Immunologic/Allergy Flashcards
Allergic reactions
An allergy is defined as an immune mediated reaction to a foreign environmental allergen.
Symptoms from this are characterized by an inflammatory response such as skin, respiratory tree.
It may cause a systemic reaction.
Atopy
is a term used that is an immunoglobulin (Ig)E immune response that is exaggerated or out of character in comparison to the exposure in comparison to the innocuous environmental allergens.
Allergic Skin Reactions
usually appear as a raised, erythematous plaque, or atopic dermatitis, and there are several different manifestations whose pathophysiology extends beyond IgE mediated allergic processes.
Allergies- Epidemiology and Causes
Autoimmune responses tend to be more common with females than males.
- Allergies are more evenly distributed with both males and females. However, allergies tend to be more common in children than adults. (most likely due to the immaturity of immune responses in children, and the tendency toward humorally mediated T helper cell-2 (TH2)- type response. - Seasonal allergies vary according to hemispheric geography, which is pollen, mold, and fungal spores affect individuals according to seasonal patterns of exposure in the Northern and Southern hemispheres. - Regardless of the source, the allergen invades the body, either locally or systemically, and will cause an immune regulated response that results in either local or systemic effects.
Pathophysiology of Allergic Reactions
- All allergens are foreign substances to the body. The cellular and humoral immune response will occur after the exposure of the foreign body.
Key cell types involved releasing proteins , which signal cytokines. Key cell types signal an allergic reaction, which includes histamine containing mast cells and basophils, in addition to granular eosinophils.
It is also important to understand antibody screening plasma cells designed to produce monoclonal antibodies of single antigenic specificity.
CD4+ T helper cells are also antigen-specific and produce an array of regulatory cytokines ( interleukin (IL)-4. O;-5. (IL)-13 that upregulate humeral antibody mediated immune response, where as Th1 helper T cells predominantly produce a separate set of cytokines .
Four Types of Immune Responses According to Gell-Coombs Classification System
Hypersensitivity responses- Classic allergic responses. Type I immune responses. Classic allergic hypersensitivity reactions. These are Type 1-3.
Type 3 are drug and food allergy responses or allergies.
Type 4 are immune reactions mediate contact dermatitis, a response to certain skin irritants, such as poison ivy or poison oak.
When diagnosing someone with a type one response, the provider should obtain a good history. Describe any dietary changes in the diet, soaps, detergents, skin care products, or environmental activities that preceded the reaction.
* Type I response recommend initial skin testing.
* Later to test specific allergens that were thought to be suspicious, and initially resulted to be negative on prick testing. (this is called patch testing).
Type 2 Response
* Rh testing of the blood during pregnancy.
Type 3 Response
Initial test are used to detect compliment activation
T4 Response
Skin testing is the initial test of preference for cell mediated hypersensitivity, i.e. TB. These allergens are typically injected intradermally, and monitored for 48-72 hours for a patch.
Differential diagnosis
Allergies are triggered by exposure to environment.
A classic allergic disease is discerned from : skin tests, antigen specific IgE levels, and other diagnostic tests.
Management of Allergies
Management is focused around symptomatic relief and prevention.
One should identify the allergen or trigger, and avoid. Whether it is respect to respiratory symptoms (asthma, allergic rhinitis, cutaneous, uticaria, ocular allergies) or systematic allergic response, i.e. anaphylaxis. Atopic dermatitis, is another core atopic disorder.
Or both allergic rhinitis and asthma patients- long-term immunomodulatory therapy with allergy vaccines offer effective prophylaxis and attenuation of future atopic situations.
The pt . Must avoid irritating factors.
Skin testing, IgE testing must be instituted.
IF a pt is allergic to PCN, must also avoid Cephalosporins.
Ongoing symptom control, and immunotherapy. This can be accomplished via OTC RX., Sympathomimetics, antihistamines, corticosteroids. (new antihistamines have less anticholinergic effects. Less CNS penetration, less tachycardia and sedation.
Immunotherapy.
Allergist referral.
Rheumatoid Allergies
RA is a chronic, progressive systemic inflammatory disease that primarily affects the synovial joints, but can affect many organ systems.
Joints are destroyed over a long period of the disease, causing emotional, and physical trauma.
R.A. Epidemiology
RA is one of the most common Connective tissue diseases in the U.S., and the most destructive on the joints.
- It occurs in Women more often than men, with a ratio of 2.5 to 3.1:1, or 3 in 10,000 people worldwide.
Prevalence:
- Increases with age
- Peak of cases occur between 40-60 years of age.
- Onset 20-40 years of age.
It can be genetic- noted in first degree relatives of affected patients having a two fold to threefold higher risk of developing the disease.
There is a link between RA and human leukocyte antigen (HLA) linked to the 6th chromosome.
Although there has been known genetic risk factors, the cause of the disease is not known.
Triggers- infection, autoimmunity, environmental triggers, and hormonal influences.
RA Clinical Presentation
Patients may in the early stage of disease may complain of the following:
*Malaise
*Diffuse arthritis
*Weight loss
*Anorexia
*Low grade fever.
*Neuropathic pain in the extremities.
Pts will typically awaken with joint pain and stiffness, but improves as the day progresses.
The swelling associated with the joint pain will also abate.
However, as the day progresses over time, recurrent pain and swelling in both small and large peripheral joints may result, as well as diminished activity, and increased pain and immobility.
RA Physical Findings
Peripheral symmetric polyarthritis, and morning stiffness, lasting > 1 hour.
Commonly you may note PIP-proximal interphalangeal joints and MCP – metacarpophalangeal joints in the hands and wrists as well as the knees. In addition to the toes and ankles.
The provider should inspect and palpate the interphalangeal joints for erythema, tenderness, and edema. ( an xray should be taken, but may not show anything). However, an MRI is more promising.
As the disease progresses the affected joints will become more evidently deformed, rigid, and immobile.
PE may also show other organ disease such as: cardiac rub- with pericarditis, visceral pulmonary friction rub- inflammation of the visceral pleura, or crackles- chronic lung disease. Injected sclera- scleritis, Peripheral neuropathy. Etc.
RA Diagnostic Testing
Preferred Initial test: - Rheumatoid factor – RF, IgM class auto antibody that binds to the Fc portion of IgG molecules.
The test result provides both qualitative and quantitative information that is useful in correlating with physical markers of RA.
i.e. a positive RF titer > 1:150 is indicative of a poor prognosis, and severe disease such as rheumatoid nodules.
It is necessary to interpret both the presence of RF (qualitative) with a dilutional titer (quantitative)because RF may be present in other diseases, and this may increase with age.
It is said that only 75% of RA patients are positive for RF. Therefore RF is not diagnostic for RA.
It is said that only 75% of RA patients are positive for RF. Therefore RF is not diagnostic for RA.
More specific tests for RA:
Circulating anti-CCP antibodies (anti cyclic citrullinated peptide)- This can be more specific and can be detected earlier for RA detection.
However, they do not correlate well with the severity of the disease.
Other testing to include:
Erythrocyte sedimentation rate (ESR)- Will elevate if disease is active, but can elevate with other inflammatory disorders going on as well. So not as specific.
C-reactive protein- (CRP) – will elevate in an acute reactant of inflammation, similar as ESR.
Complete Blood Count (CBC)- Rule out anemia as a potential cause of fatigue. Also check for Leukocytosis, or Neutropenia.
Platelets – will elevate with joint inflammation.
Antinuclear Antibodies (ANA)- may help to differentiate RA from SLE. Lower titers are indicative of Rheumatoid disease.
RA Differential Diagnosis
There is an array of connective tissue diseases, which must be included in the diagnosis of RA. Below is a list of diagnoses to include: Osteoarthritis Gout Chronic Lyme disease Systemic Lupus Erythematosus (SLE) Infection by human parvovirus B19 Polymyalgia rheumatic(PMR) Sjogren’s syndrome Sarcoidosis Various neoplasms
Management of RA
Management progresses from conservative to aggressive, according to the patient’s symptoms.
The disease is quite debilitating, but so are some to the treatments of immunosuppressives, and anti-inflammatory therapies. Some things to be cautious of: * hepatotoxicity Increased risk for infection GI tract inflammation and irritation
- ** The overall goal is to manage, or reduce pain and inflammation.
- ** Preserve joint function.
Initial Management of RA
Early disease can be managed by : Physical and occupational therapy. Heat and cold therapy Exercise Rest Assistive devices Splints Meditation Chiropractic Adjustments Weight loss
Subsequent Management of RA
Drug therapies to include analgesics, NSAIDS, coriticosteroids, nonbiologic, and biologic disease- modifying antirheumatic drugs (DMARDS)
Analgesics- Tylenol, or capsaicin cream gel, lotion, or roll- on may be effective. However, they do not have any anti-inflammatory effect.
Opioids- may be used but should only be used in severe pain, and should be noted that they are addictive.
NSAIDs- Should be taken on a prn schedule when non pharmacologic agents are not effective. (They can have significant negative effects on the GI system).
EC Extra strength ASA (1000mg)can be taken if baseline LFTs, Plt counts, renal studies, as well as Hgb are all normal. Pts on anticoagulant Rx should avoid these meds. *** it is advisable that pts take this with H2 blocker such as zantac, or PPI.
Corticosteroids- upto 7.5 mg daily po, or Triamcinolone injected intra-articularly. (be cautious of side effects: adrenal insufficiency, hyperglycemia, osteoporosis, increased infection risk, and skin discoloration.
Should not be given for more than 6 months.
Calcium and Vitamin D are recommended to be given in addition.
Disease-Modifying Antirheumatic Drugs- DMARDS- these drugs include immunosuppressants. And immunmodulators of various types. They have been used for decades.
The newest of the DMARDS are the bilogid immunotherapeutic agents, including anticytokine immunotherapies and anti- B cell and anti –T cell agents. Active disease is treated early with DMARDs, within 3 mo. Of the onset.
***The provider must do a TB screening- as a potential side effect is reactivation of latent (dormant) TB infection.
Combination Rx is more effective than monotherapy with DMARDs., such as Methotrexate, sulfasalazine, and hydroxychloroquine vs methotrexate mono therapy.
One should monitor patients for the potential for infection.
Older Therapies
Other DMARDs are a possible option for treatment failure with ASA and othe NSAIDs, such as:
Azathioprine (Imuran), Gold sodium thiomalate (Myochrysine), antimalarials, penicillamine (Depen), Sulfasalazine (Azulfidine), and minocycline hydrochloride (Minocin). Hydroxchloroquine (Plaquenil) which is an antimalarial drug used in milder cases.
Most COX-2 inhibitors use to be a mainstay of Rx, are no longer due to cardiovascular risks, except Celebrex.
Follow Up and Referral RA
When following your patient with RA, you will need to involve:
Clinical evaluation and episodic adjustments
Routine laboratory evaluation at least every 3 mo which will include:
- CBC
- Platelet count
- Liver function test
- Renal function test
- Fasting glucose
- CRP you may follow for the severity and course of inflammatory process,
although, nonspecific
- ESR same as CRP rationale.
Primary care may refer to Rheumatology for initial management if NSAIDs fails, and further management with DMARDs, and methotrexate.
RA Patient Education
Patient Education:
Should encompass the emotional, social, and spiritual sequelae of living with recurrent bouts of pain and disability.
Promote self care practices.
Encouraging therapeutic goals of therapy, which should be reviewed with each visit.
Chronic Fatigue Syndrome and Fibromyalgia
Myalgic encephalomyelitis/ chronic fatigue syndrome
A disorder that is poorly misunderstood, yet has been studied by many scientists, and lay press.
- The Institute of Medicine (IOM)has recommended that it be renamed the systemic exertion disease.
- This is due to the lack of laboratory markers, and not documented in many texts.
- There is a large overlap between of CFS and Fibromyalgia syndrome.
- Over 70 % of Fibromyalgia pts meet the criteria for CFS.
- Both disorders meet recognition in people who have comorbid psychiatric illness, because 2/3 of the Fibromyalgia pts, meet criteria for depression, or anxiety disorders.
CFS Epidemiology
The etiology is difficult to discern as the definition of both disorders is not clear.
10% of these patients meet criteria for CFS.
Women are 2 times more often than men, and it affects younger women more often than older women.
CFS is considered to be an autoimmune and infectious in etiology, but the cause has not been determined.
