Chapter 14: Med Surg Flashcards
immunity
a state of responsiveness to foreign substances such as microorganisms and tumor proteins; fx: defense, homeostasis, surveillance
homeostasis
damaged cellular substances are digested and removed, but the body’s different cell types remain unchanged
surveillance
mutations continually arise, but are normally recognized as foreign cells and destroyed
active immunity
takes awhile to develop, but long lasting
passive immunity
short lived because the host did not synthesize the antibodies and does not retain memory cells for the antigen
antigen
body recognizes a foreign substance and elicits an immune response; most composed of protein
thymus gland
central (primary) lymphoid organ- shrinks with age and is important in the differntiation and maturation of t lymphocytes
bone marrow
central (primary) lymphoid organ- produces RBCs, WBCs, and platelets
lymphoid tissue
found in submucosa of the respiratory, genitourinary, and GI tract- protects body surface from external microorganisms e.g. tonsils
spleen
primary site for filtering foreign substances from blood and major site of immune responses to blood-borne antigens
lymphnodes
filtrate foreign material brought to site and circulate lymphocytes
mononuclear phagocytes
monocytes & macrophages; capture through phagocytosis and the macrophage bound antigen is presented to lymphocytes which triggers an immune response
B lymphocytes
produced in bone and differentiate into plasma cells which produce antibodies (immunoglobulins)
T lymphocytes
migrate from bone marrow to thymus, compose 70%-80% of lymphocytes and provide immunity to intracellular viruses, tumor cells, and fungi; long term immunity
T cytotoxic cells
CD8 attack antigens on cell membrane of foreign pathogens and destroy, antigen specific and sensitized by exposure to the antigen
T helper cells
CD4 regulate cell-mediated immunity and the humoral antibody response
natural killer cells
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
antibodies
immune globulins produced by lymphocytes in response to antigens
dendritic cells
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
cytokines
soluble factors secreted by WBCs that act as messengers between cell types and instruct cells to alter their proliferation, differentiation, secretion, or activity
interferons
type of cytokine that help the body’s natural defenses attack tumors and viruses and enhance natural killer cells
what is the first antibody formed by humoral immunity?
IgM formed by the primary immune response (4-8 days after initial exposure); forms antibodies to ABO blood antigens
cell-mediated immunity
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
humoral immunity
antibody-mediated immunity produced by b lymphocytes that have memory cells- protects against bacteria, extracellular viruses, respiratory pathogens, and GI pathogens
examples of when humoral response is initiated
anaphylactic shock, atopic diseases, transfusion reactions, bacterial infections
what is the second antibody formed by humoral immunity?
IgG formed by the secondary response (1-3 days after second exposure and is more rapid & stronger) ONLY ONE TO CROSS PLACENTA
examples of when cell-mediated response is initiated
TB, fungal infections, contact dermatitis, graft rejection, destruction of cancer cells
IgA
found in body secretions and lines mucous membranes to protect body surfaces
IgD
found in plasma, assists differentiation of B lymphocytes
IgE
found in plasma and interstitial fluid & causes symptoms of allergic reaction
effects of aging on the immune system
more tumors, greater chance of infection, thymic involution, decreased cell-mediated immunity, delayed hypersensitivity reaction, decreased autoantibodies
what is relatively unaffected in the immune system of older people?
bone marrow
anergy
common in older people, lack of or dimished reaction to an antigen
type 1 hypersensitivity
IgE mediated, anaphylactic reaction, highly sensitized to pollen, food, drugs, dust
mediators to type 1 hypersensitivity
histamine, mast cells, leukotrienes, prostaglandins; short acting and reversible
locus
where the gene resides on the chromosome
allele
one of two or more alternative forms of a gene that codes inherited characteristics
dominant allele
gene that is expressed in the phenotype of a heterozygous individual, allele that is fully expressed
recessive allele
lacks the ability to express itself, no noticeable effect on the phenotype
transcription
messenger RNA is synthesized from a single strand of DNA
mitosis
results in two identical daughter cells and before duplication, each cell receives an extra replica of chromosomes from parent cell
meiosis
oocytes and sperm contain only a single copy of each chromosome
crossing over
genetic material is exchanged between homologous chromosomes in the cell; some traits from mom, some from dad
autosomal dominant disorders
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
Autosomal recessive disorders
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
X-linked recessive disorders
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
human genome project
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
carrier screening
identifies individuals who carry one copy of the gene e.g. sickle cell & hemophilia
preimplantation genetic diagnosis
allows embryos free of disease to be placed in uterus
newborn screening
phenylketonuria and allows for early diagnosis and treatment by diet
presymptomatic testing for predicting adult-onset disorders
codominant genetic disorders that have their onset in adulthood e.g. Huntington’s disease
presymtomatic testing for estimating the risk of developing disorder
testing for BRCA-1 & BRCA-2 mutations in women for break cancer, prophylactic measures can be taken
gene therapy
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)
stem cells
they divide and remain a stem cell or differentiate into specialized cells
embryonic stem cells
have the ability to become any cell; derived from human embryo cells that are 4-5 days old (adult cells are differentiated)
innate immunity
present at birth and first line defense against pathogens; nonspecific, neutrophils, monocytes, and WBCs
cells involved in humoral immunity
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)
what does the skin look like with type 1 hypersensitivity?
pale wheal containing edematous fluid surrounded by a red flare, occurs within minutes or hours of exposure aka wheal and flare skin test
anaphylaxis
type 1 hypersensitivity, mediator released systemically and reaction occurs in minutes- edema, itching, rapid & weak pulse, hypotension, dilated pupils, dyspnea, cyanosis
allergic rhinitis
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
urticaria
hives, cutaneous reaction against systemic allergens occurring in atopic persons- transient wheals (pink, raised, edematous, pruritic area), develops rapidly after exposure
angioedema
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
type 2 hypersensitivity
cytotoxic and cytolytic reactions involving the binding of IgG or IgM antibodies to an antigen activating the complement system
cellular tissue is destroyed in one of two ways in type 2 hypersensitivity:
activation of complement system resulting in cytolysis or enhanced phagocytosis
what types of cells are frequently destroyed in type 2 hypersensitivity?
RBCs, platelets, leukocytes
examples of type 2 hypersensitivity
ABO incompatibility, Rh incompatibility, hemolytic anermias, leukopenia, Goodpasture syndrome
agglutination
occurs when transfused with incompatible blood and antibodies immediately coat the foreign RBCs causing blockage of blood vessels, depletes clotting factors leading to bleeding
cytolysis occurs
when neutrophils and macrophages phagocytize the agglutainted cell and complement is fixed to the antigen- hemoglobin is released in the urine and plasma
cytotoxic reaction causes
vascular spasms in the kidneys and can block tubules causing acute renal failure
goodpasture syndrome
IgG is deposited along the basement membranes of the lungs and kidneys causing pulmonary hemorrhage and glomerulonephritis
type 3 hypersensitivity
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
type 4 hypersensitivity
delayed reaction, cell-mediated immune response, sensitized t lymphocytes attack antigens or release cytokines, which attract macrophages and cause tissue destruction
contact dermatitis
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
acute contact dermatitis
lesions are erythematous, papules, vesicles, bullae
chronic contact dermatitis
lesions are thickened, scaly, lichenified
microbial hypersensitivity reaction
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
cellular immunodeficiency is diagnosed if lymphocyte count is below
1200/uL
radioallergosorbent test
RAST, in vitro diagnostic test for IgE antibodies to specific allergens, safe, but less sensitive and takes longer than skin tests for detecting allergens
scratch test
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
intradermal testing
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)
initial intervention for anaphylactic shock
ensure patent airway, high flow oxygen via non-rebreather mask, remove allergen if possible, establish IV
antihistamines
best for rhinitis and uritcaria (edema, pruritus), will not work as well with severe conditions (will not prevent bronchoconstriction
drug of choice for anaphylactic shock
Epinephrine (Adrenalin), stimulates a&b adrenergic receptors to stabilize and prevent further degranulation, but only lasts for a few minutes (IM or IV)
immunotherapy is indicated when?
anaphylactic reactions with insect venom; administer small amounts of allergen until hyposensitivity is reached
allergens readily combine with which antibody?
IgG
when should you call physician to discuss allergen dosage?
if local reaction is larger than the size of a quarter
immunotherapy care
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
type 4 latex allergy
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
type 1 latex allergy
response to natural rubber latex proteins and occurs within minutes- skin redness, urticarial, rhinitis, asthma, even anaphylactic shock
sensitive foods in reference to latex
banana, grapes, avocado, chestnut, kiwi, tomato, potatoes, peaches, apricots
multiple chemical sensitivities
many symptoms r/t different foods and chemicals, mostly women, odor seems to be principal triggor
provocation-neutralization test
exposing pt to certain environmental substances to produce symptoms and then repeating at higher and lower dosages to initiate disappearance of symptoms
at what age do the number of autoantibodies increase and what gender is more effected?
over 50 years of age and women
apheresis
treats autoimmune disorders, separates components of blood followed by the removal of platelets, leukocytes, lymphocytes, or stem cells
plateletphresis is used for
removal of platelets in patients who develop thrombocytopenia
plasmapheresis
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
what to watch for with apheresis
hypotension and citrate toxicity (may cause hypocalcemia- headache, dizzy)
primary immunodeficiency disorders
rare, serious, caused by phagocytic defects, b or t cell deficiencies
secondary immunodeficiency disorders
drug-induced is most common (cancer treatment), malnutrition alters cell-mediated immune responses and atrophy of the thymus and lymphoid tissues occur
major histocompatibility antigens
antigens that reject genetically unlike tissues
human leukocyte antigen
occurs on the sixth chromosome and system is used in matching organs and tissues for transplants
what genes are most used for transplantation matching?
A, B, DR
what are the organs with the highest demand?
kidney, liver, heart
how many antigen matches are needed for a transplantation?
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
graft rejection is highest with what organs?
kidney and bone, heart and lung are somewhere in between
panel of reactive antibodies
determines the recipient’s sensitivity to various HLAs before receiving transplant, high PRA means person will have a harder time finding a match
what does a positive crossmatch mean?
absolute contraindication to transplant- especially important for kidneys!
how can transplant rejection be reduced?
immunosuppressant therapy, ABO & HLA matching, and ensuring crossmatch is negative
hyperacute rejection
occurs within minutes to hours of transplantation because blood vessels are being destroyed, no tx must be removed- kidney especially susceptible for this!
acute rejection
manifests in the first 6 months, lymphocytes have been activated against donated organ, usually reversible with immunosuppressant therapy and increased corticosteroid use
chronic rejection
months or even years after transplantation, repeated episodes of acute rejection, no optimistic prognosis
immunosuppressant therapy
immune system needs to be repressed to not harm the transplanted organ, but there is an increased risk of infection and malignancies
calcineurin inhibitors
tacrolimus and cyclosporine- most effective, prevent cell mediated attack on organ, do not cause bone marrow suppression or suppress the inflammatory response
graft vs. host disease
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
how to prevent graft vs host disease
immunosuppressant agents for tx and radiation of blood products before they are administered to prevent t cell replication
