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PATHO/PHARM II > Part Four: Inflammatory DX - Rheumatoid Arthritis RA > Flashcards

Part Four: Inflammatory DX - Rheumatoid Arthritis RA Flashcards

Exam 4 (Final)

1
Q

Rheumatoid Arthritis (RA): What kind of disease is this considered?

A

Autoimmune & inflammatory

Chronic, systemic

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2
Q

Rheumatoid Arthritis (RA):

Is Chronic, systemic:

What symptoms exist?

A

Fever, malaise, rash, lymph node or spleen enlargement

Joint swelling, tenderness

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3
Q

Rheumatoid Arthritis (RA):

What is there destruction of?

A

Destruction of synovial joints

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4
Q

Rheumatoid Arthritis (RA):

Destruction of synovial joints:

What does it line?

Why does destruction occur?

What else does it lead to?

A

lines the joint cavity

Immune system targets the synovium

Synovitis

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5
Q

Rheumatoid Arthritis (RA):

Destruction of synovial joints:

Synovitis- What does this lead to?

A

Membrane thickened/swollen

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6
Q

Rheumatoid Arthritis (RA):

What forms?

A

Pannus forms

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7
Q

Rheumatoid Arthritis (RA):

Pannus forms: What is this?

A

Abnormal tissue growth in synovium

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8
Q

Rheumatoid Arthritis (RA):

Pannus forms: What does this consist of?

A

Consists of inflamed synovial cells, immune cells, and blood vessels

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9
Q

Rheumatoid Arthritis (RA):

Pannus forms: What does it contribute to and how?

A

Invades & damages nearby cartilage and bone, contributing to joint erosion and deformity

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10
Q

Rheumatoid Arthritis (RA)

Predisposing Factors

A

Age (Young & middle aged)

Environmental factors

Females

Postpartum

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11
Q

Patho of RA:

How does it start (What gets activated?)

A

Synovial fibroblasts (SF) that line joint cavity get activated

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12
Q

Patho of RA

When synovial fibroblasts (SF) that line joint cavity get activated, what happens?

A

Immune system mounts an attack

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13
Q

Patho of RA

What happens to synovial fibroblasts (SF)?

A

Synovial fibroblasts (SF) proliferate & produce inflammatory cytokines & PGs

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14
Q

Patho of RA

Synovial fibroblasts (SF) proliferate & produce inflammatory cytokines & PGs

What do the cytokines do?

A

Cytokines: Pro-inflammatory (TNF-α, IL-1, and IL-6) drive the inflammatory process.

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15
Q

Patho of RA:

What does the enflamed synovium (pannus) do?

A

The inflamed synovium (pannus) grows over the cartilage and bone, releasing enzymes that degrade cartilage and bone.

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16
Q

Patho of RA:

What does the SFs do?

A

SFs attack articular cartilage –> more release of inflamm enzymes –> spreads to joint capsule, ligaments, tendons

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17
Q

Patho of RA

What do activated T-cells do?

A

Activated T cells produce pro-inflammatory cytokines

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18
Q

Patho of RA

What do B-cells do?

A

B cells produce autoantibodies which form immune complexes that further drive inflammation.

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19
Q

Pannus formation (thickened synovium)

A

Granulation tissue from the synovium spreads over the articular cartilage, releasing enzymes and inflammatory mediators that destroy the cartilage.

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20
Q

Slide 5: I don’t understand

A
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21
Q

Clinical Manifestations:

How are joints?

A

Red, swollen, warm and painful joint

Symmetrical
Insidious onset

Multiple joints (small joints in hands, wrists, feet, larger joints like knees, shoulders, hips)

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22
Q

Clinical Manifestations:

Red, swollen, warm and painful joint

Symmetrical
Insidious onset

Multiple joints (small joints in hands, wrists, feet, larger joints like knees, shoulders, hips)

What leads to this?

A

Abnormal immune response, causing inflammation of the synovial membrane with vasodilation, increased permeability

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23
Q

Clinical Manifestations:

Red, swollen, warm and painful joint

Symmetrical
Insidious onset

Multiple joints (small joints in hands, wrists, feet, larger joints like knees, shoulders, hips)

What time of day is this most common?

A

Sx most intense in the AM

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24
Q

Clinical manifestations:

How are muscles?

A

Atrophy of muscles

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25
Q

Clinical manifestations:

Atrophy of muscles: Why does this occur?

A

Disuse of muscles and stretching of tendons and ligaments related to acute inflammation

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26
Q

Clinical manifestations:

What happens to bones? why?

A

Misalignment of bones

Due to eroded cartilage and muscle imbalance

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27
Q

Clinical manifestations:

Other than muscle atrophy, what happens to muscles?

Why does this occur?

A

Muscle spasm

Inflammation and pain

28
Q

Clinical manifestations:

What happens to mobility? What else?

Why does this occur?

A

Deformity and impaired mobility

Contractures and deformity

29
Q

Clinical manifestations:

What other symptoms occur? Why?

A

Fatigue, anorexia, mild fever, generalized lymphadenopathy, and generalized aching (systemic)

From the immune factors

30
Q

Clinical manifestations:

Rheumatoid nodules – What are they?

A

Rheumatoid nodules – inflammatory tissue, consisting mainly of immune cells (macrophages, lymphocytes, fibroblasts).

They may also contain deposits of fibrin.

31
Q

Eval & Management

How to diagnose?

A

Assessment

Labs:

Synovial fluid analysis Joint X-rays, MRI, ultrasounds

32
Q

Eval & Management

Diagnose: What kind of labs are needed?

A

Serum rheumatoid factor test

Serum anticyclic citrullinated peptide antibodies test (ACPA) –
specific marker

ESR – erythrocyte sedimentation rate

Serum C-reactive protein

Serum antinuclear antibody

33
Q

Eval & Management:

What is treatment?

A

Early aggressive pharmacotherapy

Surgical repair

Non-pharm

34
Q

Eval & Management:

Early aggressive pharmacotherapy: Is there a cure?

A

⍉ cure

35
Q

Eval & Management:

Early aggressive pharmacotherapy:

What does this do?

A

Slowed progression, delayed joint destruction

Symptomatic relief

36
Q

Eval & Management:

Early aggressive pharmacotherapy:

RA is treated with three classes of drugs: What are they?

A
  1. NSAIDs for pain,
  2. glucocorticoids (may delay disease progression),
  3. disease-modifying antirheumatic drugs (DMARDs)
37
Q

Eval & Management:

Early aggressive pharmacotherapy:

Glucocorticoids: What do they do?

A

(may delay disease progression),

38
Q

Eval & Management:

Early aggressive pharmacotherapy:

NSAIDs: What are they for?

A

NSAIDs for pain

39
Q

Eval & Management:

Non-pharm treatment?
ARTHUR

A

Assistive devices

Rest & pacing activities

Therapeutic activities –

Heat/cold application

Use splints, braces for support & alignment to prevent deformities

Relaxation techniques

40
Q

Eval & Management:

Non-pharm treatment?
ARTHUR

A = Assistive devices ~

A

walkers, rails

41
Q

Eval & Management:

Non-pharm treatment?
ARTHUR

Therapeutic activities –

A

balanced exercise & rest

PT & OT ~ massage, warm baths

42
Q

Eval & Management:

Non-pharm treatment?
ARTHUR

Heat/cold application:

What is heat for? What does it do

What is cold for? What does it do?

A

Heat=vasodilation=decrease pain

Cold=vasoconstriction=dec pain, swelling

43
Q

Eval & Management:

Non-pharm treatment?
ARTHUR

Use splints, braces for what?

A

for support & alignment to prevent deformities

44
Q

DMARDs: Disease-Modifying Antirheumatic Drugs

What is the aim of these drugs?

A

Aim: reduce joint destruction & slow disease progression

45
Q

DMARDs: Disease-Modifying Antirheumatic Drugs

What are the two groups? What are they based on?

A

Nonbiologic (traditional) vs Biological (recombinant DNA)

based on molecular size & how produced
46
Q

What is the most rapid acting and first choice DMARD?

A

Methotrexate

47
Q

RA
DMARDs:

Methotrexate- MOA

How does it treat disease progression?

A

Slows disease progression (not just sx relief!!!)

Interferes with rapid growth/cell division

48
Q

RA
DMARDs:

Methotrexate- MOA

What does it do with B and T lymphocyte activity?

A

Immunosuppression of B&T lymphocyte activity

49
Q

RA
DMARDs:

Methotrexate- MOA

What does it interfere with?

A

Interferes with rapid growth/cell division

50
Q

RA
DMARDs:

Methotrexate

How long does it take therapeutic effects to occur?

A

Therapeutic effect: 3 to 6 weeks

51
Q

RA
DMARDs:

Methotrexate

What are adverse effects?

A

Hepatic fibrosis

Bone marrow
suppression

GI ulceration

pneumonitis

CVD, infection, lymphomas

52
Q

RA
DMARDs:

Methotrexate

What are fatal toxicities that can occur?

A

Fatal toxicities of bone marrow, liver, lungs, kidneys, skin reactions, hemorrhagic enteritis, GI perforation

53
Q

RA
DMARDs:

Methotrexate

What is necessary when taking this med?

A

Supplemental folic acid necessary

54
Q

RA
DMARDs:

Methotrexate

What tests are needed when taking this med?

A

Periodic liver, kidney function tests, CBC, Platelet

55
Q

RA

DMARDs:

Methotrexate

How is life expectancy effected?

A

Reduced life expectancy: CVD, cancers

56
Q

DMARDs II: Major Biologic DMARDs

What are they?

A

Tumor necrosis factor (TNF) inhibitors

57
Q

DMARDs II: Major Biologic DMARDs

Tumor necrosis factor (TNF) inhibitors:

What are TNF ?

A

TNF is an inflammatory response mediator & responsible for joint injury

58
Q

DMARDs II: Major Biologic DMARDs

In RA, what does TNF bind to?

A

In RA – TNF binds with synovial cells –

59
Q

DMARDs II: Major Biologic DMARDs

In RA – TNF binds with synovial cells – what does this lead to? (What is stimulated)

A

stimulates inflammatory mediators, promotes infiltration of neutrophils & macrophages –> inflammation & joint destruction

60
Q

DMARDs II: Major Biologic DMARDs

TNF inhibitors- What do they do?

A

Binds tightly to TNF & makes it inactive, preventing it from interacting with natural receptors on human cells in the synovium

61
Q

DMARDs II: Major Biologic DMARDs

TNF:
Some interfere with B&T lymphocytes

What does this put someone at increased risk of?

A

Increased risk of serious infection

62
Q

DMARDs II: Major Biologic DMARDs

TNF- What do some of them interfere with?

A

Some interfere with B&T lymphocytes

63
Q

DMARDs II: Major Biologic DMARDs

TNF inhibitors: How is it administered? What can it be combined with?

A

Weekly subQ injections

Can be combined with methotrexate

64
Q

DMARDs II: Major Biologic DMARDs

TNF inhibitors: Work by neutralizing TNF

Drugs include?

A

Etanercept [Enbrel]**
Adalimumab [Humira]
Certolizumab pegol [Cimzia]
Golimumab [Simponi]
Infliximab [Remicade]

  • end in ‘mab’
65
Q

Adverse effects of Etanercept

A

Injection site reactions
Serious infections
Severe allergic reactions
Heart failure
Cancer/Hematologic disorders
Liver injury
CNS demyelinating disorders

66
Q

Adverse effects of Etanercept

Serious infections include? What may need to be done if infection occurs?

A

Fungal, TB, opportunistic

Reactivation of HBV

Increased risk with DM, HIV, immunosuppressant drugs

May need to d/c if infection develops

67
Q

Adverse effects of Etanercept

Serious infections include: Fungal, TB, opportunistic

A

TNF plays crucial role in immune response to infection, especially TB

PATHO/PHARM II (27 decks)

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