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ARTHRITIS AND ITS TYPES
PRESENTED BY: GHAZIA IJAZ (DPT)
CONTENT
 Define Arthritis
 Common signs and symptoms of Arthritis
 Different kinds of arthritis
 Etiology and possible treatment
WHAT IS ARTHRITIS
 Arth means “Joint” and Tis means “Inflammation”
 Arthritis is a chronic condition inflammation of the joint
 It covers a group of more than 100 diseases that involve
inflammation of joint
SIGNS AND SYMPTOMS
 According to the US National
Arthritis foundation there are four
major signs of arthritis:
 Persistent pain and stiffness on arising
 Pain, tenderness and swelling in one or
more joint
 Recurrence of these symptoms ,
especially when they involve more than
one joint
 Recurrent or persistent pain and stiffness
in the neck, lower back, knees and other
joints
DIAGNOSIS
 Follow these steps to diagnose arthritis in
suspected person:
1. Complete health history
2. Physical examination to look for swelling and loss
of motion
3. Blood tests (this analysis will help to pinpoint the
type of arthritis)
4. X-rays(It shows cartilage loss, bone damage and
bone spurs)
TREATMENT
 Treatment focuses on relieving symptoms and
improving joint function
 Medications such as
 Painkillers help to reduce pain, but have no effect on inflammation
 Nonsteroidal anti-inflammatory drugs (NSAIDs): reduce both pain and inflammation
 Corticosteroids: this class of drugs, which includes prednisone and cortisone, reduces
inflammation and suppresses the immune system.
PHYSICAL THERAPY
 Physical therapy can be helpful for some types of arthritis.
 Exercises can improve range of motion and strengthen the muscles
surrounding joints.
 In some cases, splints or braces may be warranted.
SURGERY
 If conservative measures don't help, doctors go for:
 Joint repair: Joint surfaces can be smoothed or realigned to reduce pain and improve
function.
These types of procedures can often be performed arthroscopically — through small incisions
over the joint.
 Joint replacement:
This procedure removes your damaged joint and replaces it with an artificial
one.
Joints most commonly replaced are hips and knees.
 Joint fusion:
This procedure is more often used for smaller joints, such as those in
the wrist, ankle and fingers.
It removes the ends of the two bones in the joint and then locks
ends together until they heal into one rigid unit.
KINDS OF ARTHRITIS
 Osteoarthritis
 Rheumatoid arthritis
 Psoriatic arthritis
 Gout
 Systemic lupus Erythromatosus
1. OSTEOARTHRITIS
 The wear and tear disease
 It's the "wear and tear" that happens when your joints are overused
 It happens with age, but it can also come from joint injuries or obesity, which puts extra stress
on your joints
 Joints that bear weight -- like your knees, hips, feet, and spine -- are the most common places
it affects
SYMPTOMS
 Pain
 Stiffness
 Tenderness
 Loss of flexibility
 Bone spurs
 Swelling
CAUSE
 Osteoarthritis occurs when the cartilage that cushions the ends of bones in
your joints gradually deteriorates
 Besides the breakdown of cartilage, osteoarthritis affects the entire joint. It
causes changes in the bone and deterioration of the connective tissues that
hold the joint together and attach muscle to bone
RISK FACTORS
 Older age: Risk of osteoarthritis increases with age
 Sex: Women are more likely to develop osteoarthritis
 Obesity
 Repeated stress on the joint
 Genetics
 Bone deformities
TREATMENT
 Osteoarthritis can't be reversed, but treatments can reduce pain and help you move better
Medications:
 Acetaminophen has been shown to help some people with osteoarthritis who have mild to
moderate pain
 NSAIDs typically relieve osteoarthritis pain
 Physical Therapy: Exercises to strengthen the muscles around your joint, increase joint
flexibility and reduce pain
RHEUMATOID ARTHRITIS
 An autoimmune disorder in which immune system attacks its own body
tissues especially joints
 It leads to the joint inflammation that severely damages the joint.
 Most typical features
a) Symmetrical polyarthritis
b) Morning stiffness
c) Elevation of erythrocyte sedimentation rate ESR
d) Appearance of autoantibodies that target immunoglobins in the serum
EPIDEMIOLOGY
 Peak prevalence between the ages of
30 and 50 years
 Women are affected 3 or 4 times
more commonly than men
CAUSES
 Factors in the development of RA are
1. Genetic susceptibility
2. Autoimmune reactions
3. Inflammatory response in joints and synovial sheaths
4. Appearance of rheumatoid factor in the blood and synovium
5. Articular cartilage destruction
RISK FACTORS
 Risk factors are almost same for
every kind of arthritis.
 Sex
 Age
 Family history
 Smoking
 Environmental exposures
 Obesity
CLINICAL FEATURES
 Early feature (synovitis)
 Most commonly affect MCPJ and PIPJ, wrist, tendon sheaths around the
joint(wrist----knee----shoulder)
 Bilateral symmetrical polysynovitis
 Pain, fusiform swelling, stiffness, loss of mobility
 Deformity
 Increased pain, deformity, instability, decreased ROM
 Joint deformity---- Movement restricted and painful
 Z deformity in Thumb
 Swan neck deformity/ boutonniere's deformities, ulnar deviation in Fingers
 Radial and volar displacement in Wrist
 Limited extension in Elbow
 Limited abduction in Shoulder
 Swollen, flexion an valgus in Knees
 Clawed Toes
MEDICATION
 NSAIDs
Such as Ibuprofen, Indomethacin, COX-2 inhibitors reduce pain and
inflammation
 Analgesics
Morphine and acetaminophen reduce pain
 Glucocorticoids
Prednisolone prescribed in a small dose
 Disease modifying antirheumatic drugs DMARD
Used with NSAIDs and/or prednisolone to slow down joint destruction caused
by RA over time. For example; Azathioprine, injectable gold, chloroquine
 Protein-A Immunoadsorption Therapy
A method to remove antibodies and immune complexes triggering the
inflammation
SURGERY
 Osteotomy
 Joint replacement therapy or Arthroplasty
Surgical reconstruction or replacement of joint
 Arthrodesis or fusion
A procedure that fuses two bones together to decrease pain and increase
stability of the joint although it limits movement at a joint
PSORIATIC ARTHRITIS
 A chronic disease characterized by inflammation of skin (psoriasis) and joints
(inflammatory arthritis)
SIGNS AND SYMPTOMS
 A chronic disease that get worse with the time. Signs and symptoms of psoriatic
arthritis often resemble those of rheumatoid arthritis
 Painful, swollen, red joints especially in knees, ankle and feet
 Sausage like swelling of fingers and toes
 Low back pain
 Pitted nails or nails separating from the nail bed
 Pain at the point f ligament and tendon attachment especially at the back of the heel and sole
of the foot
CAUSE
 Psoriatic arthritis develops because of the autoimmune reaction between the
antibody and body’s own tissue
 Immune complexes trigger the inflammatory mediators to attack and cause
inflammation in certain joint
 Researchers say that certain genes are responsible for causing PA
RISK FACTORS
 Psoriasis is the single greatest risk factor for developing psoriatic arthritis.
 Family history
 More often in adults between the age of 30-50 years
 Obesity
 Smoking
 Bacterial infection
TREATMENT
 NSAIDs
 Regular exercise
 Corticosteroids
 Antimalarial drugs are also prescribed
 Disease-modifying antirheumatic drugs (DMARDs)
 Immunosuppressants
SURGICAL AND OTHER PROCEDURE
 Steroid injections to reduce inflammation quickly
 Joint replacement surgery: Psoriatic arthritis can be replaced with artificial prostheses made
of metal and plastic
GOUTY ARTHRITIS
 A chronic heterogenous disorder or urate metabolism
 Results in deposition of monosodium urate crystals in the joints and soft
tissues, with accompanying inflammation and degenerative consequences
PREDISPOSING FACTORS
 Purine rich food---Meat, kidney, liver, seafood
 Caffeine
 Drugs such as loop diuretics, NSAIDs, corticosteroids
 Trauma
 Infection
 Other disease such as diabetes mellitus, hypertension, vascular disease, renal disease or
thyroid disease
HALLMARKS OF GOUT
 Increased serum uric acid level
 Recurrent attacks of an acute inflammatory arthritis with monosodium urate
crystals demonstrated in synovial fluid leukocytes
 Bone and joint destruction in some cases
 Bone and joint destruction
 Tophus in bone leading to erosion in some cases
 Kidney disease and renal stones
STAGES
 Asymptomatic hyperuricemia
 Acute gout
 Intercritical gout
 Chronic tophaceous gout
INVESTIGATION
 Plain radiographs (may be normal)
 Serum Uric acid
 Synovial fluid analysis (shows uric acid crystals)
 BUN (blood urea nitrogen)
 Serum Creatinine
 Synovial biopsy
 Uric acid – urine
SYNOVIAL FLUID ANALYSIS
 The Gold standard
 Crystals intracellular during attacks
 Needle & rod shapes
 Strong negative birefringence
TREATMENT
 NSAIDs
Inhibits urate crystal phagocytosis by decreasing the migration of granulocytes into the inflammatory area
such as Indomethacin and Naproxen
 Colchicine
Inhibits the synthesis and release of leukotrienes
 Uricosuric agents
Such as Probenecid & Sulfinpyrazone. Increase the excretion of Uric acid.
 Allopurinol
Inhibits synthesis of uric acid by inhibiting xanthine oxidase enzyme
PREVENTION
 Avoid purine rich foods
 Reducing alcohol consumption
 Avoid Diuretic Drugs
 Maintain the concentration of Uric Acid level within the
normal range
 Drinking Plenty of Water
 Balance your weight with proper diet and exercise
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
 Systemic lupus erythematosus is a chronic, multisystem, inflammatory, autoimmune disorder
characterized by formation of autoantibodies directed against self-antigens and immune-
complex formation resulting in damage to essentially any organ.
TYPES OF LUPUS
 Systemic Lupus Erythematosus (SLE)
 Discoid Lupus Erythematosus (DLE)
 Neonatal lupus
CLINICAL FEATURES
 Cardiac
Myocarditis
Endocarditis
Pericarditis
 Constitutional
Fatigue
Fever
Weight loss
 GIT
Abdominal pain
Nausea, vomiting
 Dermatological
Alopecia
Butterfly rash
Mucus membrane rash
Photosensitivity
Purpura
Urticaria
Vasculitis
 Hematological
Anemia
Leukopenia
Thrombocytopenia
 Musculoskeletal
Arthralgia
Arthritis
Thrombocytopenia
 Pulmonary
Pleurisy
Pulmonary hypertension
Pulmonary parenchyma
 Neuropsychiatric
Cranial neuropathies
Organic brain syndrome
Peripheral neuropathies
Psychosis
Seizures
Transverse myelitis
 Renal
Hematuria
Nephrotic syndrome
Proteinuria
 Reticuloendothelial
Hepatomegaly
Lymphadenopathy
Splenomegaly
ETIOLOGY
 Etiology is still unknown
 But environment factors such as Ultraviolet light (UVB), chemicals, drugs and
infections
 Beta cell activation results in increased autoantibody
 Development of and failure to remove immune complexes
 Impaired T-cell regulation of immune response
DRUGS
 NSAIDs----Acetaminophen
 Corticosteroids----Prednisone
 Antimalarial drugs----Hydroxychloroquine
TREATMENT GOALS
 Control disease manifestation
 Prevent adverse effect of drug
 Prevent flares
 Treat flares when they occur
 Minimize organ damage
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Arthritis and its types

  • 1. ARTHRITIS AND ITS TYPES PRESENTED BY: GHAZIA IJAZ (DPT)
  • 2. CONTENT  Define Arthritis  Common signs and symptoms of Arthritis  Different kinds of arthritis  Etiology and possible treatment
  • 3. WHAT IS ARTHRITIS  Arth means “Joint” and Tis means “Inflammation”  Arthritis is a chronic condition inflammation of the joint  It covers a group of more than 100 diseases that involve inflammation of joint
  • 4. SIGNS AND SYMPTOMS  According to the US National Arthritis foundation there are four major signs of arthritis:  Persistent pain and stiffness on arising  Pain, tenderness and swelling in one or more joint  Recurrence of these symptoms , especially when they involve more than one joint  Recurrent or persistent pain and stiffness in the neck, lower back, knees and other joints
  • 5. DIAGNOSIS  Follow these steps to diagnose arthritis in suspected person: 1. Complete health history 2. Physical examination to look for swelling and loss of motion 3. Blood tests (this analysis will help to pinpoint the type of arthritis) 4. X-rays(It shows cartilage loss, bone damage and bone spurs)
  • 6. TREATMENT  Treatment focuses on relieving symptoms and improving joint function  Medications such as  Painkillers help to reduce pain, but have no effect on inflammation  Nonsteroidal anti-inflammatory drugs (NSAIDs): reduce both pain and inflammation  Corticosteroids: this class of drugs, which includes prednisone and cortisone, reduces inflammation and suppresses the immune system.
  • 7. PHYSICAL THERAPY  Physical therapy can be helpful for some types of arthritis.  Exercises can improve range of motion and strengthen the muscles surrounding joints.  In some cases, splints or braces may be warranted.
  • 8. SURGERY  If conservative measures don't help, doctors go for:  Joint repair: Joint surfaces can be smoothed or realigned to reduce pain and improve function. These types of procedures can often be performed arthroscopically — through small incisions over the joint.
  • 9.  Joint replacement: This procedure removes your damaged joint and replaces it with an artificial one. Joints most commonly replaced are hips and knees.
  • 10.  Joint fusion: This procedure is more often used for smaller joints, such as those in the wrist, ankle and fingers. It removes the ends of the two bones in the joint and then locks ends together until they heal into one rigid unit.
  • 11. KINDS OF ARTHRITIS  Osteoarthritis  Rheumatoid arthritis  Psoriatic arthritis  Gout  Systemic lupus Erythromatosus
  • 12. 1. OSTEOARTHRITIS  The wear and tear disease  It's the "wear and tear" that happens when your joints are overused  It happens with age, but it can also come from joint injuries or obesity, which puts extra stress on your joints  Joints that bear weight -- like your knees, hips, feet, and spine -- are the most common places it affects
  • 13. SYMPTOMS  Pain  Stiffness  Tenderness  Loss of flexibility  Bone spurs  Swelling
  • 14.
  • 15. CAUSE  Osteoarthritis occurs when the cartilage that cushions the ends of bones in your joints gradually deteriorates  Besides the breakdown of cartilage, osteoarthritis affects the entire joint. It causes changes in the bone and deterioration of the connective tissues that hold the joint together and attach muscle to bone
  • 16. RISK FACTORS  Older age: Risk of osteoarthritis increases with age  Sex: Women are more likely to develop osteoarthritis  Obesity  Repeated stress on the joint  Genetics  Bone deformities
  • 17. TREATMENT  Osteoarthritis can't be reversed, but treatments can reduce pain and help you move better Medications:  Acetaminophen has been shown to help some people with osteoarthritis who have mild to moderate pain  NSAIDs typically relieve osteoarthritis pain  Physical Therapy: Exercises to strengthen the muscles around your joint, increase joint flexibility and reduce pain
  • 18. RHEUMATOID ARTHRITIS  An autoimmune disorder in which immune system attacks its own body tissues especially joints  It leads to the joint inflammation that severely damages the joint.  Most typical features a) Symmetrical polyarthritis b) Morning stiffness c) Elevation of erythrocyte sedimentation rate ESR d) Appearance of autoantibodies that target immunoglobins in the serum
  • 19. EPIDEMIOLOGY  Peak prevalence between the ages of 30 and 50 years  Women are affected 3 or 4 times more commonly than men
  • 20. CAUSES  Factors in the development of RA are 1. Genetic susceptibility 2. Autoimmune reactions 3. Inflammatory response in joints and synovial sheaths 4. Appearance of rheumatoid factor in the blood and synovium 5. Articular cartilage destruction
  • 21.
  • 22.
  • 23. RISK FACTORS  Risk factors are almost same for every kind of arthritis.  Sex  Age  Family history  Smoking  Environmental exposures  Obesity
  • 24.
  • 25. CLINICAL FEATURES  Early feature (synovitis)  Most commonly affect MCPJ and PIPJ, wrist, tendon sheaths around the joint(wrist----knee----shoulder)  Bilateral symmetrical polysynovitis  Pain, fusiform swelling, stiffness, loss of mobility
  • 26.  Deformity  Increased pain, deformity, instability, decreased ROM  Joint deformity---- Movement restricted and painful  Z deformity in Thumb  Swan neck deformity/ boutonniere's deformities, ulnar deviation in Fingers  Radial and volar displacement in Wrist  Limited extension in Elbow  Limited abduction in Shoulder  Swollen, flexion an valgus in Knees  Clawed Toes
  • 27.
  • 28. MEDICATION  NSAIDs Such as Ibuprofen, Indomethacin, COX-2 inhibitors reduce pain and inflammation  Analgesics Morphine and acetaminophen reduce pain  Glucocorticoids Prednisolone prescribed in a small dose
  • 29.  Disease modifying antirheumatic drugs DMARD Used with NSAIDs and/or prednisolone to slow down joint destruction caused by RA over time. For example; Azathioprine, injectable gold, chloroquine  Protein-A Immunoadsorption Therapy A method to remove antibodies and immune complexes triggering the inflammation
  • 30. SURGERY  Osteotomy  Joint replacement therapy or Arthroplasty Surgical reconstruction or replacement of joint  Arthrodesis or fusion A procedure that fuses two bones together to decrease pain and increase stability of the joint although it limits movement at a joint
  • 31. PSORIATIC ARTHRITIS  A chronic disease characterized by inflammation of skin (psoriasis) and joints (inflammatory arthritis)
  • 32. SIGNS AND SYMPTOMS  A chronic disease that get worse with the time. Signs and symptoms of psoriatic arthritis often resemble those of rheumatoid arthritis  Painful, swollen, red joints especially in knees, ankle and feet  Sausage like swelling of fingers and toes  Low back pain  Pitted nails or nails separating from the nail bed  Pain at the point f ligament and tendon attachment especially at the back of the heel and sole of the foot
  • 33. CAUSE  Psoriatic arthritis develops because of the autoimmune reaction between the antibody and body’s own tissue  Immune complexes trigger the inflammatory mediators to attack and cause inflammation in certain joint  Researchers say that certain genes are responsible for causing PA
  • 34.
  • 35. RISK FACTORS  Psoriasis is the single greatest risk factor for developing psoriatic arthritis.  Family history  More often in adults between the age of 30-50 years  Obesity  Smoking  Bacterial infection
  • 36. TREATMENT  NSAIDs  Regular exercise  Corticosteroids  Antimalarial drugs are also prescribed  Disease-modifying antirheumatic drugs (DMARDs)  Immunosuppressants
  • 37. SURGICAL AND OTHER PROCEDURE  Steroid injections to reduce inflammation quickly  Joint replacement surgery: Psoriatic arthritis can be replaced with artificial prostheses made of metal and plastic
  • 38. GOUTY ARTHRITIS  A chronic heterogenous disorder or urate metabolism  Results in deposition of monosodium urate crystals in the joints and soft tissues, with accompanying inflammation and degenerative consequences
  • 39. PREDISPOSING FACTORS  Purine rich food---Meat, kidney, liver, seafood  Caffeine  Drugs such as loop diuretics, NSAIDs, corticosteroids  Trauma  Infection  Other disease such as diabetes mellitus, hypertension, vascular disease, renal disease or thyroid disease
  • 40. HALLMARKS OF GOUT  Increased serum uric acid level  Recurrent attacks of an acute inflammatory arthritis with monosodium urate crystals demonstrated in synovial fluid leukocytes  Bone and joint destruction in some cases  Bone and joint destruction  Tophus in bone leading to erosion in some cases  Kidney disease and renal stones
  • 41. STAGES  Asymptomatic hyperuricemia  Acute gout  Intercritical gout  Chronic tophaceous gout
  • 42. INVESTIGATION  Plain radiographs (may be normal)  Serum Uric acid  Synovial fluid analysis (shows uric acid crystals)  BUN (blood urea nitrogen)  Serum Creatinine  Synovial biopsy  Uric acid – urine
  • 43.
  • 44. SYNOVIAL FLUID ANALYSIS  The Gold standard  Crystals intracellular during attacks  Needle & rod shapes  Strong negative birefringence
  • 45. TREATMENT  NSAIDs Inhibits urate crystal phagocytosis by decreasing the migration of granulocytes into the inflammatory area such as Indomethacin and Naproxen  Colchicine Inhibits the synthesis and release of leukotrienes  Uricosuric agents Such as Probenecid & Sulfinpyrazone. Increase the excretion of Uric acid.  Allopurinol Inhibits synthesis of uric acid by inhibiting xanthine oxidase enzyme
  • 46. PREVENTION  Avoid purine rich foods  Reducing alcohol consumption  Avoid Diuretic Drugs  Maintain the concentration of Uric Acid level within the normal range  Drinking Plenty of Water  Balance your weight with proper diet and exercise
  • 47. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)  Systemic lupus erythematosus is a chronic, multisystem, inflammatory, autoimmune disorder characterized by formation of autoantibodies directed against self-antigens and immune- complex formation resulting in damage to essentially any organ.
  • 48. TYPES OF LUPUS  Systemic Lupus Erythematosus (SLE)  Discoid Lupus Erythematosus (DLE)  Neonatal lupus
  • 50.  GIT Abdominal pain Nausea, vomiting  Dermatological Alopecia Butterfly rash Mucus membrane rash Photosensitivity Purpura Urticaria Vasculitis
  • 52.  Pulmonary Pleurisy Pulmonary hypertension Pulmonary parenchyma  Neuropsychiatric Cranial neuropathies Organic brain syndrome Peripheral neuropathies Psychosis Seizures Transverse myelitis
  • 53.  Renal Hematuria Nephrotic syndrome Proteinuria  Reticuloendothelial Hepatomegaly Lymphadenopathy Splenomegaly
  • 54.
  • 55. ETIOLOGY  Etiology is still unknown  But environment factors such as Ultraviolet light (UVB), chemicals, drugs and infections  Beta cell activation results in increased autoantibody  Development of and failure to remove immune complexes  Impaired T-cell regulation of immune response
  • 56.
  • 58. TREATMENT GOALS  Control disease manifestation  Prevent adverse effect of drug  Prevent flares  Treat flares when they occur  Minimize organ damage