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MICR 270 > module 4: adverse reaction and immune defects > Flashcards

module 4: adverse reaction and immune defects Flashcards

1
Q

what is immunodeficiency

A
  • disorder/condition where the immune system has reduced function or is absent and can be traced to the failure of one more more parts of the immune system
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2
Q

what are the 2 main types of immunodeficiencies?

A
  • primary immunodeficiency
  • secondary immunodeficiency
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3
Q

primary immunodeficiency

A
  • are congenital and derive from a genetic or developmental defect
  • leads to abnormal maturation of the immune system
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4
Q

what does primary immunodeficiency lead to?

A

leads to abnormal maturation of the immune system

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5
Q

what are primary immunodeficiency associated with?

A

defects in the innate or adaptive immune systems

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6
Q

lists the primary immunodeficiency- deficiencies

A

b-cell deficiencies: 65%
t-cell deficiencies: 5%
complement deficiencies 5%
phagocytic deficiencies: 10%
combines T- and B-cell deficiencies: 15%

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7
Q

secondary immunodeficiency

A

are acwuired and result from environmental factors affecting and compromising the immune system

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8
Q

what are causes of the secondary immunodeficiency

A
  • undergoing chemotherapy treatment
  • taking immunosuppressive medication
  • contracting a chronic infection (HIV/AIDS)
  • developing cancer
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9
Q

classification of primary immunodeficiencies

A
  • B-cell deficiencies
  • T-cell deficiencies
  • complement deficiencies
  • phagocytic deficiencies
  • combined T-and B-cell deficiencies
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10
Q

B-cell deficiencies- classification of primary

A
  • characterized by dysfunctional B lymphocytes or a decrease in their prevalence
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11
Q

what would a deficiency in B-cell development result in?

A

increased susceptibility to infection, especially by encapsulated bacteria

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12
Q

congenital

A

present from birth

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13
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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14
Q

when does the first symptoms of b-cell deficiencies appear

A

age of 7-9 months old

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15
Q

clinical example of b-cell deficiencies

A

X-linked agammaglobulinemia (XLA)
- genetic disorder
- mostly in males
- don’t develop mature b-cells and results have low levels of IgG and lack all other immunoglobulins
- fine to viral and fungal infections, because their cell-meditated immune response remain normal

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16
Q

T-cell deficiencies- primary classification

A
  • dysfunctional T-lymphocytes or a decrease in their prevalence
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17
Q

what does a deficiency in T-cells result in?

A

increased susceptibility to viruses, protozoan’s, and fungi

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18
Q

when are t-cell deficiencies often identify in a person

A

by frequent infections beginning 3-4 months after birth

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19
Q

clinical example of t-cell deficiencies

A

DiGeorge syndrome
- caused by the deletion of a small segment of chromosome 22

  • they have absent or undeveloped thymus, which results in the absence of mature t-cells
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20
Q

complement deficiencies- primary deficiencies

A
  • performs multiple functions and involves the intricate regulation of nine components
  • genetic deficiencies have been described for each of these complement components
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21
Q

what people with complement deficiencies prone to

A

frequent severe bacterial infections and complications arising from inability to clear immune complexes
- C3 deficiencies display the severest symptoms, reflective of the central role played by this component in complement activities

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22
Q

phagocytic deficiencies- primary classification

A
  • can appear at various stage of this process
  • bacterial and fungal infections are unusually frequent infections and severe, often causing deep abscesses
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23
Q

combined T-cell and B-cell deficiencies

A
  • have dysfunctional and/or low number of lymphocytes
  • both humoral and cell mediated responses of the adaptive immune system are comprised
  • little or no resistance to infection thus pathogens that cause mild disease in the average human may be life threatening.
  • people suffer fatal infections within the first year of life
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24
Q

what are easier to classify? primary or secondary

A

primary

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25
Q

what does the acronym AIDS stand for?

A

Acquired
Immunodeficiency
syndrome

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26
Q

acquired- AIDS

A

individuals do not inherit this disease.

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27
Q

immunodeficiency- AIDS

A

the one disease characteristic AIDS victims have common is the breakdown of their immune system

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28
Q

syndrome- AIDS

A

the plethora of rare but ravaging disease that take advantage of the body collapsed defenses

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29
Q

secondary immunodeficiency: AIDS/HIV

A

AIDS is the final stage of following an acute and chronic HIV infection.
- many AIDS patients die from opportunistic infections as their immune system is compromised and unable to effectively protect and defend the body

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30
Q

mode of transmission of HIV

A
  • depends on the location
  • regards of the portal of entry, without treatment, the outcome is the same
  • immunosuppression, neuropsychiatric, abnormalities and death
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31
Q

north America - transmission of HIV

A

sexual intercourse

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32
Q

sub-Africa mode of transmission of HIV

A

through heterosexual sex with a concomitant epidemic in children through vertical transmission (mother to child)

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33
Q

eastern Europe and central Asia - transmission of HIV

A

use of non-sterile injecting drug parapherila

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34
Q

HIV and the immune response stages

A
  • primary infection
  • acute infection
  • chronic infection
  • AIDS
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35
Q

primary infection- HIV response

A
  • will mount an effective immune response to the virus for the first couple weeks
  • over time, response will prove ineffective through the various stages of the disease
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36
Q

Acute infection- HIV

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
  • within 2 to 4 weeks after exposure, ppl experience flu like symptoms
  • level of HIV in blood is very high during the acute infection phase
  • increases the risk of HIV transmission
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37
Q

clinical latency- HIV

A
  • HIV continues to multiply in the body at a steady state
  • ppl often do not experience HIV related symptoms, transmission still possible
  • Anti HIV antibodies are detectable
  • HIV can begin to evade the immune response that is present by changing their antigens through high mutation rates
  • about 8-10 years
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38
Q

AIDS- HIV

A
  • through clinical latency, CD4+ T helper cells get ‘exhausted’ and depleted while constantly fighting chronic HIV infection
  • HIV patients are diagnosed with AIDS if they have a CD4+ t helper t cell level of less than 200cells/mm3
  • viral load INCREASES as the virus continues to acquire mutations that allow it to further avoid immune defenses
  • patients get susceptible to infections
  • with no treatment AIDS ppl survive 3 years
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39
Q

when was the first antiretroviral therapy approved?

A

1987

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40
Q

what do the antireviral therapy- for HIV ppl do?

A
  • do not kill or cure the human immunodeficiency virus, but prevent it from replicating
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41
Q

retroviral therapy (ART) and highly antiretroviral therapy (HAART) functions

A
  • utilizes a panel of antiretroviral drugs in different combinations to prevent drug resistance by rapidly-mutating virus
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42
Q

what has retroviral therapy (ART) and highly antiretroviral therapy (HAART) led too?

A
  • staggering declines in the rate of AIDS and AIDS- associated deaths
  • HAART maintains function of the immune system, and prevents opportunistic infections that often lead to death
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43
Q

what is the benefits of retroviral therapy (ART) and highly antiretroviral therapy (HAART)

A
  • reduces the amount of HIV
  • protects the immune system
  • prevents HIV from advancing to AIDs
  • reduces the risk of HIV transmisison
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44
Q

what are screening techniques for immunodeficiencies

A
  • methods or strategies used to identify the possible presence of a disease in individuals who may be pre-symptomatic or have unrecognized symptoms
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45
Q

what do screening techniques for immunodeficiencies allow?

A

for early intervention and management of the disease

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46
Q

types of screening techniques for immunodeficiencies

A
  • complete blood counts
  • quantitative serum immunoglobulin
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47
Q

what is complete blood counts (CBC)

A

shows how many of each cell type are present in a sample of patients blood
- number then compared to a reference range of values in healthy ppl

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48
Q

what is complete blood count used for

A

to highlight any severe defect in the blood that could potentially be caused by an immunodeficiency.

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49
Q

what is quantitative serum immunoglobin?

A

tests measure the levels of IgG, IgA, IgM in a patients blood serum and compare them to a control
- if levels of antibodies are lower than normal (hypoantibody) this could be an indication of a humoral immunodeficiency

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50
Q

what does quantitative serum immunoglobin? further testing mean

A

further testing would be complete blood counts and urine protein electrophoresis which could be used to pinpoint the source of the hypogammaglobulinemia

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51
Q

urine protein electrophoresis

A

a screening test to evaluate the amount of certain protein in urine

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52
Q

step 2 of case study

A
  • review of symptoms
  • clinical findings
  • clinical history
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53
Q

what specific immune cell does HIV preferentially replicate in?

A
  • helper t-cells
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54
Q

what is autoimmunity

A
  • the immune system initiates a reaction in response to its own cells.
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55
Q

what is autoimmune disease

A

failure of an orgnaims to distinguish self from non-self causes the immune system to initiate a response against its own cells and tissues
- any disease that results from such aberrant immune response

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56
Q

what is the number of autoimmune disease within the general population

A

affects 5-7% of the human population

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57
Q

what is the number of autoimmune diseases within the affected population

A

they more commonly affect females than males. appox. 78% of individuals infected with an autoimmune disease are women

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58
Q

what is the main cause of autoimmune disease

A

the development of an autoimmune disease is highly dependent on genetics, but many other factors such as infection by bacteria or virus or chemical exposure can play a role in their development

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59
Q

how are autoimmune diseases classified

A

organ specific autoimmune diseases or systemic autoimmune diseases

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60
Q

what do autoimmune diseases often involve?

A

autoantibodies, is an antibody produces by the immune system that is directed against a self-antigen

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61
Q

what is organ specific autoimmune diseases

A

involve an immune response that is directed to an antigen that is unique to a single organ or gland.

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62
Q

target organ specific autoimmune diseases

A
  • thyroid gland
  • stomach
  • adrenal gland
  • pancreas
63
Q

example of organ specific autoimmune disease

A
  • graves disease
  • leads to overactivity of the thyroid gland known as hyperthyroidism
64
Q

normal function of thyroid stimulating hormone

A
  • produced by pitutuary gland, regulates thyroid hormones
  • binding of TSH by receptors on thyroid cells stimulate the production of thyroid hormones which control metabolism
65
Q

graves disease- normal function of thyroid stimulating hormone

A

grave patients produce autoantibodies to the receptor for TSH
- these autoantibodies continuously engage TSH receptors but unlike TSH cannot be moderated
- results in unregulated overproduction of thyroid hormones (create metabolism dysfunction)

66
Q

cause and symptoms of graves disease

A
  • cause unknown but maybe genetic and environemnt factors
  • enlargement of thyroid glands (goiter)
  • weight loss, rapid heartbeat, poor regulation of body temp, muscle weakness, irritability
67
Q

what is systemic autoimmune disease

A
  • the immune response is directed towards a broad range of antigens that are characterisiic of a number of organs and tissues
68
Q

example of systemic autoimmune disease

A
  • rheumatoid arthritis
  • typically presents as a chronic inflammation in joints but organs can be affected
69
Q

rheumatoid arthritis

A
  • women ages 40-60
  • many patients produce autoantibodies, most commonly IgM to portion of the Fc receptor of IgG, which are referred as rheumatoid factors
  • rheumatoid dfactors bind to circulating IgG forming immune complexes that become deposited within joints
  • these deposits can activate the complement cascade leading to prolonged inflammation and ultimately joint tissue damage
70
Q

can autoimmunity be cured and/or treated?

A

no it cannot be cured
- only can treat and try to reduce reactions by immunosuppresion but secondary effects may occur

71
Q

how do immunosuppressions work?

A

the drugs reduce the strength of the body’s immune response
- ideal would be suppressing the erroneous autoimmune response but that way hasn’t been found yet

72
Q

when are immunosuppression also used?

A

when people undergo a organ transplant
(so the body doesn’t see it as a foreign object and try to fight it) the drugs are used to reduce rejection by inhibiting the immune response and allowing the organ to remain healthy in its new environemnt

73
Q

what are the four classes of immunosuppressive drugs

A
  • corticosteroids
  • cytotoxic drugs
  • immunophilins
  • lymphocyte-depleting therapies
74
Q

corticosteroid action

A

anti-inflammatory; kills T-cells

75
Q

cytotoxic drugs action

A

blocks cell division nonspecificially

76
Q

immunophilins action

A

blocks T-cell responses

77
Q

lymphocyte-depleting therapies action

A

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

78
Q

mechanism of immunosuppreive drugs
1. reception, kills T-cells

A

corticosteroid

79
Q
  1. activation- blocks t-cell responses
A

immunophilin

80
Q
  1. antibody receptivity- kills T-cells nonsepcifically
A

lymphocyte-depleting therapy

81
Q
  1. antibody receptivity- nonspecifically
A

cytotoxic drug

82
Q

downside of immunosuppressive degus

A

immunophilin
cytotoxic drugs
corticosteroids

83
Q

down side - immunophilin

A

drug: cyclosporine
side effects: nephrotoxicity, hypertension, hirsutism, hypertrichosis, gingival hyperplasia

84
Q

downside- cytotoxic drugs

A

drug: cyclophosphamide
side effects: nausa, vomiting, no appetitie, diarrhea, skin darker

drug: methotrxate
side effects: hair loss, puking, tiredness, dizziness, chills, headache, rash, stuffy nose, low blood cells levels

85
Q

downsides- corticosteroids

A

drug: prednisone
side effects: osteoporosis, hirsutism, hypertrichosis, diabetogenic

86
Q

infections caused by immunosuppression

A

latent infections
opportunistic infections

87
Q

latent infections

A
  • individuals that are on immunosuppressive therapy have increased risk of pathogens that are usually assoicated with latent infections
  • infections that are inactive, hidden, or dormant
88
Q

what are the most common pathogens with latent infections

A
  • TB
  • HSV1/2 (herpes)
  • CMV (cyomegalovirus)
  • EBV (epstein-barr virus)
  • VZV (varicella zoster virus)
89
Q

opportunistic infections

A
  • commonly occur when there is reactivation of a pathogen that is already present in the host
  • result in the pathogen is picked up from environemnt, but the blunted immune response of the host is unable to combat the pathogen
  • arise from bacteria, viruses, parasites, fungi
90
Q

opportunistic infections- fungal- pneumocytis Jiroveci pneumonia

A

common name: PCP
infects: pneumonia of lings

91
Q

opportunistic infections- fungal- crytococcosis

A

common name: crytococcal disease
infects: lungs- can spread to brain

92
Q

opportunistic infections- fungal- candidiasis

A

common name: thrush
infects: mouth, throat, vagina

93
Q

opportunistic infections- fungal- aspergillosis

A

common name: N/A
infects: lungs

94
Q

opportunistic infections- parastic- toxoplasmosis

A

common name: N/A
infects: skeletal muscle, myocardium, brain, and eyes

95
Q

opportunistic infections- bacterial- TB

A

common name: consumption
infects: lungs

96
Q

opportunistic infections- bacterial- mycobacterium Avium complex

A

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

97
Q

opportunistic infections- viral- cytomegalovirus

A

CN: CMV
infects: eyes, brain, other internal organs

98
Q

opportunistic infections- viral- herpres simplex virus

A

CN: herpes
infects: skin, mouth, lips, eyes, genitals

99
Q

opportunistic infections- viral- varicella zoster virus

A

CN: chickenpox
infects: skin, sometimes organs

100
Q

opportunistic infections- viral- mononucleosis

A

CN: Epstein-Barr virus or kissing disease
infects: lymph nodes, throat, salivary glands, liver, spleen, blood

101
Q

what is hypersensitivities

A

refers to excessive reactions produced by the normal immune system

102
Q

classifications of hypersensitivities

A

type I, II, III, IV

103
Q

type I

A

immediate/anaphylaxis

104
Q

example of type I

A

allergic reactions
- food allergies

105
Q

type II

A

cytotoxic

106
Q

examples of type II

A

blood diseases:
- transfusion reactions
- hemolytic disease of the newborn

107
Q

type III

A

Immune complex mediated

108
Q

examples of type III

A

contribute to development of autoimmune diseases
- systemic lupus erythematosus
- rheumatoid arthritis

109
Q

type IV

A

delayed-type

110
Q

examples of type IV

A

skin reactions
- contract dermatitis

111
Q

type I hypersensitivity- mediators

A
  • milk
  • eggs
  • fish
  • crustacean shelfish
  • tree nuts
  • peanuts
  • wheat
  • soya
112
Q

type I hypersensitivity- mediators- immune cells

A
  • IgE
  • basophils
  • Mast cells
113
Q

type I hypersensitivity- primary exposure to an allergen

A
  • the allergen induces a humoral immune response wherein plasma cells secrete an excessive amount of IgE antibodies which bind to mast cells and basophils
114
Q

type I hypersensitivity- secondary exposure to the same allergen

A

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

115
Q

type I hypersensitivity- reaction time

A
  • can be immediate
  • can led to death in as little as 15min
  • rare are 24h after
116
Q

degranulation

A

release of granules

117
Q

type I hypersensitivity- clinical manifestation

A
  • allergic rhinitis
  • asthma
  • atopic dermatitis (eczema)
  • hives (urticaria)
118
Q

allergic rhinitis

A

generalized irritation of the nose when the immune system overreacts to allergens in the air

119
Q

atopic dermatitis (eczema)

A

a condition where an individual develops skin eruptions accompanied by redness

120
Q

asthma

A

respiratory condition in which the airway narrow, swell and produce extra mucus

121
Q

hives (urticaria)

A

a rash of itchy round, red welts on the skin that may also burn, sting, swell

122
Q

type II hypersensitivity- mediators

A
  • IgG
  • IgM
  • NK cells
  • the complement system
123
Q

type II hypersensitivity- mechanism of reaction

A
  • IgGs/IgMs bind to antigens on the surface of cells (ex. erythrocytes)
  • once antibodies are attached through their antigen binding region, the Fc region is free and can activate 2 processes
  1. classical complement activation
  2. antibody-dependent cell-mediated cytotoxicity
124
Q

classical complement activation

A

leads to opsonization or membrane attack complexes

125
Q

what do the mechanism of reaction in type II hypersensitivity do?

A

these processes mediate the destruction of the cells, leading to an excessive inflammatory response

126
Q

type II hypersensitivity- reaction time

A

is min to hours

127
Q

type II hypersensitivity- clinical manifestations

A
  • drug induced hemolytic anemia
  • transfusion reactions
128
Q

drug induced hemolytic anemia

A
  • some antibodies can bind nonspecifically to proteins on RBC membranes and form a complex which sometimes induces completement-mediated lysis
  • as the RBCs rupture, the number of RBCs decrease resulting in anemia
  • anemia is gone when drug is removed
  • penicillin is notable
129
Q

transfusion reactions

A
  • depending on your blood type, you will only be able to safely receive certain blood types during a blood transfusion
  • this is partly due to the presence or absences of expression of a specific antigen (A or B) on your RBCs (meaning you don’t express the antigen, you don’t have antibodies)
130
Q

type III hypersensitivity- mediators

A
  • immune complexes (antigen-antibody complexes)
  • neutrophils
  • complement proteins
131
Q

type III hypersensitivity- mechanism of reaction

A
  • of antibodies with antigens generates immune complexes. when not cleared, they build up and deposit in the tissue
  • the immune complexes will activate the complement which will induce inflammatory reactions through neutrophil attraction to the site of depositions
  • neutrophils release lytic enzymes as they attempt to phagocytose the immune complexes, which weakened surrounding cells membranes ultimately causing tissue damage
132
Q

type III hypersensitivity- reaction time

A
  • 3 to 10 hours after exposure to the antigen
  • sometime (days to weeks)
133
Q

type III hypersensitivity- clinical manifestation

A

serum sickness

134
Q

what is serum sickness

A

observed after administration of antitoxins containing foreign serum

135
Q

what happen with serum sicknees to the recipient?

A

develop antibodies specific for this protein. when these antibodies circulate, they form immune complexes with the protein
- after days-weeks, the symptoms occur

136
Q

what are serum sickness symptoms?

A
  • fever
  • weakness
  • generalized vasculitie (rash)
  • edema
137
Q

what happen when complexes accumulate in tissues

A

filtration of plasma occur and can contribute to the pathogensis of many other conditions such as autoimmune disease (hepatitis, malaria)

138
Q

when would clinicial effect of type III hypersensitivity subside

A

when the antigen has been completely broken down

139
Q

type IV hypersensitivity- mediators

A
  • CD8+ tcells
  • CD4+ t cells
  • macrophages
140
Q

why is type IV hypersensitivity different for mediators

A

not mediated by antibodies

141
Q

type IV hypersensitivity- mechanism of reaction

A
  • after exposure to an antigen, T-cells will become activated and initiate an immune response
  • sensitized helper T-cells (TH1) will release cytokines that activate macrophages or cytotoxic T-cells which mediate direct cellular damage
142
Q

type IV hypersensitivity- reaction time

A
  • delay response
  • 2-3 days to develop after exposure
143
Q

type IV hypersensitivity- clinical manifestation

A
  • inflammatory bowel disease (IBD)
  • contact dermatitis
144
Q

what is inflammatory bowel disease

A
  • a group of conditions that is characterized by chronic inflammation of all or parts of the digestive tract
145
Q

what are the most common inflammatory bowel disease

A
  • ulcerative colitis
  • crohns disease
146
Q

does inflammatory bowel disease fall into a autoimmune disease?

A

yes- immune system attack own body

147
Q

what is contact dermatitis?

A
  • type of DTH response causing red itchy rash that has been in contact with small, reactive molecules whihc create complexes with skin proteins
148
Q

common inducers of contact dermatitis

A
  • poison ivy
  • formaldehyde
  • nickel
  • cosmetics
149
Q

erythrocyte sedimentation rate (ESR)

A
  • the rate at which red blood cells sediment in one hour
  • useful for diagnostic test marker for inflammation can help confirm the presence of a variety of diseases
150
Q

C-reactive protein levels

A
  • a marker of inflammation in the body
  • CRP is a more accurate relfection of acute phase immune response (early induced innate immunity) than ESR
  • more inflammation present in the body is reflected by increased levels of CRP
151
Q

microcytic anemia

A

presence of small red blood cells

152
Q

albuterol

A

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

153
Q

AGPAR

A

is a score method to quickly summarize the health of a new born child
- is determined by evaluating the new born baby on five criteria
- appearance, pulse, grimace, activity, respiration on scale 0-2
a score above 7 is NORMAL

MICR 270 (4 decks)

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