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MICR 270 > Module 4 - Adverse Reactions and Immune Defects > Flashcards

Module 4 - Adverse Reactions and Immune Defects Flashcards

1
Q

What is immunodeficiency?

A

a disorder or condition where the IS has reduced function or is absent and can be traced to the failure of one or more parts of the immune system

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2
Q

2 types of immunodeficiencies

A

primary and secondary

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3
Q

Primary Immunodeficiency

A

Cogenital and derive from a genetic or developmental defect leading to abnormal maturation of the IS. May be associated with defects in innate or adaptive immunity

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4
Q

cogenital

A

present from birth

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5
Q

why are primary immunodeficiencies rare?

A

in most cases, the foetus will not survive

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6
Q

Secondary Immunodeficiency

A

acquired and a result from environemental factors affectong and compromising the IS

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7
Q

what is the most well studied secondary immunodeficiency?

A

AIDS, the causitave agent being HIV

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8
Q

causes of secondary immunodeficiency?

A

-undergoing chemo
-immunosuppressive medication
-chronic infection
-cancer

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9
Q

Grouping primary immunodeficiecies

A

according to the faulty component of the immune system. Deficiencies:
-B-cell
-T-cell
-Complement
-Phagocytic
-Combined B and T cell

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10
Q

B-cell deficiencies

A

-characterized by dysfunctional B lymphocytes or a decrease in their prevalence
-deficiency in B-cell development results in an increased susceptability to infection, especially by encapsulated bacteria

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11
Q

encapsulated bacteria

A

encompass both Gram-positive and Gram-negative bacteria with the unifying feature being the production of capsule composed of polysaccharides

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12
Q

T-cell deficiencies

A

-characterized by dysfunctional T-lymphocytes or a decrease in their prevalence
-a deficiency in T-cell development results in an increased susceptability to viruses, protozoans and fungi

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13
Q

why do first symptoms of B-cell deficiencies usually appear around 7-9 months old?

A

during breastfeeding, the mother transfers IgG to the baby, around 7-9 months the antibody pool from the mother decreases. Because of B-cell deficiency, the infant is not able to synthesize normal levels of antibodies to compensate

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14
Q

when do T-cell deficiencies occur?

A

-3-4 months after birth

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15
Q

Complement Deficiencies

A

-prone to frequent severe bacteria infections and complications arising from inability to clear immune complexes

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16
Q

C3 deficiencies

A

-display severest symptoms

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17
Q

Phagocytic Deficiencies

A

-deficiencies can appear at various stages
-bacterial and fungal infections are frequent and severe
- causing deep abscesses

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18
Q

Combined B and T cell deficiencies

A

-dysfunctional and/or low numbers of lymphocytes
-both hummoral and cell-mediated responses of ADAPTIVE IS are compromised
-characterized by little or no resistance to infection, thus pathogens that cause mild diseases in average human may be life threatening (chickenpox)
-suffer fatal infections in the first year of life

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19
Q

what does AIDS stand for

A

Acquired Immunodeficiency Syndrome

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20
Q

what does Acquired in AIDS stand for?

A

individuals do not inherit this type of disease, which is a major difference between AIDS and other primary immunodeficiencies

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21
Q

what does Immunodeficiency stand for in AIDS

A

the one disease characteristic AIDS has in common is the breakdown of their immune system

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22
Q

what does Syndrome stand for in AIDS

A

the plethora of rare but ravaging diseases that take advantage of the body’s collapsed defences

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23
Q

Mode of transmission of HIV in north america

A

sexual intercourse is primary transmission of HIV

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24
Q

Mode of transission of HIV in eastern europe and central asia

A

non-sterile injecting drug paraphenalia is the parimary mode of transmisison

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25
Q

Mode of transmission of HIV in Africa

A

heterosexual sex with a contaminant epidemic in children (mother to child)

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26
Q

HIV outcomes without treatment

A

immunosuppression, neuropsychiatric abnormalities and death

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27
Q

HIV: primary infection

A

-mount an effective immune response for first couple weeks
-over time this response will provide ineffective through the various stages of the disease, as the HIV virus compromises the individuals IS

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28
Q

stages of HIV infection

A
  1. Primary Infection
  2. Acute Infection
  3. Chronic Infction
  4. AIDS
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29
Q

CD4 T lmphoyte count at primary infection

A

HIGH

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30
Q

HIV: acute infection

A

-HIV targets and infects cells with CD4 on their surface, including CD4+ helper T cells
-Viral infection causes a drastic decrease in the level of CD4+ helper T cells while the level of virus in the blood increases
-HIV in blood is HIGH increasing risk of transmission

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31
Q

2-4 weeks after primary exposure to HIV

A
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32
Q

why do CD4+ cell levels stop crashing?

A

CD4+ helper T cell levels increase after the initial decrease, as some antibodies are formed against the virus allowing the immune system to recover some of the lost cell population

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33
Q

HIV: Chronic Infection

A

-clinical latency
-HIV continues to multiply in the body at a steady state
-do not experience any HIV-related symptoms, transmission is still possible
-Anti-HIV antibodies are detectable
-HIV can begin to evade the immune response that is present by changing antigens through high mutation rates
-8-10 years

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34
Q

HIV: AIDS

A

-CD4 helper t cells get exhausted
-diagnosed with AIDS if CD4 level less than 200 cells/mm3
-viral load drastically increases as the virus continues to acquire mutations that allow it to further avoid immune defenses
-as the IS is weakened, patients become susceptible to infections
-survive for about 3 years

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35
Q

Antiretroviral therapy

A

-firs twas approved in 1987
-do not sure or kill HIV but prevent it from replicating
-led to declines in AIDS

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36
Q

which immune cell does HIV preferably replicate in?

A

Helper T cells

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37
Q

Autoimmunity

A

when the IS initiates a reaction in response to its own cells (overactivated and attacks healthy cells)

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38
Q

Autoimmune Disease

A

-failure of an organism to distiguish self from non-self and any disease that results from this is an autoimmune disease

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39
Q

how much of the human population do autoimmune diseases affect

A

5-7%

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40
Q

Gender Rates wthin autoimmune disease population

A

78% of people with autoimmune disease are female

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41
Q

What is the main cause of an autoimmune disease

A

-genetics (mainly)
-infection by bacteria/virus
-chemical exposure

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42
Q

two classifications of autoimmune diseases

A

organ-specific and systemic

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43
Q

Autoantibody

A

produced by the immune system that is directed against a self antigen

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44
Q

Organ-specific Autoimmune diseases

A

-immune response directed to an antigen that is unique to a single organ or gland
-disease manifestations are limited to specific organ

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45
Q

Most common target organs of auntoimmune diseases

A

-thyroid
-stomach
-adrenal glands
-pancreas

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46
Q

Thyroid organ specific autoimmune disease

A

Graves, overactivty of thyroid gland, known as hyperthyroidism

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47
Q

Graves Disease

A

Thyroid-stimulating hormone (TSH) is produced by pituitary gland to regulate hormone production. Graves patients produce autoantibodies that engage TSH receptors resulting in an overproduction of thyroid hormones

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48
Q

Goiter

A

enlarged thyroid due to overstimulation of thyroid cells. Other symptoms include weightloss, rapid heartbeat, irritability, poor regulation of body temp etc

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49
Q

Systemic Autoimmune Diseases

A

-immune response is directed towards a broad range of antigens that are characteristic of a number of organs and tissues

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50
Q

Rheumatoid arthritis

A

-systemic autoimmune disorder that presents as chronic inflammation of joints, other organ systems can be affected
-common women age 40-60

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51
Q

How does Rheumatoid arthritis ocurr?

A

-produce autoantibodies most commonly IgM to portion of the Fc receptor of IgG (rheumatoid factors)
-factors bind to ciculating IgG forming immune complexes that become deposited in joints
-deposits activate cascade leading to prolonged inflammation and joint tissue damage

52
Q

cure for autoimmune diseases

A

none

53
Q

treatment for autoimmune disease

A

immunosuppression; reducing strength of bodys immune response

54
Q

in additon to autoimmune drugs, when would immunosuppressants be used

A

organ transplant, during this time paitents may not be able to fight infection as their immune system is inhibited

55
Q

Understanding rejection: 3 signals of inflammation

A

T-cell activation signal:
1. Antigen Presentation
2. Co-stimulation
3. Proliferation

56
Q

4 main classes of immunosupressive drugs

A
  1. Corticosteriods
  2. Cytotoxic drugs
  3. Immunophils
  4. Lymphocyte-depleting Therapies
57
Q

Corticosteriods

A

Anti-imflammatory; kills T-cells

58
Q

Cytotoxic Drugs

A

Blocks cell division nonspecifically

59
Q

Immunophilin

A

blocks T cell response

60
Q

Lymphocyte-depleting Therapies

A

Kills T-cells non-specifically, kills activated T-cells

61
Q

Side effects of immunophilin

A

Drug: Cylosporine
Effects: nephrotocicity, hypertension, hirsutism, hypertrichosis, gingival hyperplasia

62
Q

Side effects of Cytotoxic drugs

A

Drug: Methotrexate
effects: nausea, vomitting, hair loss, tired, dizzy, chills, headache, sores, skin infection, sun sensitivity, rash, stuffy, low blood cell levels…

Drug: Cyclophosphamide
Effects: nausea, vomitting, loss appetite, stomach ache, diarrhea, darkening of skin/nails

63
Q

Side effects of corticosteriods

A

Drug: Prednisone
Effects: osteoperosis, hirsutism, hypertrichosis, diabetogenic

64
Q

types of infections immunosupressive drugs can have on the host due to weakend immune system

A

Latent or Opportunistic infections

65
Q

Latent Infections

A

-infections that are inactive, hidden or dormant

Most common: TB, HSV1/2, CMV, EBV and VZV

66
Q

Opportunistic Infections

A

-commonly occur when there is reactivation of pathogen that is already present in the host
-also result when pathogen is picked up but the blunted immune response of host is unable to combat pathogen
-can arise from bacteria, viruses, parasites or fungi

67
Q

FUNGAL opportunistic infections

A

-Pneumocystis
-Cryptococcosis
-Candidiasis
-Aspergillosis

68
Q

Pneumocystis Jiroveci

A

common name: PCP
Infects: pneumonia of lungs

69
Q

Cryptococcosis

A

common name: Crytptococcal Disease
Infects: Lungs, may spread to brain

70
Q

Candidiasiss

A

Common name: thrush
Infects: mouth, throat & vagina

71
Q

Aspergillosis

A

Infects: Lungs

72
Q

BACTERIAL opportunistic Infections

A

-tuberculosis
-Mycobacterium Avium COmplex

73
Q

Tuberculosis

A

common name: consumption
Infects: Lungs

74
Q

Mycobacterium Avium Complex

A

common name: MAC
Infects: lungs, lymph nodes, or entire body depending on site of infection

75
Q

PARASITIC opporitunistic infections

A

Toxoplasmosis

76
Q

Toxoplasmosis infects:

A

skeletal muscle, myocardium, brain and eyes

77
Q

VIRAL opporitunistic infections

A

-Cytomegalovirus
-Herpes simplex virus
-Varicella Zoster Virus
-Mononucleosis

78
Q

Cytomegalovirus

A

common name: CMV
infects: eyes, brain, other internal organs

79
Q

Herpes Simplex Virus (HSV)

A

common name: herpes
infects: mouth, skin, lips, eyes & genitals

80
Q

Varicella Zoster Virus

A

common name: chickenpox
Infects: skin or internal organs

81
Q

Mononucleosis

A

Common name: Epstein Barr virus or kissing disease
infects: lymph nodes, throat, salivary glands, liver, spleen & blood

82
Q

Hypersensitivity

A

excessive reactions produced by the normal immune system. Clinical conditions cary based on the mechanisms involved and time taken for rxn to develop

83
Q

Hypersensitivity Type I

A

Immediate/Anaphylaxis

ex. allergies

84
Q

Hypersensitivity Type II

A

Cytotoxic

ex. blood diseases like transfusion reactions OR Hemolytic disease of the newborn

85
Q

Hypersensitivity Type III

A

Immune complex-mediated

ex. Comtribute to development of autoimmune diseases: systemic lypus OR rheumatoid arthritis

86
Q

Hypersensitivity Type IV

A

Delayed Type

ex. Skin reactions: contact dermatitis

87
Q

Mediators for type I hypersensitivity

A

Allergens: normally a harmless substance, but in this case produces an abnormal immune response called allergic reaction

88
Q

8 major food allergens

A

-milk
-eggs
-wheat
fish
-crustacean shellfish
-tree nuts
-peanuts
-soya

89
Q

what cells do allergens affect

A

IgE, Basophils and mast cells

90
Q

Mechanisms of reactions to allergens

A

primary and secondary

91
Q

primary exposure to an allergen

A

the allergen induces hummoral response where plasma cells secrete an excessive amount of IgE antibodies whiich bind to mast cells and basophils

92
Q

secondary exposure to same allergen

A

membrane-bound IgE cross-links with the allergen which initiates degranulation of basophils and mast cells, releasing vasoactive mediators causing vasodilation and smooth muscle contraction

93
Q

degranulation

A

release of granules

94
Q

Reaction time of Type I hypersensitivty reactions

A

can be immediate (minutes for anaphylatic) and can lead to death in as little as 15 mins. Rarely type 1 reactions take longer (after 24 hrs) but most occur soon after exposure

95
Q

Clinical manifestations of Type I hyper sensitivity

A

-Allergic rhinitis
-Atopic dermititis (eczema)
-Asthma
-Hives (urticaria)

96
Q

Mediators of type II hypersensitivity

A

-IgG
-IgM
-NK cells
-the complement system

97
Q

Mechanism of reaction for type II hypersensitivity

A

-IgGs/IgMs bond to antigens on the surface of cells such as erythrocytes
-once antibodies attached through antigen-binding regions, the Fc region is free and can activate 2 processes: CLASSICAL COMPLEMENT ACTIVATION (leading to MAC or opsonization) & ANTIBODY DEPENDENT CELL MEDIATED TOXICITY
-these mediate destruction of cells, leading to excessive inflammatory response

98
Q

Membrane Attack complex

A

creates holes in cell membrane leading to cell lysis

98
Q

Opsonization

A

leads to phagocytosis by phagocytes such as macrophages

99
Q

Type II hypersensitivity reaction time

A

minutes to hours

100
Q

clinical manifestation type II hypersensitivity

A

-Drug induced hemolytic anemia
-Transfusion rxns

101
Q

Transfusion rxns

A

Depending on blood type, you will only be able to safely recieve ceratin blood types during a blood transfusion. This is due to expression of specific antigen on your RBCs, meaning if you dont express antigens, you have the antibodies against them

101
Q

Drug Induced Hemolytic anemia

A

-Some antibiotics can bind nonspecifically to proteins on RBC membranes and form complex which sometimes induced complement-mediated cell lysis
-As RBCs rupture, the # of RBCs decrease resulting in anemia
-anemia disappears when drug removed
*pennicillin

102
Q

universal donor

A

O negative

103
Q

Universal reciepnt

A

AB

104
Q

Type III hypersensitivity mediators

A

-Immune complexes (antigen-antibody complexes)
-Neutrophils
-Complement proteins

105
Q

Mechanism of reaction type III hypersensitivity

A

-the reaction of antibodies with antigens generates immune complexes. When immune complexes are not cleared, they can accumulate and deposit in tissue

-the immune complexes will activate the complement which will induce inflammatory reactions through neutrophil attraction to the site of deposition

-Neutrophils release lytic enzymes as they attempt to phagocytose the immune complexes, which weakens surrounding cell membranes causing tissue damage

106
Q

Type III hypersensitivity reaction time

A

3 to 10 hours after exposure to an antigen (sometimes days to weeks)

107
Q

Clinical manifestation Type III hypersensitivity

A

Serum sickness

108
Q

Serum sickness

A

-rxns are observed after administration of antitoxins containing foreign serum

-recipent of antiserums develop specific antibodies for this protein & form immune complexes

-after days -week symptoms occur

-complexes accumulate in tissues where filtration of plasma occur and can contribute to pathogenesis

-clinical efects subside when antigen broken down

109
Q

whats an antitoxin

A

and antibody that counteracts a toxin

110
Q

Type IV hypersensitivity mediators

A

-CD8+ cytotoxic T cells
-CD4+ Helper T cells
-Macrophages
***only type of hypersensitivity NOT mediated by antibodies

111
Q

Type IV Hypersensitivtiy mechanism of Reaction

A

-after exposure to antigen, T cells become activated and initiate an immune response
-sensitized helper T cells will release cytokines that activate macrophages or cytotoxic T cells which mediate direct cellular damage

112
Q

Type IV Hypersensitivtiy Reaction time

A

two - three days

113
Q

Type IV hypersensitivity clinical manifestation

A

-Inflammatory Bowel Disease
-Contact Dermatitis

114
Q

Inflammatory Bowel Disease

A

group of conditions characterized by chronic inflammation of all or parts of digestive tract
2 most common: chrons & collitis
-falls into class of autoimmune disease

115
Q

Contact Dermatitis

A

-type of DTH response causing red itchy rash on skin that has been in contact with small, reactive molecules which create complexes with skin proteins
-poison ive, formaldehyde, nickel …

116
Q

Erythrocyte sedimentation rate (ESR)

A

rate at which RBC sediment in one hour
*non-specific measure of inflammation

117
Q

Microcytic anemia

A

presence of small RBC

118
Q

what type of hypersensitivity does not involve antibodies and is only cell-mediated

A

type IV

119
Q

Albuterol

A

used to relax muscles found in the airways to increase airflow to the lungs

120
Q

Asthma

A

-abnormal inflammatory response to a specific or nonspecific stimuli in the bronchial lining, resulting inn obstruction of small and large airways
-muscles contract and become inflammed
-increase in mucous secretion

121
Q

which immunoglobin is responsible for asthma

A

IgE

122
Q

what type of hypersensitivity is asthma

A

Type I

123
Q
A

MICR 270 (5 decks)

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