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Human Pathophysiology > Chapter 3 > Flashcards

Chapter 3 Flashcards

1
Q

types of T lymphocytes

A

Helper T cells, cytotoxic T cells, suppressor T cells

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2
Q

how many binding sites does the T cell receptor have

A

1

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3
Q

antigen presentation

A

required for T cells

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4
Q

APC

A

antigen presenting cells

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5
Q

types of APC

A

macrophages
dendritic cells
B cells

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6
Q

what is the best type of APC

A

dendritic cell

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7
Q

major histocompatibility proteins (MHC)

A

present antigen to responding cells of immune system (T cells)

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8
Q

MHC Class I

A

present on all cells w/nucleus
CD8+

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9
Q

what are MHC I not present on

A

red blood cells

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10
Q

MHC Class II

A

only on APCs
CD4+

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11
Q

sequence of humoral immunity (B lymphocyte)

A
  1. B cell sees virus (must interact w/helper T cell)
  2. B cell becomes plasma cell
  3. Memory B cells are formed
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12
Q

sequence of cellular immunity (T lymphocyte)

A
  1. Cytotoxic T cells kill epithelial cells attacked by virus (helper T cells assist)
  2. Memory cells are left over
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13
Q

types of immune response

A

primary and secondary

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14
Q

primary immune response

A

first exposure
naive cells

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15
Q

secondary immune response

A

follows initial encounter’s formation of memory cells
AKA activating memory cells
basis of vaccines

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16
Q

what immunoglobulin is made first

A

IgM

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17
Q

hypersensitivity

A

too much of a response to the wrong antigen

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18
Q

immunodeficiency

A

too little of a response to antigen

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19
Q

autoimmune disease

A

inappropriate response to antigen

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20
Q

malignancy

A

cancer of immune tissues

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21
Q

types of hypersensitivity reactions

A

type 1, 2, 3, 4

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22
Q

what types of hypersensitivity reactions are mediated by B cells and antibodies

A

types 1, 2, 3

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23
Q

what type of hypersensitivity reaction is mediated by T cells

A

type 4

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24
Q

time frame of Type 1 hypersensitivity

A

immediate/instantly

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25
Q

what kind of antibodies are involved in hypersensitivity

A

preformed antibodies (already encountered antigen)
IgE antibody is made after first exposure

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26
Q

what does the IgE antibody do in Type 1 hypersensitivity

A

becomes embedded in mast cell, binds, degranulates

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27
Q

what cells are involved in Type 1

A

mast cells and basophils

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28
Q

mast cells in Type 1

A

affect smooth muscle because they are full of granules, also mediated by prostaglandins (derivatives of arachidonic acid)

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29
Q

effect of granules in mast cells (Type 1)

A

degranulation (histamine and serotonin)
vasodilation, increased capillary permeability, edema accumulation BLOOD VESSELS

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30
Q

is Type 1 hypersensitivity systemic or local?

A

both

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31
Q

systemic Type 1 hypersensitivity effects

A

enters blood, activating massive amounts of mast cells, leading to constriction, decreasing BP

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32
Q

local Type 1 hypersensitivity effects

A

nose, sinuses, GI tract

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33
Q

phase of IgE-mediated allergic reaction (Type 1)

A

immediate (wheel & flare)
late (eosinophil chemotaxis)

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34
Q

what is the main ‘disease’ of Type 1 hypersensitivity

A

allergic
hypersensitivity to environmental substance

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35
Q

atopy

A

genetic sensitivity

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36
Q

what is the most common allergen?

A

dust mites

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37
Q

examples of Type 1 hypersensitivity

A

hay fever, hives, atopic dermatitis (eczema), systemic anaphylaxis, asthma

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38
Q

why are mast cells important for parasitic infections

A

IgE ejects parasites

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39
Q

helminth

A

parasitic

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40
Q

hygiene hypothesis

A

westernized countries have allergic disorders vs. developing countries do not

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41
Q

treatment for Type 1 hypersensitivity

A

avoidance, drugs
anti-histamines, corticosteroids, anti-IgE therapy, beta adrenergics, desenstitization

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42
Q

anti-histamine

A

blocks vasoactive histamine receptors

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43
Q

corticosteroids

A

decreases immune system by decreasing cortisol levels

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44
Q

anti-IgE therapy

A

IgE to IgG antibodies

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45
Q

beta adrenergics

A

albuterol, opens airways by SNS

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46
Q

what is Type 2 hypersensitivity

A

cytotoxic (attacks host cell)
tissue specific antibody attaches directly to antigen in target tissue

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47
Q

what cells mediate Type 2

A

B cells

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48
Q

what antibodies are included in Type 2

A

IgG or IgM

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49
Q

types of interaction in Type 2

A

death of target cells
antibodies block receptor function (myasthenia gravis)

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50
Q

examples of Type 2 hypersensitivity

A

transfusion reactions, hemolytic disease of newborn (Rh factor), autoimmune reaction (myasthenia gravis)

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51
Q

what is Type 3 hypersensitivity

A

normal immune complex

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52
Q

what is Type 3 mediated by

A

antibody and antigen (forms immune complex)

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53
Q

what is Type 3 cleared by

A

red blood cells

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54
Q

main point of Type 3

A

failure to clear complexes
- deposition induced inflammatory response in blood vessels, kidneys, joints

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55
Q

is Type 3 deposition local or systemic?

A

can be distant (systemic)
circulates via blood to different site from formation
can also be local
remains at site (farmer’s lung)

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56
Q

what is Type 3 influenced by

A

size of complex (smaller complexes circulate longer, increasing immune response)
vascular permeability

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57
Q

what is a good word to describe Type 4 hypersensitivity

A

delayed

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58
Q

does Type 4 depend on antibodies?

A

no

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59
Q

what mediates Type 4

A

T lymphocytes

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60
Q

steps of Type 4 hypersensitivity

A
  1. initial sensitization via antigen uptake, hapten, presentation by APC
  2. APCs present to Helper T cells
  3. memory T cells migrate to site
  4. second exposure releases mediators, attracting other cells
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61
Q

hapten

A

part of antigen binding to normal protein

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62
Q

examples of Type 4 hypersensitivity

A

poison ivy, metallic injury, tuberculosis test

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63
Q

what is an autoimmune disease

A

attacks self, self becomes foreign

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64
Q

examples of autoimmune diseases

A

SLE, RA, myasthenia gravis, Type I Diabetes, MS

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65
Q

why does the body turn on itself?

A

imperfect B/T cell programming
inaccessible self-antigens
altered antigen
molecular mimicry
infection and inflammation (viral)
decrease suppressor T cell function
genetic susceptibility (MHC proteins)

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66
Q

molecular mimicry

A

Type 2 hypersensitivity
foreign antigen resembles pathogen and host antigen, immune response initiated by microbe becoming directed at self cells

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67
Q

what is the most common autoimmune disease

A

type 1 diabetes

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68
Q

examples of molecular mimicry

A

rheumatic fever

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69
Q

Systemic Lupus Erythematosus (SLE)
Lupus

A

systemic autoimmune disease

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70
Q

hallmarks of lupus

A

butterfly rash
women (20-40yrs)
fever
weakness
photosensitivity
arthritis and kidney dysfunction can develop

71
Q

is lupus age associated?

A

no

72
Q

what type of hypersensitivity is lupus

A

Type 3 hypersensitivity

73
Q

what antibodies are associated with lupus

A

antinuclear antibodies (ANA) in blood
highly sensitive, low specificity

74
Q

what do ANA do in lupus

A

binding of ANA forms soluble immune complexes, leading to deposition

75
Q

what does the deposition of immune complexes cause in lupus

A

inflammation (in the arteries, results in vasculitis)

76
Q

is lupus a chronic inflammatory disease?

A

yes. it affects all tissues of body KIDNEYS

77
Q

clinical findings of lupus

A

cytopenia
vasculitis
skin lesions
myocarditis
glomerunephritis
arthritis
brain (microinfarcts, psychosis, dementia)

78
Q

cytopenia

A

decrease in # of WBC

79
Q

vasculitis

A

inflammation of blood vessels, weakens and causes redness of skin

80
Q

myocarditis

A

inflammation of heart muscle

81
Q

microinfarcts

A

decrease in blood flow, leads to cell death

82
Q

how do you diagnose lupus

A

blood work
look for presence of ANA
high ESR and CRP levels

83
Q

clinical outcome of lupus

A

variable and unpredictable,
30% mortality rate in first 10 yrs (reduced life expectancy)
death due to organ failure (kidneys, brain)

84
Q

treatment for lupus

A

mild=NSAIDs
severe= corticosteroids, antineoplastic

85
Q

what do NSAIDs do

A

decrease inflammation

86
Q

antineoplastic

A

cancer treatment drugs, decrease cell division to reduce # of WBC

87
Q

drug induced lupus

A

following exposure to drugs, lupus-like symptoms form
~10% of cases

88
Q

rheumatoid arthritis

A

systemic autoimmune disease
1-3% of population
episodic

89
Q

what type of hypersensitivity is rheumatoid arthritis

A

Type 3

90
Q

group most susceptible to RA

A

women, 20-40yrs

91
Q

is RA age-associated

A

no

92
Q

episodic

A

relapse to remission to relapse to remission

93
Q

what organs/tissues does rheumatoid arthritis affect

A

lungs, bone, cartilage, pericardium

94
Q

rheumatoid factor

A

autoimmune antibodies

95
Q

progression of RA

A

starts in small joints of hands and feet, synovial membrane is attacked with T cell deposition

96
Q

Sjogren syndrome

A

autoimmune disease of lacrimal and salivary glands

97
Q

characteristics of Sjogren syndrome

A

dry irritated red eyes, dry mouth, difficulty swallowing, extraglandular (vasculitis, neuropathy, lymphoma)

98
Q

neuropathy

A

nerve destruction

99
Q

lymphoma

A

cancer of lymphocytes

100
Q

Sjogren syndrome treatment

A

eye drops, drinking fluids

101
Q

amyloidosis

A

amyloid proteins are abnormally deposited on organs and interfere w/function

102
Q

types of amyloidosis

A

primary
secondary

103
Q

primary amyloidosis

A

no known cause
antibodies form amyloid light chain which breaks down

104
Q

secondary amyloidosis

A

secondary to some other condition (SLE, RA)

105
Q

amyloidosis treatment

A

replace bone marrow

106
Q

symptoms of amyloidosis

A

depends on tissue/organ of deposits

107
Q

types of transplantation

A

autograft
homograft
allograft
xenograft

108
Q

autograft

A

own skin

109
Q

homograft

A

genetically identical twin

110
Q

allograft

A

genetically different but same species

111
Q

xenograft

A

different species
pig valve

112
Q

what is transplantation rejection mediated by

A

immune system

113
Q

what causes transplantation rejection

A

mismatch of MHC

114
Q

what causes transplantation rejection

A

mismatch of MHC

115
Q

types of transplantation rejection

A

hyperacute organ rejection, acute organ rejection, chronic transplant rejection

116
Q

hyperacute organ rejection

A

preformed antibodies react w/graft endothelial cells
INSTANT

117
Q

what causes hyperacute organ rejection

A

previous organ transplant, blood transfusion, pregnancy

118
Q

acute organ rejection

A

happens within weeks of transplant, attach to mismatch of MHC

119
Q

what mediates acute organ rejection

A

T cells

120
Q

chronic transplant rejection

A

months to years post transplant
T cell mediated

121
Q

what happens w/chronic transplant rejection

A

ischemia and hypoperfusion of organ

122
Q

graft vs. host reaction (GVH)

A

bone marrow transplants
recipients must have pretransplant treatment (killing off bone marrow for space)

123
Q

mechanisms of GVH

A

immune cells in graft recognize host as foreign
transplanted graft lymphocytes attack host cells

124
Q

what tissues are affected by GVH

A

GI tract (diarrhea)
skin (red/rash)
liver (jaundice)

125
Q

how do you minimize GVH

A

matching MHC proteins prior to transplant

126
Q

blood transfusion

A

most common form of transplantation
blood type for matching of donors and recipients

127
Q

transfusion reaction

A

antibodies mismatch

128
Q

ABO

A

antigens on surface of RBC

129
Q

Type A

A

A antigen makes B antibodies
can receive A, O

130
Q

Type B

A

B antigen makes A antibodies
B, O

131
Q

Type AB

A

no antibodies to A or B
UNIVERSAL RECIPIENT A, B, AB, O

132
Q

Type O

A

no antibodies on surface but makes antibodies to A and B
UNIVERSAL DONOR O

133
Q

major transfusion reaction

A

hemolysis, thrombosis
life threatening

134
Q

hemolysis

A

RBC destruction

135
Q

thrombosis

A

abnormal blood clot due to stickiness

136
Q

minor transfusion reaction

A

fever, chills
not life threatening
not due to ABO mismatch (due to other antibodies)

137
Q

Rh incompatability

A

D/d antigens
hemolytic disease of newborn (Rh+)

138
Q

crossmatch

A

donor blood is compatible w/recipient blood

139
Q

major crossmatch

A

donor’s RBC in recipient’s serum
checks for preformed antibodies in recipient’s serum against donor’s RBC

140
Q

minor crossmatch

A

donor’s serum in recipient’s RBCs
preformed antibodies in donor serum that could hemolyse recipient’s RBC

141
Q

types of immunodeficiency diseases

A

primary (born w/it) or secondary (acquired)

142
Q

deficiency of T cells

A

prone to infections, cancer (T cells kill cancer cells)
SCID (severe combined immunodeficiency diseases)

143
Q

immunodeficiency diseases

A

entire immune system or subsets of cells are effected

144
Q

deficiency of B cells

A

lack of antibodies
sensitive to bacteria

145
Q

X-linked Agammaglobulinemia (XLA)

A

primary immunodeficiency disease

146
Q

what does XLA lack

A

antibodies, tyrosine kinase which leads to B cell development

147
Q

is XLA an SCID

A

no

148
Q

what results from XLA

A

recurrent bacterial infections (no B cells, no antibodies)

149
Q

DiGeorge Syndrome

A

deletion of Q arm on chromosome 22 (primary immunodeficiency disease)

150
Q

is DiGeorge Syndrome an SCID

A

yes

151
Q

what happens with DiGeorge Syndrome

A

missing genes, no thymus development, no T cells

152
Q

causes of secondary immunodeficiency diseases

A

secondary to something else:
nutrition, infection, radiation, age

153
Q

AIDS

A

secondary immunodeficiency disease
caused by HIV

154
Q

characteristics of AIDS

A

low Helper T cell count
recurrent infections (opportunistic infections)
neoplasms
cachexia

155
Q

cachexia

A

wastes away

156
Q

transmission of AIDS

A

blood and bodily fluids (semen, blood transfusions, mom to baby)

157
Q

highest risk groups for AIDS

A

homosexual or bisexual males
IV drug users
patients w/hemophilia (missing coagulation factors)
blood transfusion recipients
heterosexual contacts w/those above

158
Q

HIV

A

secondary immunodeficiency disease
virus (nucleic acid in protein coat)

159
Q

how does HIV enter cells

A

binding to receptors through retrovirus of RNA and DNA

160
Q

what does HIV entry depend on

A

CD4 receptor AND CCR5 (or CXCR4) co-receptor

161
Q

progression of HIV

A

acute, latent, crisis

162
Q

opportunistic infections of AIDS

A

candidasis, tuberculosis, salmonella, herpes

163
Q

neoplasms of AIDS

A

kaposi sarcoma, lymphoma brain

164
Q

neurological symptoms of AIDS

A

dementia, seizures, mood swings

165
Q

HIV resistant mutation

A

CCR5 mutation
virus can’t get into cell

166
Q

heterozygous

A

in latent period for longer, cell can still enter

167
Q

homozygous

A

virus doesn’t progress at all

168
Q

ethnicity of HIV

A

white
10% hetero 1% white

169
Q

HIV/AIDS diagnosis

A

anti-HIV antibodies, HIV antigens in blood and saliva

170
Q

clinical diagnosis of AIDS

A

definitive w/out confirming lab data (kaposis sarcoma < 60yrs)

definitive w/confirming data (CD4+ <200 cells/mL)

presumptive w/conforming lab data (recurrent pneumonia)

171
Q

goals of HIV treatment

A

control virus and other infections

172
Q

HIV treatment

A

highly active antiretroviral therapy (HAART)

173
Q

HAART

A

suppresses virus replication, acts on different stages of HIV life cycle, increases latency period

Human Pathophysiology (8 decks)

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