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LCCC Nursing > Chapter 14: Med Surg > Flashcards

Chapter 14: Med Surg Flashcards

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1
Q

immunity

A

a state of responsiveness to foreign substances such as microorganisms and tumor proteins; fx: defense, homeostasis, surveillance

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2
Q

homeostasis

A

damaged cellular substances are digested and removed, but the body’s different cell types remain unchanged

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3
Q

surveillance

A

mutations continually arise, but are normally recognized as foreign cells and destroyed

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4
Q

active immunity

A

takes awhile to develop, but long lasting

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5
Q

passive immunity

A

short lived because the host did not synthesize the antibodies and does not retain memory cells for the antigen

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6
Q

antigen

A

body recognizes a foreign substance and elicits an immune response; most composed of protein

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7
Q

thymus gland

A

central (primary) lymphoid organ- shrinks with age and is important in the differntiation and maturation of t lymphocytes

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8
Q

bone marrow

A

central (primary) lymphoid organ- produces RBCs, WBCs, and platelets

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9
Q

lymphoid tissue

A

found in submucosa of the respiratory, genitourinary, and GI tract- protects body surface from external microorganisms e.g. tonsils

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10
Q

spleen

A

primary site for filtering foreign substances from blood and major site of immune responses to blood-borne antigens

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11
Q

lymphnodes

A

filtrate foreign material brought to site and circulate lymphocytes

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12
Q

mononuclear phagocytes

A

monocytes & macrophages; capture through phagocytosis and the macrophage bound antigen is presented to lymphocytes which triggers an immune response

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13
Q

B lymphocytes

A

produced in bone and differentiate into plasma cells which produce antibodies (immunoglobulins)

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14
Q

T lymphocytes

A

migrate from bone marrow to thymus, compose 70%-80% of lymphocytes and provide immunity to intracellular viruses, tumor cells, and fungi; long term immunity

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15
Q

T cytotoxic cells

A

CD8 attack antigens on cell membrane of foreign pathogens and destroy, antigen specific and sensitized by exposure to the antigen

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16
Q

T helper cells

A

CD4 regulate cell-mediated immunity and the humoral antibody response

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17
Q

natural killer cells

A

involved in cell-mediated immunity, large lymphocytes, do not require prior sensitization for activation, recognize and kill virus-infected cells, tumor cells, and transplanted grafts

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18
Q

antibodies

A

immune globulins produced by lymphocytes in response to antigens

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19
Q

dendritic cells

A

capture antigens at sites of contact with the external environment and then transport the antigen to a T cell with specificity for the antigen and activate the immune response

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20
Q

cytokines

A

soluble factors secreted by WBCs that act as messengers between cell types and instruct cells to alter their proliferation, differentiation, secretion, or activity

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21
Q

interferons

A

type of cytokine that help the body’s natural defenses attack tumors and viruses and enhance natural killer cells

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22
Q

what is the first antibody formed by humoral immunity?

A

IgM formed by the primary immune response (4-8 days after initial exposure); forms antibodies to ABO blood antigens

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23
Q

cell-mediated immunity

A

t cells. macrophages, and natural killer cells that are initiated through specific antigen recognition by t cells; memory cells- protects against fungus, intracellular viruses, chronic infections, and tumor cells

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24
Q

humoral immunity

A

antibody-mediated immunity produced by b lymphocytes that have memory cells- protects against bacteria, extracellular viruses, respiratory pathogens, and GI pathogens

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25
Q

examples of when humoral response is initiated

A

anaphylactic shock, atopic diseases, transfusion reactions, bacterial infections

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26
Q

what is the second antibody formed by humoral immunity?

A

IgG formed by the secondary response (1-3 days after second exposure and is more rapid & stronger) ONLY ONE TO CROSS PLACENTA

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27
Q

examples of when cell-mediated response is initiated

A

TB, fungal infections, contact dermatitis, graft rejection, destruction of cancer cells

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28
Q

IgA

A

found in body secretions and lines mucous membranes to protect body surfaces

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29
Q

IgD

A

found in plasma, assists differentiation of B lymphocytes

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30
Q

IgE

A

found in plasma and interstitial fluid & causes symptoms of allergic reaction

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31
Q

effects of aging on the immune system

A

more tumors, greater chance of infection, thymic involution, decreased cell-mediated immunity, delayed hypersensitivity reaction, decreased autoantibodies

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32
Q

what is relatively unaffected in the immune system of older people?

A

bone marrow

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33
Q

anergy

A

common in older people, lack of or dimished reaction to an antigen

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34
Q

type 1 hypersensitivity

A

IgE mediated, anaphylactic reaction, highly sensitized to pollen, food, drugs, dust

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35
Q

mediators to type 1 hypersensitivity

A

histamine, mast cells, leukotrienes, prostaglandins; short acting and reversible

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36
Q

locus

A

where the gene resides on the chromosome

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37
Q

allele

A

one of two or more alternative forms of a gene that codes inherited characteristics

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38
Q

dominant allele

A

gene that is expressed in the phenotype of a heterozygous individual, allele that is fully expressed

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39
Q

recessive allele

A

lacks the ability to express itself, no noticeable effect on the phenotype

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40
Q

transcription

A

messenger RNA is synthesized from a single strand of DNA

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41
Q

mitosis

A

results in two identical daughter cells and before duplication, each cell receives an extra replica of chromosomes from parent cell

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42
Q

meiosis

A

oocytes and sperm contain only a single copy of each chromosome

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43
Q

crossing over

A

genetic material is exchanged between homologous chromosomes in the cell; some traits from mom, some from dad

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44
Q

autosomal dominant disorders

A

mutation of single gene pair, has variable expression (people may have same mutated gene, but different symptoms), and incomplete penetrance (skips generations or a completely new gene) e.g. Huntington’s disesase

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45
Q

Autosomal recessive disorders

A

mutations of two gene pairs, if you only receive one half of the gene, you do not have the disease, but you are a carrier e.g. Cystic fibrosis, sickle cell disease

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46
Q

X-linked recessive disorders

A

usually only effect men, daughters of effected male will be carrier, sons of affected male are unaffected unless mother is a carrier e.g. hemophilia

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47
Q

human genome project

A

help to improve the diagnosis of diseases, allow for earlier detection of disease, help determine risk assessment on individuals at risk for disease, can assist in matching organ donors to transplant recipients

48
Q

carrier screening

A

identifies individuals who carry one copy of the gene e.g. sickle cell & hemophilia

49
Q

preimplantation genetic diagnosis

A

allows embryos free of disease to be placed in uterus

50
Q

newborn screening

A

phenylketonuria and allows for early diagnosis and treatment by diet

51
Q

presymptomatic testing for predicting adult-onset disorders

A

codominant genetic disorders that have their onset in adulthood e.g. Huntington’s disease

52
Q

presymtomatic testing for estimating the risk of developing disorder

A

testing for BRCA-1 & BRCA-2 mutations in women for break cancer, prophylactic measures can be taken

53
Q

gene therapy

A

replaces or repairs defective or missing genes with normal genes, needs a carrier molecule (vector) to deliver therapeutic gene to target cell (most often a genetically altered virus)

54
Q

stem cells

A

they divide and remain a stem cell or differentiate into specialized cells

55
Q

embryonic stem cells

A

have the ability to become any cell; derived from human embryo cells that are 4-5 days old (adult cells are differentiated)

56
Q

innate immunity

A

present at birth and first line defense against pathogens; nonspecific, neutrophils, monocytes, and WBCs

57
Q

cells involved in humoral immunity

A

monocytes or macrophages may phagocytize bacteria and present its antigens to B lymphocytes, becoming activated, turns into plasma, and fights with immunoglobulins (which later turn into memory cells)

58
Q

what does the skin look like with type 1 hypersensitivity?

A

pale wheal containing edematous fluid surrounded by a red flare, occurs within minutes or hours of exposure aka wheal and flare skin test

59
Q

anaphylaxis

A

type 1 hypersensitivity, mediator released systemically and reaction occurs in minutes- edema, itching, rapid & weak pulse, hypotension, dilated pupils, dyspnea, cyanosis

60
Q

allergic rhinitis

A

hay fever, most common type 1 hypersensitivity, pollen, dust, mold most common cause, lesions are more generalized and involve vasodilation of blood vesicles resulting in interstitial edema and vesicle formation

61
Q

urticaria

A

hives, cutaneous reaction against systemic allergens occurring in atopic persons- transient wheals (pink, raised, edematous, pruritic area), develops rapidly after exposure

62
Q

angioedema

A

similar to hives, but involves deeper layers of skin and submucosa, swelling usually begins in face, progresses to airways, and then to rest of body, lesions may burn or itch and skin appears normal or reddish

63
Q

type 2 hypersensitivity

A

cytotoxic and cytolytic reactions involving the binding of IgG or IgM antibodies to an antigen activating the complement system

64
Q

cellular tissue is destroyed in one of two ways in type 2 hypersensitivity:

A

activation of complement system resulting in cytolysis or enhanced phagocytosis

65
Q

what types of cells are frequently destroyed in type 2 hypersensitivity?

A

RBCs, platelets, leukocytes

66
Q

examples of type 2 hypersensitivity

A

ABO incompatibility, Rh incompatibility, hemolytic anermias, leukopenia, Goodpasture syndrome

67
Q

agglutination

A

occurs when transfused with incompatible blood and antibodies immediately coat the foreign RBCs causing blockage of blood vessels, depletes clotting factors leading to bleeding

68
Q

cytolysis occurs

A

when neutrophils and macrophages phagocytize the agglutainted cell and complement is fixed to the antigen- hemoglobin is released in the urine and plasma

69
Q

cytotoxic reaction causes

A

vascular spasms in the kidneys and can block tubules causing acute renal failure

70
Q

goodpasture syndrome

A

IgG is deposited along the basement membranes of the lungs and kidneys causing pulmonary hemorrhage and glomerulonephritis

71
Q

type 3 hypersensitivity

A

tissue damage in immune-complex reactions- soluble antigens bind with IgG or IgM and are too small to be removed by phagocytosis, they’re deposited in tissue or small blood vessels and cause inflammation and destruction of involved tissue

72
Q

type 4 hypersensitivity

A

delayed reaction, cell-mediated immune response, sensitized t lymphocytes attack antigens or release cytokines, which attract macrophages and cause tissue destruction

73
Q

contact dermatitis

A

skin is exposed to substances that easily penetrate the skin to combine with epidermal proteins, within 7-14 days memory cells form and on subsequent reactions, skin lesions form in about 48 hours; LOCAL NOT GENERALIZED

74
Q

acute contact dermatitis

A

lesions are erythematous, papules, vesicles, bullae

75
Q

chronic contact dermatitis

A

lesions are thickened, scaly, lichenified

76
Q

microbial hypersensitivity reaction

A

microbial cell-mediated immune reaction, the organism does not directly damage tissue, rather the antigenic material from the organism interacts with t cells initiating the cell mediated response- memory cells are then formed

77
Q

cellular immunodeficiency is diagnosed if lymphocyte count is below

A

1200/uL

78
Q

radioallergosorbent test

A

RAST, in vitro diagnostic test for IgE antibodies to specific allergens, safe, but less sensitive and takes longer than skin tests for detecting allergens

79
Q

scratch test

A

saline or other diluent is applied to control site and then the allergen is placed on the skin and a pricking device is used to embed the allergen is skin; results in 5 to 10 minutes

80
Q

intradermal testing

A

allergen injected under the skin, results available in 5 to 10 minutes, tourniquet needed to be applied in case of severe reaction (may need epinephrine)

81
Q

initial intervention for anaphylactic shock

A

ensure patent airway, high flow oxygen via non-rebreather mask, remove allergen if possible, establish IV

82
Q

antihistamines

A

best for rhinitis and uritcaria (edema, pruritus), will not work as well with severe conditions (will not prevent bronchoconstriction

83
Q

drug of choice for anaphylactic shock

A

Epinephrine (Adrenalin), stimulates a&b adrenergic receptors to stabilize and prevent further degranulation, but only lasts for a few minutes (IM or IV)

84
Q

immunotherapy is indicated when?

A

anaphylactic reactions with insect venom; administer small amounts of allergen until hyposensitivity is reached

85
Q

allergens readily combine with which antibody?

A

IgG

86
Q

when should you call physician to discuss allergen dosage?

A

if local reaction is larger than the size of a quarter

87
Q

immunotherapy care

A

always inject away from a joint, so tourniquet can be applied in case of emergency, aspirate to make sure not injecting in blood vessel, carefully observe pt for 20 minutes, but educate that reaction may occur within 24 hours

88
Q

type 4 latex allergy

A

caused by the chemicals used in latex, delayed reaction that occurs within 6-48 hours, dryness, pruritus, cracking of the skin, redness, swelling, and crusting at 24-48 hours

89
Q

type 1 latex allergy

A

response to natural rubber latex proteins and occurs within minutes- skin redness, urticarial, rhinitis, asthma, even anaphylactic shock

90
Q

sensitive foods in reference to latex

A

banana, grapes, avocado, chestnut, kiwi, tomato, potatoes, peaches, apricots

91
Q

multiple chemical sensitivities

A

many symptoms r/t different foods and chemicals, mostly women, odor seems to be principal triggor

92
Q

provocation-neutralization test

A

exposing pt to certain environmental substances to produce symptoms and then repeating at higher and lower dosages to initiate disappearance of symptoms

93
Q

at what age do the number of autoantibodies increase and what gender is more effected?

A

over 50 years of age and women

94
Q

apheresis

A

treats autoimmune disorders, separates components of blood followed by the removal of platelets, leukocytes, lymphocytes, or stem cells

95
Q

plateletphresis is used for

A

removal of platelets in patients who develop thrombocytopenia

96
Q

plasmapheresis

A

removal of plasma thought to be causing disease and replaced by saline, fresh frozen plasma, or albumin; also prevents antibody rebound and may remove inflammatory mediators that cause tissue damage

97
Q

what to watch for with apheresis

A

hypotension and citrate toxicity (may cause hypocalcemia- headache, dizzy)

98
Q

primary immunodeficiency disorders

A

rare, serious, caused by phagocytic defects, b or t cell deficiencies

99
Q

secondary immunodeficiency disorders

A

drug-induced is most common (cancer treatment), malnutrition alters cell-mediated immune responses and atrophy of the thymus and lymphoid tissues occur

100
Q

major histocompatibility antigens

A

antigens that reject genetically unlike tissues

101
Q

human leukocyte antigen

A

occurs on the sixth chromosome and system is used in matching organs and tissues for transplants

102
Q

what genes are most used for transplantation matching?

A

A, B, DR

103
Q

what are the organs with the highest demand?

A

kidney, liver, heart

104
Q

how many antigen matches are needed for a transplantation?

A

Since A, B, and DR are currently the only genes tested and each gene has 2 alleles, we are testing 6 antigens. 5 or 6 matched antigens are preferred, but some 4 matched antigens will suffice in kidneys and bone transplants

105
Q

graft rejection is highest with what organs?

A

kidney and bone, heart and lung are somewhere in between

106
Q

panel of reactive antibodies

A

determines the recipient’s sensitivity to various HLAs before receiving transplant, high PRA means person will have a harder time finding a match

107
Q

what does a positive crossmatch mean?

A

absolute contraindication to transplant- especially important for kidneys!

108
Q

how can transplant rejection be reduced?

A

immunosuppressant therapy, ABO & HLA matching, and ensuring crossmatch is negative

109
Q

hyperacute rejection

A

occurs within minutes to hours of transplantation because blood vessels are being destroyed, no tx must be removed- kidney especially susceptible for this!

110
Q

acute rejection

A

manifests in the first 6 months, lymphocytes have been activated against donated organ, usually reversible with immunosuppressant therapy and increased corticosteroid use

111
Q

chronic rejection

A

months or even years after transplantation, repeated episodes of acute rejection, no optimistic prognosis

112
Q

immunosuppressant therapy

A

immune system needs to be repressed to not harm the transplanted organ, but there is an increased risk of infection and malignancies

113
Q

calcineurin inhibitors

A

tacrolimus and cyclosporine- most effective, prevent cell mediated attack on organ, do not cause bone marrow suppression or suppress the inflammatory response

114
Q

graft vs. host disease

A

when immunocompromised pt is transfused with immunocompetent cells, graft rejects the host 7-30 days after transplantation, evidenced by maculopapular rash that can be itchy and painful on palms and soles of feet

115
Q

how to prevent graft vs host disease

A

immunosuppressant agents for tx and radiation of blood products before they are administered to prevent t cell replication

LCCC Nursing (15 decks)

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