CLASS 12 - IMMUNE DISORDERS + RELATED THERAPIES Flashcards

1
Q

What is immunity? What are the 2 types?

A

The body’s ability to resist disease.

The 2 types are innate and acquired / adaptive.

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2
Q

Describe innate immunity.
Which cells are involved?
Is this response antigen-specific?

A

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.

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3
Q

Describe Acquired/Adaptive Specific Immunity. What are the 2 types?

A

Development of immunity either actively or passively.

2 types are active + passive.

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4
Q

Describe Active Acquired Immunity

Does this immunity develop quickly or slowly? Is it short or long lasting?

A
  • 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
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5
Q

Describe Passive Acquired Immunity

Does this immunity develop quickly or slowly? Is it short or long lasting?

A

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.

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6
Q

What are mononuclear phagocytes?

What is the role of mononuclear phagocytes in the immune reponse?

A

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.

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7
Q

Where are B Lymphocytes located?

What is the role of B Lymphocytes in the immune response?

A

Produced in the bone marrow

B Lymphocytes convert to plasma cells when activated and produce antibodies

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8
Q

Where are T Lymphocytes located?

What is the role of T Lymphocytes in the immune response?

A

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

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9
Q

Where are Cytotoxic T (CD8) cells located?

What role do they play in the immune response?

Are these cells antigen-specific?

A

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.

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10
Q

Where are T Helper (CD4) cells located?

What is the role of T Helper Cells in the immune response?

A

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
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11
Q

Where are natural killer cells located?

Are these cells antigen-specific?

A

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.

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12
Q

Where are dendritic cells located in the body?

What role do they play in the immune response?

A

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

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13
Q

What are cytokines? What is their function?

A

messengers between the cell types; instruct other cells to alter their proliferation, differentiation, secretion, or activity.

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14
Q

What are the 4 types of cytokines?

A
  • interleukins
  • interferons
  • tumor necrosis factor
  • colony stimulating factors
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15
Q

describe the function and effect of interleukins.

A
function - enhances immune response
effect - promotes B + T cell proliferation
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16
Q

describe the function and effect of interferons

A

anti-viral (inhibits viral replication)

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17
Q

describe the function and effect of tumor necrosis factor (TNF)

A

enhance inflammation and immune response

kill tumor cells

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18
Q

describe the function of Colony stimulating factors

give 2 examples of CSFs.

A

stimulate proliferation and differentiation of cells

ex - erythropoietin, neupogen

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19
Q

Compare the humoral immune response and cell-mediated immune response. What cells are involved? What does each response protect us against?

A

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.

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20
Q

Describe the process of the humoral immune response

A
  • 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
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21
Q

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
A

Primary immune response: primarily IgM

Secondary immune response: primarily IgG

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22
Q

Identify the 4 classes of antibodies

A
  • IgM
  • IgG
  • IgA
  • IgE
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23
Q

Identify the locations of the following immunoglobulins in the body:

  • IgM
  • IgG
  • IgA
  • IgE
A
  • IgM (plasma)
  • IgG (plasma, ISF)
  • IgA (body secretions such as tears, saliva, breast milk)
  • IgE (plasma, ISF)
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24
Q

Describe the function of IgM.

A
  • Responsible for primary + early immune response

- forms antibodies to ABO blood antigens

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25
Q

Describe the function of IgG.

A
  • responsible for secondary immune response; predominant in late immune response
  • only immunoglobulin that crosses the placenta
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26
Q

Describe the function of IgA.

A

lines mucous membranes + protects body surfaces

useful in defending the airways

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27
Q

Describe the function of IgE.

A

causes symptoms of allergic rxns by releasing histamine
fixes to mat cells and basophils
assists in defense against parasitic infections

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28
Q

Describe the process of the Cell-Mediated Immune Response. What cells are involved?

A

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.

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29
Q
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
A
  • 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)
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30
Q

Describe the normal immune response (7 steps)

A
  1. Virus invades the body through a break in the skin or another portal of entry.
  2. 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.
  3. T-Helper Cells recognize the antigen displayed on the macrophages which stimulates the production of cytokines: IL1 and IL2, TNF, and interferon.
  4. 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.
  5. The antibodies bind to the virus and mark it for macrophage destriction.
  6. Cytotoxic T Cells and NK cells destroy the infected body cells.
  7. 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.
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31
Q

Identify the 3 types of altered immune responses.

A
  1. immunodeficiencies / immuno-incompetencies (severe infections, cancers, immune deficiency diseases)
  2. hypersensitivity (allergies, autoimmune disorders)
  3. active acquired immune responses
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32
Q

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?

A
  • 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.

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33
Q

What is neutropenia? What is severe neutropenia?

A

neutropenia = ANC less than 1.5

severe neutropenia = ANC less than 0.5

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34
Q

What are the clinical implications of severe neutropenia? What steps should the nurse take?

A

Patient is at high risk for sepsis due to limited ability to fight infection and shows diminished signs of inflammation.

Administer broad spectrum antibiotics.

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35
Q

What is the normal range for WBC count?

A

5-10 x 109 / L

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36
Q

What are the possible causes of a higher WBC count?

What are the possible causes of a lower WBC count?

A

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.

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37
Q

What is the normal range of band neutrophils?

What are the possible causes of an increased band neutrophil count?

A

0-1 x 109 / L (0%-9%)

Acute infections

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38
Q

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?

A

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

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39
Q

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?

A

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

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40
Q

What is the normal range of monocytes?

What are the possible causes of an increased monocyte count?

A

0.1-0.7 x 109 / L

causes of increased monocyte count: 
•	Acute infections
•	Chronic inflammatory
•	Hodgkin’s disease
•	Malaria
•	Monocytic leukemia
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41
Q

What is the normal range of segmented neutrophils?

What are the possible causes of an increased segmented neutrophil count?

A

2.5-7.5 x 109 / L (62%-68%)

increased count:
• Bacterial infections
• Collagen diseases
• Hodgkin’s disease

decreased count:
• Aplastic anemia
• Viral infections

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42
Q

What is hypersensitivity?

What is an autoimmune disease?

A

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.

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43
Q

Describe Type I Hypersensitivity. Which antibodies mediate this rxn?

A

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.

44
Q

Describe the process of an anaphylactic rxn upon the first exposure to an allergen and subsequent exposures.

A

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.

45
Q

What are the clinical symptoms of allergy?

A
  • sm muscle contraction
  • increased vascular permeability
  • vasodilation
  • hypotension
  • increased secretion of mucous
  • itching
46
Q

What skin allergy test is used to test for type I hypersensitivity?

A

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.

47
Q

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?

A

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.

48
Q

What are the symptoms of anaphylaxis in the following systems:

  • neurological
  • skin
  • respiratory
  • cardiovascular
  • GI
A

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
49
Q

What are 2 potential drugs used to treat anaphylaxis?

A

Epinephrine (IM, IV)

Antihistamines

50
Q

Describe the MOA of epinephrine

A

Epinephrine is sympathomimetic (mimics SNS response)
Adrenergic agonist
Alpha receptors (heart, blood vessels)
beta receptors (lungs)

51
Q

What does it mean to be atopic?

What disease can result from being atopic?

A

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
52
Q

Describe allergic rhinitis.

What substances cause it?

A

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.

53
Q

What are the targeted areas effected by allergic rhinitis? What are the symptoms?

A

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.

54
Q

Describe the link between asthma and atopic disorders.

A

Many patients w asthma have a history of atopic disorders.

55
Q

What is atopic dermatitis? Describe this condition in terms of the type of lesions.

A

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

56
Q

Describe urticaria (hives)

A

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.

57
Q

Describe angioedema. How does it differ from urticaria?

Which body parts does it effect?

A

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

58
Q

Describe Type II Hypersensitivity. What antibodies mediate it?

A

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.

59
Q

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?

A

RBCs, platelets, and WBCs

Cellular tissue can be destroyed by:

  • activation of complement cascade resulting in cytolysis
  • enhanced phagocytosis

Tissue damage occurs rapidly

60
Q

Identify 3 pathophysiological disorders characteristic of type II hypersensitivity rxns.

A
  • hemolytic transfusion rxns
  • goodpasture’s syndrome
  • Myasthenia gravis
61
Q

What is a hemolytic transfusion rxn?

A

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.

62
Q

What is Goodpasture’s syndrome?

A

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.

63
Q

Describe Type III Hypersensitivity.
Which antigens predominate this response?

Is this rxn local or systemic? Can it be immediate or is it delayed?

A

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

64
Q

What are the 5 common sites for antigen-antibody complex deposition in the body during a type III hypersensitivity rxn?

A
Kidneys
Skin
Joints
Blood Vessels
Lungs
65
Q

Which 3 autoimmune disorders are associated with severe type III hypersensitivity rxns?

A
  • systemic lupus erythematosus (SLE)
  • acute glomerulonephritis
  • rheumatoid arthritis
66
Q

Describe Type IV Hypersensitivity rxns.

Which antibodies mediate this response?

How long does this rxn take?

A

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)

67
Q

Describe Allergic Contact Dermatitis as a type IV hypersensitivity rxn.

A

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.

68
Q

Describe the ABCDs of hypersensitivity rxns.

A

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

69
Q

Identify and describe the 2 types of latex allergies.

A
  • 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).
70
Q

Describe Latex-Food Syndrome.

A

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

71
Q

What is Multiple Chemical Sensitivity?

What are the common causative substances? What are the symptoms?

A

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

72
Q

Identify the 6 drug classes that can be used to treat allergic disorders.

A
Antihistamines
Antipruritic drugs
Corticosteroids
Leukotriene receptor antagonists
Mast cell-stabilizing drugs
Sympathomimetic / decongestant drugs
73
Q

Identify the 4 types of blood transfusion rxns.

A

acute hemolytic rxn
febrile rxn
mild allergic rxn
anaphylactic rxn

74
Q

describe the cause of acute hemolytic rxns

A

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.

75
Q

Identify the clinical manifestations of acute hemolytic rxns

A
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
76
Q

how can we treat acute hemolytic rxns?

A

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

77
Q

of the 4 types of blood transfusion rxns, which is the most common?

A

febrile rxns

78
Q

Describe the cause of febrile rxns. Is this a hemolytic rxn?

A

not hemolytic.

febrile rxns are caused by either leukocyte incompatibility or sensitization to donor WBCs, platelets, or plasma proteins

79
Q

What are the clinical manifestations of febrile rxns?

A
Sudden chills and fever (rise in temp greater than 1 degree C)
Headache
Flushing
Anxiety
Muscle pain
Vomiting
80
Q

How can we treat febrile rxns? When should we restart the transfusion?

A

Administer antipyretics
Avoid giving ASA in patients w thrombocytopenia
Do not restart the transfusion unless the physician orders it.

81
Q

What are some preventative measures we can take to prevent febrile rxns?

A

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

82
Q

What is the cause of mild allergic rxns?

In which population are these rxns more common in?

A

Caused by sensitivity to foreign plasma proteins

More common in people with a history of allergies.

83
Q

Identify the clinical manifestations of mild allergic rxns.

A

Flushing
Itching
Urticaria (hives)

84
Q

How can we treat mild allergic rxns (3 drug classes)?

When can we restart tthe transfusion?

A

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

85
Q

What are the potential preventative measures we can take to prevent mild allergic rxns?

A

Consider using washed RBCs and platelets

86
Q

What are the causes of anaphylactic blood transfusion rxns?

A

Sensitivity to donor plasma proteins

Infusion of IgA proteins to IgA deficient recipient who has developed IgA antibodies.

87
Q

What are the clinical manifestations of anaphylactic blood transfusion rxns?

A
Anxiety
Urticaria
Dyspnea, wheezing, cyanosis
Bronchospasm
Hypotension
Shock
Possible cardiac arrest
88
Q

How can we treat anaphylactic blood transfusion rxns?

A
Initiate CPR is indicated
Administer oxygen
Have epinephrine ready for injection
Antihistamines, corticosteroids, beta2-agonists
- do not restart transfusion
89
Q

What are some preventative measures we can take to prevent anaphylactic blood transfusion rxns?

A

Transfuse extensively washed RBC products from which all plasma has been removed

Use plasma from IgA-deficient donors

90
Q

Identify 4 other types of acute transfusion rxns.

A

Circulatory overload rxn
Sepsis rcn
Transfusion-releated acute lung injury (TRALI) rxn
Massive (multi) blood transfusion rxn

91
Q

What is autoimmunity?

What causes it?

A

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.

92
Q

Define immunodeficiency

A

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
93
Q

What are the 2 types of Immunodeficiency disorders?

A

Primary + Secondary

94
Q

Describe Primary Immunodeficiency Disorders and the 4 categories.

A

Primary Immunodeficiency Disorders are rare and often serious

Categories are:

  • Phagocytic defects
  • B-cell deficiency
  • T-cell deficiency
  • Combined B and T cell deficiency
95
Q

Describe Secondary Immunodeficiency Disorders.

A

More common, less severe than primary immunodeficiency disorders.

96
Q
  • 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?

A

Primary Immunodeficiency Disorders.

97
Q

What are the 4 types of Antibody Dependent Immunity?

A
Natural Active
- natural antigen trigger
Artificial Active
- vaccine
Natural Passive
- from mother
Artificial Passive
- immunoglobulins given ex snake venom
98
Q

Describe vaccinations.

A

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

99
Q

Identify the 5 types of vaccines

A
Bacterial
Viral
Attenuated
Inactivated
Toxoids
100
Q

Describe bacterial vaccines

A

Inactivated bacterial exotoxins (ex - tetanus)

Killed bacteria

Live attenuated bacteria (increased response, increased risk)

101
Q

Describe viral vaccines

A

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.

102
Q

Describe attenuated (live) vaccines

A

Infectious agent is intact but unable to cause disease or reproducem safer than attenuated

103
Q

Describe inactivated (killed) vaccines

A

Infectious agent is intact but anable to cause disease or reproduce; safer than attenuated

104
Q

Describe toxoids

A

Bacterial toxin / agent only

Has been modified in such a way that prevents it from causing disease

105
Q

What are the 3 precautions + contraindications associated with vaccines?

A

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)

106
Q

What are the common adverse effects of vaccines?

What is a rare adverse effect?

A
Redness, swelling, soreness, tenderness at site of injection
Fever
Fatigue
Poor appetite
Headache

Rare: anaphylaxis

107
Q

What is the MOA of glucocorticoids?

A

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.