Term
| Rheumatoid Arthritis (RA) |
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Definition
CHRONIC and PROGRESSIVE inflammatory disorder.
Affects synovium of joints.
Leads to pain, stiffness, joint damage and disagbility.
Severity of disease and progression vary.
Tx: anti-inflammatory, immunosuppressives, biologic response modifiers. |
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Term
| RA, clinical presentation |
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Definition
Slow progressing symptoms
- fatigue, weakness
- low grade fever
- joint pain
- stiffness of the hands (symmetrical)
- erythematous appearing joints
Symmetrical joint involvement of small joints (hands, wrists, feet) but can involve large joints too |
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Term
| RA clinical presentation cont.. |
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Definition
Inflam and swelling may be visible/palpable.
Soft tissue around joints spongy warm, and erythematous (red).
Eventually destruction of tendons and ligaments leads to various deformities.
Extra-articular Sx may be present:
pleural effusion, pericarditis, lymphadenopathy |
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Term
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Definition
Considered auto-immune disease
Involves T lymphocytes (T cells) in the inflamed joint and proinflammatory cytokines.
Genetically mediated process involving:
- antigen presentation to T cells alert it to inflammation
- T cells infiltrate joint and secrete TOXIC PROTEASES
- activates cellular and humoral immune responses that include cytokines, etc. and ultimately results in loss and damage of cartilage and bone. |
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Term
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Definition
Proteins that act as intracellular messengers for immune system.
Include interleukins (IL) and interferons, and tissue necrosis factor. (TNF)
Produced in response to cytokines or microbes.
Act locally, but also can lead to systemic effects |
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Term
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Definition
Heavily involved in inflammation and joint destruction.
TNFalpha and IL-1 most abundant cytokines in synovial fluid |
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Term
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Definition
NSAIDs
- NSAIDs and COX-2 inhibitors used early for symptom relief, but do not prevent joint destruction.
DMARD's (disease modifying antirheumatic drugs)
- Methotrexate, leflunomide, sulfasalazine
- takes time to see clinical improvement
Corticosteroids
- Prednisone is the SYNTHETIC VERSION OF CORTISOL
- produces quick and significant improvement in inflammation
Biologic Response Modifiers |
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Term
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Definition
Stress hormone - physical emotional or chemical stress triggers its release.
Secreted from the adrenal cortex.
Increases gluconeogenesis and lipolysis for fuel.
Enhances epinephrine synthesis and sensitizes tissues to the effects of catecholamines. |
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Term
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Definition
Prednisone (Deltasone)
Dexamethasone (Decadron)
Hydrocortisone (SoluCortef)
Methylprednisolone (SoluMedrol)
PrednisOLONE (Orapred) |
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Term
Corticosteroid MOA
**look at slide 19 for adverse effects table |
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Definition
Decreases inflammation by suppressing migrations of polymorphonuclear leukocytes (PMLs).
Reversal of increased capillary permeability.
Immunosuppression by decreasing activity and volume of the lymphatic system
- neutropenia, leukopenia and eosinopenia |
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Term
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Definition
Lowest possible dose is used.
Bone scan used for long-term disease monitoring.
Patients need Ca and Vitamin D supplementation.
Alternate day dosing used to minimize adverse effects, but difficult to adhere to.
Must be tapered off |
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Term
| Sulfasalazine (Azulfidine) |
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Definition
MOA: suppress immune system and may inhibit TNFalpha. ultimately inhibits prostaglandin synthesis
Adverse Effects
- nausea rash (lupus like rxn)
- pneumonitis, BONE MARROW SUPPRESION.
- headache, GI upset, leukopenia, megaloblastic anemia
Contraindicated for pts with sulfa allergy |
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Term
| Hydroxychloroquine (Plaquenil) |
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Definition
MOA: suppresses T cells, improves Sx's, but doesn't delay bony lesions.
ADE's
- dyspepsia, nausea, abdominal pain
- rashes, nightmares, visual disturbances |
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Term
| Methotrexate (MTX) (Rheumatrex) |
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Definition
MOA: folic acid antagonists that impairs DNA synthesis of leukotrienes? IMMUNOSUPPRESSANT. Inhibits leukotriene synthesis, and decreases TNFalpha and IL-1
Used in lower dose than when its used for cancer
ADE's
- abdominal cramping and stomatitis.
- NEED concomitant folic acid therapy
- potential toxicity w/renal insufficiency
- avoid using NSAIDS w/MTX if possible to avoid GI and Renal issues |
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Term
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Definition
MOA: prodrug w/an active metabolite that interferes w/the cell cycled and synthesis of lymphocytes.
Must be taken with cholestyramine
ADE's
- Diarrhea
- Alopecia
- Nausea and headache
drug has greater than 14 day half life |
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Term
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Definition
MOA: prodrug that is IMMUNOSUPPRESSANT
reducing the function of bodys immune response
Blocks purine metabolism and inhibits DNA, RNA and protein synthesis
ADE's
- fatigue and nausea |
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Term
Biologic Response Modifiers (BRM)
"TNFalpha Inhibitors) |
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Definition
TNF promotes inflammatory response that causes most RA problems.
Artificial bioengineered molecule.
- Etanercept (ENBREL) decoy receptor that binds TNFalpha
Monoclonal antibodies (MAbs)
- infliximab (REMICADE)
- adalimumab (HUMIRA)
ADE's
- all TNF inhibitors increase risk of serious life-threatening infections due to fungi, TB and some bacteria. |
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Term
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Definition
Abatacept (Orencia) - blocks T cell stimulation
Rituximab (Rituxan) - depletes B cells
Anakinra (Kineret) - IL-1 inhibitor
Newer agents: Tocilizumab, Ocrelizumab |
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Term
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Definition
Unusual or easy bruising is sign of bone marrow suppression.
Lowered Exercise tolerance is a sign of bone marrow suppression.
infections, skik rashes (inspect regularly)
Hydration is important for renal function and skin tone.
Pain level
Catabolic effects of DMARDs |
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Term
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Definition
Uric acid is produced by degradation of nucleic acids.
Gout is when plasma urate concentration is elevated due to overproduction, decreased elimination or combo.
Hyperuricemia does not always lead to gout, but patients cannot have gout w/out hyperuricemia. |
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Term
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Definition
Uric acid >7mg/dL in males and 6 in females.
Common in men 30-50 and postmenopausal women.
Associated w/CV disease, alcoholism, obesity, hypertriglyceridemia, insulin resistance, and renal insufficiency.
Meds that cause gout:
- Thiazide diuretics, ARB's and aspirin can all interfere with urinary excretion of urate.
Pain is often described as intense and excruciating. |
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Term
| Gout pathogenesis and clinical manifestations |
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Definition
Intermittent monoarthritis
- sodium urate in joint synovial fluid (bundle of crystal in soft tissue)
- classical 1st metatarsophalangeal joint, but knee and carpal tunnel too
Rapid onset of monoarthritis
- joint warms swells and is painful with redness
Inflammatory response to phagocytize crystals which releases proteolytic enzymes that DAMAGE TISSUE |
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Term
Drugs used to treat gout;
NSAIDS and corticosteroids |
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Definition
NSAIDs
- indomethacin most common, be
- cautious cause gout is associated with worsening renal function
- COX-2 inhibitors also effective
- opioids for pain
Corticosteroids
- prednisone, methylprednisolone for acute gout that are unresponsive to NSAIDs |
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Term
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Definition
old drug, prevents neutrophil migration, DECREASING PHAGOCYTOSIS AND PERHAPS COX-2 EXPRESSION
ADE's
- diarrhea, nausea, vomiting
- large doses may produce GI hemorrhage or renal failure
- long term use - bone marrow suppression |
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Term
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Definition
Used for chronic gout or prevent recurrence.
PROBENECID (BENEMID) AND SULFINPYRAZONE
MOA: lower blood uric acid lvls by increasing excretion by blocking reabsorption of filtered in renal tubules.
ADE's Gi discomfort and rash
Avoid regular dose aspirin (blocks uricosuric effect)
HYDRATE ESPECIALLY DURING EXERCISE |
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Term
| Xanthine Oxidase Inhibitor |
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Definition
only used for long term management and prevention of gout
ALLOPURINOL
MOA: blocks enzyme xanthine oxidase which catalyzes final steps of purine metabolism
Better for gout due to excessive production
ADE's headache heartburn and diarrhea |
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Term
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Definition
aka Systemic lupus erythematosus (SLE)
Autoimmune disease affects variety of organs.
Common constitutional Sx's
- fever, weight loss, fatigue
Promotes B cell activity to SELF AND FOREIGN antigens (destructive immune system) |
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Term
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Definition
NSAIDs
- help reduce pain and inflammation and combat fever
Corticosteroids
- inflammation
MTX, leflunomide previously discussed |
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Term
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Definition
Severe SLE involves major organs
- glomerular nephritis, pneumonitis, neurological disease, hematologic disorders
Prompt treatment with high dose IV Corticosteroids or other medications such as Chemotherapy or Immunosuppressives |
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Term
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Definition
May be able to identify S&S
Treatments involve immmunosuppressives
- infection, monitor skin for reddened and warm areas
- report low grade fever
- keep equipment clean
- patient isolation when possible
May be taking drugs that cause photosensitivity |
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Term
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Definition
Caused by aging process/repetitive joint use on cartilage.
Involves subchondral bone, menisci, ligaments, periarticular muscle and capsule/synovium |
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Term
| Osteoarthritis Treatments |
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Definition
Aspirin, Acetaminopen, NSAID's, Cox-2 inhibitors like Celecoxib (Celebrex).
Hyaluronate, Glucosamine, and Chondroitin |
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Term
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Definition
Site: localized joint.
Pathology: biomechanical, leads to loss of cartilage
Sx: pain, stiffness <20 min, limited motion
Inflammation: Usually limited, may be present in advanced disease
Osteophytes: usually present
Rheuatoid factors: absent |
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Term
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Definition
Site: articular, systemic and extraarticular manifestations
Pathology: autoimmune response leads to joint destruction
Sx: pain, joint swelling >1 hr, limited motion
Inflammation: chronic
Osteophytes: absent
Rheuatoid factors: frequently present |
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