RHEMATOID NURSING

2. ⦿ Rheumatoid arthritis is
autoimmune disorder in
which Immune system
identifies the synovial
membrane as "foreign"
and begins attacking it.
⦿ Synovial membrane shown in
picture

3. ⦿ Rheumatoid Arthritis (RA) is a chronic
inflammatory disorder that may affect many
tissues and organs, but mainly attacks the
joints producing an inflammatory synovitis.

6. ⦿ Idiopathic
⦿ Positive family history
⦿ Inherited tissue type major
histocompatibility complex (MHC) antigen
⦿ Smoking
⦿ Bacterial and Fungal Infection
⦿ Herpes simplex virus infections
⦿ Epstein-Barr virus (EBV)
⦿ Vitamin D deficiency

7. ⦿ RA affects 0.5-1.0% of population in USA
⦿ Females > males 3:1
⦿ but people of any age can be affected
⦿ Peak age 45-65 but onset early from age 20-45
yrs
⦿ About 75% of these are women.
⦿ The disease strikes women three times more
often than men

8. ⦿ Presentation of antigen to T cells
⦿T- and B-cell Proliferation Angiogenesis in
synovial lining
⦿ Neutrophil accumulation in synovial fluid.
⦿ Synovitis.
⦿ Early pannus Formation(The pannus is a
sheet of inflammatory granulation tissue that
spreads from the synovial membrane and
invades the joint)

9. ⦿ Subchondral bone erosion.
⦿ Pannus invasion of cartilage Chondrocyte
proliferation.
⦿ Laxity of ligaments
⦿ Joint instability
, contractures, decreased
ROM, systemic complications

10. In chronically affected joints, the normally
thin synovium proliferates, thickens, and
develops many villous folds.
The synovial lining cells produce various
materials, including collagenase and
stromelysin(distroys connective tissues).
These contribute to cartilage destruction,
and interleukin-1 (IL-1) and TNF-alpha,
which stimulate cartilage destruction,
osteoclast-mediated bone absorption,
synovial inflammation, and prostaglandins
(which potentiate inflammation).

11. Sign and Symptoms

12. ⦿The joints of the
hands are often the
very first joints
affected by
rheumatoid arthritis.
These joints are
swollen red and
tender when
squeezed.
⦿ Swelling due to synovitis

15. ⦿The deformity arises
from hyperextension
of the proximal
interphalangeal joint,
while the distal
interphalangeal joint
is flexed.

17. ⦿Mallet finger is a
simple flexion
deformity of the
distal
interphalangeal
joint preventing
extension.

18. ⦿ Severe
hyperextension of
the interphalangeal
joint of the thumb

19. ⦿ Fatigue
⦿ Joint pain
⦿ Joint tenderness
⦿ Joint swelling
⦿ Joint redness
⦿ Joint warmth

20. ⦿ Joint stiffness
⦿ Loss of joint range of motion
⦿ Many joints affected (polyarthritis)
⦿ Limping
⦿ Joint deformity
⦿ Both sides of the body affected (symmetric)

21. • Extra articular s/s – low grade
fevr,fatigue,anorexia, chest
pain,numbness tingling ,vasculitis,
pericarditis,osteoporosis,neoropathy
etc.

22. Diagnosis

23. ⦿ X Rays
◾X rays of hands and feet are generally performed in
people with RA.
⦿ Magnetic Resonance Imaging (MRI)
⦿ Ultrasounds

24. ⦿ Blood Tests
◾Rheumatoid Factor (RF)
 RF is a specific antibody in the blood.
 A negative RF does not rule out RA. The arthritis is then called
seronegative, most common during the first year of illness and
converting to seropositive status over time.
◾Anti-citrullinated Protein Antibodies (ACPAs)
 Like RF
, this testing is only positive in a proportion of all RA
cases.
 Unlike RF
, this test is rarely found positive if RA is NOT present,
giving it a specificity of about 95%.

25. ◾Other blood tests performed when RA is suspected:
 Erythrocyte Sedimentation Rate (ESR)
⚫The rate at which red blood cells precipitate in a 1
hour period.
 C-Reactive Protein
⚫A protein found in the blood in response to
inflammation.
 Full Blood Count
⚫Gives information about all blood cells.
 Renal Function
⚫Kidney Function
 Liver Enzymes
⚫Gives information on the state of a patient’s liver

26. Arthroscopic examination
synovial fluid analysis
ANA Antibodies

27. ⦿ Salicylates
⦿ Acetylated
◾aspirin
⦿ Nonacetylated
◾choline magnesium
◾trisalicylate (Trilisate)
◾choline salicylate (Arthropan)

28. ⦿Nonsteroidal Anti-inflammatory Drugs
(NSAIDs)
◾diclofenac (Voveran)
◾etodolac (Lodine)
◾flurbiprofen (Ansaid)
◾ibuprofen
◾meclofenamate (Meclomen)
◾meloxicam
◾nabumatone (Relafen)

29. ⦿ Disease-Modifying Antirheumatic Drugs (DMARDs)
⦿ Antimalarials
 Action: Anti-inflammatory, inhibits lysosomal enzymes
◾hydroxychloroquine
◾chloroquine

30. ⦿ Gold-containing compounds
 Action: Inhibits T- and B-cell activity, suppresses
synovitis during active stage of rheumatoid
◾aurothioglucose (Solganol)
◾gold sodium thiomalate
◾auranofin (Ridaura)
◾sulfasalazine (Azulfidine)
◾penicillamine (Cuprimine)

31.  Immunosuppressives
⦿ Action: Immune suppression, effects DNA
synthesis and other cellular effects
 methotrexate (Rheumatrex)
 azathioprine (Imuran)
 cyclophosphamide (Cytoxan)

32. ⦿ Corticosteroids
⦿ Action: Anti-inflammatory, analgesic Used
for shortest duration and at lowest dose
possible to minimize adverse effects
◾prednisone
◾prednisolone
◾hydrocortisone
◾intra-articular injections

33. ⦿ Topical Analgesics
◾capsaicin (Zostrix)

34. TNF alpha inhibitors
infliximab, adalimumab, etanercept,
golimumab, and certrolizumab.
These agents can be used by themselves or
in combination with other medications such
as prednisone, methotrexate,
hydroxychloroquine, leflunomide or
sulfasalazine.

35. Surgeries considered for people who
have severe rheumatoid
arthritis include:
⦿ Arthroplasty
, to replace part or all of a joint, such
as the hip or knee.
⦿Arthroscopy, which uses a small lighted instrument
to remove debris or inflamed tissue from a joint.
⦿ Carpal tunnel release, to relieve pressure on the
median nerve in the wrist.

36. ⦿ Cervical spinal fusion, to treat severe neck
pain and nerve problems.
⦿ Finger and hand surgeries, to correct joint
problems in the hand.
⦿ Foot surgery such as phalangeal head
resection.
⦿ Synovectomy
, to remove inflamed joint
tissue.

37. Arthrodesis
In this process, any diseased cartilage
between the two bones is removed, the
bone ends are cut off, and the two bone
ends are connected to one another using
metal internal fixation, such as screws and
plates.
The two bones eventually grow into one
another, fusing to become one.

38. Other treatments
physiotyherapy
Exercise
Joint protection splints
Complementary therapies-
acupuncture,meditation,relaxation
Nutrition- omega 3 fatty acids

39. ⦿ NURSING DIAGNOSES
• Acute and chronic pain related to inflammation
and increased disease activity, tissue damage,
fatigue, or lowered tolerance level
• Fatigue related to increased disease activity,
pain, inadequate sleep/rest, deconditioning,
inadequate nutrition, emotional
stress/depression
• Disturbed sleep pattern related to pain,
depression, and medications
• Self-care deficits related to contractures,
fatigue, or loss of motion

40. ⦿ Impaired physical mobility related to
decreased range of motion, muscle
weakness, pain on movement, limited
endurance, lack of or improper use of
ambulatory devices
⦿ Disturbed body image related to physical and
psychological changes and dependency
imposed by chronic illness
• Ineffective coping related to actual or
perceived lifestyle or role changes

42. Ankylosing spondylitis

43. Ankylosing spondylitis, also known as axial
spondyloarthritis, is an inflammatory
disease that, over time, can cause some of
the bones in the spine, called vertebrae, to
fuse.
This fusing makes the spine less flexible and
can result in a hunched posture. If ribs are
affected, it can be difficult to breathe
deeply

44. Family history and genetics. If you have a
family history of ankylosing spondylitis, you
are more likely to develop the disease.
Age. Most people develop symptoms of
ankylosing spondylitis before age
45. However, some people develop the
disease when they are children or teens.
Other conditions. People who have Crohn’s
disease, ulcerative colitis, or psoriasis may
be more likely to develop the disease.

45. As ankylosing spondylitis worsens, new bone
forms as part of the body's attempt to heal.
The new bone gradually bridges the gaps
between vertebrae and eventually fuses
sections of vertebrae together.
Fused vertebrae can flatten the natural
curves of the spine, which causes an
inflexible, hunched posture.

46. There is no cure for ankylosing spondylitis,
but treatments can lessen symptoms and
possibly slow progression of the disease.

47. Early symptoms –
might include back pain and stiffness in the lower back
and hips, especially in the morning and after periods of
inactivity.
Neck pain and fatigue also are common. Over time,
symptoms might worsen, improve or stop at irregular
intervals.
The areas most commonly affected are:
The joint between the base of the spine and the pelvis.
The vertebrae in the lower back.
The places where tendons and ligaments attach to bones,
mainly in the spine, but sometimes along the back of the
heel.
The cartilage between the breastbone and the ribs.
The hip and shoulder joints.

48. Causes
genetic factors seem to be involved. In
particular, people who have a gene
called HLA-B27 are at a greatly increased
risk of developing ankylosing spondylitis.
Onset generally occurs in late adolescence
or early adulthood.

49. Pathophysiology
This chronic inflammation involves
infiltrating immune cells such as CD4 and
CD8 T lymphocytes and macrophages.
Cytokines, particularly tumor necrosis
factor-α (TNF-α) and transforming growth
factor-β (TGF-β), are also important in the
inflammatory process.
They contribute to inflammation, fibrosis,
and ossification at sites affected
by enthesitis (Enthesitis is the medical term
for inflammation of one or more entheses,
which are sites where tendons and
ligaments attach to bones.)

50. Lab studies
erythrocyte sedimentation rate (ESR) and
elevated C-reactive protein (CRP).
Presence of HLA –B 27 gene

51. • Common treatments for ankylosing
spondylitis include:
Exercise: Regular physical activity can
reduce stiffness and stop AS from getting
worse.
Nonsteroidal anti-inflammatory drugs
(NSAIDs): Over-the-counter (OTC)
NSAIDs, including ibuprofen and
naproxen ease pain and inflammation.
Biologic disease-modifying anti-
rheumatic drugs (DMARDs)
Corticosteroids: Joints
Surgery: joint replacement

52. GVHD (Graft-versus-host disease)
Graft-versus-host disease (GvHD) is a
systemic disorder that occurs when the
graft's immune cells recognize the host as
foreign and attack the recipient’s body
cells.
“Graft” refers to transplanted, or donated
tissue, and “host” refers to the tissues of
the recipient

53. GVHD has been classically classified based on the
timing of presentation into acute and chronic using
a cutoff of 100 days post-transplant.
Acute classic GVHD: Presents within 100 days of
transplantation.
Persistent, recurrent, or late-onset acute GVHD:
Manifests after 100 days of transplantation.
Overlap syndrome: May present at any time post-
transplant with features of both acute and chronic
GvHD

54. GvHD occurs in the following settings:
Following allogeneic bone transplantation
(most common)
Following transplantation of solid organs that
are rich in lymphoid cells (eg. liver)
Following transfusion of un-irradiated blood

55. Pathophysiology
The ability to recognize "non-self" cells
depends on a set of genes knows as the
histocompatibility genes that provide
instructions for making a group of related
proteins known as major histocompatibility
complex (MHC proteins) or human
leukocyte antigens (HLA).

56. During transplantation, the donor tissue is
usually obtained from a genetically
different individual known as an "allograft".
Immune cells in the graft recognize
the MHC proteins of the recipient tissue as
"non-self" and triggers an immune response
between the donor and the recipient.

57. Donor cytotoxic CD-8 t cells recognize host
tissue as foreign and proliferate to cause
severe organ damage (type IV cytotoxic T
cell hypersensitivity reaction).

58. Treatment / Management
Most treatment options focus on
immunosuppression of donor T cells and
must be balanced to reduce the symptoms
of GVHD while avoiding decreasing the
beneficial graft vs. tumor (GVT) response.
Corticosteroids remain the most commonly
used treatment.

59. Most commonly methylprednisolone 2
mg/kg/day in divided doses. In cases of GI
involvement, the addition of a
nonabsorbable corticosteroid (budesonide
or beclomethasone) is more effective than
systemic treatment alone.
Steroids should be avoided if a GI infection
is present.