Arthiritis Treatments And Managment Flashcards

1
Q

What roles does the muscoskeletal system play?

A

protects organs
Enables movement
Stores essential minerals
Produces red blood cells within bone marrow

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2
Q

What is included in the muscoskeltal system other than bones and muscle?

A

Joints, cartilage and ligaments

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3
Q

What is a joint and what are its 3 main categories

A

A point where two bones meet.

Fibrous joints connect bones whilst allowing NO movement e.g Skull and Pelivis

Cartilaginous Joints, Bones are attached by Cartilage allow little movement Spine + Ribs

Synovial Joints are tissues comprised of cartilage and a synovial membrane that can produce synovial fluid; that helps lubricate the surfaces allowing free movement. E.g the knee, shoulder, neck etc

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4
Q

What type of synovial joint allows a wide rotation of movement?

A

Ball and socket

Examples include the shoulder and hip.

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5
Q

What type of synovial joint allows rotational movement?

A

Pivot

An example is the neck.

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6
Q

Which synovial joint is similar in range of movement to a door hinge?

A

Hinge

Examples include the knee and elbow.

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7
Q

What type of synovial joint allows a small amount of sideways movement between two flat bones?

A

Gliding

Examples include some bones in the wrist and ankle.

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8
Q

Which synovial joint allows movement in two planes but has a smaller range of movement than a ball and socket joint?

A

Condyloid

Examples include the wrist and ankle.

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9
Q

What type of synovial joint allows movement but no rotation?

A

Saddle

An example is the base of the thumb.

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10
Q

What is osteoarthritis?

A

A common, disabling disease that usually affects large, weight-bearing joints, causing pain and limitations to movement and mobility.

Osteoarthritis (OA) is primarily due to wear and tear on a joint caused by ageing or excessive usage.

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11
Q

What is the most common joint disorder?

A

Osteoarthritis (OA)

OA begins in the second or third decades of life and becomes extremely common by age 70.

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12
Q

At what age do changes in weight-bearing joints typically begin?

A

By age 40

Although relatively few individuals have symptoms at this age.

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13
Q

How many people in the UK are affected by osteoarthritis?

A

Approximately 8.5 million people

This statistic highlights the prevalence of OA in the UK population.

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14
Q

Which gender is more commonly affected by osteoarthritis over the age of 55?

A

Women

However, the onset of symptoms often occurs earlier in men.

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15
Q

What factors contribute to the development of osteoarthritis?

A

Wear and tear on a joint due to ageing or excessive usage

This wear and tear leads to pain and mobility limitations.

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16
Q

True or False: Osteoarthritis symptoms usually begin in the second or third decades of life.

A

True

OA is commonly asymptomatic until later in life.

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17
Q

Fill in the blank: Osteoarthritis mainly occurs due to _______.

A

wear and tear on a joint

This is caused by ageing or excessive usage.

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18
Q

What joints does osteoarthritis primarily affect?

A

Large, weight-bearing joints

This includes joints like the hips and knees.

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19
Q

What characterizes osteoarthritis (OA)?

A

Destruction of articular cartilage, bony erosion with narrowing of the joint space, and new bone formation (osteophytes)

OA is mainly a degenerative disease.

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20
Q

What are the two classifications of osteoarthritis?

A

Primary and secondary

OA is classified based on the presence of a discernible cause.

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21
Q

What is primary osteoarthritis?

A

Osteoarthritis that occurs without an obvious cause; it is idiopathic

Primary OA most commonly affects the hip, knees, spine, and interphalangeal joints.

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22
Q

Which joints are most commonly affected by primary osteoarthritis?

A
  • Hip
  • Knees
  • Spine
  • Interphalangeal joints (fingers and toes)

Primary OA is often idiopathic.

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23
Q

What are Heberden’s and Bouchard’s nodes?

A

Hard swellings that form on the fingers and toes affected by OA

Heberden’s nodes occur at the distal interphalangeal joints, while Bouchard’s nodes occur at the proximal interphalangeal joints.

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24
Q

What is secondary osteoarthritis?

A

Osteoarthritis that occurs due to a change in the structure or function of a joint

This often follows a joint injury or can be due to other conditions.

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25
What are some causes of secondary osteoarthritis?
* Joint injury * Congenital joint malformations * Inflammatory conditions (e.g., rheumatoid arthritis, gout) * Obesity * Diabetes * Connective tissue disorders (e.g., Ehler-Danlos syndrome, Marfan syndrome) ## Footnote Secondary OA is linked to changes in joint structure or function.
26
Explain the pathophysiology of normally functioning cartilage and osteoarthritis
• Normal cartilage absorbs shock and reduces friction, relying on balanced ECM turnover by chondrocytes. • Osteoarthritis disrupts this balance, leading to cartilage breakdown, inflammation, and joint degeneration. It involves mechanical, inflammatory, and biochemical processes. College health and function is dependent on change changes of pressure that occur during the movement of a joint compression pumps fluids from the cartilage into the joint space and into the capillaries and venues whereas release allows the cartilage to re-expand hydrate and absorb necessary nutrients In osteoporosis, the balance between cartilage breakdown and its production by chondrocytes is lost and erosion of cartilage occurs. Chandra sites die and repair is attempted from adjacent cottage with the process is disordered cartilage surface displays roughening and pitting proceeding in cartilage ulcer ratio leaving the bone vulnerable to wear and tear. The bone attempts to repair itself but cannot perform as perfectly in produces overgrowth and joint margins. These are called osteophytes by the time symptoms have appeared. This I know has often thickens producing more so I know your fluid to attempt to protect a joint swelling and inflammation of the joint is referred to as Synovitis
27
What is the function of chondrocytes?
Cartilage producing cells
28
What are osteophytes?
Overgrowth at the joint margin caused by attempted bone repair when cartilage suffers while and the bone becomes vulnerable
29
What is the main difference between osteoarthritis and other diseases such as rheumatoid arthritis?
Osteoarthritis as a condition where the burns become weak and brittle due to the balance of Conrow sites production of cartilage and cartilage breakdown collapsing and it’s characterised by the loss of cartilage which leads to the bones being vulnerable to wear and tear and override in the margins OA is essentially a war intensity whereas rheumatoid authorise information disease
30
What are the key diagnosis signs and symptoms and tools used to diagnose osteoarthritis?
Diagnosis tools include blood test which may rule out identifiable causes of arthritis, e.g. gout or to arthritis, synovial fluid analysis would disclose a viscous joint to fluid characterise in OA, x-ray would reveal narrowing joint space in the formation of osteophytes at the peripheral joints
31
What does nice recommend as the treatment for osteoarthritis?
As asked you arthritis is a progressive disease treatment focuses on rehabilitation techniques and preventing dysfunction before disability develops to decrease the duration of disability Three treatment stages First treatment stage is based on the individual needs of the patient and includes education advice information strengthening exercise, aerobic fitness training weight loss if overweight Secondary treatment relies on relatively safe pharmacological options such as paracetamol and topical NSAIDS Final stage treatments focus on adjunctive treatments including pharmacological options, self management techniques, surgery and other non-pharmacy treatments . Final stage refers to treatment such as opioids intra articular corticosteroid injections physical treatment such as supporting braces, shock absorbing shoes, manual therapy, including stretching. This joint osteoplasty assistive devices, local heat and cold sources.
32
List some of the primary treatments for osteoarthritis.
Primary treatments are focused on education, strengthening weight loss and fitness. The patient should be educated on physiology and by a mechanics prognosis of optimal physical fitness . A patient with hip or knee OA should be instructed to avoid soft deep chairs recliners which arising is difficult use pillows under the knees regularly sit straight and chairs without slumping sleep on a firm bed with a bed board use a car seat designed for comfort well well supported athletic shoes and continue employment and physical activity Healthy cartilage is maintained by exercise and can help increase the range of motion and strengthen muscles and connective tissues to improve stability of the joint immobilisation can accelerate and worsen the clinical course
33
Name the secondary treatment for osteoarthritis and its goal. In addition to further treatments
Secondary treatment is based around pain relief usually paracetamol is adequate and should be used first alternative treatments topical non-steroidal anti-inflammatory medicine or NSAID. Which may be used with paracetamol often for hand and knee. NSAID names or ibuprofen felbinac piroxicam and diclofenac Further treatment includes these farm pharmacological options Capsaicin - used if topical NSA IDs are ineffective for hand and knee Oral NSAID - fenoprofen, naproxen, etodolac, diclofenac can be used with or substitute paracetamol Cox -2 inhibitors - celecoxib are used for patients that cannot tolerate NSAID side-effects but are associated with increased risk of cardiac side-effects therefore should be used with caution Intra articular corticosteroid injection - DexaMethasone, triamcinolone, prednisolone produce temporary benefit in soft tissue inflammation Low dose opioid- codeine, morphine tramadol dihydrocodeine buprenorphine act on Central nervous system to reduce pain can result in opioid dependency, constipation, nausea, confusion particularly in elderly
34
When should surgery be considered for osteoarthritis?
Joint surgery should be considered for patients who experience joint symptoms that have an impact on quality of life and do not respond to non-surgical management Surgery should be performed before prolonged an established functional limitation and severe pain Surgical options may include total joint replacement, partial joint replacement joint resurfacing or fusion in terms of hand or foot surgeries to few small bones together
35
Who is at the highest risk of rheumatoid arthritis and what is it?
Rheumatoid arthritis is a chronic inflammatory autoimmune condition that affects all races however women are three times more likely to be affected than men and most frequently start after the age of 35
36
What does early stage rheumatoid arthritis look like?
Initially the disease prevents painful inflammation of the Sino joints often starting with symmetrical inflammatory arthritis which affects multiple joints and maybe associated with a general symptoms of uncomfortability and illness As the disease progresses more joints become affected it often affects the distal joints further away from the centre of the body such as the hands and feet first as the disease progresses it affects larger and more proximal joints such as the knees, hips and shoulders
37
Describe mid to late stage rheumatoid arthritis and its symptoms
Joint inflammation will cause heat swelling, redness, and pain in addition to stiffness which is worse in the mornings or after period inactivity As the disease progresses synovial membranes become thickened chronic swelling and inflammation may cause joint deformities loss of function contractions muscle wasting and burst tendons due to inflammation of tendon sheets . Patients will potentially become very disabled if not treated quickly. In late stages are a can involve other organs such as eye skin, lungs, nerves, blood vessels and heart and it may cause psychological issues such as depression and it sometimes referred to as rheumatoid disease rather than rheumatoid arthritis due to affecting different parts of body
38
Describe the different ways that rheumatoid arthritis can present
Sudden and severe – acute onset Develop quickly over a few weeks – sub acute onset Develop slowly over a long period of time insidious onset
39
Although rheumatoid arthritis can affect all of your choice, it is more common for it to affect what joints initially
Distal joints such as hands and feet
40
What causes rheumatoid arthritis?
Rheumatoid arthritis and autoimmune disorders which is caused by the bodies owner immune system forming antibodies which attack and destroy its own cells. The causes not fully understood but it is seem to be a combination between genetic and environmental factors. These factors can be as diverse as birthweight smoking diabetes and even infections.
41
Explain the connection between genetic markers and rheumatoid arthritis
Arthritis was tendency to run in families. How many cases occur without a family history? No family history cases are referred to as sporadic RA. Family history RA associated with jeans called HLA – DR4 and HLA – DR1 the inheritance of these dreams make an individual more susceptible to external factors triggering RA
42
What are the theories that link rheumatoid arthritis to hormones
The fact that women have a higher incident than men Are usually develops between the onset of puberty and the menopause RA seems to improve during pregnancy when a hormone levels are significantly modified Responses of exceed by the male sex are giving during treatment
43
Explain the diagnosis for rheumatoid arthritis by the American College of rheumatology in 1987
This is the previously used way to diagnose rheumatoid arthritis and it includes seven steps Stiffness lasting at least one hour of getting out of bed for at least six weeks Swelling of soft tissue at least three joints for at least six weeks Swelling of specific joints in the hands, especially in the middle finger knuckle and wrist for at least six weeks Symmetrical arthritis for at least six weeks Swelling under the skin Positive blood test for rheumatoid factor X-ray evidence of destruction or loss of bone in around the joints in the hands
44
explain the diagnosis by ARC European league against rheumatoid ism for rheumatoid arthritis and how it works
Using the ARC/EULAR criteria for scoring RA you need at least a score of 6 to have definite RA Firstly, joint involvement One large joint equals score 0 2 to 10 large joints equals score 1 1– 3 small joints equals score 2 4 to 10 small giants equals score 3 More than 10 joints with at least one small joint score 5 Serology Negative rheumatoid factor (RF) and negative anti citrullinated protein antibody (ACPA) equals score 0 Low positive RF or low positive ACPA equals score 2 High positive RF or high positive ACPA equals score three Acute phase reactants Normal C reactive protein (CRP) and normal erythrocyte sedimentation rate test (ESR) equals score 0 Abnormal CRP or abnormal ESR equals score 1 Duration of symptoms Less than six weeks equals zero Greater than or equal to 6 weeks equals score one
45
Explain rheumatoid factor and its significance in rheumatoid arthritis
Rheumatoid factor is the name given to an antibody found in the blood of up to 85% of people diagnosed with RA. The antibody forms with Emilio goblin G to form RF – IgG. Raise is found in patients with out RA however RF contributes to disease process in patients with RA patients who have raised RF on blood testing and the active disease have the poorest prognosis or long-term prospect.
46
Explain the influence of anti citrullinated protein antibodies (ACPA) on rheumatoid arthritis and name 2 other important makers
ACPA are important by a marker for RA as they rarely unless RA is present however occur detection limits show that ACPA appear to be present in less than 70% of RA patients Additionally, two cytokines tumour necrosis factor alpha TNF – Alpha and interleukin six I also raised before symptoms appear
47
Why is RA considered a serious disease?
Arthritis can lead to a serious reduction and quality and mainly to significant disability leading people to potential have to give up on Work particularly aggressive for the disease can affect the heart and circular system and other organs which means that RA patients are increased risk of cardiovascular disease, including heart attacks and strokes Approximately 40% of patients suffer a degree of disability 10 years after diagnosis
48
Describe the four distinct stages of rheumatoid arthritis
The inflammatory stage characterised by pain swelling and stiffness, but no joint destruction. Blood vessels close to the joint allow cytokines & protogladins to enter joint which causes white blood cells to enter the joint. Proliferative stage Inflamed synovium begins to proliferate inflammatory cells and fluid causes the synovium to thicken which starts to road tendons, cartilage blood vessels and bone the joint space narrows Destructive stage . The infiltrating cells of the synovium release destructive chemicals that are capable of breaking down cartilage and bone. pannus tissue (thicken synovium) invades and erodes joining bone and cartilage leading to loss of function and deformities. And stage disease, the inflammatory process and leaving to form disabled joints and commonly rheumatoid nodules in the skin
49
Explain the inflammatory stage within rheumatoid arthritis as well as if the key chemical mediators and substances involved. Extra points if you can name how these substances lead to non-steroidal anti-inflammatories or NSAIT
Acute information is a normal process which is in response to injury or infection and is supposed to minimise damage to tissue or eliminate cause through a self limiting process which is supposed to be over a few hours or days In our E blood vessels in close proximity to the joint allow inflammatory cytokines fluid white blood cells to enter the joint. The cells in the synovium start to proliferate faster and produce more sign over your fluid. An important substance in this is prostaglandins which are formed and released into the joint The RA treatment NSAID or non-steroidal anti-inflammatories are based on affecting the formation of prostaglandins
50
Describe and explain the main differences between the inflammatory stage and proliferative stage of rheumatoid arthritis
In the inflammatory stage cytokines white blood cells and fluid flood the joint which leads to inflammation and pain, especially prostaglandins however in the proliferative stage this inflammation leads to the synovium thickening and secreting even more synovial fluid as it becomes infiltrated by cells from the immune system such as white blood cells. The proliferative stage is characterised by thickening of the sign of him that begins to a road articular cartilage and adjacent structures.
51
Describe the main differences between the destructive stage and the stage is that lead up to it finishing with end stage disease
The inflammatory stage is characterised by a release of cytokines from blood vessels that are of close proximity to the joint which causes inflammation as white blood cells get released on Prostogladins get released. The proliferative stage is characterised by this inflammation causing the sign of him to become further thickened and more side of your fluids secreted as well as infiltrated joint space by the immune system such as white blood cells this thickening of the side of him begins to a road articular cartilage and adjacent structures Finally, the destructive stage is worth thickened. Synovium becomes known as invasive pannus the infiltrating cells in the synovial tissue release several kinds of destructive chemicals that are capable of breaking down bone and cartilage. Pace tissue arose are joining bone and cartilage ultimate leading to loss of function and joint deformities which are typical for RA. End stage disease the informative process is largely finished or referred to as burnt out but the burning joint destruction caused by inflammatory process remains often given the patient significant to form pain and disability
52
What are the three main drug classes used to treat rheumatoid arthritis?
Non-steroidal anti-inflammatory drugs (NSAID) and analgesic agent (paracetamol) Disease modifying anti-rheumatic drugs (DMARD) sometimes referred to as slow acting anti-rheumatic drugs (SAARD) Corticosteroids
53
Describe the first line of treatment for rheumatoid arthritis giving specific pharmacological approaches
The main approach is to treat the symptom of pain. The approach taken is a cascade approach which is usually begins with analgesic agent such as paracetamol then following with non-steroid anti-inflammatory drugs (NSAID) NSAID include traditional painkillers such as ibuprofen and naproxen and diclofenac however they have been known to cause gastrointestinal problems Alternatively, cyclo oxygenate 2 inhibitors or COX2 inhibitors such as seller Celecoxib or rofecoxib referred to as coxibs can we use if patients don’t respond to NSAID however they have been linked to cardiovascular issues increased risk of myocardial infarction Full analgesic affect is expected within a few days however if a patient is going through severe pain which is harder to control opioid analgesic may be required at initially low dose but increasing the dose necessary and tolerated whereas anti-inflammatory can be up to 3 weeks and alternative NSAID should be tried
54
Describe the effect of DMARD in rheumatoid arthritis
Disease modifying anti-rheumatic drugs aim to alter the progression of rheumatoid arthritis minimising disability and is often prescribed from the outset with a combination of NSAID
55
Describe how small molecule DMARD function and give example examples
Small molecule DMARD or disease modifying rheumatic drugs such as penacillamine, azathioprine, ciclosporin, hydroxychloroquine, leflunomide, minocycline and sulfasalazine Work as immuno suppressants dumpling down the bodies immune system therefore reducing inflammation due to this they should only be initiated by an expert and monitored regularly through blood test
56
Explain how DMARD biologics work against rheumatoid arthritis
Disease modifying antirheumatic drugs, biologic such as infliximab, adalimumab and etanercept act as site to kind modulators to block TNF Alpha one of the main inflammatory mediators Rituximab is a Monaco antibody which kills B cells by binding to an antigen on their surface Abatcept disrupt the activation of T lymphocytes Anakinra and tocilizumab affect interleukins Methotrexate a small molecule DMRD is used in combination with the biologics
57
Explain corticosteroid use for rheumatoid arthritis
Corticosteroids are often injected into troublesome giant during flareup or acute onset of disease in two separate ways Short term or systematic cortical steroids such as prednisolone which is used when other anti-inflammatory drugs are not successful Alternatively, a local injection such as hydrocortisone betamethasone DEXA methadone and prednisolone ( most common steroid)
58
Explain the cases in which surgery will be needed for rheumatoid arthritis
Surgery is last line and is used to relieve severe pain and improve function of deformed joints but haven’t responded well to medication exercise Surgical options include Finger and hand surgery to join problems arthroscopy (keyhole surgery) which removes inflamed tissue in a joint Hip or knee replacement (arthroplasty) Cervical spinal fusion to treat severe neck pain Removing deformed bones from feet
59
Describe and explain the term juvenile idiopathic arthritis and the seven main types
JIA is the most common type of arthritis occurring in children’s between the ages of seven and 12 and teenagers before the age of 16 It is not a single condition, but as a collection of all forms of arthritis that begin before the age of 16 and possess for more than six weeks of unknown origin The seven sub categories include Systematic arthritis Poly arthritis RF negative Polyarthritis RF positive Oligo arthritis (persistent extended) the most common Psoriatic arthritis Enthesitis related arthritis Other arthritis
60
Describe and explain oligoarticular JIA
oligoarticular JIA is the most common type of JIA occurring in roughly 50% of JIA patients and is diagnosed impatience with arthritis in one to 4 joints during the first six months of disease It develops in very young children with peak onset age of 2 to 4 years old affecting primarily the knees and ankles girls are more affected than boys Arthritis confined to 4 or fewer Jones is designated as persistent oligoarticular JIA A child’s with active arthritis and five or more joints after the first six months of disease is considered to have extended oligoarticular JIA up to 50% of patients develop this Alternatively mono articular onset affecting only the knee is common seen in half of patience and is associated with patient’s functioning well and do not complain of pain
61
Describe poly articular JIA
Polyarticular JIA is impatience with five more joints within the first six months affected by arthritis This is split between RF negative which is around 11 to 28% of JIA patients which peaks at onset age of 2 to 4 Alternatively RF positive which is more for adolescence and represents 2 to 7% of JIA patients And can be seen as an early presentation of adult RA Affects girls more than boys
62
Explain enthesitis related JIA
enthesitis related JIA affects boys more than girls and they found in 10 to 15% of all children with JIA It affects areas where tendons attach particularly in legs and spine and is usually seen in late childhood/adolescence 8 to 15 years of age Children with ERA Jetter have arthritis in the lower lip is the hip knee and foot and arthritis of the spine (spondylitis) can occur later and cause lower back or buttock pain which is worse with the rest and better with activity
63
Explain systematic onset JIA
Systematic onset JIA affects the whole body and causes general tiredness fever and rushes children with this typically have two weeks of high spiking fever usually with two peaks daily (double quotidian) as well as a transient rash which comes and goes with fever spikes Depending on the type of arthritis usually polyarticular usually appears within six months of the initial fever and rush symptoms variable course with 60 to 85% of patients going into remission and 37% developing chronic and destructive poly arthritis It causes inflammation, swelling, pain, stiffness, and restrictive movement which start fairly non-specific depending on the type of arthritis as well as swollen, painful joints fever lethargy loss of appetite weight loss reluctance to use the affected limb Lastly, complications include eye inflammation known as uveitis which is left untreated can result in glaucoma cataracts and even blindness however it can be asymptomatic or regular eye checks are needed
64
Explain treatment of juvenile idiopathic arthritis (JIA)
Treatment is based on a combination of pharmacological interventions, physical occupation, no therapy and psychosocial support physical therapy is to be encouraged to prevent joint deformities, especially in hands and feet Initial treatment or NSAID e.g. naproxen ibuprofen indometacin for pain relief DMARD that suppress the immune system and help control inflammation to prevent joint damage prednisolone methotrexate sulfasalazine NSAD and DMARD can be used alone or with combination in the following Entarercept four children age aged 4 to 17 with active poly articular JIA who have not responded adequately to methotrexate Tocilizumab treats systemic JIA and young people age 2 and older who have not responded to NSAID corticosteroids and methotrexate
65
Describe Anklosing spondylitis the affected groups and symptoms
AS is a chronic arthritis that primarily affects part of the spine causing pain information and eventually fusion of the vertebrae usually in the lower back Men are affected more than women in the age of 20 to 40 commonly although the causes not known it’s their eyes the HLA – B27 gene involved Symptoms include back pain but but the disease can begin a typically in the peripheral joints, especially in children and women, board stiffness typically relieved by activity. Bent over posture sometimes eases back pain and muscle spasms thus some degree of kyphosis (curving of the spine) is expected assuming a question mark Posture with a stooped forward neck loss of curvature at the base of the spine and atrophy of the buttock muscles Proper treatment in most patients results and minimal or no disability however complications such as Uevitis ( inflammation of the uvea in the eye) and posture remaining fixed. Lastly, osteoporosis, cardiac problems, lung disease and occasionally kidney problems.
66
Explain the treatment process for ankylosing spondylitis
Treatment involves intense physiotherapy and occupational therapy with the aim of relieving symptoms and maintaining mobility of the spine. Strengthening of muscle groups that oppose the direction of deformities such as the extensor rather than the flexor muscle groups is crucial. Pharmacologically long-term corticosteroids should not be used instead NSAIDs should be used to treat inflammation, pain and muscle spasms and the choice should be based on tolerance and toxicity rather than no differences in efficacy. With the daily dose of NSA IDs being as low as possible until withdrawal of NSAID can be attempted. Patients who are not responding to NSAD analgesia and physical therapy can be put on tumour necrosis alpha inhibitors enteracept, golimumab and adalimumab
67
Explain gout and what causes it as well as the risk factors?
Gout is a form of arthritis in which crystals of monosodium urate form in one of several joints due to improper uric acid clearance. Uric acid is formed when the body breaks down purines and buildup in the bloodstream where it can be excreted via the kidneys in the case of gout not enough is excreted and microscopic crystals of mono sodium urate form in and around joints triggering the inflammatory reaction from synovium Risk factors include Diabetes one and two, high blood pressure, hypercholesteraemia, long-standing kidney disease, Familia history of gout Medication, including diuretics and niacin , diet foods with natural high purines (beef pork bacon, lamb seafood liv a kidney) , alcohol, sugary drinks
68
Explain the signs and symptoms of gout
Acute gout occurs without warning, but maybe precipitated by lifestyle risk factors as well as medical conditions. Acute pain (normally in one joint) often nocturnal is usually the first symptom pain becomes progressively more painful and is often excruciating signs resemble acute infection with swelling heat redness and tenderness. The overly skin is tense warm and shiny and red or purple. Fever chills and Molly may occur. Common joints affected for initial flareup or the Metatarsophalangeal joint of the big toe and the first few attacks affect only a single joint to lasting a few days later attacks may affect several joints, simultaneous and persist four weeks of untreated. Local symptoms and signs eventually regress however this asymptomatic period is in intervals and often becomes shorter as the disease progresses and without treatment several attacks may occur each year and permanent erosive joint deformity may happen limiting motion as multiple joints are involved. Urate deposits are common in the walls of the bursae and tending sheets as the MSU crystals enlarge (enlarging tophi) the nodes may erupt and discharge chalky masses of urate crystals leading to irreversible joint damage. Under the microscope, a joint aspiration would look like a needle shaped crystals of uric acid
69
What are the three main ways that gout is treated?
The main goal is a preventative program to prevent both acute attacks and disability from bone and cartilage erosion and treatment depends on stage and severity as well as specific therapy rest abundant fluid intake to combat dehydration and ate crystal precipitation or indicated NSAD is used to treat pain inflammation - naproxen, diclofenac, indometacin, etericoxib Prevention of requiring acute attacks is treated with daily colchicine which causes a dramatic effect where joint pain subsides after 12 hours and sees 36 to 48 hours. It is not a painkiller but reduces the ability of MSU crystals to inflame the sign of reducing inflammation and pain associated with gout should be given before NSAID if the patient cannot take an NSAID. Xanthine oxidise inhibitor such as Allopurinol and febuxostat reduce formation of uric acid from periods
70
Dez describe and explain psoriatic arthritis
Studies suggest 42% of people with psoriasis suffer from psoriatic arthritis although difficult to gauge as it overlaps other inflammatory arthropathies It’s not understood how it develops however the inflammation follows an autoimmune pattern genetics. I thought to play an important part as it may run in families and has been linked to genetic complexes HLA – B 27 and HLA – B 16 Symptoms include Pain swelling, stiffness, inflammation, and joints Sausage like swelling and fingers or toes known as dactylitis Tendinitis in the Achilles tendon or plantar fisciitis in sole foot Changes in nails such as pitting or separation from nail bed (onycholisis) Pain in the lower back
71
How to treat psoriatic arthritis
MSA ideas are used to treat pain and stiffness and inflammation in addition to paracetamol, steroids can be injected into the joint or tendon in the case of inflammation/flareup. Systemic steroid treatment is useful for reducing inflammation while starting DMARD therapy. DMARD use as soon as possible to prevent joint damage reduce information methotrexate and sulfasalazine are commonly used If the patient has not responded to at least two DMARD’s and the person has peripheral arthritis with three or more tender joints entanercept, inflixiximab, adalimumab are recommended Golimumab is also a treatment for active and progressive forms and in extensive damage surgery can be an option or joint replacement
72
Explain reactive arthritis and the causes
Reactive arthritis sometimes referred to his reiters syndrome is an auto immune response from an infection elsewhere in the body usually after the infection itself has been treated and it is associated with HLA – B 27 and 75% of cases Common infections types include sexually transmitted and dysergenic Sexually transmitted usually affects men aged 20 to 40 and consist of the genital infections with chlamydia trachomatis and there’s less common in women children and elderly Dysenteteric can occur in both men and women and is mostly caused by gastrointestinal infections primarily shigella salmonella yersinia Campylobacteria
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What are the symptoms of reactive arthritis? And how old do we treat?
Sexually transmitted usually leads to urethritis inflammation of the urethra, 14 days after sexual contact followed by low-grade fever, conjunctivitis arthritis over the next few weeks although not all symptoms will appear It affects the knees, ankles and toes most commonly and may cause backpain as a common sight of information is the spine tendons and ligaments may become inflamed and spondylitis and sacroilitis may occur Although this usually resolves in 3 to 6 months treating the infection should be first chlamydia can be treated with doxycycline or azithromycin. NSA IDs to relieve joint information as well as other analgesia such as paracetamol or even opioid depending on pain
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Explain septic arthritis and describe the five main types and how it’s treated
Septic arthritis is when the infection is within the joint itself and be caused by viruses, bacteria and fungi. It’s can even affect joint replacements creating a biofilm on the prosthetic joint. Bacterial septic arthritis Commonly caused by Staffler cockle bacteria which can damage the joint irreparably within a few days infections and lead to systemic sepsis and even death commonly used antibiotics include flucloxacillin, clarithromycin, co-amoxiclav and gentamicin Fungal arthritis is very rare and large joints are commonly affected antifungal agents such as amphotericin can be used Viral arthritis is short-lived and disappears without having any detrimental or lasting effects. The HIV virus is implicated. Gonococcal arthritis is caused by gonorrhoea and is treated by ceftriaxone or azithromycin Tuberculosis arthritis develop slowly intends to not be as severe as other bacterial infections it is treated with anti-tuberculosis agents isonaizid, rifampicin, pyrazinamide, ethambutol