testing muscle strength is difficult as the patient experiences pain on resisted movements.Rotator cuff pathology. Pain arc often present, where pain is experienced on active abudction between 70 and 120 degrees.
- 150This patient complains of anteriorly situated shoulder pain when lifting heavy objects, they work in a factory. On examination pain is provoked on resisted elbow flexion.Bicipital tendonitis.
- 151What are the common offensive organisms in acute septic arthritis?-S. aureus
-H. influenzae
-N. gonnorrhoeae
-streptococci
-enterococci - 152What are the common offensive organisms in chronic septic arthritis?-Mycobacterium tuberculosis
-atypical mycobacteria
-invasive fungi (histoplasma, candida)
-brucella - 153Describe the pathogenesis of crystal † crystal arthropathyInsoluble crystals undergo attempted neutrophil phagocytosis, which results in the release of pro-inflammatory cytokines such as IL-1 and TNF alpha. Clinical result is pain, heat, swelling and redness.
- 154Which types of food are high in purines and can predispose to gout?-red meat
-strawberries
-certain shellfish - 155What may be the causes of impaired urate excretion leading to gout?-renal disease
-drugs especially diuretics and low dose aspirin
-HTN
-lead toxicity
-hypothyroidism
-primary hyperparathyroidism
-raised lactic acid = EtOH, exercise, starvation
-glucose-6-phosphatase deficiency - 156What are the causes of increased urate production that may predispose to ogut?-increased purine turnover
-myeloproliferative disease
-lymphoproliferative disease
-carcinoma
-severe psoraiasis
-inborn errors of metabolism eg lesch nyhan syndrome - 157Treatment of acute gout-important to stop any precipitating drugs, such as diuretics or low dose aspirin. NSAIDs are treatment f choice.
-colchcine may be useful in patients who are unable to tolerate NSAIDS, but its use is limited by the development of GI side effects, particularly abdominal pain and diarrhoea. - 158treatment of long term goutAllopurinol - inhibits xanthine oxidase which catalyses hypoxanthine to uric acid. Purines excreted through the kidneys as hypoxanthine and xanthine
Allopurinol indicated - recurrent attacks
-tophi
-bony damage
-coexistant renal disease, nephrolithiasis
-v high urate levels. - 159What are the causes of chondrocalcinosis on radiographic finding/-hyperparathyroidism
-hyperuricaemia
-haemochromatosis
-wilson's disease
-hypothyroidism
-ochronosis
-acromegaly
-paget's disease
-renal failur
-hypophosphatasia - 160What are the causes of haemoarthrosis?-haemphilia
-other bleeding disorder
-anticoagulant therapy
-trauma
-pseudogout may cause a slightly blood stained aspirate - 161management of haemoarthrosisInitially, patient should be made comfotable with ice packs, rest and appropriate analgesia. Any precipitating causes (such as clotting factor insufficiency) should be treated, and anticoagulant therapy should be optimised or stopped if possible.
- 162What is the nerve supply for the corneal reflexcorneal sensation is mediated by the trigeminal nerve, motor sensation for the blink itself is mediated by the facial nerve.
- 163What are the causes of RAP?-optic neuritis
-optic atrophy
-papillitis
-retinal detachments
-central retinal artery occlusion
-widespread retinal disease
-optic nerve compression - 164What is belpharitis? How do patients generally present and what is foundfound on eximination?Common condition of the lids. usually a combination of: infection of the lid margins by staph bacteria
-overproduction of sebum by the glands at the lid margin
Presents with - chronic ocular irritation, watery eye, red eye
O/E - crusting and scaling of the lash line
-careful examination can demonstrate plugs of sebum in the meibomian gland orifices. - 165What is a chalazion? How is it treated?-meibomian cyst (lipogranuloma)
-v common condition caused by meibomian gland dysfunction. Occurs with increased frequency in patient with acne rosacea and seborrhoeic dermatitis.
-treated initially with hot spoon bathing and abx but often chalazia require surgical incision and curettage. - 166What is entropion and the causes?-turning inwards of lid margin
-can affect upper or lower lid
-normal eyelashes cause corneal abrasion
Causes
-ageing
-conjunctival scarring (cicatricial) (trachoma, stevens johnson syndrome, ocular pemphigoid)
-acute spastic entropion - spasm of orbicularis muscle. - 167What is ectropion and how does it present?-turning outwards of lid margins
-almost always affects lower lid
-exposed conjunctiva may become inflamed, scarred and keratinised
Causes - ageing (involutional)
-conjunctival scarring (cicatricial)
-paralytic - facial nerve palsy
-mechanical - caused by large lower lid tumours - 168Causes of conjunctivitisOH GLAD SCABS
O - ocular cicatricial pemphigoid
H - herpes
G - gonococcal infection
L - ligneous
A - adenoviral infection
D - diptheria infection
S - stevens johnson syndrome
C - candida or chlamydia infection (newborn only)
A - alkali burn
B - beta haemolytic streptococci infection
S - springtime (allergic conjunctivitis) - 169Symptoms and signs of bacterial conjunctivitis? What are the most common organisms? Treatment-red eye
-eyelids stuck together
-minimal pain
-purulent discharge
-conjunctival papillae
-Most commonly caused for S. aureus, S. epidermidis and step pneumoniae
-Treating usually via broad spec topical abx such as chloramphenicol or fucithalmic acid - 170Signs of symptoms of viral conuncitivits?-red eye
-watery discharge
-usually bilateral
-often preceding coryzal symptoms
-conjunctival follicles
-preauricular lymph nodes
-keratitis - 171What organisms usually cause viral conjunctivitis? how is it treated?-adenovirus
-HSV-1
-Treatment usually conservative and usually spontaneously resolves in approx 2 weeks. Most cases will require no treatment other than lubricants.
-If HSV-1 has been isolated, topical aciclovir drops
Extremely contagious - 172Describe chlamydia causes of conjunctivitis?Serotypes A-C cause trachoma (chronic cojuncitivitis, endemic to africaand asia)
Serotypes D-K cause adult inclusion conjunctivitis - 173What is adult inclusion conjunctivitis?-caused by chalmydia serotypes D-K
-young adults
-possible concomitant urethral or vaginal symptoms
-transmission is via autoinnoculation from genital secretions, although eye to eye spread may occur. - 174signs and symptoms of adult inclusion conjunctivitis. how is it treated-unilateral mucopurulent discharge
-large conjunctival follicles
-preauricular lympadenopathy
-subepithelial corneal deposits
-can become chronic and persist for months if left untreated
Treatment - topical erythromycin for 2 weeks
-referral to GUM clinic for various systemic abx treatment - 175Symptoms signs and treatment of allergic conjunctivitis-rapid onset
-itching
-red eye
-usually bilateral
-conunctival papillae (massive)
-conjunctival chemosis (oedema)
-preauricular lymphadenopathy
Treatment - topical antihistamine eg levocabastine
-topical mast cell stabiliser eg sodium cromoglycate
-combo of two above eg olopatadine
-systemic antihistamine
-topical steroid use under specialist advice - 176What is the difference between conunctival papillae and follicles?1) Follicles - significant diagnostic importance
-hyperplasia of lymphoid tissue
-translucent avascular mounds of plasma cells and lymphocytes
-each follicles is encircled by small blood vessel
2) non specific and of less diagnostic value
-hyperplastic conjunctival epithelium thrown into numerous folds
-central vascular tuft
-can be large - cobblestone or giant - 177What are the main causes of conjunctival follicles?-viral infections including HSV
-chlamydia infections
-molloscum contagiosum
-hypersensitivity to topical meds - 178What are the main causes of conjunctival papillae?-non specific and can be seen in any conjunctival irritation or conjunctivitis
-allergic conjunctivitis
-bacterial infection
-contact lens related problems - 179What is vernal and atopic keratoconjunctivitis and how are they treated?Both chronic conjunctivitis, within a spectrum. Both result from repeated exposure to allergen.
1) Vernal - occurs in children
-seasonal (warm months)
-associated with atopic fam history
-bilateral
-ulceration and infiltration of upper cornea
2) Atopic - occurs in adult
-associated with atopy
-bilateral
-can also cause corneal ulceration and scarrng
Treatment - similar to acute conjunctivitis but use of topical and oral steroids in required more often. - 180What is neonatal conjunctivitis?Ophthalmia neonatorum.
usually secondary to N gonorrhoea or C trachomatis - 181Signs symptoms and treatment of episcleritisCommon, self limiting, frequently recurrent and occasionally there is an underlying systemic disorder.
-mild discomfort
-epiphora (watering)
-unilateral redness
Treatment - observation, lubricants, oral NSAIDs. topical steroids may be required in persistent cases - 182How do you distinguish symptomatically between scleritis and episcelritis?Scleritis is extremely painful and often wakes the patient up at night. C
- 183What is scleritis? What are the complications? What is the treatment?Characterised by cellular infiltrate of the entire thickness of the sclera. Frequently part of a general inflammatory reaction associated with a system immune mediated collagen vascular disease. Covers a spectrum of disease, ranging from self limiting episodes of inflammation to necrotisation of the sclera and potential loss of vision.
Inflammation of the sclera can progress to ischaemia and necrosis, eventually leading to scleral thinning and perforation of the globe.
Oral pred, immunosuppresion eg mycophenolate or azathioprine - 184What is the aetiology of scleritis?1) systemic association - wegener's granulomatosis, RA, PAN
2) infections - secondary to corneal ulcers - often pseudomonas aeruginosa
3) post ocular surgery - - 185Aetiology of keratitis?-bacterial
-viral
-fungal
-acanthamoeba - 186What are the risk factors for bacterial keratitis?-contact lens wear
-trauma
-compromised occular surface eg dry eye or blepharitis
-corneal exposure eg facial nerve palsy
-immunosuppression eg topical steroid use - 187Signs and symptoms of bacterial kertitis?-purulent conjunctivitis
-reduced vision
-corneal ulcer/opacity
-hypopyon - 188What are the common offensive organisms in keratitis?1) P. aeruginosa - causes aggressive infections
2) S. epidermidis
3) S. pneuominae
4) H. influenzae - 189Treatment of a bacterial corneal ulcerSight threatening condition, patients often admitted for intensive treatment
1) corneal scrape - should always be taken for M C and S
2) Broad spectrum topical antibiotics eg ofloxacin - initially every hour day and night
3) topical steroid therapy - should only be undertaken under ophthalmological supervision. Can be given to help with scarring and necrosis. - 190Describe the pathogenesis of herpes simplex virus causing keratitisPrimary infection usually occurs in childhood. Caused by direct transmission of virus through infected HSV secretion. Primary infection usually occurs in childhood. It is caused by direct transmission of virus through infected HSV secretion. Primary infection is usually subclinical. HSV then lies dormant within the trigeminal ganglion. Recurrent epithelial keratitis is then caused by reactivation of the latent virus and invasion of corneal epithelium.
- 191Signs and symptoms of herpes simplex keratitis-painful red eye
-dendritic (branching pattern) ulcer which may develop into a geographic ulcer
-decreased corneal sensation - 192What are the ocular complications of herpes zoster ophthalmicus?-conjunctivitis
-keratitis
-iritis
-scleritis
-secondary glaucoma
-cranial nerve palsies
-retinitis
-post herpetic neuralgia
-recurrent keratitis - 193Management of herpes zoster ophthalmicus-oral aciclovir - reduces duration and severity of disease as well as post herpetic neuralgia
-topical steroid - often used for ocular inflammation - 194What are adenospots?Adenoviral conjunctivitis is very common. In some cases, a keratitis can develop which consists of multiple faint subepithelial white deposits.
Patients will complain of blurring of vision, as well as glare and the lesions may persist following resolution of the conjunctivitis.
The adenospots often spontaneously resolves but occassionally topical steroids can be utilised to speed up resolution. - 195What are the common pathogens, signs ,symptoms and management of fungal keratitis?1)Pathogens - filamentous fungi eg aspergillus, fusarium
-candida albicans
2) symptoms - red eye, photophobia, blurred vision, discharge
3) signs -Filamentous fungi - greying stromal infiltrate with satellite lesions, hypopyon
-Candida - yellow white ulcer similar to bacterial keratitis picture
4) management - topical antifungal agents eg natamycin, amphoteracin
- corneal graft in unresponsive cases - 196When should you think about acanthamoeba keratitis and what are the signs and symptoms?should always be considered in individuals who have been swimming in their contact lenses.
-pain is often disproportionate to occular signs
-red eye
-dendritiform epithelial lesions
-non suppurative ring with variable epithelial breakdown - 197Definition and classification of uveitisDefined as inflammation of the uveal tract which includes the iris, ciliary body and the choroids.
Can be subclassified into 1) anterior uveitis (irits) - iris and anterior chamber
2) intermediate uveitis - localised to the vitreous and peripheral retina
3) posterior uveitis - posterior part of uveal tract and overlying retina - 198What is the mnemonic for HLA-B27 associated arthopathies?PUBCAR
P - psoriatic arthritis
U -UC
B - behcets
C - crohn's
A - ank spon
R - reiters - 199Aetiology of uveitis?1) idiopathic
2) HLA-B27 associated arthropathies
3) infectious - syphilis, TB, herpes simplex/zoster
4) sarcoidosis
5) juvenile idiopathic arthritis - 200Signs and symptoms of uveitis?-photophobia
-red eye
-pain
-blurred vision
-circumcorneal injection (redness)
-cells within the anterior chamber
-keratic precipitates (KPs), clumps of cells on the corneal endothelium
-posterior synchiae, adhesions between the lens and iris. Can lead to an irregular pupil
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