Module 4 Flashcards
(236 cards)
1
Q
immunodeficiency
A
disorder or conditions where the IS has reduced function or is absent and can be traced to the failure of one or more parts of IS
2
Q
two main types of immunodeficiencies
A
- primary immunodeficiency
- secondary immunodeficiency
3
Q
primary immunodeficiency
A
congenital and derive from a genetic or developmental defect leading to abnormal maturation of IS
- may be associated with defects in innate or adaptive IS
4
Q
congenital
A
present from birth
5
Q
B-cell deficiencies prevalence
A
65%
6
Q
T-cell deficiencies prevalence
A
5%
7
Q
complement deficiencies
A
5%
8
Q
phagocytic deficiencies
A
10%
9
Q
combined T- and B-cell deficiencies
A
15%
10
Q
why are primary immunodeficiencies rare?
A
because the fetus doesn’t usually survive the defect
11
Q
secondary immunodeficiency
A
acquired and result from environmental factors affecting and compromising the IS
12
Q
causes of secondary immunodeficiency
A
- undergoing chemotherapy treatment
- taking immunosuppressive medication
- contracting a chronic infection (HIV/AIDS)
- developing cancer
13
Q
B-cell deficiencies
A
characterized by dysfunctional B lymphocytes or a decrease in prevalence
- B-cells are key cells of humoral immunity as they produce large quantities of antibodies
14
Q
deficiency in B-cell development
A
results in an increased susceptibility to infection, especially by encapsulated bacteria
15
Q
ex of B-cell deficiencies
A
During pregnancy and breastfeeding, the mother transfers IgGs to baby and around 7-9 months the antibody pool from mother decreases and due to B-cell deficiency, the infant is not able to synthesize normal levels of antibodies to compensate
16
Q
encapsulated bacteria
A
Gram-positive and Gram-negative bacteria with the unifying feature of being the production of capsule composed of polysaccharides
17
Q
clinical example of B-cell deficiencies
A
X-linked agammaglobulinemia (XLA)
18
Q
x-linked agammaglobulineamia (xla)
A
- rare genetic disorder
- linked and recessive, therefore occurs almost exclusively in males
- patients do not develop mature B cells and as a result have extremely low levels of IgG and lack all other immunoglobins
19
Q
XLA and infection
A
- XLA patients are extremely susceptible to bacterial infections
- their susceptibility to viral and fungal infections remains unchanged – due to cell-mediated response remaining normal
20
Q
T-cell deficiencies
A
characterized by dysfunctional T-lymphocytes or a decrease in their prevalence
- T-lymphocytes are key cells of cell-mediated immunity as they kill infected or abnormal cells
21
Q
deficiency in T-lymphocytes
A
results in an increased susceptibility to viruses, protozoans and fungi
- often characterized by frequent infections beginning 3-4 months after birth
22
Q
example of T-cell deficiencies
A
pneumonia and candidiasis
23
Q
clinical example of T-cell deficiencies
A
digeorge syndrome
24
Q
digeorge syndrome
A
complex disease caused by the deletion of a small segment of chromosome 22
25
symptoms of digeorge syndrome
1. patients have an absent or underdeveloped thymus which results on absence of mature T-cells
2. experience abnormalities in the heart, face and palate + learning disabilities
26
complement deficiencies
1. complement system involves intricate regulation of nine components
2. genetic deficiencies have been described for each of these complement components
27
patients with complement deficiencies are prone to what?
frequent sever bacterial infections and complications arising from inability to clear immune complexes
28
C3 deficiencies
C3 deficiencies display the severest symptoms, reflective of the central role played by this component in complement activities
29
clinical example of complement deficiencies
hereditary angioedema (HAE)
30
hereditary angioedema (HAE)
deficiencies in proteins that regulate complement pathways
- patients with HAE lack a regular of C1
31
symptoms of HAE
1. swelling of face
2. lips
3. larynx
4. GI tract
***swelling of larynx and GI tract are concerning cause this can lead to suffocation or acute abdominal pain
32
phagocytic deficiencies
can appear at various stages of phagocytosis
- phagocytosis is an important part of innate immunity as extracellular pathogens are engulfed and destroyed within a phagocyte
33
defective phagocytosis and infection
bacterial and fungal infections are frequent and severe often causing deep abscesses in patients
34
clinical example of phagocytic deficiencies
chronic granulomatous disease (CGD)
35
chronic granulomatous disease (CGD)
rare inherited disease where the body’s phagocytes do not make the chemicals needed to kill phagocytosed bacteria
36
where does CGD derive its name from?
tendency of patients with this disease to form non-malignant granulomas in order to attempt to separate foreign materials from the rest of the body
37
non-malignant granulomas
small, nodular aggregations of immune cells
38
combined T-cell and B-cell deficiencies
1. individuals with both deficiencies have dysfunctional and/or low numbers of lymphocytes
2. both humoral and cell-mediated responses of the adaptive immune system are compromised
39
what is combined T-cell and B-cell deficiencies characterized by?
1. too little or no resistence to infection thus pathogens that cause mild diseases in average human may be life threatening
2. patients with this often suffer fatal infections within first year of life
40
clinical example of combined T-cell and B-cell deficiencies
severe combined inherited immunodeficiency (SCID)
41
severe combined inherited immunodeficiency (SCID)
1. david Vetter suffered from SCID and was rained in a sterile room to prevent him from getting infections for 12 years
2. a space suit invented by NASA allowed him to venture a short distance away from the room
3. passed away at age of 12, after bone marrow transplant (intended to treat SCID) that contained an unexpected infectious agent
42
acquired immunodeficiency syndrome (AIDS)
defined by describing combination of words used to make up its name
43
aquired (AIDS)
individuals do NOT inherit this type of disease (big difference between AIDS and primary ID)
44
immunodeficiency (AIDS)
one disease characteristic that is common is breakdown of immune system
45
sydrome (AIDS)
the plethora of rare but ravaging diseases that take advantage of the body’s collapsed deficiencies
46
AIDS
1. final stage of an acute and chronic HIV infection
2. many AIDS patients die from opportunistic infections as their IS is compromised and unable to effectively protect and defend the body
47
mode of transmission of HIV
1. varies depending on location
2. without treatment the outcome is the same regardless of portal of entry
48
outcome of HIV
1. immunosuppression
2. neuropsychiatric abnormalities
3. death
49
mode of transmission in north america
sexual intercourse
50
mode of transmission in eastern europe and central asia
use of non-sterile injections of drugs
51
mode of transmission in sub-saharan africa
heterosexual sex with a concomitant epidemic in children through vertical transmission (mother-to-child)
52
HIV primary infection
1. most people mount an effective IR to virus for the first couple weeks
2. over this time this response will prove ineffective through the various stages of disease as HIV virus compromises individuals IS
53
HIV acute infection
1. HIV targets and infects cells with CD4 on their surface including CD4+ helper T cells
2. viral infection causes a drastic decrease in level of CD4+ helper T cells while the level of virus in blood increases
54
what happens within 2-4 weeks after primary exposure to HIV?
some people will experience flu-like symptoms including fever, headache, and rash
55
level of HIV in blood during acute infection phase
high
- this greatly increases risk of HIV transmission
56
why do CD4+ helper T-cells increase after initial decrease?
because some antibodies are formed against the virus allowing IS to recover some of lost cell population
57
chronic infection
1. HIV continues to multiply in the body at a steady state
2. anti-HIV antibodies are detectable during this phase
3. HIV can begin to evade the immune response that is present by changing their antigens through high mutation rates
58
HIV chronic infection symptoms
people with chronic HIV don't have symptoms but transmission is still possible
59
length of chronic infection phase of HIV
8-10 years
60
HIV - AIDS
1. CD4+ helper T-cells get “exhausted” and depleted while constantly fighting a chronic HIV infection
2. viral load drastically increases as the virus continues to acquire mutations that allow it to further avoid immune defenses
3. as IS is severely weakened patient become susceptible to opportunistic infections
61
when do HIV patients get diagnosed with AIDS?
when they have CD4+ helper T-cell level of less than 200 cells/mm3
62
how long do AIDS patients survive in the absence of treatment?
about 3 years
63
when was the first antiretroviral therapy approved?
1987
64
what does antiretroviral therapy do?
these drugs do not kill or cure human human immunodeficiency virus, but prevent it from replicating
65
combination retroviral therapy (types)
antiretroviral therapy (ART) and highly active antiretroviral therapy (HAART)
66
combination retroviral therapy
utilizes a panel of antiretroviral drugs in different combinations to prevent drug resistance by the rapidly-mutating virus
67
benefit of combination retroviral therapy
this treatment has led to staggering declines in rates of AIDS and AIDS-associated deaths
68
HAART
maintains function of immune system and prevents opportunistic infections that often lead to death
69
WHO and HAART
700 000 lives saved in 2010 alone due to increased availability of antiretroviral therapy
- since HAART, HIV almost never progresses into AIDS
70
4 things ART does
1. reduced amount of HIV in the body
2. protects immune system
3. prevents HIV from advancing to AIDS
4. reduces the risk of HIV transmission
71
what do B-cell deficiencies increase susceptibility to?
bacterial infections (encapsulated bacteria)
72
what do phagocytic deficiencies increase susceptibility to?
frequent, severe bacterial and fungal infections (deep abscesses)
73
what do T-cell deficiencies increase susceptibility to?
1. viruses
2. protozoan
3. fungal infections
74
what do complement deficiencies increase susceptibility to?
bacteria infections (accumulation of immune complexes)
75
what do B- and T-cell deficiencies increase susceptibility to?
all infectious agents
76
what immune components are compromised with B-cell deficiencies?
antibodies
77
what immune components are compromised with phagocytic deficiencies?
innate immunity
78
what immune components are compromised with T-cell deficiencies?
cell-mediated immunity
79
what immune components are compromised with complement deficiencies?
proteins C1 to C9
80
what immune components are compromised with B- and T-cell deficiencies?
lymphocytes
81
screening techniques for immunodeficiencies
methods or strategies used to identify the possible presence of a disease in individuals who may be pre-symptomatic or have unrecognized symptoms of the disease
82
what is the purpose of screening techniques for immunodeficiencies?
allows for early intervention and management of disease in effort to reduce suffering and/or mortality
83
2 major screening methods for primary and secondary immunodeficiency
1. complete blood counts (CBC)
2. quantitative serum immunoglobin
84
complete blood counts (CBC)
1. shows how many of each cell type are present in a small sample of patient’s blood – these number are then compared to a reference range of values commonly found in healthy people
2. used to highlight any severe defects in the blood that could potentially be caused by an immunodeficiency
85
quantitative serum immunoglobin
1. measure the levels of IgG, IgA and IgM in a patients blood serum and compare them to a control
2. complete blood counts and urine protein electrophoresis can be used to pinpoint the source of the hypogammaglobulinemia
86
what does it mean if levels of antibodies are lower than normal (hypogammaglobulinemia)
could be an indication of a humoral immunodeficiancy
87
urine protein electrophoresis
a screening test to evaluate the amount of certain proteins in urine
88
mononucleosis
a contagious infectious disease often cause by Epstein-Barr virus (EBV)
89
how is mononucleosis spread?
saliva (kissing-disease)
90
symptoms of mononucleosis
causes a glandular fever and extended feeling of tiredness even months after initial infection is resolved
91
white blood count
count of all immune cells (white blood cells or leukocytes)
92
what is low WBC indicative of?
weakened IR
- means there is a decreased number of WBC present to fight infection
93
HIV and test window
9-14 day window so it does not show its positive on the HIV test
- if HIV was acquired in the last 9-14 days it will say you’re negative
94
self-regulation
allows the body to regulate and maintain a healthy immune system
- BODY must be capable of recognizing its own healthy cells as well as infected/abnormal cells that may be harmful and subsequently destroy them
95
autoimmunity
immune system is over-activated and attacks healthy cells and tissues
(reaction to self)
96
autoimmune disease
1. failure of an organism to distinguish self from non-self causes the immune system to initiate a response against its own cells and tissues
2. any disease that results from such an aberrant IR
97
prevalence of autoimmune diseases within general population
5-7%
98
is the prevalence of autoimmune diseases more common in male or females?
females
- 78% are females
99
main cause of autoimmune diseases
- highly dependent on genetics
- BUT other factors such as infection by bacteria and/or viruses or chemical exposure can play a role
***often involve autoantibodies
100
autoantibodies
antibody produces by immune system that is directed against a self-antigen
101
two main categories of autoimmune diseases
1. organ specific autoimmune disease
2. systemic autoimmune disease
102
organ-specific autoimmune disease
involve an IR that's directed to an antigen that is unique to a single organ or gland
103
what does an organ-specific autoimmune disease result in?
the disease manifestations being largely limited to the specific organ
104
target organs affected by autoimmune disease
1. Thyroid gland
2. Stomach
3. Adrenal glands
4. Pancreas
105
example of an organ-specific autoimmune disease
graves disease
106
graves disease
frequently leads to overactivity of thyroid gland known as hyperthyroidism
107
thyroid-stimulating hormone (TSH)
produced by pituitary gland and is crucial for regulating production of thyroid hormones
108
what does binding of TSH by receptors on thyroid cells stimulate?
the production of thyroid hormones which control many aspects of metabolism
109
negative feedback of thyroid hormones
allows TSH production from pituitary gland to be moderated
110
grave TSH function
1. produce autoantibodies to receptor for TSH
2. autoantibodies continuously engage TSH receptors, but unlike TSH cannot be moderated
111
what does TSH that cannot be moderated result in?
an unregulated overproduction of thyroid hormones leading to metabolic dysfunction
112
cause of graves disease
both genetic and environmental factors
113
what does overstimulation of the thyroid gland cause?
enlargement of thyroid gland, a condition referred to as a goiter
114
symptoms of graves
1. Weight loss
2. Rapid heartbeat
3. Poor regulation of body temperature
4. Muscle weakness
5. Irritability
115
pituitary gland
1. pea-sized major endocrine gland
2. found attached to base of brain
3. source of trophic hormones that regulate growth, metabolism and regulation and responds to feedback
116
systemic autoimmune diseases
IR is directed towards a broad range of antigens that are characteristic of a number of organs and tissues
117
ex of a systemic autoimmune disease
rheumatoid arthritis
118
rheumatoid arthritis
common autoimmune disorder that presents as chronic inflammation of joints
- however other organ systems can be affected
119
what population is rheumatoid arthritis most common in?
women ages 40-60
120
rheumatoid factors
patients produce autoantibodies (IgM) to portions of the Fc receptor of IgG
- bind to circulating IgG forming immune complexes that become deposited within joints
121
what can the deposited rheumatoid factors do?
activate the complement cascade leading to prolonged inflammation and joint tissue damage
122
is there is a cure for autoimmune diseases?
NO CURE - but are not as life-threatening as they used to be
123
why are autoimmune diseases not as life threatening as they used to be?
scientists have come up with therapies to reduce symptoms of autoimmune diseases and provide patients with an improved quality of life
124
immunosuppressants purpose
treat autoimmune diseases
125
immunosuppressants function
suppress or reduce strength of body’s IR
126
when are immunosuppressants commonly administered?
to individuals who have undergone an organ transplant
127
immunosuppressants and organ transplants
after transplantation the body recognizes the new organ as a foreign object and IS will initiate a response against it
128
what are immunosuppressants used for?
reduce risk of rejection by inhibiting IR allowing organ to remain healthy in its new environment
129
why is it important for individuals on immunosuppressants to remain healthy and avoid infection?
because their IS may not be capable of fighting off foreign microbes
130
corticosteroids action
1. anti-inflammatory
2. kills T-cells
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corticosteroids example
prednisone
132
prednison (corticoid) clinical use
provides relief for inflamed areas of the body
133
prednison (corticoid) possible side effects
1. osteoporosis
2. hirsutism
3. hypertrichosis
4. diabetogenic
134
cytotoxic drugs action
blocks cell division non-specifically
135
cytotoxic drugs examples
1. cyclophosphamide
2. methotrexate
136
cyclophosphamide and methotrexate (cytotoxic drugs) clinical use
treats cancer by slowing or stopping cell growth
137
cyclophosphamide and methotrexate (cytotoxic drugs) possible side effects
1. hair loss
2. chills
3. mouth and lung sores
4. skin infection and sun sensitivity and rash
5. low blood cell levels
138
immunophilins action
blocks T-cell responses
139
immunophilins example
cyclosporine
140
cyclosporine (immunophilins) clinical use
used to prevent rejection in those receiving a transplanted organ
141
cyclosporine (immunophilins) possible side effects
1. nephrotoxicity
2. hypertension
3. hirsutism
4. hypertrichosis
5. gingival hyperplasia
142
lymphocyte-depleting therapies action
1. kills T-cells non-specifically
2. kills activated T-cells
143
lymphocyte-depleting therapies examples
monoclonal antibodies
144
monoclonal antibodies clinical use
used to prevent acute rejection in organ transplantation
145
classes of immunosuppressive drugs
1. corticosteroids
2. cytotoxic drugs
3. immunophilins
4. lymphocyte-depleting therapies
146
impact of immunosuppression on the host
1. some patients may develop latent or opportunistic infections
2. these infections tend develop because of the hosts weakened immune system
147
latent infections
1. infections that are inactive, hidden or dormant
2. immunosuppressive therapy increases risk of reactivation of pathogens associated with latent infections
148
most common pathogens
1. TB: tuberculosis
2. HSV1/2: herpes simplex 1/2
3. CMV: cytomegalovirus
4. EBV: Epstein-barr virus
5. VZV: varicella zoster virus
149
opportunistic infections
1. commonly occur when there is reactivation of a pathogen that is already present in the host
2. can also result when a pathogen is picked up from the environment, but the blunted IR of host is unable to combat the pathogen
150
what can opportunistic infections arise from?
1. bacteria
2. viruses
3. parasites
4. fungi
151
fungal opportunistic infections
1. pneumocystis jiroveci pneumonia
2. cryptococcosis
3. aspergillosis
152
pneumocystis jiroveci pneumonia common name
PCP
153
what does pneumocystis jiroveci pneumonia infect?
pneumonia of lungs
154
cryptococcosis common name
cryptococcal disease
155
what does cryptococcosis infect?
lungs which may spread to the brain
156
candidiasis common name
thrush
157
what does candidiasis infect?
1. mouth
2. throat
3. vagina
158
what does aspergillosis infect?
the lungs
159
parasitic opportunistic infections
1. toxoplasmosis
160
what does toxoplasmosis infect?
1. skeletal muscle
2. myocardium
3. brain
4. eyes
161
bacterial opportunistic infections
1. tuberculosis
2. mycobacterium avium complex
162
tuberculosis common name
consumption
163
what does tuberculosis infect?
the lungs
164
mycobacterium avium complex common name
MAC
165
what does mycobacterium avium complex infect?
1. lungs
2. lymph nodes or entire body depending on site of infection
166
viral opportunistic infections
1. cytomegalovirus
2. herpes simplex virus (HSV)
3. varicella zoster virus
4. mononucleosis
167
cytomegalovirus common name
CMV
168
what does cytomegalovirus infect?
1. eyes
2. brain
3. other internal organs
169
herpes simplex virus (HSV) common name
herpes
170
what does herpes simplex virus (HSV) infect?
1. skin
2. mouth
3. lips
4. eyes
5. genitals
171
varicella zoster virus common name
chickenpox
172
what dies varicella zoster virus infect
skin or in more extreme cases, internal organs
173
mononucleosis common name
epstein-barr virus or kissing disease
174
what does mononucleosis infect?
1. lymph nodes
2. throat
3. salivary glands
4. liver
5. spleen
6. blood
175
are immunosuppressive therapies good?
YES, but must be used cautiously
176
hypersensitvity
excessive reactions produced by the normal IS
177
Type I hypersensitivity
immediate or anaphylactic hypersensitivity
178
type I hypersensitivty - mediators
allergens
- normally a harmless substance
- produces an abnormal IR = allergic reaction
179
8 major food allergens
1. milk
2. eggs
3. fish
4.crustacean shellfish
5. tree huts
6. peanuts
7. wheat
8. soya
180
primary exposure to an allergen - type I hypersensitivity
allergen induces a humoral response wherein plasma cells secrete an excessive amount of IgE antibodies which bind to mast cells and basophils
181
secondary exposure to an allergen - type I hypersensitivity
1. membrane-bound IgE cross-links with the allergen which initiates the degranulation of basophils and mast cells
2. this releases vasoactive mediators causing vasodilation and smooth muscle contraction
182
what does vasodilation and smooth muscle contraction cause?
difficulty breathing associated with asthma
183
degranulation
release of granules
184
reaction time of type I hypersensitivity
1. immediate - minutes until anaphylactic reaction
2. can lead to death as little as 15 minutes
3. rare type I reactions can take longer (24 hours) but must occur soon after exposure
185
clinical manifestations of type I hypersensitivity
1. allergic rhinitis
2. asthma
3. atopic dermatitis (eczema)
4. hives (utricaria)
186
allergic rhinitis
generalizes irritation of the nose when IS overeacts to allergens in air
187
asthma
a respiratory condition in which the airways narrow, swell, and produce extra mucus
188
atopic dermatitis (eczema)
a condition where an individual develops skin eruptions accompanied by redness
189
hives (utricaria)
a rash of itchy round, red welts on skin that may also burn, sting or swell
190
type II hypersensitivity
antibody-mediated cytotoxic hypersensitivity
191
mediators of type II hypersensitivity
1. IgG
2. IgM
3. NK cells
4. the complement system
192
mechanism of reaction for type II hypersensitivity
1. IgG and/or IgMs bind to antigens on surface of cells such as erythrocytes (ex. following blood transfusion)
2. once antibodies are attached to cell through their antigen binding region, the Fc region is free and can activate two processes called classical complement activation and antibody-dependent cell-mediated cytotoxicity (ADCC)
193
what does classical complement activation lead to?
leading to opsonization of membrane attack complexes (MAC)
194
what happens when erythrocytes are destroyed?
lead to an excessive inflammatory response
195
MAC
creates holes in cell membrane leading to cell lysis
196
opsonization
leads to phagocytosis by phagocytes such as macrophages
197
reaction time of type II hypersensitivity
minutes to hours
198
clinical manifestations of type II hypersensitivity
1. drug-induced hemolytic anemia
2. transfusion reactions
199
drug-induced hemolytic anemia
1. some antibiotics can bind nonspecifically to proteins on RBC membranes and form a complex which sometimes induces complement-mediated lysis
2. as RBCs rupture, number of RBCs decrease resulting in anema
3. anemia disappears when drug is removed
200
what drug typically induces hemolytic anemia?
penicillin
201
transfusion reactions
depending on blood type, you will only be able to safely receive certain blood types during a blood transfusion
202
why can you only safely receive certain blood types during a blood transfusion?
due to presence or absence of expression of a specific antigen (A or B) on your RBCs, meaning if you don’t express the antigens, you have antibodies against them
203
universal donor
person with O negative blood type
- an give blood to all the other blood types cause they don’t have A or B antigens on the surface of their RBCs
204
universal recipient
person with AB positive blood type
- can receive blood from all other blood types cause they don’t have antibodies against A or B antigens
205
RBC
red blood cell or erythrocyte
206
anemia
a condition characterized by a deficiency of red blood cells or hemoglobin in the blood
207
type II hypersensitivity
immune-complex mediated hypersensitivity
208
mediators of type II hypersensitivity
1. immune complexes (antigen-antibody complexes)
2. neutrophils
3. complement proteins
209
mechanism of reaction for type II hypersensitivity
1. reaction of antibodies with antigens generates immune complexes
2. when immune complexes are not cleared, they can accumulate and deposit it the tissue
3. these immune complexes will activate the complement which will induce inflammatory reactions through neutrophil attraction to sire of deposition
4. neutrophils release lytic enzymes as they attempt to phagocytose the immune complexes, which weakens surrounding cell membranes ultimately causing tissue damage
210
reaction time of type II hypersensitivity
1. may take 3-10 hours after exposure to the antigen
2. sometimes reaction can take longer to develop (days to weeks)
211
clinical manifestations of type II hypersensitivity
serum sickness
212
serum sickness
1. reactions are often observed after administration of antitoxins containing foreign serum
2. recipient of these antiserums develop antibodies specific for this protein
3 . when these antibodies circulate, they form immune complexes with protein
4. often complexes accumulate in tissues where filtration of plasma occur and can contribute to pathogenesis of many other conditions such as autoimmune diseases, hepatitis and malaria
213
how long does it take for symptoms of serum sickness to occur?
after a couple days to a week
214
symptoms of serum sickness
1. fever
2. weakness
3. generalized vasculitis (rashes) with edema
215
when do clinical effects of serum sickness subside?
when the antigen has been completely broken down
216
antitoxins
an antibody that counteracts a toxin
217
antiserums
blood serum containing antibodies against specific, injected to treat to protect against specific diseases
218
type IV hypersensitivity
cell-mediated or delayed-type hypersensitivity (DTH)
219
mediators of type IV hypersensitivity
1. CD8+ cytotoxic T-cells
2. CD4+ helper T-cells
3. macrophages
***not mediated by antibodies
220
mechanism of reactions
1. after exposure to an antigen, T-cells become activated and initiate an IR
2. sensitized helper T-cells (TH1) will release cytokines that activate macrophages or cytotoxic T-cells which mediate direct cellular damage
221
reaction time of type IV hypersensitivity
1. delayed response
2. can take 2-3 days to develop after exposure to a particular substance
222
clinical manifestations of type IV hypersensitivity
1. inflammatory bowel disease (IBD)
2. contact dermatitis
223
two most common diseases of IBD
1. ulcerative colitis
2. chron's disease
224
inflammatory bowel disease (IBD)
1. a group of conditions that is characterized by chronic inflammation of all or parts of the digestive tract
2. autoimmune disease
225
contact dermatitis
type of DTH response causing a red itchy rash on the skin that has been in contact with small, reactive molecules which create complexes with skin proteins
226
common inducers of contact dermatitis
1. poison ivy
2. formaldehyde
3. nickel
4. cosmetics
227
synovitis
inflammation of a synovial membrane which is a component of the synovial joint that attaches bones with fibrous joint capsule
228
erythrocyte sedimentation rate (ESR)
1. rate at which red blood cells sediment in one hour
2. used as a marker for inflammation and can help confirm presence of a variety of disease states
3. inflammation causes RBC to clump more = higher ESR
229
C-reactive protein levels
a marker of inflammation in the body
- a more accurate reflection of acute phase immune response than ESR
- more inflammation is reflected by increased levels of CRP
230
microcytic anemia
presence of small RBCs
231
colonoscopy
a procedure in which a flexible fiber-optic instrument is inserted through the anus in order to examine the colon
232
albuterol
used to relax muscles found in airways to increase airflow to the lungs
233
AGPAR score
method to quickly summarize the health of a newborn child
- determined by evaluating the newborn baby on 5 criteria from zero to two
- 5 values are then summed up to give the AGPAR score
- a score of 7 and above is considered normal
234
what does the AGPAR score stand for?
1. Appearance
2. Pulse
3. Grimace
4. Activity
5. Respiration
235
asthma
abnormal inflammatory response to a specific or nonspecific stimuli in the bronchial lining, resulting in obstruction of small and large airways
236
what happens during an asthma attack?
the muscles in the airway contract and the walls become inflamed, resulting in a narrow airway with thickened walls
