Chapter 3 Flashcards
(173 cards)
1
Q
types of T lymphocytes
A
Helper T cells, cytotoxic T cells, suppressor T cells
2
Q
how many binding sites does the T cell receptor have
A
1
3
Q
antigen presentation
A
required for T cells
4
Q
APC
A
antigen presenting cells
5
Q
types of APC
A
macrophages
dendritic cells
B cells
6
Q
what is the best type of APC
A
dendritic cell
7
Q
major histocompatibility proteins (MHC)
A
present antigen to responding cells of immune system (T cells)
8
Q
MHC Class I
A
present on all cells w/nucleus
CD8+
9
Q
what are MHC I not present on
A
red blood cells
10
Q
MHC Class II
A
only on APCs
CD4+
11
Q
sequence of humoral immunity (B lymphocyte)
A
- B cell sees virus (must interact w/helper T cell)
- B cell becomes plasma cell
- Memory B cells are formed
12
Q
sequence of cellular immunity (T lymphocyte)
A
- Cytotoxic T cells kill epithelial cells attacked by virus (helper T cells assist)
- Memory cells are left over
13
Q
types of immune response
A
primary and secondary
14
Q
primary immune response
A
first exposure
naive cells
15
Q
secondary immune response
A
follows initial encounter’s formation of memory cells
AKA activating memory cells
basis of vaccines
16
Q
what immunoglobulin is made first
A
IgM
17
Q
hypersensitivity
A
too much of a response to the wrong antigen
18
Q
immunodeficiency
A
too little of a response to antigen
19
Q
autoimmune disease
A
inappropriate response to antigen
20
Q
malignancy
A
cancer of immune tissues
21
Q
types of hypersensitivity reactions
A
type 1, 2, 3, 4
22
Q
what types of hypersensitivity reactions are mediated by B cells and antibodies
A
types 1, 2, 3
23
Q
what type of hypersensitivity reaction is mediated by T cells
A
type 4
24
Q
time frame of Type 1 hypersensitivity
A
immediate/instantly
25
what kind of antibodies are involved in hypersensitivity
preformed antibodies (already encountered antigen)
IgE antibody is made after first exposure
26
what does the IgE antibody do in Type 1 hypersensitivity
becomes embedded in mast cell, binds, degranulates
27
what cells are involved in Type 1
mast cells and basophils
28
mast cells in Type 1
affect smooth muscle because they are full of granules, also mediated by prostaglandins (derivatives of arachidonic acid)
29
effect of granules in mast cells (Type 1)
degranulation (histamine and serotonin)
vasodilation, increased capillary permeability, edema accumulation *BLOOD VESSELS*
30
is Type 1 hypersensitivity systemic or local?
both
31
systemic Type 1 hypersensitivity effects
enters blood, activating massive amounts of mast cells, leading to constriction, decreasing BP
32
local Type 1 hypersensitivity effects
nose, sinuses, GI tract
33
phase of IgE-mediated allergic reaction (Type 1)
immediate (wheel & flare)
late (eosinophil chemotaxis)
34
what is the main 'disease' of Type 1 hypersensitivity
allergic
hypersensitivity to environmental substance
35
atopy
genetic sensitivity
36
what is the most common allergen?
dust mites
37
examples of Type 1 hypersensitivity
hay fever, hives, atopic dermatitis (eczema), systemic anaphylaxis, asthma
38
why are mast cells important for parasitic infections
IgE ejects parasites
39
helminth
parasitic
40
hygiene hypothesis
westernized countries have allergic disorders vs. developing countries do not
41
treatment for Type 1 hypersensitivity
avoidance, drugs
anti-histamines, corticosteroids, anti-IgE therapy, beta adrenergics, desenstitization
42
anti-histamine
blocks vasoactive histamine receptors
43
corticosteroids
decreases immune system by decreasing cortisol levels
44
anti-IgE therapy
IgE to IgG antibodies
45
beta adrenergics
albuterol, opens airways by SNS
46
what is Type 2 hypersensitivity
cytotoxic (attacks host cell)
tissue specific antibody attaches directly to antigen in target tissue
47
what cells mediate Type 2
B cells
48
what antibodies are included in Type 2
IgG or IgM
49
types of interaction in Type 2
death of target cells
antibodies block receptor function (myasthenia gravis)
50
examples of Type 2 hypersensitivity
transfusion reactions, hemolytic disease of newborn (Rh factor), autoimmune reaction (myasthenia gravis)
51
what is Type 3 hypersensitivity
normal immune complex
52
what is Type 3 mediated by
antibody and antigen (forms immune complex)
53
what is Type 3 cleared by
red blood cells
54
main point of Type 3
failure to clear complexes
- deposition induced inflammatory response in blood vessels, kidneys, joints
55
is Type 3 deposition local or systemic?
can be distant (systemic)
circulates via blood to different site from formation
can also be local
remains at site (farmer's lung)
56
what is Type 3 influenced by
size of complex (smaller complexes circulate longer, increasing immune response)
vascular permeability
57
what is a good word to describe Type 4 hypersensitivity
delayed
58
does Type 4 depend on antibodies?
no
59
what mediates Type 4
T lymphocytes
60
steps of Type 4 hypersensitivity
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
61
hapten
part of antigen binding to normal protein
62
examples of Type 4 hypersensitivity
poison ivy, metallic injury, tuberculosis test
63
what is an autoimmune disease
attacks self, self becomes foreign
64
examples of autoimmune diseases
SLE, RA, myasthenia gravis, Type I Diabetes, MS
65
why does the body turn on itself?
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)
66
molecular mimicry
Type 2 hypersensitivity
foreign antigen resembles pathogen and host antigen, immune response initiated by microbe becoming directed at self cells
67
what is the most common autoimmune disease
type 1 diabetes
68
examples of molecular mimicry
rheumatic fever
69
Systemic Lupus Erythematosus (SLE)
Lupus
systemic autoimmune disease
70
hallmarks of lupus
butterfly rash
women (20-40yrs)
fever
weakness
photosensitivity
arthritis and kidney dysfunction can develop
71
is lupus age associated?
no
72
what type of hypersensitivity is lupus
Type 3 hypersensitivity
73
what antibodies are associated with lupus
antinuclear antibodies (ANA) in blood
highly sensitive, low specificity
74
what do ANA do in lupus
binding of ANA forms soluble immune complexes, leading to deposition
75
what does the deposition of immune complexes cause in lupus
inflammation (in the arteries, results in vasculitis)
76
is lupus a chronic inflammatory disease?
yes. it affects all tissues of body *KIDNEYS*
77
clinical findings of lupus
cytopenia
vasculitis
skin lesions
myocarditis
glomerunephritis
arthritis
brain (microinfarcts, psychosis, dementia)
78
cytopenia
decrease in # of WBC
79
vasculitis
inflammation of blood vessels, weakens and causes redness of skin
80
myocarditis
inflammation of heart muscle
81
microinfarcts
decrease in blood flow, leads to cell death
82
how do you diagnose lupus
blood work
look for presence of ANA
high ESR and CRP levels
83
clinical outcome of lupus
variable and unpredictable,
30% mortality rate in first 10 yrs (reduced life expectancy)
death due to organ failure (kidneys, brain)
84
treatment for lupus
mild=NSAIDs
severe= corticosteroids, antineoplastic
85
what do NSAIDs do
decrease inflammation
86
antineoplastic
cancer treatment drugs, decrease cell division to reduce # of WBC
87
drug induced lupus
following exposure to drugs, lupus-like symptoms form
~10% of cases
88
rheumatoid arthritis
systemic autoimmune disease
1-3% of population
episodic
89
what type of hypersensitivity is rheumatoid arthritis
Type 3
90
group most susceptible to RA
women, 20-40yrs
91
is RA age-associated
no
92
episodic
relapse to remission to relapse to remission
93
what organs/tissues does rheumatoid arthritis affect
lungs, bone, cartilage, pericardium
94
rheumatoid factor
autoimmune antibodies
95
progression of RA
starts in small joints of hands and feet, synovial membrane is attacked with T cell deposition
96
Sjogren syndrome
autoimmune disease of lacrimal and salivary glands
97
characteristics of Sjogren syndrome
dry irritated red eyes, dry mouth, difficulty swallowing, extraglandular (vasculitis, neuropathy, lymphoma)
98
neuropathy
nerve destruction
99
lymphoma
cancer of lymphocytes
100
Sjogren syndrome treatment
eye drops, drinking fluids
101
amyloidosis
amyloid proteins are abnormally deposited on organs and interfere w/function
102
types of amyloidosis
primary
secondary
103
primary amyloidosis
no known cause
antibodies form amyloid light chain which breaks down
104
secondary amyloidosis
secondary to some other condition (SLE, RA)
105
amyloidosis treatment
replace bone marrow
106
symptoms of amyloidosis
depends on tissue/organ of deposits
107
types of transplantation
autograft
homograft
allograft
xenograft
108
autograft
own skin
109
homograft
genetically identical twin
110
allograft
genetically different but same species
111
xenograft
different species
pig valve
112
what is transplantation rejection mediated by
immune system
113
what causes transplantation rejection
mismatch of MHC
114
what causes transplantation rejection
mismatch of MHC
115
types of transplantation rejection
hyperacute organ rejection, acute organ rejection, chronic transplant rejection
116
hyperacute organ rejection
preformed antibodies react w/graft endothelial cells
INSTANT
117
what causes hyperacute organ rejection
previous organ transplant, blood transfusion, pregnancy
118
acute organ rejection
happens within weeks of transplant, attach to mismatch of MHC
119
what mediates acute organ rejection
T cells
120
chronic transplant rejection
months to years post transplant
T cell mediated
121
what happens w/chronic transplant rejection
ischemia and hypoperfusion of organ
122
graft vs. host reaction (GVH)
bone marrow transplants
recipients must have pretransplant treatment (killing off bone marrow for space)
123
mechanisms of GVH
immune cells in graft recognize host as foreign
transplanted graft lymphocytes attack host cells
124
what tissues are affected by GVH
GI tract (diarrhea)
skin (red/rash)
liver (jaundice)
125
how do you minimize GVH
matching MHC proteins prior to transplant
126
blood transfusion
most common form of transplantation
blood type for matching of donors and recipients
127
transfusion reaction
antibodies mismatch
128
ABO
antigens on surface of RBC
129
Type A
A antigen makes B antibodies
can receive A, O
130
Type B
B antigen makes A antibodies
B, O
131
Type AB
no antibodies to A or B
*UNIVERSAL RECIPIENT* A, B, AB, O
132
Type O
no antibodies on surface but makes antibodies to A and B
*UNIVERSAL DONOR* O
133
major transfusion reaction
hemolysis, thrombosis
life threatening
134
hemolysis
RBC destruction
135
thrombosis
abnormal blood clot due to stickiness
136
minor transfusion reaction
fever, chills
not life threatening
not due to ABO mismatch (due to other antibodies)
137
Rh incompatability
D/d antigens
hemolytic disease of newborn (Rh+)
138
crossmatch
donor blood is compatible w/recipient blood
139
major crossmatch
donor's RBC in recipient's serum
checks for preformed antibodies in recipient's serum against donor's RBC
140
minor crossmatch
donor's serum in recipient's RBCs
preformed antibodies in donor serum that could hemolyse recipient's RBC
141
types of immunodeficiency diseases
primary (born w/it) or secondary (acquired)
142
deficiency of T cells
prone to infections, cancer (T cells kill cancer cells)
SCID (severe combined immunodeficiency diseases)
143
immunodeficiency diseases
entire immune system or subsets of cells are effected
144
deficiency of B cells
lack of antibodies
sensitive to bacteria
145
X-linked Agammaglobulinemia (XLA)
primary immunodeficiency disease
146
what does XLA lack
antibodies, tyrosine kinase which leads to B cell development
147
is XLA an SCID
no
148
what results from XLA
recurrent bacterial infections (no B cells, no antibodies)
149
DiGeorge Syndrome
deletion of Q arm on chromosome 22 (primary immunodeficiency disease)
150
is DiGeorge Syndrome an SCID
yes
151
what happens with DiGeorge Syndrome
missing genes, no thymus development, no T cells
152
causes of secondary immunodeficiency diseases
secondary to something else:
nutrition, infection, radiation, age
153
AIDS
secondary immunodeficiency disease
caused by HIV
154
characteristics of AIDS
low Helper T cell count
recurrent infections (opportunistic infections)
neoplasms
cachexia
155
cachexia
wastes away
156
transmission of AIDS
blood and bodily fluids (semen, blood transfusions, mom to baby)
157
highest risk groups for AIDS
homosexual or bisexual males
IV drug users
patients w/hemophilia (missing coagulation factors)
blood transfusion recipients
heterosexual contacts w/those above
158
HIV
secondary immunodeficiency disease
virus (nucleic acid in protein coat)
159
how does HIV enter cells
binding to receptors through retrovirus of RNA and DNA
160
what does HIV entry depend on
CD4 receptor AND CCR5 (or CXCR4) co-receptor
161
progression of HIV
acute, latent, crisis
162
opportunistic infections of AIDS
candidasis, tuberculosis, salmonella, herpes
163
neoplasms of AIDS
kaposi sarcoma, lymphoma brain
164
neurological symptoms of AIDS
dementia, seizures, mood swings
165
HIV resistant mutation
CCR5 mutation
virus can't get into cell
166
heterozygous
in latent period for longer, cell can still enter
167
homozygous
virus doesn't progress at all
168
ethnicity of HIV
white
10% hetero 1% white
169
HIV/AIDS diagnosis
anti-HIV antibodies, HIV antigens in blood and saliva
170
clinical diagnosis of AIDS
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
goals of HIV treatment
control virus and other infections
172
HIV treatment
highly active antiretroviral therapy (HAART)
173
HAART
suppresses virus replication, acts on different stages of HIV life cycle, increases latency period
