AH II Test 1 Flashcards
Immunity
- **Innate: **exists at birth without prior contact with antigen; includes skin, mucous membranes, cilia, gastric juice, enzymes in tears and sliva, coughing, sneezing; WBCs (neurtrophils and monocytes), inflammatory process.
- Acquired:
active=body develops antibodies and sensitized lymphocytes to foreign substance after invasion (may be natural or artificial), long term–memory!
passive=host receives antibodies (temporary-no memory agent)-can be natural or artificial (antibodies are administered)
Functions of the
Immune Response
- Defense (protects against microo’s, prevents infection, attacks foreign antigens/pathogens)
- Homeostasis (digest damaged cellular substances)
- Surveillance (recognize/destroy cell mutations, prevent malignancies)
Spleen
lymphoid tissue that stores lymphocytes, filters foreign substances from the blood
Phagocytes
-include monocytes and macrophages (capture and present antigen to lymphocytes to stimulate immune response)
Interferon
Interferon=immunomodulator
a cytokine protein that activates components of the immune system, also modifies the immune response by (at times) suppressing antibody production, used to treat some immune disorders.(alpha, beta, gamma)
examples–inhibit viral replication, activate NK cells and macrophages, antiproliferative effects on tumor cells, promotes B-cell differentiation
Tachycardia and orthostatic hypotension are also commonly reported, also depression and suicidal ideation, photosensitivity.
Complement= enzymatic proteins in serum that, when activated, destroy cell membrane of antigen.
Humoral Immunity
=antibody mediated immunity
- antibodies are produced by plasma cells (B-cells)
- immunoglobulins are antibodies
- 20-30% of lymphocytes
- responsible for immunity to bacteria (and some extra-cellular viruses)
- have memory cells
Cell-Mediated Immunity
- immune response is initiated through specific antigen recognition by T cells
- 70-80% of lymphocytes are T lymphocytes
- responsible for immunity to viruses, fungi and malignancies
- attack antigen directly
- responsible for organ rejection
- have memory cells
- T Helper cells are responsible for regulation activity of all immune cells (activate antibody-producing B cells)
Immunosuppressed/
Immunocompromised
- high dose steroids
- immunosuppressants
- chemo
- AIDS/HIV
- organ/bone marrow transplant
- asplenic
- very young/old
- severe infection
- chronic dz (DM or SLE)
Labs that indicate infection
- WBC’s elevated and shift to left (neutrophils)
- lower Total Complement Assay normal is75-160 (used up when fighting infection)
- increased ESR (sed rate)-normal is <30
- increased CRP-normal is 6.8-820
- ANA should be neg
- RF should be neg
- Serum Lactate Level-increased when there’s generalized infection in the blood stream.
SLE
- multi-system inflm autoimmune dz
- cause-UV radiation, drugs, chems, viral inf, stess, increased estrogen activity
- pattern of remission/exacerbations, chronic, unpredictable course
- production of autoantibodies against nucleic acids (ANA); B and T cell hyperactivity
- white less freq than others, women 20-40
- dz of connective tissue: polyarthralgia, rash, alopecia, oral/nasal ulcers, proteinurea, fibrosis of heart valves, neuropathy, psych, cognitive dys, Raynauds, seizures, anemia of chronic dz, fever, weight loss, fatigue
- Dx-Anti-Smith ab’s and Anti-DNA ab’s are very specific to Lupus-LE cells present-ESR-CRP-decreased complement-RF+-ANA+-pancytopenia-UA shows proteinurea
- Tx=NSAIDs, glucocorticoids, immunosuppressants (azathioprine,cyclophosphamide, methotrexate, mycophenolate), antimalarial drugs (hydroxychloroquine), biologic agents (belimumab), vit D
- Avoid sun!, photosens meds, avoid stress
- cause of death=renal failure (nephritis), cardiovascular thrombotic event, generalized infection
- ND’s=fatigue, acute pain, impaired skin integrity
MS
- autoimmune dz of CNS (not periphery), chronic, progressive; tx by neurologist
- cause=viral, immunologic, genetic
- onset is insidous, gradual
- demylination of nerve fibers of white and gray matter in brain and spinal cord…sclerotic plaques (seen on MRI)
- over-active t-lymphocytes, antigen-ab rxns in CNS
- initial sx-blurred vision, tinnitus, paresthesias, sensation changes, vertigo, Lhermitte’s sign
- Northern climates
- adults age 20-50, more women
- lack of or altered nerve conduction (spacity)
- 4 types
- Key features=charcot triad (nystagmus, dysarthia (slurred speech), intention tremors (shake when reach)), muscle weakness/spacsticity, fatigue, ataxia, paresthesia, bowel/bladder dys, cognitive changes, dysphagia, heat exacerbates MS, neuropathic pain (trigeminal neuralgia, HA, extremity pain, pain from spasms), constipation
- Tx for pain=anticonvulsants, **antidepressants, **benzos, anti-arrhythmics, anti-inflam, muscle relax
- other Tx=glucocorticoids (reduce inflm at site of demylenation-given IV), immunosuppressants (methotrexate, azathioprine), immunomodulators (betaseron, avonex-given sub Q), antispasmotics (baclofen–pump), valium, botox, surgery
- Dx=MRI, CSF-spec IgG and elevated protein level, presence of WBC, electromyography (nerve conduction study), [elevated ANA or ESR or Lyme titer to r/o other causes]
- Nursing Mgt-constipation (from meds, < fluids, immobility), bladder dysfunction (failure to store-hypertonic bladder), failure to empty (hypotonic bladder*=neurogenic bladder, lack nerve impulses to contract bladder)
- exacerbated by PMS and post-partum; no sx during PG
Surgeries for MS
- tenonotomy-cut tendon
- rhizotomy-chemically ablate nerve
- myelotomy-cut nerve at spinal level
- motor point blocks-interupt impulses bye anesthesia or destroy nerve at motor point to relieve spasicity
Guillain-Barre Syndrome
(acute idiopathic polyneuritis)
- affects PERIPHERAL nervous system, cranial nerves
- autoimmune, inflammatory
- demylelination of the axons (temporary)
- pain, tingling , crawling skin
- ascending* or descending
- abrupt onset, acute, NOT chronic
- self-limiting, complete recovery possible (85-95%)
- often follows acute illness such as URI, CMV or epstein-barr, post immunization, Campylobacter jejuni
- Dx-LP with elevated CSF proteins, leukocytosis, EMG shows nerve conduction delays, PFT-worry about breathing if chest muscles paralyze
- Nursing Mgt-vent, plasmapheresis to remove antibodies, high dose immunoglobulins (Sandoglobulin)
- pain mgt (neuropathic), immobility, eye care (no blink)
- death-PE (immobility), upper GI bleed (?)
Myasthenia gravis
- autoimmune-ab’s attack Ach receptors at neuromuscular jnct; not enough Ach or too much cholinesterase; chronic, no cure
- fluctuating skeletal muscle weakness
- triggered by viral infection, hyperplasia of thymus (t-cells), genetic component
- age 10-65, more women-peak age is childbearing years.
- highly variable course of dz
- affects muscles of resp, swallow, chew, speak, eyes, facial
- death=resp failure
- Dx-EMG (electromyography), tensilon test, muscle biopsy (shows Ach receptor antibodies)
- Tensilon Test-inject tensilon (anticholinesterase), if muscle response improves=MG, no response-not MG; must have atropine available due to brady from tensilon
- Meds= anticholineserase drugs (Mestinon and Neostigmine) must be taken on time, 30-60 min bf meal with water only, immunosuppressants (azathioprine, cyclosporine), corticosteroids
- plasmaphersis, thymectomy to remove thymus
- Nursing Mgt-monitor resp status, aspiration precautions, myesthenic crisis (not enough meds vs cholinergic crisis–too much med), monitor blood levels
- myesthenic crisis-may need vent support, s/s weak skeletal muscles, ptosis, diff swallowing, dyspnea, resp failure; results from not enough meds vs. cholinergic crisis which is from too many meds
- monitor resp function with PFT (neg inspiratory pressure, tidal volumes, vital capacity), 25% reduction from baseline=resp failure
Aspiration
-may cause temperature elevation after meals!
Rheumatoid Arthritis
- chronic, systemic, nonsuppurative (=inflm without pus) inflammation of diarthrodial joints due to infiltration of immune cells (t lymphocytes) into synovial fluid where they release cytokines: TNF
- triggered by environment, virus, antigen, stress, genetic
- 2-3 x more common in women
- mostly muskuloskeletal, but anywhere connective tissue is present, vasculitis if bv involvement
- AM stiffness, bilateral, symmetrical, usually upper extremeties first,generalized weakness, anorexia, wt loss, fever, pain*, ulnar drift
- Dx=RF+, ANA+, CRP elevated, ESR elevated, CBC (anemia of chronic dz), decreased serum complement, elevated IgG, arthrocentesis with synovial fluid analysis, Xray, CT, MRI, bone scan
- Tx-focus on early intervention, prevent inflm and erosion…remission
- Meds-NSAIDs, steroids (for exacerbations), biologic therapies, immunosuppressants (DMARDs)–leflunomide, Enbrel, Methotrexate, Cyclosporine
- Non-drug=PT, OT, heat/cold, water exercise, min joint stress, splinting, massage, balanced nutr, incr mobility
- Nursing-med compliance to preent joint destruction
- RA-systemic, swollen, small, stiff
- OA-large, obese, asymmetric, degenerative, osteophytes (spurs)