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MICR 270 > Module 4 > Flashcards

Module 4 Flashcards

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

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2
Q

two main types of immunodeficiencies

A
  1. primary immunodeficiency
  2. secondary immunodeficiency
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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

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4
Q

congenital

A

present from birth

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5
Q

B-cell deficiencies prevalence

A

65%

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6
Q

T-cell deficiencies prevalence

A

5%

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7
Q

complement deficiencies

A

5%

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8
Q

phagocytic deficiencies

A

10%

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9
Q

combined T- and B-cell deficiencies

A

15%

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10
Q

why are primary immunodeficiencies rare?

A

because the fetus doesn’t usually survive the defect

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11
Q

secondary immunodeficiency

A

acquired and result from environmental factors affecting and compromising the IS

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12
Q

causes of secondary immunodeficiency

A
  1. undergoing chemotherapy treatment
  2. taking immunosuppressive medication
  3. contracting a chronic infection (HIV/AIDS)
  4. developing cancer
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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

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14
Q

deficiency in B-cell development

A

results in an increased susceptibility to infection, especially by encapsulated bacteria

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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

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16
Q

encapsulated bacteria

A

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

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17
Q

clinical example of B-cell deficiencies

A

X-linked agammaglobulinemia (XLA)

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18
Q

x-linked agammaglobulineamia (xla)

A
  1. rare genetic disorder
  2. linked and recessive, therefore occurs almost exclusively in males
  3. patients do not develop mature B cells and as a result have extremely low levels of IgG and lack all other immunoglobins
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19
Q

XLA and infection

A
  1. XLA patients are extremely susceptible to bacterial infections
  2. their susceptibility to viral and fungal infections remains unchanged – due to cell-mediated response remaining normal
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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

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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

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22
Q

example of T-cell deficiencies

A

pneumonia and candidiasis

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23
Q

clinical example of T-cell deficiencies

A

digeorge syndrome

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24
Q

digeorge syndrome

A

complex disease caused by the deletion of a small segment of chromosome 22

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25
Q

symptoms of digeorge syndrome

A
  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
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26
Q

complement deficiencies

A
  1. complement system involves intricate regulation of nine components
  2. genetic deficiencies have been described for each of these complement components
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27
Q

patients with complement deficiencies are prone to what?

A

frequent sever bacterial infections and complications arising from inability to clear immune complexes

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28
Q

C3 deficiencies

A

C3 deficiencies display the severest symptoms, reflective of the central role played by this component in complement activities

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29
Q

clinical example of complement deficiencies

A

hereditary angioedema (HAE)

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30
Q

hereditary angioedema (HAE)

A

deficiencies in proteins that regulate complement pathways
- patients with HAE lack a regular of C1

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31
Q

symptoms of HAE

A
  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
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32
Q

phagocytic deficiencies

A

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

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33
Q

defective phagocytosis and infection

A

bacterial and fungal infections are frequent and severe often causing deep abscesses in patients

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34
Q

clinical example of phagocytic deficiencies

A

chronic granulomatous disease (CGD)

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35
Q

chronic granulomatous disease (CGD)

A

rare inherited disease where the body’s phagocytes do not make the chemicals needed to kill phagocytosed bacteria

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36
Q

where does CGD derive its name from?

A

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

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37
Q

non-malignant granulomas

A

small, nodular aggregations of immune cells

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38
Q

combined T-cell and B-cell deficiencies

A
  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
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39
Q

what is combined T-cell and B-cell deficiencies characterized by?

A
  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
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40
Q

clinical example of combined T-cell and B-cell deficiencies

A

severe combined inherited immunodeficiency (SCID)

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41
Q

severe combined inherited immunodeficiency (SCID)

A
  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
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42
Q

acquired immunodeficiency syndrome (AIDS)

A

defined by describing combination of words used to make up its name

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43
Q

aquired (AIDS)

A

individuals do NOT inherit this type of disease (big difference between AIDS and primary ID)

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44
Q

immunodeficiency (AIDS)

A

one disease characteristic that is common is breakdown of immune system

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45
Q

sydrome (AIDS)

A

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

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46
Q

AIDS

A
  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
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47
Q

mode of transmission of HIV

A
  1. varies depending on location
  2. without treatment the outcome is the same regardless of portal of entry
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48
Q

outcome of HIV

A
  1. immunosuppression
  2. neuropsychiatric abnormalities
  3. death
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49
Q

mode of transmission in north america

A

sexual intercourse

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50
Q

mode of transmission in eastern europe and central asia

A

use of non-sterile injections of drugs

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51
Q

mode of transmission in sub-saharan africa

A

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

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52
Q

HIV primary infection

A
  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
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53
Q

HIV acute infection

A
  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
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54
Q

what happens within 2-4 weeks after primary exposure to HIV?

A

some people will experience flu-like symptoms including fever, headache, and rash

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55
Q

level of HIV in blood during acute infection phase

A

high
- this greatly increases risk of HIV transmission

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56
Q

why do CD4+ helper T-cells increase after initial decrease?

A

because some antibodies are formed against the virus allowing IS to recover some of lost cell population

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57
Q

chronic infection

A
  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
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58
Q

HIV chronic infection symptoms

A

people with chronic HIV don’t have symptoms but transmission is still possible

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59
Q

length of chronic infection phase of HIV

A

8-10 years

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60
Q

HIV - AIDS

A
  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
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61
Q

when do HIV patients get diagnosed with AIDS?

A

when they have CD4+ helper T-cell level of less than 200 cells/mm3

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62
Q

how long do AIDS patients survive in the absence of treatment?

A

about 3 years

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63
Q

when was the first antiretroviral therapy approved?

A

1987

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64
Q

what does antiretroviral therapy do?

A

these drugs do not kill or cure human human immunodeficiency virus, but prevent it from replicating

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65
Q

combination retroviral therapy (types)

A

antiretroviral therapy (ART) and highly active antiretroviral therapy (HAART)

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66
Q

combination retroviral therapy

A

utilizes a panel of antiretroviral drugs in different combinations to prevent drug resistance by the rapidly-mutating virus

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67
Q

benefit of combination retroviral therapy

A

this treatment has led to staggering declines in rates of AIDS and AIDS-associated deaths

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68
Q

HAART

A

maintains function of immune system and prevents opportunistic infections that often lead to death

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69
Q

WHO and HAART

A

700 000 lives saved in 2010 alone due to increased availability of antiretroviral therapy
- since HAART, HIV almost never progresses into AIDS

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70
Q

4 things ART does

A
  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
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71
Q

what do B-cell deficiencies increase susceptibility to?

A

bacterial infections (encapsulated bacteria)

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72
Q

what do phagocytic deficiencies increase susceptibility to?

A

frequent, severe bacterial and fungal infections (deep abscesses)

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73
Q

what do T-cell deficiencies increase susceptibility to?

A
  1. viruses
  2. protozoan
  3. fungal infections
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74
Q

what do complement deficiencies increase susceptibility to?

A

bacteria infections (accumulation of immune complexes)

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75
Q

what do B- and T-cell deficiencies increase susceptibility to?

A

all infectious agents

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76
Q

what immune components are compromised with B-cell deficiencies?

A

antibodies

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77
Q

what immune components are compromised with phagocytic deficiencies?

A

innate immunity

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78
Q

what immune components are compromised with T-cell deficiencies?

A

cell-mediated immunity

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79
Q

what immune components are compromised with complement deficiencies?

A

proteins C1 to C9

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80
Q

what immune components are compromised with B- and T-cell deficiencies?

A

lymphocytes

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81
Q

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 of the disease

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82
Q

what is the purpose of screening techniques for immunodeficiencies?

A

allows for early intervention and management of disease in effort to reduce suffering and/or mortality

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83
Q

2 major screening methods for primary and secondary immunodeficiency

A
  1. complete blood counts (CBC)
  2. quantitative serum immunoglobin
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84
Q

complete blood counts (CBC)

A
  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
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85
Q

quantitative serum immunoglobin

A
  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
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86
Q

what does it mean if levels of antibodies are lower than normal (hypogammaglobulinemia)

A

could be an indication of a humoral immunodeficiancy

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87
Q

urine protein electrophoresis

A

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

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88
Q

mononucleosis

A

a contagious infectious disease often cause by Epstein-Barr virus (EBV)

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89
Q

how is mononucleosis spread?

A

saliva (kissing-disease)

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90
Q

symptoms of mononucleosis

A

causes a glandular fever and extended feeling of tiredness even months after initial infection is resolved

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91
Q

white blood count

A

count of all immune cells (white blood cells or leukocytes)

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92
Q

what is low WBC indicative of?

A

weakened IR
- means there is a decreased number of WBC present to fight infection

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93
Q

HIV and test window

A

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

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94
Q

self-regulation

A

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

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95
Q

autoimmunity

A

immune system is over-activated and attacks healthy cells and tissues
(reaction to self)

96
Q

autoimmune disease

A
  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
Q

prevalence of autoimmune diseases within general population

A

5-7%

98
Q

is the prevalence of autoimmune diseases more common in male or females?

A

females
- 78% are females

99
Q

main cause of autoimmune diseases

A
  • 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
Q

autoantibodies

A

antibody produces by immune system that is directed against a self-antigen

101
Q

two main categories of autoimmune diseases

A
  1. organ specific autoimmune disease
  2. systemic autoimmune disease
102
Q

organ-specific autoimmune disease

A

involve an IR that’s directed to an antigen that is unique to a single organ or gland

103
Q

what does an organ-specific autoimmune disease result in?

A

the disease manifestations being largely limited to the specific organ

104
Q

target organs affected by autoimmune disease

A
  1. Thyroid gland
  2. Stomach
  3. Adrenal glands
  4. Pancreas
105
Q

example of an organ-specific autoimmune disease

A

graves disease

106
Q

graves disease

A

frequently leads to overactivity of thyroid gland known as hyperthyroidism

107
Q

thyroid-stimulating hormone (TSH)

A

produced by pituitary gland and is crucial for regulating production of thyroid hormones

108
Q

what does binding of TSH by receptors on thyroid cells stimulate?

A

the production of thyroid hormones which control many aspects of metabolism

109
Q

negative feedback of thyroid hormones

A

allows TSH production from pituitary gland to be moderated

110
Q

grave TSH function

A
  1. produce autoantibodies to receptor for TSH
  2. autoantibodies continuously engage TSH receptors, but unlike TSH cannot be moderated
111
Q

what does TSH that cannot be moderated result in?

A

an unregulated overproduction of thyroid hormones leading to metabolic dysfunction

112
Q

cause of graves disease

A

both genetic and environmental factors

113
Q

what does overstimulation of the thyroid gland cause?

A

enlargement of thyroid gland, a condition referred to as a goiter

114
Q

symptoms of graves

A
  1. Weight loss
  2. Rapid heartbeat
  3. Poor regulation of body temperature
  4. Muscle weakness
  5. Irritability
115
Q

pituitary gland

A
  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
Q

systemic autoimmune diseases

A

IR is directed towards a broad range of antigens that are characteristic of a number of organs and tissues

117
Q

ex of a systemic autoimmune disease

A

rheumatoid arthritis

118
Q

rheumatoid arthritis

A

common autoimmune disorder that presents as chronic inflammation of joints
- however other organ systems can be affected

119
Q

what population is rheumatoid arthritis most common in?

A

women ages 40-60

120
Q

rheumatoid factors

A

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
Q

what can the deposited rheumatoid factors do?

A

activate the complement cascade leading to prolonged inflammation and joint tissue damage

122
Q

is there is a cure for autoimmune diseases?

A

NO CURE - but are not as life-threatening as they used to be

123
Q

why are autoimmune diseases not as life threatening as they used to be?

A

scientists have come up with therapies to reduce symptoms of autoimmune diseases and provide patients with an improved quality of life

124
Q

immunosuppressants purpose

A

treat autoimmune diseases

125
Q

immunosuppressants function

A

suppress or reduce strength of body’s IR

126
Q

when are immunosuppressants commonly administered?

A

to individuals who have undergone an organ transplant

127
Q

immunosuppressants and organ transplants

A

after transplantation the body recognizes the new organ as a foreign object and IS will initiate a response against it

128
Q

what are immunosuppressants used for?

A

reduce risk of rejection by inhibiting IR allowing organ to remain healthy in its new environment

129
Q

why is it important for individuals on immunosuppressants to remain healthy and avoid infection?

A

because their IS may not be capable of fighting off foreign microbes

130
Q

corticosteroids action

A
  1. anti-inflammatory
  2. kills T-cells
131
Q

corticosteroids example

A

prednisone

132
Q

prednison (corticoid) clinical use

A

provides relief for inflamed areas of the body

133
Q

prednison (corticoid) possible side effects

A
  1. osteoporosis
  2. hirsutism
  3. hypertrichosis
  4. diabetogenic
134
Q

cytotoxic drugs action

A

blocks cell division non-specifically

135
Q

cytotoxic drugs examples

A
  1. cyclophosphamide
  2. methotrexate
136
Q

cyclophosphamide and methotrexate (cytotoxic drugs) clinical use

A

treats cancer by slowing or stopping cell growth

137
Q

cyclophosphamide and methotrexate (cytotoxic drugs) possible side effects

A
  1. hair loss
  2. chills
  3. mouth and lung sores
  4. skin infection and sun sensitivity and rash
  5. low blood cell levels
138
Q

immunophilins action

A

blocks T-cell responses

139
Q

immunophilins example

A

cyclosporine

140
Q

cyclosporine (immunophilins) clinical use

A

used to prevent rejection in those receiving a transplanted organ

141
Q

cyclosporine (immunophilins) possible side effects

A
  1. nephrotoxicity
  2. hypertension
  3. hirsutism
  4. hypertrichosis
  5. gingival hyperplasia
142
Q

lymphocyte-depleting therapies action

A
  1. kills T-cells non-specifically
  2. kills activated T-cells
143
Q

lymphocyte-depleting therapies examples

A

monoclonal antibodies

144
Q

monoclonal antibodies clinical use

A

used to prevent acute rejection in organ transplantation

145
Q

classes of immunosuppressive drugs

A
  1. corticosteroids
  2. cytotoxic drugs
  3. immunophilins
  4. lymphocyte-depleting therapies
146
Q

impact of immunosuppression on the host

A
  1. some patients may develop latent or opportunistic infections
  2. these infections tend develop because of the hosts weakened immune system
147
Q

latent infections

A
  1. infections that are inactive, hidden or dormant
  2. immunosuppressive therapy increases risk of reactivation of pathogens associated with latent infections
148
Q

most common pathogens

A
  1. TB: tuberculosis
  2. HSV1/2: herpes simplex 1/2
  3. CMV: cytomegalovirus
  4. EBV: Epstein-barr virus
  5. VZV: varicella zoster virus
149
Q

opportunistic infections

A
  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
Q

what can opportunistic infections arise from?

A
  1. bacteria
  2. viruses
  3. parasites
  4. fungi
151
Q

fungal opportunistic infections

A
  1. pneumocystis jiroveci pneumonia
  2. cryptococcosis
  3. aspergillosis
152
Q

pneumocystis jiroveci pneumonia common name

A

PCP

153
Q

what does pneumocystis jiroveci pneumonia infect?

A

pneumonia of lungs

154
Q

cryptococcosis common name

A

cryptococcal disease

155
Q

what does cryptococcosis infect?

A

lungs which may spread to the brain

156
Q

candidiasis common name

A

thrush

157
Q

what does candidiasis infect?

A
  1. mouth
  2. throat
  3. vagina
158
Q

what does aspergillosis infect?

A

the lungs

159
Q

parasitic opportunistic infections

A
  1. toxoplasmosis
160
Q

what does toxoplasmosis infect?

A
  1. skeletal muscle
  2. myocardium
  3. brain
  4. eyes
161
Q

bacterial opportunistic infections

A
  1. tuberculosis
  2. mycobacterium avium complex
162
Q

tuberculosis common name

A

consumption

163
Q

what does tuberculosis infect?

A

the lungs

164
Q

mycobacterium avium complex common name

A

MAC

165
Q

what does mycobacterium avium complex infect?

A
  1. lungs
  2. lymph nodes or entire body depending on site of infection
166
Q

viral opportunistic infections

A
  1. cytomegalovirus
  2. herpes simplex virus (HSV)
  3. varicella zoster virus
  4. mononucleosis
167
Q

cytomegalovirus common name

A

CMV

168
Q

what does cytomegalovirus infect?

A
  1. eyes
  2. brain
  3. other internal organs
169
Q

herpes simplex virus (HSV) common name

A

herpes

170
Q

what does herpes simplex virus (HSV) infect?

A
  1. skin
  2. mouth
  3. lips
  4. eyes
  5. genitals
171
Q

varicella zoster virus common name

A

chickenpox

172
Q

what dies varicella zoster virus infect

A

skin or in more extreme cases, internal organs

173
Q

mononucleosis common name

A

epstein-barr virus or kissing disease

174
Q

what does mononucleosis infect?

A
  1. lymph nodes
  2. throat
  3. salivary glands
  4. liver
  5. spleen
  6. blood
175
Q

are immunosuppressive therapies good?

A

YES, but must be used cautiously

176
Q

hypersensitvity

A

excessive reactions produced by the normal IS

177
Q

Type I hypersensitivity

A

immediate or anaphylactic hypersensitivity

178
Q

type I hypersensitivty - mediators

A

allergens
- normally a harmless substance
- produces an abnormal IR = allergic reaction

179
Q

8 major food allergens

A
  1. milk
  2. eggs
  3. fish
    4.crustacean shellfish
  4. tree huts
  5. peanuts
  6. wheat
  7. soya
180
Q

primary exposure to an allergen - type I hypersensitivity

A

allergen induces a humoral response wherein plasma cells secrete an excessive amount of IgE antibodies which bind to mast cells and basophils

181
Q

secondary exposure to an allergen - type I hypersensitivity

A
  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
Q

what does vasodilation and smooth muscle contraction cause?

A

difficulty breathing associated with asthma

183
Q

degranulation

A

release of granules

184
Q

reaction time of type I hypersensitivity

A
  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
Q

clinical manifestations of type I hypersensitivity

A
  1. allergic rhinitis
  2. asthma
  3. atopic dermatitis (eczema)
  4. hives (utricaria)
186
Q

allergic rhinitis

A

generalizes irritation of the nose when IS overeacts to allergens in air

187
Q

asthma

A

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

188
Q

atopic dermatitis (eczema)

A

a condition where an individual develops skin eruptions accompanied by redness

189
Q

hives (utricaria)

A

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

190
Q

type II hypersensitivity

A

antibody-mediated cytotoxic hypersensitivity

191
Q

mediators of type II hypersensitivity

A
  1. IgG
  2. IgM
  3. NK cells
  4. the complement system
192
Q

mechanism of reaction for type II hypersensitivity

A
  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
Q

what does classical complement activation lead to?

A

leading to opsonization of membrane attack complexes (MAC)

194
Q

what happens when erythrocytes are destroyed?

A

lead to an excessive inflammatory response

195
Q

MAC

A

creates holes in cell membrane leading to cell lysis

196
Q

opsonization

A

leads to phagocytosis by phagocytes such as macrophages

197
Q

reaction time of type II hypersensitivity

A

minutes to hours

198
Q

clinical manifestations of type II hypersensitivity

A
  1. drug-induced hemolytic anemia
  2. transfusion reactions
199
Q

drug-induced hemolytic anemia

A
  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
Q

what drug typically induces hemolytic anemia?

A

penicillin

201
Q

transfusion reactions

A

depending on blood type, you will only be able to safely receive certain blood types during a blood transfusion

202
Q

why can you only safely receive certain blood types during a blood transfusion?

A

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
Q

universal donor

A

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
Q

universal recipient

A

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
Q

RBC

A

red blood cell or erythrocyte

206
Q

anemia

A

a condition characterized by a deficiency of red blood cells or hemoglobin in the blood

207
Q

type II hypersensitivity

A

immune-complex mediated hypersensitivity

208
Q

mediators of type II hypersensitivity

A
  1. immune complexes (antigen-antibody complexes)
  2. neutrophils
  3. complement proteins
209
Q

mechanism of reaction for type II hypersensitivity

A
  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
Q

reaction time of type II hypersensitivity

A
  1. may take 3-10 hours after exposure to the antigen
  2. sometimes reaction can take longer to develop (days to weeks)
211
Q

clinical manifestations of type II hypersensitivity

A

serum sickness

212
Q

serum sickness

A
  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
  3. 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
Q

how long does it take for symptoms of serum sickness to occur?

A

after a couple days to a week

214
Q

symptoms of serum sickness

A
  1. fever
  2. weakness
  3. generalized vasculitis (rashes) with edema
215
Q

when do clinical effects of serum sickness subside?

A

when the antigen has been completely broken down

216
Q

antitoxins

A

an antibody that counteracts a toxin

217
Q

antiserums

A

blood serum containing antibodies against specific, injected to treat to protect against specific diseases

218
Q

type IV hypersensitivity

A

cell-mediated or delayed-type hypersensitivity (DTH)

219
Q

mediators of type IV hypersensitivity

A
  1. CD8+ cytotoxic T-cells
  2. CD4+ helper T-cells
  3. macrophages
    ***not mediated by antibodies
220
Q

mechanism of reactions

A
  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
Q

reaction time of type IV hypersensitivity

A
  1. delayed response
  2. can take 2-3 days to develop after exposure to a particular substance
222
Q

clinical manifestations of type IV hypersensitivity

A
  1. inflammatory bowel disease (IBD)
  2. contact dermatitis
223
Q

two most common diseases of IBD

A
  1. ulcerative colitis
  2. chron’s disease
224
Q

inflammatory bowel disease (IBD)

A
  1. a group of conditions that is characterized by chronic inflammation of all or parts of the digestive tract
  2. autoimmune disease
225
Q

contact dermatitis

A

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
Q

common inducers of contact dermatitis

A
  1. poison ivy
  2. formaldehyde
  3. nickel
  4. cosmetics
227
Q

synovitis

A

inflammation of a synovial membrane which is a component of the synovial joint that attaches bones with fibrous joint capsule

228
Q

erythrocyte sedimentation rate (ESR)

A
  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
Q

C-reactive protein levels

A

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
Q

microcytic anemia

A

presence of small RBCs

231
Q

colonoscopy

A

a procedure in which a flexible fiber-optic instrument is inserted through the anus in order to examine the colon

232
Q

albuterol

A

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

233
Q

AGPAR score

A

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
Q

what does the AGPAR score stand for?

A
  1. Appearance
  2. Pulse
  3. Grimace
  4. Activity
  5. Respiration
235
Q

asthma

A

abnormal inflammatory response to a specific or nonspecific stimuli in the bronchial lining, resulting in obstruction of small and large airways

236
Q

what happens during an asthma attack?

A

the muscles in the airway contract and the walls become inflamed, resulting in a narrow airway with thickened walls

MICR 270 (5 decks)

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