Question 1

Are MBP and CRP present in the blood all the time?

Accepted Answer

yarp. MRP= Mannose-binding lectin.

Question 2

what cytokine causes fever? and what one causes increase acute phase reaction?

Accepted Answer

TNF alpha IL6

Question 3

Why does liver failure put you at increased risk of infection?

Accepted Answer

poor APR or decreased neutrophil count

Question 4

How long does it take APC to migrate to regional lymph node?

Accepted Answer

1 day.

Question 5

what happens in lymph node?

Accepted Answer

certain CD4+ receptor on naive T cells bind to MHC class 2 on APC. Costimulatory molecules are needed to activate T cell as well - rapid division and maturation.

Question 6

What is B cell receptor? How do they interact with T cells?

Accepted Answer

surface bound IgD. T cells provide necessary signals and cytokines for B cell development. B cells help T cells and vice versa - take out B cells Stop T cell development

Question 7

What happens to IgD on B cells after activation? What process occurs during this?

Accepted Answer

swapped for IgM. And B cells start proliferating. somatic hypermutuation - during igD-IgM switch - immunoglobulin modified to provide better match.

Question 8

whats happening when lymph nodes swell and become painful?

Accepted Answer

T and B cells proliferate

Question 9

What do immature B cells express? what drug make use of this and for what?

Accepted Answer

CD20 surface marker. and anti CD20 antibody (rituximab) - used for leukaemias

Question 10

where do similar reactions to those in the lymph nodes occur?

Accepted Answer

spleen - always palpate it!

Question 11

If child gets lots of sore throats, ear infections or conjuctivitis what would you check?

Accepted Answer

IgA

Question 12

Describe responses to intracellular pathogens?

Accepted Answer

virus invades. dendritic cells on epithelial surfaces pick up virus via sampling ECS (pinocytosis) which are recognised by Intracellular PRR which cause innate response. interferon alpha produce which makes protein synthesis inefficient. NK cells can detect when MHC are switched off by cells. cells fall apart debris eaten by macrophages TNF alpha released makes you ill. Infected cell presents some viral proteins on HLA class 1 receptors are taken in by dendritic cell which changes to spherical shape and heads to lymph node.

Question 13

What key cell is activated in lymph node by HLA class 1 molecules in viral infection? How long does it take CTLs to start killing cells?

Accepted Answer

CTLs 1 week

Question 14

what is the costimulatory mechanism in activating a naive T cell?

Accepted Answer

Cd28-CD80/86 pathway. c28 om naive T ce and CD80 and 86 on pro APCs.

Question 15

what turns off T cell activation? when does it appear?

Accepted Answer

after a few days CTLA4 appears which are similar to CD28 but binds more strongly to CD80/86, stopping further activation of T helper and CTLs.

Question 16

What other pathways turn off immune response?

Accepted Answer

FAS/FAS-ligand after 10 days lymphocytes start expressing FAS and FAS-ligand. once pair of activated T cells meet and combine with their FAS and FAS ligand - cause cell death

Question 17

How quick are memory responses compared to primary responses?

Accepted Answer

4 days instead of 7

Question 18

How does CTLA4 Ig work with memory cells?

Accepted Answer

memory cells no longer require presence of costimulation for activation

Question 19

what type of joint is the sternoclavicular and the AC joint?

Accepted Answer

SC = saddle type joint AC=plane joint

Question 20

How is AC dislocated?

Accepted Answer

direct blow or fall on outstretched hand

Question 21

what causes winged scapula?

Accepted Answer

damage to long thoracic nerve - serratous ant loses innervation

Question 22

what type of joint is the elbow joint?

Accepted Answer

synovial hinge joint

Question 23

what is the carrying angle?

Accepted Answer

Deviation of forearm from midline in the anatomical position usually 5-15 degrees

Question 24

Whats cubitus varus? and cubitus valgus?

Accepted Answer

cubitus varus is deviation of forearm towards midline (smaller carrying angle) = supracondylar fracture of humerus cubitus valgus = opposite - Turner or Noonan syndrome

Question 25

how do you get colles fracture? and what is the opposite type called?

Accepted Answer

Fall with extended arm and outstretched hand - dorsal displacment of distal fragments Reverse colles or Smiths fracture - lands on wrist in flexion

Question 26

is ulnar part of wrist joint?

Accepted Answer

No

Question 27

what structures form the cubital fossa?

Accepted Answer

imaginary line between 2 humeral epicondyles, pronator teres and brachioradialis and supinator

Question 28

what is apex of palmar aponeurosis continuous with?

Accepted Answer

palmaris longus tendon

Question 29

What one action is entirely due to the intrinsic muscles of the hand?

Accepted Answer

flex mcp while extending ip joints

Question 30

what is increased pain with mild noxious stimuli called and pain evoked by non noxious stimuli?

Accepted Answer

hyperalgesia and allodynia

Question 31

Where do tricyclic antidepressants act? where do pain fibres go in the thalamus? desribe descending inhibition pathway?

Accepted Answer

Locus coeruleus - nucleus in pons - opoids inhibit it Medial and ventral thalamus PAG area of midbrain which receives inputs from hypothalamus, amygdala and cortex - descending inhibition goes 1st fo Rostroventral medulla.

Question 32

What are opoids? and opiates?

Accepted Answer

opoids - any substance tht has morphine like effects opiate - compounds such as morphine and codeine that are found in the opium poppy

Question 33

what % of people are resistant to codeine?

Accepted Answer

10%

Question 34

How does botulism work?

Accepted Answer

Botox binds to Ach or inhibits release

Question 35

how long does it take igm to increase to level that can be detected?

Accepted Answer

10 days

Question 36

what is annual incidence of back pain? whats prognosis? What are the 2 worrying things with back pain? How long does it take for chronic back pain to get better?

Accepted Answer

Annual incidence of back pain is 10-15%. Lifetime prevalence of 70% to 85%. Despite its widespread prevalence, the general prognosis of acute LBP is favourable, as 90% of patients recover without sequelae. Usually gets better in 6 weeks. 2 worrying things are infection and malignancy.

Question 37

What are 6 most common aetiological causes of back pain? Describe generally the AETIOLOGY? 3 main categories?

Accepted Answer

1. lumbar strain/sprain. strain is disruption of muscle fibers In muscle belly or musculotendinous junction. Sprain is subcatastrophic stretch of spinal ligaments. It is themost common mechanical cause. 2. Degenerative discs and or facets. 3. Herniated nucleus pulposus: L5/S1 is the most common place. 4. spinal stenosis. 5. spondylolysis (defect in pars interarticularis of vertebral arch which is the part between sup and inf articular processes) spondylolisthesis is forward displacement of vertebrae. 6. systemic: infection such as osteomyelitis, epidural abscess. Malignancy, ankylosing spondylitis. AETIOLOGY: 3 groups: mechanical, systemic, and referred. By far, the most common cause is mechanical (97%). MECHANICAL: Mechanical back pain is defined as pain that is elicited with spinal motion and decreases with rest. Lumbar strain/sprain: The most common cause of mechanical back pain. Strain: disruption of the muscle fibres at various locations within the muscle belly or musculotendinous junction. Patients experience intense pain for 24 to 48 hours then experience muscle spasm. Sprain: subcatastrophic stretch of 1 or more spinal ligaments. Some fibres are injured but the overall continuity of the ligament is maintained. Degenerative disc and/or facets: The pain generator is yet to be discovered, but the disc, ligaments, and facets have all been implicated. The disc is presumed to be the primary source of pain (discogenic). Unfortunately, many patients have asymptomatic degenerative discs. Discogenic pain increases with flexion, sitting, and coughing/sneezing due to an increase in intradiscal pressures. Facet joints may cause back pain that increases with extension as the facet joints are mechanically loaded. The facet capsule has been demonstrated anatomically to contain nociceptive fibres. The sacroiliac joint also has been implicated in low back pain. Herniated nucleus pulposus (HNP): Natural history is of clinical improvement in most patients with only 10% requiring surgical intervention. Leg pain is usually greater than back pain with pain radiating into the lower extremity in a dermatomal distribution. Leg pain may be reproduced with a straight-leg raise or a contralateral straight-leg raise. Back pain may occur as a result of referred pain from a corresponding tear in the annulus fibrosus. Spinal stenosis: A narrowing of the anatomical dimensions of the spinal canal secondary to disc osteophyte formation and facet/ligamentum flavum hypertrophy. Patients may manifest back pain that is often referred to as neurogenic secondary to mechanical constriction of the lumbar nerve roots. Spondylolysis and/or spondylolisthesis: General population has a pars interarticularis defect incidence of 3% to 6%, but most are asymptomatic. Patients have pain in the lower back with occasional radiation to the posterior thigh. Pain is aggravated by extension. If spondylolisthesis is severe, an exaggerated lordosis, heart-shaped buttock, or midline step off of the spinous processes may be present. Patients have pain with single-leg hyperextension test. Patient stands on 1 leg while extending the other leg. If pain is reproduced on the side of the extended leg, the test is positive. Compression fracture: May occur without recognised trauma and patients should have a medical work-up performed for the evaluation of osteoporosis, osteomalacia, and malignancy, depending on the fracture mechanism. Work-up for osteoporosis is key for future prevention. May be associated with a radiculopathy secondary to neuroforaminal encroachment from vertebral body height loss. Most commonly treated non-operatively. SYSTEMIC: Systemic aetiologies are much less common (1%) than mechanical back pain, but these causes usually warrant further work-up and signal possible urgent referral to a spine surgeon. Tumour and infection are the more common causes of systemic aetiologies of LBP. IT INCLUDES: Infection: Untreated discitis, osteomyelitis, or epidural abscess can lead to sepsis, progressive kyphotic deformity, and/or neurological deficit. Malignancy. Inflammatory spondyloarthropathy (i.e., ankylosing spondylitis). Connective tissue disorder. REFERRED: Sources are typically non-spine related and include intra/retroperitoneal pathologies. Much like systemic causes, these aetiologies are less common (2%) than mechanical back pain. Includes: Aortic aneurysm, Acute pancreatitis, Acute pyelonephritis, Renal colic, Peptic ulcer disease.

Question 38

Name 4 causes of referred pain to the back?

Accepted Answer

aortic aneurysm, acute pancreatitis, acute pylenonephritis, peptic ulcer

Question 39

what is radiculopathy and what is a compression fracture? how is a compression fracture Tx?

Accepted Answer

mechanical compression of nerve root, collapse of a vertebrae - kyphoplasty - inject cement into bone

Question 40

What are emergency (urgent) considerations with back pain?

Accepted Answer

cauda equina syndrome - bowel or bladder dysfunction, bilateral sciatica, saddle anaesthesia. - aetiology - large herniated disc or pathological or traumatic fracture Infection or tumour = other considerations

Question 41

STEP by STEP approach to Lower Back pain? What are 5 red flags with back pain?

Accepted Answer

HISTORY: The primary purpose of the initial encounter is to evaluate whether the patient requires immediate surgical evaluation and if the symptoms suggest a more serious underlying condition. Red flags in the history to warrant additional diagnostic imaging include: Systemic ailments, including fever, chills, night sweats, and/or unexplained weight loss (infection/malignancy), Profound or progressive neurological deficit, Trauma/high-speed injury, Pain that is refractory to medicine/injections, Older age, Prolonged corticosteroid drugs, Presence of contusion or abrasions over the spine, Aged under 20 or over 50, sphincter disturbances, nocturnal pain, worse pain on being supine. Patients should also be asked about intravenous drug use, immunocompromise, and history of cancer. Intravenous drug use or an immunocompromised state increases the risk of osteomyelitis of the spine and the possibility of epidural abscess. Metastasis to the spine needs to be excluded if a patient has a history of cancer and back pain. Patient’s age can also help in narrowing the differential, as older patients are at high risk of developing metastasis to the spine and spinal stenosis. EXAMINATION: Gait observed. Spine palpated to localise any tenderness. A thorough Neuro exam should then be performed. Specific maneouvres include: A positive straight-leg raise or contralateral straight-leg raise indicates a possible herniated nucleus pulposus (HNP). A straight-leg raise is performed with the patient supine and the hip flexed gradually with the knee extended. Pain that is reproduced below 60° of hip flexion on the ipsilateral side is considered a positive straight-leg raise and is more sensitive. Reproduced pain on the contralateral side indicates a positive contralateral straight-leg raise and is more specific. Pain that occurs above 60° is usually secondary to hamstring tightness. All patients with disc herniation do not exhibit the classic straight-leg raise. Because of the absence of a straight-leg raise and dermatomal pain, the clinician should not assume the patient is not suffering from a disc herniation. Specific neurological deficits, such as weakness, spasticity, or hyper/hyporeflexia, should be noted. These suggest more profound neurological compression; prompt referral to a spinal surgeon is indicated for further evaluation and management. Decreased rectal tone is an important examination finding, as it suggests sacral root encroachment from significant intraspinal compression. A vascular examination is important in differentiating vascular versus neurogenic claudication. Vascular claudication typically worsens with ambulation in any position and is relieved immediately by rest. Neurogenic claudication worsens with ambulation in an extended posture and improves with forward flexion of the lumbar spine. Patients with claudication may have concomitant vascular and spinal pathologies. CLINICAL TESTS FOR SACROILIITIS: SACROILIAC STRETCH TEST: Pain on adduction of the hip, with the hip and knee flexed. STRAIGHT LEG TEST tests L4, L5, S1. The femoral stretch test (L4 and above): pain in front of thigh on lifting the hip into extension with patient lying face downwards with knee flexed. LAB TESTS: Routine laboratory studies are not necessary in the evaluation of back pain unless the physician is concerned about the possibility of malignancy or infection (i.e., non-mechanical back pain, fever, chills, night sweats, and/or weight loss). In these cases FBC, ESR, C-reactive protein (CRP), and blood cultures are typically obtained. MRI is image of choice. High risk patients, Patients with unrelenting pain despite recumbency, systemic ailments (i.e., fevers, chills, general malaise, history of malignancy, unexplained weight loss), and profound neurological deficits warrant urgent advanced imaging studies such as MRI or CT. Lastly, imaging is indicated in patients with trauma, especially minor trauma in older adults, those with osteoporosis, and those on chronic treatment with corticosteroids. Most patients should be reassured that their symptoms will respond to conservative treatment. If symptoms persist longer than 6 to 8 weeks, plain x-rays at that time should be obtained, as most patients with benign low-back pain aetiology should have improved. More advanced imaging, such as MRI or CT, should be reserved if neurological compromise, infection, or tumour is considered, as degenerative and disc abnormalities are found in many asymptomatic patients, causing over-diagnosis and unwarranted patient anxiety. If a patient has metal in their spine or is unable to undergo an MRI, a CT myelogram is usually warranted. In trauma situations, the standard AP pelvis and cervical spine radiographs should be obtained. If patients have back pain, AP and lateral radiographs of the lumbar spine should be ordered. Furthermore, neurological compromise, gross spinal deformities, or manual step-off on spinal palpation also warrant CT to understand the bony anatomy.

Question 42

what does decreased rectal tone indicate? Whats the NICE guidance on back pain and cancer? If patient has simple back pain that has not improved after 6 weeks what should you do?

Accepted Answer

significant intraspinal compression. In patients with back pain and weight loss who are 60 years and over, you should also consider a possible diagnosis of pancreatic cancer and arrange an urgent direct access CT scan (to be performed within two weeks) or an urgent ultrasound if CT is not available. You should consider a possible diagnosis of myeloma in patients with persistent back pain who are 60 years and over. You should offer a full blood count, blood tests for calcium and plasma viscosity or erythrocyte sedimentation rate. Perform an ESR. If raised or has new risk factors then do imaging.

Question 43

Is CT preferred over MRI in back pain? Does losing weight help lower back pain? What is the NICE guidance on lower back pain and use of X rays? What is the advice on rest for lower back pain? How should analgesics be taken in lower back pain? When is MRI indicated in back pain? What antidepressants can you give in back pain?

Accepted Answer

No. Obesity is not a risk factor for developing low back pain and no data suggest that weight loss improves back pain. The dose of radiation from a set of lumbar spine x rays is 120 times that of a chest x ray, should not use it in non specific lower back pain saids NICE. Only rest if absolutely necessary. Analgesics are often more effective if patients use them regularly rather than only when the pain is at its worst.Radiographic imaging for chronic non-specific low back pain is not recommended. However, MRI scans are recommended for the investigation of patients who may have malignancy or sepsis as a cause of their pain and for the investigation of radicular symptoms. Tricyclic antidepressants.

Question 44

How does lumbar strain/sprain present? what percentage of people who see their GP with back pain come back within three months? What does NICE recommend with back pain lasting less than one year that has failed to improve with physical therapy and have significant distress or pain? When should surgery be offered in back pain?

Accepted Answer

sharp intense pain for 1-2 days muscle spasms most recover within 3 months. 30%. NICE guidance advises that patients with back pain lasting for less than one year who have failed to improve after one or more courses of physical therapy and who have significant pain or distress should be referred for an intensive programme of combined physical and psychological treatment lasting around 100 hours. European guidelines advise that surgery should only be considered for patients with severe pain for whom two years of conservative treatment have failed.

Question 45

Describe HNP?

Accepted Answer

Herniated lumbar disc is a displacement of disc material (nucleus pulposus or annulus fibrosus) beyond the intervertebral disc space. The highest prevalence is among people aged 30 to 50 years. More common in Males. In people aged 25 to 55 years, about 95% of herniated discs occur at the lower lumbar spine (L4-L5 and L5-S1 level); disc herniation above this level is more common in people aged over 55 years. Risk factors for disc herniation include smoking, weight-bearing sports (e.g., weight lifting, hammer throw), and certain work activities, such as repeated lifting. Presence of HNP on MRI does not predict pain. PROGNOSIS: Sequential MRIs have shown that the herniated portion of the disc tends to regress over time, with partial to complete resolution after 6 months in two-thirds of people. A herniated nucleus pulposus is most common in those aged below 40 years, whilst degeneration of discs tends to affect those aged over 40 years, with the prevalence increasing with advancing age. The term sciatica is used for the pain, tingling and numbness that arise due to nerve root entrapment in the lumbosacral spine. The symptoms may be felt in one or more of the lumbar nerve roots. About 90% of cases of sciatica are caused by a herniated intervertebral disc. This most commonly occurs at the L5/S1 level. CLINICAL FEATURES: If there is nerve entrapment in the lumbosacral spine, this leads to symptoms of sciatica which include: Unilateral leg pain which radiates below the knee to the foot/toes. The leg pain being more severe than the back pain. Numbness, paraesthesia, weakness and/or loss of tendon reflexes, which may be present and are found in the same distribution and only in one nerve root distribution. A positive straight leg raising test (there is greater leg pain and/or more nerve compression symptoms on raising the leg). Pain which is usually relieved by lying down and exacerbated by long walks and prolonged sitting. Large herniations can compress the cauda equina, leading to symptoms/signs of saddle anaesthesia, urinary retention and incontinence. Bowel or bladder dysfunction, Bilateral sciatica and saddle anaesthesia (last 2=severe compression) +ve straight leg (supine if pain with less than 60 degrees of elevation=positive) or contralateral (more specific) (ipsilateral is more sensitive) straight leg. CT is normal. MRI shows disc. Note: should not exclude HNP if straight leg -ve and no dermatomal distribution. Leg pain greater than back pain. 10% = surgery. Management: ANALGESIA: Simple analgesics as first line (paracetamol/non-steroidal anti-inflammatory drug). These may be used in combination. A weak opioid such as codeine or tramadol may be added if pain is still present. Consider a benzodiazepine (eg, diazepam) if there is muscle spasm. Consider a trial of a tricyclic antidepressant or gabapentin if there is persistent sciatica. Encouragement to keep active: swimming is a good exercise. Avoidance of activities that may aggravate pain - eg, lifting, prolonged sitting. Physiotherapy. Surgery: Pain due to a herniated lumbosacral disc may settle within six weeks. If it does not, or there are red flag signs such as the possibility of cauda equina syndrome, referral to an orthopaedic surgeon or a neurosurgeon should be considered. Interventions for people with chronic intractable pain or neurological complications include removal of the protruding disc (discectomy) and/or spinal fusion. IN DISC PROLAPSE: typically one is seized by severe pain on coughing, sneezing or twisting a few days after a back strain. Pain may be confined to lower back, lumbar area (lumbago) or may radiate to buttock or leg (sciatica). WITH L5/S1 prolapse, S1 root compression causes calf pain, weak foot plantar flexion, decreased sensation over sole of foot and back of calf and decreased ankle jerk. WITH L4/L5 (L5 root compression). Hallux extension is weak and decreased sensation on outer dorsum of the foot.

Question 46

what are features of spinal stenosis?

Accepted Answer

Lumbar spondylosis refers to degenerative conditions of the lumbar spine that narrow the spinal canal, lateral recesses, and neural foramina. Facet joint and ligamentous hypertrophy, intervertebral disc protrusion, and spondylolisthesis may all contribute to the stenosis, and symptoms result from neural compression of the cauda equina, exiting nerve roots, or both. Patients present with symptoms of neurogenic claudication or radiculopathy. Acquired degenerative spinal stenosis typically becomes symptomatic in patients in their 50s and 60s. AETIOLOGY: In nearly all patients, lumbar stenosis is the consequence of degenerative changes in the lumbar spine. With normal ageing, the intervertebral disc loses proteoglycans and water, leading to diminished disc height and circumferential disc bulging. This, in turn, results in altered biomechanical stress on the facet joints leading to facet hypertrophy and thickening of the ligamentum flavum, along with collagen and calcium deposition. CLINICAL FEATURES: walk with forward gait, intermittent pain radiating to thigh or legs, worse with prolonged standing/activity or lumbar extension. pain relieved lying down. MRI - can see it. X rays may show diffuse osteophyte formation of scoliosis. MANAGEMENT: Initially treated with non-steroidal anti-inflammatory drugs (NSAIDs) and physiotherapy. Epidural corticosteroid injections may provide symptomatic relief. More severe or persistent symptoms that significantly interfere with function are likely to benefit from decompressive spinal surgery, possibly with fusion if there is degenerative spondylolisthesis or degenerative scoliosis.

Question 47

Describe the features of a compression fracture?

Accepted Answer

Most osteoporotic spinal compression fractures represent an isolated failure of the anterior spinal column due to a combination of flexion and axial compression loading. The stability of the spine is not compromised with this type of fracture. These fractures are traditionally considered benign injuries that heal without complications. Rarely, osteoporotic compression fractures can also involve the middle and/or posterior spinal columns, in addition to the anterior column. This type of fracture is potentially unstable and requires surgical intervention. Vertebral compression fractures in osteoporotic patients are usually due to low-energy trauma in weakened bone. Consequently, these fractures are most common in older people and in patients taking corticosteroid therapy. It is important to rule out a pathological fracture due to tumour infiltration (e.g., multiple myeloma, metastatic disease), metabolic disease (e.g., osteomalacia), or osteomyelitis. Wedge compression (isolated anterior column failure). Stable burst (anterior and middle-column compression failure, posterior column intact). Unstable burst (compressive failure of anterior and middle columns, disruption of posterior column). The most frequent site for spinal compression fracture is the thoracolumbar junction, followed by the mid-thoracic spine. Anterior column: consists of the anterior two-thirds of the annulus and vertebral body, along with the anterior longitudinal ligament. Middle column: consists of the posterior one third of the annulus and vertebral body, along with the posterior longitudinal ligament. Posterior column: consists of all bony and tissue elements posterior to the anterior and middle column. CLINICAL FEATRUES: trauma history, pain at rest and night. tenderness to palpate over midline, normal neuro unless retropulsion of fragments.The pain may radiate bilaterally to the abdomen, although, unlike pain from a herniated intervertebral disc, it rarely radiates to the legs. Typically the pain resolves gradually over 4 to 6 weeks. Initial investigation involves radiographic evaluation with AP and lateral spine x-rays. The causative mechanism is a combination of flexion and axial compression loading. Treatment frequently involves pain relief, temporary use of an orthosis (e.g., Jewett/Lumbar brace or thoracolumbosacral orthosis) and walking aids (e.g., stick, elbow crutches, all-terrain rollator). Radiographic and clinical follow-up is required every 6 weeks for 3 months post-injury.

Question 48

what does red hot swollen joint indicate?

Accepted Answer

septic or crystal arthritis

Question 49

Name 5 DMARDS - describe each?

Accepted Answer

methotrexate - folic acid antagonist - 1st line drug Sulfasalazine - scavenges toxic O2 - common 1st line drug penicillamine - decreases immune response IL1 generation +/- collagen synthesis. Has metal chelating properties - Wilsons disease Gold compounds - auranofin antimalarial drugs - hydroxycholoroquine

Question 50

Name 6 immunosuppressive drugs and describe each one?

Accepted Answer

ciclosporin - decreases clonal proliferation of T cells - inhibits IL2 synthesis, decreases production of CTL, and T cell mediated B cell responses. ciclosporin binds to cyclophilin - complex then binds to and inhibits calcineurin and therefore prevents Th cell activation and production of IL2. TAcrolimus - macrolide antiBiotic - more potent than ciclosporin. Azathioprine - interferes with purine synthesis. mycophenolate mofetil - inhibits enzyme crucial for purine synthesis. Leflunomide - inhibits pyrimidine synthesis. Glucocorticoids - decrease IL2, TNFalpha and others underfgoing transcription also release antiinflammatory proteins like annexin 1. - effects mediated through inhibition of activator protein 1 and NFKB.

Question 51

Name 3 anti TNF alpha drug and 1 anti IL1 drug?

Accepted Answer

Adalimumab, infliximab, etanercept Anakinra

Question 52

When do u get fever?

Accepted Answer

within 10 days of infection

Question 53

Name drugs used in gout and describe each?

Accepted Answer

Allopurinol - analogue of hypoxanthine - reduces urate through inhibition of xanthine oxidase. Uricosuric agents (increase urate excretion) probenecid and sulfinpyrazone colchicine - prevents migration of neutrophils into the joint by binding to tubulin. - used in Acute gout

Question 54

how does rasburicase work?

Accepted Answer

contains uric acid oxidase - converts uric acid - allantoin - more soluble and readily excreted

Question 55

describe the pathway to uric acid formation?

Accepted Answer

hypoxanthine - xanthine - uric acid each step is catalysed by xanthine oxidase

Question 56

Name a H1 receptor antagonist that is used as an antiemetic? and one for allergies?

Accepted Answer

cyclizine cetirizine

Question 57

Where is CRP made? how does it work? when does it appear? when does its conc peak? whats normal conc?

Accepted Answer

Made in the liver - following IL6 secretion it binds to phosphocholine on surface of dead or dying cells and some bacteria which activates complement system and promotes phagocytosis. It rises within 2 hours of onset of inflammation. peaks at 48 hours normal conc is 10mg/L. higher levels in preg, viral infections, bacterial infections, burns. more sensitive than esr - returns to normal more quickly.

Question 58

what % have backpain in lifetime?

Accepted Answer

90%

Question 59

where do HNP most commonly occur? describe the management of back pain?

Accepted Answer

L4/L5 or L5/S1. lifestyle NSAIds back support physio, steroid injection remain mobile.

Question 60

how is compression fracture commonly treated non operatively?

Accepted Answer

back brace - jewet brace

Question 61

Describe sciatica?

Accepted Answer

shooting pain or numbness and tingling in buttock down back of knee and into foot pain worse on coughing sneezing

Question 62

where does spondylolisthesis occur? wht is tx? wht is spondyloarthropathy? What is Spondylolysis? What is spondylolisthesis? What is spondylosis?

Accepted Answer

L5/S1 . lumbosacral fusion. spondyloarthropathy is any disease of the vertebrae. Spondylolysis is a bony defect (commonly due to a stress fracture but it may be a congenital defect) in the pars interarticularis of the vertebral arch, separating the dorsum of the vertebra from the centrum. It may occur unilaterally or bilaterally. It most commonly affects the fifth lumbar vertebra and may cause back pain. Spondylolisthesis refers to the anterior slippage of one vertebra over another (or the fifth vertebra over the sacrum). There are five forms: Isthmic: the most common form, usually acquired in adolescence as a consequence of spondylolysis but often unnoticed until adulthood. Degenerative: developing in older adults as a result of facet joint osteoarthritis and bone remodelling. Traumatic (rare): resulting from fractures of the neural arch. Pathologic: from metastases or metabolic bone disease. Dysplastic: (rare): congenital, resulting from malformation of the pars. Spondylosis is a general term for degenerative osteoarthritic changes in the spine. It involves dehydration of the intervertebral discs with consequent narrowing of the intervertebral spaces. There may be changes in the facet joints with osteophyte formation and this may put pressure on the nerve roots, causing motor and sensory disturbance. Isthmic spondylolisthesis is a lumbar spinal condition in which a fracture of the isthmus causes one vertebral body to slip forward on top of the vertebral body below it. The isthmus, or pars interarticularis, is a small, thin segment of bone that connects the facet joints at the back of the spine. Spondylolysis affects 3-6% of the population but up to 12% of young athletes like gymnasts, presumably due to impact-related stress fractures. Isthmic spondylolisthesis affects around 5% of the population but is more common in young athletes. 60-80% of people with spondylolysis have associated spondylolisthesis. 90% of cases of spondylolysis and spondylolisthesis affect L5 and most of the remainder affect L4. Degenerative spondylolisthesis is more common in older people, particularly women. Traumatic, metastatic and dysplastic spondylolistheses are relatively rare. RISK FACTORS: Young. female. Athlete. Most cases of spondylolysis are asymptomatic and identified incidentally. It may present with low back pain provoked by lumbar extension, paraspinal spasm and tight hamstrings. It frequently does not show on X-ray. It is important to consider it in the differential diagnosis of back pain, as its identification can prevent progression and avoid the potential need for aggressive intervention The presentation of spondylolisthesis varies slightly by type although common symptoms include exercise-related back pain, radiating to the lower thighs, which tends to be eased by rest, particularly in positions of spinal flexion. Blood tests: looking for infection, myeloma, hypercalcaemia/hypocalcaemia. Lateral spinal X-rays - will show spondylolisthesis. These are best performed in the position of maximal pain. Management: Conservative 1st: activity modification, analgesia, sleep on side, physio, Bracing: a brace or corset may be recommended for a pars interarticularis fracture which is likely to heal. Then surgery. Surgical therapy involves fusing the affected vertebra with a neighbouring normally aligned vertebra (both anteriorly and posteriorly). The intervertebral disc is usually also removed, as it is inevitably damaged. The slipped vertebra may be realigned. PROGNOSIS: Spondylolisthesis is generally a benign condition; however, it runs a chronic course and is therefore a cause of much morbidity and disability.

Question 63

Describe ankylosing spondylitis? who gets it? what other features present? treatment?

Accepted Answer

Ankylosing spondylitis (AS) is a chronic progressive inflammatory arthropathy predominantly affecting the spine and sacroiliac joints. Patients present with severe pain and spinal stiffness, which ultimately may lead to spinal fusion.AS mainly affects the axial skeleton, although peripheral joints, entheses (tendon or ligament attachments to bone), and extra-articular sites such as the eye and bowel are frequently affected. Levels of disability are comparable with those who have rheumatoid arthritis. A diagnosis of established AS requires definitive evidence of sacroiliitis on plain radiographs. Such x-ray changes represent established damage and take many years to develop. Thus, the concept of non-radiographic axial spondyloarthritis (nr-axSpA) was developed to account for the earlier changes of axial inflammation visible on MRI, in the hope that earlier recognition and treatment of these patients will improve outcomes. Peak onset is between 20-30 years of age. More common in Males. The prevalence of ankylosing spondylitis in white people is about 0.15%. It is lower in women and higher in some other ethnic groups. AETIOLOGY: There is a strong genetic component in the risk of developing AS, with heritability of 97%. PATHOPHYSIOLOGY: In contrast to rheumatoid arthritis, where inflammation and erosion are the only pathological processes present, AS involves inflammation, cartilage erosion, and an additional process, which is subsequent repair (ossification). CLINICAL FEATURES: AS usually manifests as back pain in patients aged 20 years and older. Inflammatory back pain comprises a variety of symptoms, which can include: Early morning back stiffness, Improvement of stiffness with exercise, Resolution of symptoms using non-steroidal anti-inflammatory drugs (NSAIDs), Alternating buttock pain, Waking in the second half of the night with back pain. At least 2 of these symptoms need to be present to be highly suggestive of inflammatory back pain. Primary care physicians should refer patients with back pain that appears to be inflammatory and has lasted more than 3 months to a specialist with an interest in spondyloarthropathy. Most patients have mild chronic disease or intermittent flares with periods of remission. Morning stiffness is characteristic. The spinal disease starts in the sacroiliac joints (bilateral lumbosacral region) and may be felt as diffuse nonspecific buttock pain. In the advanced stages, patients develop loss of lumbar lordosis, buttock atrophy, and an exaggerated thoracic kyphosis with a stooped forward neck sometimes referred to as a 'question mark posture'. Peripheral enthesitis: Occurs in approximately a third of patients. Common sites - behind the heel (Achilles tendonitis), the heel pad (plantar fasciitis) and the tibial tuberosity. Lesions tend to be painful, especially in the morning. Peripheral arthritis: Also occurs in about a third of patients. Joint involvement is usually asymmetric, involving the hips, shoulder girdle (glenohumeral, acromioclavicular, and sternoclavicular joints), joints of the chest wall (costovertebral joints, costosternal junctions) and symphysis pubis. Other peripheral joints are less often and less severely affected, usually as asymmetrical oligoarthritis. In children, AS tends to commence with arthritis prior to spinal disease developing. TMJ is occasionally involved. Further history should also be obtained to establish the presence of disease-associated features such as: Iritis, Enthesitis (affecting tendon or ligament attachments to bone), FHx spondyloarthropathy, Psoriasis, Uveitis, Inflammatory bowel disease, Dyspnoea, Fatigue, Sleep disturbance. EXAMINATION: Findings on examination may include: Loss of lumbar lordosis and flexion, Tenderness at sacroiliac joints, Kyphosis (in chronic cases), Peripheral joint involvement. Measure chest expansion, lateral lumbar flexion and forward lumbar flexion. Schober's test: shows restriction of lumbar flexion. Palpate and stress the sacroiliac joints. Aortitis of the ascending aorta may lead to distortion of the aortic ring, causing aortic regurgitation. Patients with AS are prone to atlanto-axial subluxation, which may lead to cervical myelopathy. There is no test that is diagnostic of AS. test that is diagnostic of AS. A history suggestive of inflammatory back pain should prompt the clinician to request an x-ray of the pelvis to confirm the presence of radiographic sacroiliitis. A negative radiograph does not exclude the diagnosis. Should refer to a specialist, and they may suggest MRI. DIAGNOSIS: NEW YORK CLASSIFICAITON USED IN THE UK: Definite AS if criterion 4 and any one of the other criteria are fulfilled. 1. Low back pain of at least 3 months' duration that is improved by exercise and not relieved by rest. 2. Limited lumbar spinal motion in sagittal and frontal planes.3. Chest expansion decreased relative to normal values for sex and age. 4. Bilateral sacroiliitis grade 2 to 4, or unilateral sacroiliitis grade 3 or 4. Bamboo spine develops when outer fibres of annulous fibrosis ossify (occurs in 20%). TREATMENT: A positive response to non-steroidal anti-inflammatory drugs (NSAIDs) is characteristic of most patients. Physiotherapy and NSAIDs are the cornerstone of treatment. In refractory patients, tumour necrosis factor (TNF)-alpha inhibitors play a key role.

Question 64

name 2 common organisms that cause bone infections? what is infection of intervertebral disc called?

Accepted Answer

s aureus or tuberculous, and potts disease

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2.10 Funny turn and fall: OA, spinal stenosis, Gout, Paget's Disease, SLE, Systemic Sclerosis, Reactive Arthritis, Enteropathic Arthritis, Psoriatic Arthritis, Sciatica, Back pain, HNP, RA, Osteomalacia, osteoporosis. Ankylosing Spondylitis, Vasculitis, Behcets. Flashcards

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