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Disorders of Immune Function (3)
Hypersensitivity (too much of a response):
exaggerated immune response to a foreign substance.
mistakes self as non-self (will fight itself)
inadequate immune reaction
What is the body damaged by as opposed of?
What are the four types?
Excessive or inappropriate activation of the immune response
The body is damaged by the immune response, rather than by the antigen, (often called allergen)
Commonly divided into four types (I, II, III, IV)
- Type I: Immediate Hypersensitivity Disorders
- Type II: Antibody-Mediated Disorders
- Type III: Immune Complex-Mediated Disorders
- Type IV: Cell-Mediated Hypersensitivity Disorders
Differ in terms of type of immune response and nature/location of the antigen that is the target
Type I Hypersensitivity
What type of mediated response? Binds to what kind of cells?
What is it commonly called?
What type of treatment is necessary?
- Commonly called "allergic reactions"; produces an immediate response (within minutes of an antigen challenge)
- Systemic or anaphylactic; local or atopic reaction
- Allergen activate IgE which bind to mast cells
- At next exposure, the antigen binds with the surface of IgE releasing mediators and triggering the complement system
-hay fever, food allergies, hives, atopic dermatitis and anaphylaxis (high risk of death)
Treatment: includes epinephrine, antihistamines, corticosteroids, and desensitizing injections
desensitizing injections = allergy shots.
exposed to something and then exposed a second time to produce a response
Eosinophils, mast cells, and B cells
Type I Allergies are Mediated by IgE
What two types of cells are involved?
What kind of cells are they?
What are released to initiate response and what do they contain?
What are mast cells sources of?
Two types of cells
involved: type 2 helper T and mast cells or basophils
are tissue cells; basophils
are blood cells derived from hematopoietic precursor cells; both have granules that contain mediators that are released to initiate the response
Type 1 reaction begins with mast cell or basophil sensitization
; allergen-specific IgE antibodies attach to cell receptors; with subsequent exposure, the allergen binds and triggers a series of events that lead to degranulation
- Mast cells are source of prostaglandins (hormone-like lipid compounds), histamine (contraction of smooth muscle, and dilation of capillaries), acetylcholine (causes constriction of the lungs, difficulty breathing), adenosine (treats irregular hearbeat), chemotactic mediators, leukotrienes, and cytokines (important for cell signaling).
- That continue the rxn
Histamine is one of the first chemical mediators released during the inflammatory response as a result of...
Mast cell degranulation.
Mast cell stabilizers (used to treat asthma) prevent the histamine from being released; antihistamines (compete with histamine receptors; used to treat allergies) compete with histamine for receptor sites, lessening the inflammatory response.
What type of reaction is it?
What is it a response to?
What produces vasodilation? bronchoconstriction?
What will happen when arterioles vasodilate throughout the body?
What will happen when the bronchioles constrict?
Systemic response to the inflammatory mediators released in type 1 hypersensitivity
- histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation
- acetylcholine, kinins, leukotrienes, and protaglandins all can cause bronchoconstriction
Life-threatening hypersensitivity reaction characterized by widespread edema, difficulty breathing, and vascular shock secondary to vasodilation.
Rapid vasodilation lowers blood pressure so HR will increase to compensate.
Constriction of bronchioles will impair airway which means less oxygen for the body
Management of Anaphylaxis
What should you initially do?
If happened in the past, what are some ways to manage?
- stable airway (getting them breathing is important)
- IV access (fluid=volume to help BP)
- administer epinephrine (dilation of airways and constriction of blood vessels)
- need preloaded syringes
- prevent exposure
- educate family
- wear medical alert bracelet
What type of reaction is this? What are the antibodies and what does it react to?
What occurs in blood cells?
What type of treatment is necessary?
Cytotoxic Hypersensitivity Reaction
IgG or IgM type antibodies that react to foreign tissue of cells
Lysis (breaking/bursting) of blood cells occurs because of the activation of the complement
Usually immediate responses
Ex: blood transfusion reaction and erythroblastosis fetalis (Rh disease); drug reactions
Treatment includes ensuring blood compatibility and administering medication to prevent maternal antibody development
What type of reaction is this? What type of antibodies and what do they do?
What happens to blood vessels?
(flow through blood and gets stuck in tissues)
A systemic or local reaction
Immune complex-mediated hypersensitivity reaction
Circulating antigen-antibody complexes
accumulate and are deposited in the tissue
Triggers the complement system and inflammation
- Autoimmune conditions (e.g. systemic lupus erythematosus); Autoimmune vasculitis; Glomerulonephritis; Serum sickness
Treatment is disease specific
- Systemic: IgM, IgG, and occasionally IgA
- Local: IgG
- immune complexes deposit on walls of blood vessels and activate complement.
- blood vessels are damaged
What type of reaction is this?
What two types are there and what is there corresponding T cell?
cell-mediated hypersensitivity reaction
Cell-mediated: sensitized T cells attack antigen
- Direct cell-mediated cytotoxicity (CD8 Tcells)
- --Viral reactions
- Delayed-type hypersensitivity (activated CD4 helper Tcells)
- --Tuberculin Test
- --Allergic contact dermatitis: ex: "poison ivy", reaction to metal in jewelry
- --hypersensitivity pneumotitis
Treatment is disease specific
takes 48-72 hours to develop symptoms of delayed-type hypersensitivity
What happens? What is destroyed?
What appears in the blood?
Immune system attacks self-antigens
**Normally, self-reactive immune cells are killed in the lymphoid organs or suppressed by regulatory T cells
Anti-tissue antibodies appear in blood
- In autoimmunity, this self-tolerance breaks down
- Immune system destroys body tissues
(e.g. antithyroid antibodies)
What happens to the immune system?
Defenses are against...
What are the known characteristics (4)
Immune system looses the ability to recognize self
Defenses are directed against host
Can affect any tissue
Mechanism that triggers this response is not clear
- Known characteristics:
- --Genetics play a role
- --More prevalent in females
- --Onset is frequently associated with an abnormal stressor, either physical or psychological
- --Are frequent progressive disorders characterized by periods of exacerbation (worsening) and remission (improvement)
What assures best chance of success?
What are the 3 categories of transplants?
Best match of tissue antigens helps assure best chance of success (so the body will not fight the tissue coming in)
Donor sources may be living or a cadaver
- 3 categories:
- --Allogenic-donor and recipient are related or unrelated, but share similar tissue types
- --Synergenic-donor and recipient are identical twins
- --Autologous-donor and recipient are the same person; most successful
Patterns of Transplant Rejections
What are the three types of rejections?
- --immediate or 3 days after transplant; circulating antibodies react to graft.
- --produced by existing recipient antibodies to graft antigens that initiate a type III
- --Most common; treatable; occurs between 4 days and 3 months after transplant; Exposure to transplant causes activation of immune system, especially T cells
- --T cells cause direct lysis of graft cells and recruit and activate inflammatory cells that injure the graft.
- --Manifestations; fever, erythema, edema, site tenderness, and impaired function of organ
- --Occurs 4 months to years after transplant; likely antibody-mediated response; Antibodies and complements deposit in vessel walls of transplanted tissue, resulting in ischemia
- --It manifests with dense intimal fibrosis of blood vessels of the transplanted organ.
Host VS Graft
Host Vs Graft Disease
-host fights the graft
-The recipient's immune system attempts to eliminate the donor cells
Graft VS Host
When does this occur
What transplant is this common?
What has to occur for GVHD to develop?
What are the acute organs and how are they effected?
Transplanted immune cells attack host
- --Graft fights the host
- --Frequent and potentially fatal complication of bone marrow transplants
- --Occurs when immunocompetent fatal cells recognize host tissue as foreign and mount a cell-mediated immune response
- --Host usually immunocompromised and unable to fight graft cells, and the host's cells are destroyed
Acute or chronic
Skin: Most commonly effected; frequent desquamation (skin peeling)
GI: Nausea, bloody diarrhea, and abdominal pain
Liver: Painless jaundice, hyperbilirubinemia, sepsis, coma
Immunodeficiency (low response or no response)
What can this make people susceptible to?
Diminished or absent immune response
Renders the person susceptible to disease normally prevented; Opportunistic infections
May be acute or chronic
- --Primary: B-cell deficiencies; Ig deficiencies; T-cell deficiencies; Combined immunodeficiencies
- --Secondary (Acquired): HIV
What type of deficiency is this?
What does it infect?
What are the two types?
How is it transmitted? (3)
What age group is HIV high in?
Secondary Acquired Immunodeficiency
--Parasitic retrovirus that infects CD4 and macropahges
- Two primary types:
- --Type 1 is the most common strain
- --Type 2 is more common in West Africa; progresses to disease more slowly
In the US, rates rising among women and African Americans
HIV high in elderly
- Transmitted by body fluids (anything sticky)
- --sexual contact
- --breast milk
- --blood-to-blood contact - contaminated needles, transfusions, during pregnancy or birth
Course of HIV Infection
(How HIV infection progresses)
What are the three different stages?
Course varies from person-to-person
Without treatment most HIV+ progress to AIDS in 7-10 years
1) Stage 1/Primary infection phase
- Signs of systematic infection; fever, fatigue, myalgias, sore throat, night sweats, GI problems, swollen lymph nodes, rash, headache
- --Seroconversion: immune system responds and antibodies against HIV appear (1 month - 6 months); high viral loads
2) Stage 2/Latency (chronic asymptomatic) phase
Virus is replicating
, TH cell count gradually falls
: may last 10-11 years or longer
3) Stage 3/Overt AIDS
- Without therapy usually leads to death in 2-3 years.
- Infections begin as the viral number rise destroying the CD4
- --TH cell count <200 cells/mL or AIDS-defining illness
It takes a while for the immune system to let the world know you have HIV
asymptomatic- w/o symptoms
AIDS Classification System
What are the two types of systems?
What are the 3 sub categories in these systems?
Two systems, one based on lab findings and the other based on clinical manifestations
- --Category 1: >500 cells/microL
- --Category 2: 200-499
- --Category 3: <200
- --Category A: asymptomatic
- --Category B: some less serious manifestations of immune deficiency
- --Category C: AIDS defining illnesses present
Is there a cure?
What therapy works best?
What is the leading cause of death with HIV?
What do people with AIDS need?
Combination therapy works best⇢Highly Active Antiretroviral Therapy (HAART)
May have to change meds because of viral adaptation
Other meds and vaccines will be used to prevent (prophylactic) opportunistic infections as needed
Screen for TB; tuberculosis leading cause of death for people with HIV worldwide; often first manifestation
Emotional support (make people aware of their options and medications)
Hopsice (for anyone w/ a diagnosis and prognosis of 6mos or less)
messed up immune system
What are the three systems of opportunistic infections?
What are some malignancies associated?
What is wasting syndrome?
What are some metabolic disorders?
What is TORCHES?
- --Respiratory: bacterial pneumonia, P.Jiroveci pneumonia, TB
- --Gastrointestinal: esophageal candiasis, CMV, herpes simplex, mouth ulcers, diarrhea, gastroenteritis, cryptospiridium
- --Nervous system: toxoplasmosis (cat poop/liter), leukoencephlopathy, neurocognitive disorders, AIDS dementia complex; neuropathies
, Kaposi Sarcoma
; noninvasive cervical carcinoma
; function of impaired cell-mediated immunity
Wasting Syndrome (losing weight; "wasting away"):
--AIDS-defining illness; involuntary weight loss of at least 10% in presence of diarrhea
, >2 stools per day
, or chronic weakness and fever.
--many associated with treatment; lipodystrophy a problem, insulin-resistance/diabetes
, mitochondrial disorders
- toxoplasmosis, other infections, rubella, cytomegalovirus infection, and herpes simplex
- Epstein-Bar, and syphilis
At-Risk Individuals for Immune Dysfunction
- Very young and very old
- Poor nutrition (good nutrition necessary)
- Impaired skin integrity (break in skin)
- Circulatory issues (imflammatory reaction, blood needs to get there and clean everything out)
- Alterations in normal flora due to antibiotic therapy
- Chronic diseases especially diabetes mellitus
- Corticosteroid therapy (steroid that stops inflammation)
- Smoking (causes vasoconstriction; can mess up vitamin C)
- Alcohol consumption (liver)
- Immunodeficiency states
Optimize your Immune Health
(Also good for nursing students)
- Maintain adequate fluid intake
- Balanced diet high in monosaturated fats, whole grains, fruits, vegetables
- Moderate exercise
- Weight control
- Limit caffeine and refined sugar
- Increase antioxidants, daily source of Vitamin C
- Increase protein intake (to make antibodies)
- Get adequate sleep
- Good hygiene practices
- Manage stress
- Avoid toxins: negativity, environmental pollution, smoking