CLASS 12 - IMMUNE DISORDERS + RELATED THERAPIES Flashcards
What is immunity? What are the 2 types?
The body’s ability to resist disease.
The 2 types are innate and acquired / adaptive.
Describe innate immunity.
Which cells are involved?
Is this response antigen-specific?
The innate immune response is the body’s “first line of defense”.
Involves neutrophils + monocytes.
This response is not antigen-specific, therefore it can respond w/in minutes to an invading microorganism w/o prior exposure to it.
Describe Acquired/Adaptive Specific Immunity. What are the 2 types?
Development of immunity either actively or passively.
2 types are active + passive.
Describe Active Acquired Immunity
Does this immunity develop quickly or slowly? Is it short or long lasting?
- Active: results from the invasion of the body by foreign substances which leads to the development of antibodies and synthesized lymphocytes.
- W/ each reinvasion of the microorganisms, the body responds more rapidly and vigorously to fight it off.
- This can result naturally from a disease or artifically through vaccines.
- This immunity takes time time to develop but is long lasting
Describe Passive Acquired Immunity
Does this immunity develop quickly or slowly? Is it short or long lasting?
The host receives antibodies rather than synthesizing them.
Can happen through injection of immunoglobulin (antibodies) or transfer of antibodies across the placental membrane.
Immediate response but short-lived bc no antibodies are synthesized.
What are mononuclear phagocytes?
What is the role of mononuclear phagocytes in the immune reponse?
Includes monocytes in the blood and macrophages throughout the body.
Mononuclear phagocytes capture (via phagocytosis), process, and present antigens to the T or B lymphocytes which stimulate an immune response.
Where are B Lymphocytes located?
What is the role of B Lymphocytes in the immune response?
Produced in the bone marrow
B Lymphocytes convert to plasma cells when activated and produce antibodies
Where are T Lymphocytes located?
What is the role of T Lymphocytes in the immune response?
T Lymphocytes are produced in the bone marrow and mature in the thymus.
They play a role in long-term immunity
Responsible for immunity to intracellular viruses, tumour cells, and fungi
Where are Cytotoxic T (CD8) cells located?
What role do they play in the immune response?
Are these cells antigen-specific?
Cytotoxic T cells are produced in the bone marrow and mature in the thymus.
They attack antigens on the cell membrane of foreign pathogens and release cytolytic substances to destroy them.
These cells are antigen-specific and are sensitized by exposure to the antigen.
Where are T Helper (CD4) cells located?
What is the role of T Helper Cells in the immune response?
Produced in the bone marrow and mature in the thymus.
- Play a role in the regulation of cell-mediated immunity and the humoral response.
- produce cytokines
- stimulate phagocyte-mediated ingestion + killing of microbes
- stimulate eosinophil-mediated immunity
Where are natural killer cells located?
Are these cells antigen-specific?
NK cells are located in the cytoplasm.
Prior sensitization is not required. These cells play a role in the recognition and killing of virus-infeced cells, tumor cells, and transplanted graphs. They “survey” for malignant cell changes.
Where are dendritic cells located in the body?
What role do they play in the immune response?
Dendritic cells are located in the skin, nose, lungs, stomach, and intestines. When immature, they are located in the blood.
Dendritic cells capture antigens at sites of contact w the external environment such as the skin + mucous membranes and transport them to T cells w specificity for those antigens.
Play a role in activating the immune response
What are cytokines? What is their function?
messengers between the cell types; instruct other cells to alter their proliferation, differentiation, secretion, or activity.
What are the 4 types of cytokines?
- interleukins
- interferons
- tumor necrosis factor
- colony stimulating factors
describe the function and effect of interleukins.
function - enhances immune response effect - promotes B + T cell proliferation
describe the function and effect of interferons
anti-viral (inhibits viral replication)
describe the function and effect of tumor necrosis factor (TNF)
enhance inflammation and immune response
kill tumor cells
describe the function of Colony stimulating factors
give 2 examples of CSFs.
stimulate proliferation and differentiation of cells
ex - erythropoietin, neupogen
Compare the humoral immune response and cell-mediated immune response. What cells are involved? What does each response protect us against?
homoral response: antibody-mediated, involves B lymphocytes.
Protects us from bacteria, extracellular viruses, and respiratory + GI pathogens.
cell-mediated response: antigen mediated, involves T lymphocytes. Protects us from intracellular viruses, chronic infectious agents, and tumour cells.
Describe the process of the humoral immune response
- The B cells convert to plasma cells when activated and produce antibodies IgM and IgG
- antibodies attach to their antigens and either interfere w their function or mark them for phagycytosis
- Results in the production of memory B cells for quicker rxn w second exposure
In the humoral response:
- which antibodies are primarily produced in the primary immune response (first exposure to antigen)?
- which antibodies are primarily produced upon the secondary immune response
Primary immune response: primarily IgM
Secondary immune response: primarily IgG
Identify the 4 classes of antibodies
- IgM
- IgG
- IgA
- IgE
Identify the locations of the following immunoglobulins in the body:
- IgM
- IgG
- IgA
- IgE
- IgM (plasma)
- IgG (plasma, ISF)
- IgA (body secretions such as tears, saliva, breast milk)
- IgE (plasma, ISF)
Describe the function of IgM.
- Responsible for primary + early immune response
- forms antibodies to ABO blood antigens
Describe the function of IgG.
- responsible for secondary immune response; predominant in late immune response
- only immunoglobulin that crosses the placenta
Describe the function of IgA.
lines mucous membranes + protects body surfaces
useful in defending the airways
Describe the function of IgE.
causes symptoms of allergic rxns by releasing histamine
fixes to mat cells and basophils
assists in defense against parasitic infections
Describe the process of the Cell-Mediated Immune Response. What cells are involved?
Involves antigen recognition by T cells. T Lymphocytes attack infected cells.
Includes T-Lymphocytes (Cytotoxic and T Helper Cells), macrophages, and NK cells.
Cytotoxic T cells attach antigens on the cell membrane of foreign pathogens and release cytolytic substaces that destroy the pathogen. They then produce Memory Cytotoxic T Cells.
T Helper cells stimulate pahocyte-mediated ingestion + killing of microbes,regulate cytotoxic T cell and B cell responses, produce cytokine messengers, and produce Memory T Helper Cells.
Identify which of the following would result in a humoral response. Which would result in a cell-mediated response? - Anaphylactic shock - atopic diseases - transfusion rxns - bacterial infections - tuberculosis - fungal infections - contact dermatitis - graft rejection - destruction of cancer cells
- Anaphylactic shock (HUMORAL)
- atopic diseases (HUMORAL)
- transfusion rxns (HUMORAL)
- bacterial infections (HUMORAL)
- tuberculosis (CELL-MEDIATED)
- fungal infections (CELL-MEDIATED)
- contact dermatitis (CELL-MEDIATED)
- graft rejection (CELL-MEDIATED)
- destruction of cancer cells (CELL-MEDIATED)
Describe the normal immune response (7 steps)
- Virus invades the body through a break in the skin or another portal of entry.
- Macrophage recognizes the antigens on the surface of the virus. The macrophage then digests the virus and displays pieces of it (= antigens) on its surface.
- T-Helper Cells recognize the antigen displayed on the macrophages which stimulates the production of cytokines: IL1 and IL2, TNF, and interferon.
- IL2 instructs other T Helper cells and Cytotoxic T cells to multiply. T Helper cells release cytokines causing B cells to multiply and produce antibodies.
- The antibodies bind to the virus and mark it for macrophage destriction.
- Cytotoxic T Cells and NK cells destroy the infected body cells.
- Once the virus is gone, activated T and B cells are turned off by suppressor T cells. Memory B and T cells remain behind and respond quickly if the same virus attacks again.
Identify the 3 types of altered immune responses.
- immunodeficiencies / immuno-incompetencies (severe infections, cancers, immune deficiency diseases)
- hypersensitivity (allergies, autoimmune disorders)
- active acquired immune responses
A 40 y/o woman who completed first round of chemotherapy for breast cancer. She reports feeling malaise + chills 2 wks after her first treatment. She has been gardening and cut herself on rose bushes.
She has an oral temp of 38, a WBC count of 2.0 x 109 / L, and an ANC of 1.3 x 109 / L.
What is the appropriate term for this patient’s WBC?
What does this mean for the patient clinically?
What should be included in the assessment of this patient?
- leukopenia w mild neutropenia
- patient is very susceptible to infection
- a temp of 38 on someone who is neutropenic is probably equal to a temp of 39 on a normal patient
assesment should include wound assesment on hand, look for infection (oral, respiratory, GI, GU) culture + sensitivity of wound + blood, swab oral cavity, urine sample, bone marrow biopsy if neutropenia is unexplained.
What is neutropenia? What is severe neutropenia?
neutropenia = ANC less than 1.5
severe neutropenia = ANC less than 0.5
What are the clinical implications of severe neutropenia? What steps should the nurse take?
Patient is at high risk for sepsis due to limited ability to fight infection and shows diminished signs of inflammation.
Administer broad spectrum antibiotics.
What is the normal range for WBC count?
5-10 x 109 / L
What are the possible causes of a higher WBC count?
What are the possible causes of a lower WBC count?
WBC count could be raised due to inflammatory + infectious processes or leukemia
WBC count could be lowered due to aplastic anemia, autoimmune diseases, overwhelming infection, side effects of chemotherapy and irradiation.
What is the normal range of band neutrophils?
What are the possible causes of an increased band neutrophil count?
0-1 x 109 / L (0%-9%)
Acute infections
What is the normal range of eosiniphils?
What are the possible causes of an increased eosiniphil count?
What are the possible causes of a decreased eusinophil count?
0.00-0.5 x 109 / L (1%-4%)
Causes of an increased eosinophil count:
- Allergic rxns
- Eosinophilic and chronic granulocytic leukemia
- Hodgkin’s disease
- Parasitic disorders
Causes of a decreased eosinophil count:
- Corticosteroid therapy
What is the normal range of lymphocytes?
What are the possible causes of an increased lymphocyte count?
What are the possible causes of a decreased lymphocyte count?
1.0-4.0 x 109 / L (20%-40%)
Causes of an increased lymphocyte count: • Chronic infections • Lymphocytic leukemia • mononucleosis • Viral infections
Causes of a decreased lymphocyte count:
• Corticosteroid therapy
• Whole body irradiation
What is the normal range of monocytes?
What are the possible causes of an increased monocyte count?
0.1-0.7 x 109 / L
causes of increased monocyte count: • Acute infections • Chronic inflammatory • Hodgkin’s disease • Malaria • Monocytic leukemia
What is the normal range of segmented neutrophils?
What are the possible causes of an increased segmented neutrophil count?
2.5-7.5 x 109 / L (62%-68%)
increased count:
• Bacterial infections
• Collagen diseases
• Hodgkin’s disease
decreased count:
• Aplastic anemia
• Viral infections
What is hypersensitivity?
What is an autoimmune disease?
Hypersensitivity occurs when the immune response is overreactive against foreign tisse or reacts aginst its own tissue, resulting in tissue damage.
An autoimmune disease is a type of hypersensitivity response in which the body fails to recognize self-proteins and reacts against self-antigens.
Describe Type I Hypersensitivity. Which antibodies mediate this rxn?
Type I Hypersensitivity rxns are IgE mediated rxns - these include anaphylactic rxns (anaphylaxis, atopic rxns).
Anaphylactic rxns occur in people who are sensitized to specific allergens.
Describe the process of an anaphylactic rxn upon the first exposure to an allergen and subsequent exposures.
First exposure: IgE antibodies are produced and bind to mast cells and basophils. These cells have granules w/in them that contain potent chemical mediators such as histamine, serotonin, bradykinin, kinins, leukotrienes, eosiniphil chemotactic factor of anaphylaxis).
subsequent exposures (when the reaction actually occurs): the allergen links with the IgE bound to mast cells or basophils which triggers degranulation of the cells and the release of chemical medaitors from the granules. These chemicals attack target tissues which cause clinical symptoms of allergy.
What are the clinical symptoms of allergy?
- sm muscle contraction
- increased vascular permeability
- vasodilation
- hypotension
- increased secretion of mucous
- itching
What skin allergy test is used to test for type I hypersensitivity?
Wheal-and-flare rxn
Will result in a pale wheal (pink, raised, edematous, pruritic areas) containing edematous fluid surrouned by a red flare from hyperemia.
What is anaphylaxis?
How fast does this rxn occur? How many organ systems are involved?
What are the initial symptoms?
What is the leading cause of anaphylaxis-related deaths?
Anaphylaxic can occur when chemical mediators are released systemically (ex - injection of drugs, insect stings)
rxn occurs w/in minutes
minimum of 2 systems involved.
Can be life threatening.
Initial symptoms = edema and itching at site of exposure
Shock can occur rapidly
Death occurs if emergy treatment is not initated
Medications are the leading cause of anaphylaxis-related deaths.
What are the symptoms of anaphylaxis in the following systems:
- neurological
- skin
- respiratory
- cardiovascular
- GI
NEUROLOGICAL
- headache
- dizziness
- paresthesia
- feeling of impending doom
SKIN
- pruritis
- angioedema
- erythema
- urticaria
RESPIRATORY
- hoarseness
- coughing
- sensation of narrowed artery
- wheezing
- stridor
- dyspnea
- tachycardia
- cardiac arrest
CV
- hypotension
- dysrhythmias
- tachycardia
- cardiac arrest
GI
- cramping
- abdominal pain
- nausea
- vomiting
- diarrhea
What are 2 potential drugs used to treat anaphylaxis?
Epinephrine (IM, IV)
Antihistamines
Describe the MOA of epinephrine
Epinephrine is sympathomimetic (mimics SNS response)
Adrenergic agonist
Alpha receptors (heart, blood vessels)
beta receptors (lungs)
What does it mean to be atopic?
What disease can result from being atopic?
to be atopic means to have an inherited tendency to become sensitive to environmental allergens
atopic diseases that can result include:
- allergic rhinitis
- asthma
- atopic dermatitis
- urticaria (hives)
- angioedema
Describe allergic rhinitis.
What substances cause it?
Allergic rhinitis is the most common type I hypersensitivity rxn.
Can be year round (perennial) or seasonal.
Primary cause is airborne substances such as pollens, dusts, or moulds.
Perennial allergic rhinitis may be caused by dust, moulds, or animal dander.
Seasonal allergic rhinitis can be caused by pollens from trees, weeds, or grasses.
What are the targeted areas effected by allergic rhinitis? What are the symptoms?
Conjunctiva of eyes, mucosa of upper respiratory tract
Symptoms include nasal discharge, sneezing, lacrimation, mucosal swelling w airway obstruction, pruritis around eyes, nose, throat, and mouth.
Describe the link between asthma and atopic disorders.
Many patients w asthma have a history of atopic disorders.
What is atopic dermatitis? Describe this condition in terms of the type of lesions.
atopic dermatitis is a chronic, inherited skin disorder.
skin lesions do not represent wheal and flare rxns; lesions are more generalized and involve vasodilation of blood vessels resulting in interstitial edema w vesicle formation
Describe urticaria (hives)
cutaneous rxn
histamine causes localized vasodilation (erythema), transudation of fluid (wheal), flaring (caused by dilation of blood vessels on the edge of the wheal), and itching.
Describe angioedema. How does it differ from urticaria?
Which body parts does it effect?
Similar to urticaria but involves deeper layers of the skin + submucosa; welts not as apparent
Effects eyelids, lips, tongue, larynx, hands, feet, GI tract, and genitals.
swelling usually begins in the face and then progresses to other parts of the body
Describe Type II Hypersensitivity. What antibodies mediate it?
Consists of Cytotoxic and cytolytic rxns.
Mediated by IgG and IgM antibodies, which
bind to antigens on the cell surface. Antigen-antibody complexed activate complement systme which mediates the rxn.
What are the 3 types of target cells destroyed during a type II hypersensitivity rxn?
What are the 2 ways in which cellular tissue is detroyed?
At what rate does tissue damage occur?
RBCs, platelets, and WBCs
Cellular tissue can be destroyed by:
- activation of complement cascade resulting in cytolysis
- enhanced phagocytosis
Tissue damage occurs rapidly
Identify 3 pathophysiological disorders characteristic of type II hypersensitivity rxns.
- hemolytic transfusion rxns
- goodpasture’s syndrome
- Myasthenia gravis
What is a hemolytic transfusion rxn?
If a recipient receives a transfusion w incompatible blood, antibodies immediately coat the foreign RBCs resulting in agglutination. The clumping cells block small blood vessels in the body. The use/depletion of these clotting factors results in bleeding.
What is Goodpasture’s syndrome?
Rare disorder involving the lungs + kidneys
Antibody-mediated immune rxn ocurs involving the glomerular and alveolar basement membranes
circulating antibodies combine w tissue antigen to activate the complement system which causes deposits of IgG to form along the basement membranes of the lungs or kidneys
this rxn may result in pulmonary hemorrhage and glomerulonephritis.
Describe Type III Hypersensitivity.
Which antigens predominate this response?
Is this rxn local or systemic? Can it be immediate or is it delayed?
Type III Hypersensitivity consists of Immune-Complex rxns
IgM + IgG bind to soluble antigens forming an immune complex. These complexes are too small to be removed by the phagocyte system so they deposit in tissues + vessels.
Can be local OR systemic, immediate OR delayed
What are the 5 common sites for antigen-antibody complex deposition in the body during a type III hypersensitivity rxn?
Kidneys Skin Joints Blood Vessels Lungs
Which 3 autoimmune disorders are associated with severe type III hypersensitivity rxns?
- systemic lupus erythematosus (SLE)
- acute glomerulonephritis
- rheumatoid arthritis
Describe Type IV Hypersensitivity rxns.
Which antibodies mediate this response?
How long does this rxn take?
Delayed Hypersensitivity Rxns
This is a cell-mediated response, therefore there are no antibodies involved. Tissues are destroyed by T-Lymphocytes.
This rxn takes several days to develop (over 48 hrs)
Describe Allergic Contact Dermatitis as a type IV hypersensitivity rxn.
occurs when you are exposed to a substance that easily penetrates the skin such as nickel, rubber, poison ivy, or cosmetics
upon first exposure, the substance combines w epidermal proteins and becomes antigenic. memory cells for the antigen form.
allergic rxn occurs upon the second exposure. eczematous skin lesions occur w/in 48 hours.
Describe the ABCDs of hypersensitivity rxns.
A - type i Atopic / Allergic
B - type ii cytotoxic (antiBodies against the Body)
C - type iii ab + ag Complex deposits in tissue
D - type iv Delayed
Identify and describe the 2 types of latex allergies.
- Type IV allergic contact dermatitis (caused by chemicals used in the manufacturing of latex gloves - rxn ocurs w/in 6-48 hrs).
- Type I allergic rxns (response to the natural rubber latex proteins, occurs w/in minutes).
Describe Latex-Food Syndrome.
Some proteins in rubber are similar to food proteins. Therefore some foods may cause an allergic rxn in people who are allergic to latex.
Banana, avocado, chesnut, kiwi, tomato, water chestnut, guava, hazelnut, porato, peach, grape, and apricot
What is Multiple Chemical Sensitivity?
What are the common causative substances? What are the symptoms?
Subjective illness, symptoms are not found during physical examination.
Consists of recurrent, non-specific symptoms attributed to low levels of chemical, biological, or physical agents.
Common causative substances include smoke, pesticides, plastics, synthetic fabrics, fragrance, petroleum, paint fumes
symptoms: headache, fatigue, dizziness, nausea, congestion, itching, sneezing, sore throat, chest pain, breathing problems, muscle pain / stiffness, skin rash, diarrhea, bloating, gas, confusion, difficulty concentrating, memory problems, mood changes
Identify the 6 drug classes that can be used to treat allergic disorders.
Antihistamines Antipruritic drugs Corticosteroids Leukotriene receptor antagonists Mast cell-stabilizing drugs Sympathomimetic / decongestant drugs
Identify the 4 types of blood transfusion rxns.
acute hemolytic rxn
febrile rxn
mild allergic rxn
anaphylactic rxn
describe the cause of acute hemolytic rxns
acute hemolytic rxns are caused by the transfusion of incompatible blood
antibodies in the plasma attach to antigens on the transfused RBCs which results in the destruction of those RBCs.
Identify the clinical manifestations of acute hemolytic rxns
Fever w or w/o chills Pain in lower back, chest, abdomen, or flank Flushing Tachycardia Dyspnea Hypotension Vascular collapse Hemoglobinuria Acute jaundice Dark urine Bleeding Kidney injury Shock Cardiac arrest DIC Death
how can we treat acute hemolytic rxns?
Treat shock and DIC if present
Maintain BP with IV colloid solutions and give diuretics to maintain urine flow
Insert catheter or measure voided amounts to monitor hourly urine output - dialysis may be required if renal failure occurs
of the 4 types of blood transfusion rxns, which is the most common?
febrile rxns
Describe the cause of febrile rxns. Is this a hemolytic rxn?
not hemolytic.
febrile rxns are caused by either leukocyte incompatibility or sensitization to donor WBCs, platelets, or plasma proteins
What are the clinical manifestations of febrile rxns?
Sudden chills and fever (rise in temp greater than 1 degree C) Headache Flushing Anxiety Muscle pain Vomiting
How can we treat febrile rxns? When should we restart the transfusion?
Administer antipyretics
Avoid giving ASA in patients w thrombocytopenia
Do not restart the transfusion unless the physician orders it.
What are some preventative measures we can take to prevent febrile rxns?
consider administering leukocyte-poor blood products (filtered, washed, or frozen) for patients w a history of 2+ such rxns
give acetaminopen or diphendyramine (benadryl) 30 mins before transfusion
What is the cause of mild allergic rxns?
In which population are these rxns more common in?
Caused by sensitivity to foreign plasma proteins
More common in people with a history of allergies.
Identify the clinical manifestations of mild allergic rxns.
Flushing
Itching
Urticaria (hives)
How can we treat mild allergic rxns (3 drug classes)?
When can we restart tthe transfusion?
Give anthistamines, corticosteroids, or epinephrine
If symptoms are mild and transient, the tranfusion may be restarted slowly
Do not restart the transfusion if fever or pulmonary symptoms develop
What are the potential preventative measures we can take to prevent mild allergic rxns?
Consider using washed RBCs and platelets
What are the causes of anaphylactic blood transfusion rxns?
Sensitivity to donor plasma proteins
Infusion of IgA proteins to IgA deficient recipient who has developed IgA antibodies.
What are the clinical manifestations of anaphylactic blood transfusion rxns?
Anxiety Urticaria Dyspnea, wheezing, cyanosis Bronchospasm Hypotension Shock Possible cardiac arrest
How can we treat anaphylactic blood transfusion rxns?
Initiate CPR is indicated Administer oxygen Have epinephrine ready for injection Antihistamines, corticosteroids, beta2-agonists - do not restart transfusion
What are some preventative measures we can take to prevent anaphylactic blood transfusion rxns?
Transfuse extensively washed RBC products from which all plasma has been removed
Use plasma from IgA-deficient donors
Identify 4 other types of acute transfusion rxns.
Circulatory overload rxn
Sepsis rcn
Transfusion-releated acute lung injury (TRALI) rxn
Massive (multi) blood transfusion rxn
What is autoimmunity?
What causes it?
Immune rxn to self-proteins.
The immune system no longer differentiates self from non-self.
Immune cells that are normally unresponsive (tolerant to self-antigens) are activate
Autoantibodies and autosensitized T cells cause pathophysiological tissue damage.
Cause is unknown.
Define immunodeficiency
Immunodeficiency is a condition in which the immune system does not adequately protect the body.
Immunodeficiency disorders involve an impairment of one or more immune mechanisms such as:
- phagocytosis
- humoral response
- cell-mediated immune response
- complement system
- combined humoral and cell-mediated deficiency
What are the 2 types of Immunodeficiency disorders?
Primary + Secondary
Describe Primary Immunodeficiency Disorders and the 4 categories.
Primary Immunodeficiency Disorders are rare and often serious
Categories are:
- Phagocytic defects
- B-cell deficiency
- T-cell deficiency
- Combined B and T cell deficiency
Describe Secondary Immunodeficiency Disorders.
More common, less severe than primary immunodeficiency disorders.
- Chronic granulomatous disease
- Job syndrome
- Bruton agammaglobulinemia
- Common variable hypogammaglobulinemia
- Selective IgA, IgM, or IgG deficiency
- DiGeorge syndrome (thymic hypoplasia)
- Severe combined immunodeficiency disease
- Ataxia-telangiectasia
- Wiskott-Aldrich syndrome
- Graft-versus-host disease
… are all types of which immunodeficiency disorder?
Primary Immunodeficiency Disorders.
What are the 4 types of Antibody Dependent Immunity?
Natural Active - natural antigen trigger Artificial Active - vaccine Natural Passive - from mother Artificial Passive - immunoglobulins given ex snake venom
Describe vaccinations.
Antigen - marker, usually a protein, found on the surface of infectious agents
Introduction of foreign antigens to trigger an immune response, allowing the immune system to react more effectively the next time it is exposed to the antigen
Vaccinations sometimes require boosters
Identify the 5 types of vaccines
Bacterial Viral Attenuated Inactivated Toxoids
Describe bacterial vaccines
Inactivated bacterial exotoxins (ex - tetanus)
Killed bacteria
Live attenuated bacteria (increased response, increased risk)
Describe viral vaccines
Live attentuated virus (increased response, increased risk)
Killed (inactivated) virus
Recombinant - cultured vaccine (needs booster)
- most safe
- vaccine made from specific part of the germ and put in yeast culture rather than from human blood
Live viral vaccines produce increased protection and longer immunity and production of IgAs, IgGs, and cellular immunity
Killed virus only produces IgGs.
Describe attenuated (live) vaccines
Infectious agent is intact but unable to cause disease or reproducem safer than attenuated
Describe inactivated (killed) vaccines
Infectious agent is intact but anable to cause disease or reproduce; safer than attenuated
Describe toxoids
Bacterial toxin / agent only
Has been modified in such a way that prevents it from causing disease
What are the 3 precautions + contraindications associated with vaccines?
Immunocompromised patients who are unable to produce an active immune response
History of allergy or anaphylactic responses to vaccine components
Pregnancy (only inactivated vaccines are suitable during pregnacy)
What are the common adverse effects of vaccines?
What is a rare adverse effect?
Redness, swelling, soreness, tenderness at site of injection Fever Fatigue Poor appetite Headache
Rare: anaphylaxis
What is the MOA of glucocorticoids?
Glucocorticoid receptors are located inside of the cell rather than on the surface.
Modulate the production of regulatory proteins rather than the activity of signalling pathways.
Produce anti-inflammatory and immunosuppressive effects.
