Chap 5 Flashcards
(27 cards)
What is auto immunity
The immune system reacts against self antigens to such a degree that auto antibodies or auto reactive T cells damage the individuals tissues
What is the client at risk for when they are immuno suppressed
Increase risk of infection, increased risk of cardiovascular disease, increased risk of bone marrow suppression, increased risk of cancer development
What adverse effects should the nurse be careful about when giving glucocorticoids 
-Skin breakdown, atrophy, acne, mild hair growth, facial redness, impaired wound healing, development of diabetes, osteoporosis, peptic ulcer’s, hypertension, obesity, increase protein breakdown resulting in muscle wasting
why is glucocorticoid dangerous
It is dangerous because It can mask signs of information which means that active infection present in the body will be undetected
What kind of pts would you never give glucocorticoids to
Patients that have an active infection 
Describe hypersensitivity reaction 1 (antibody mediated?, mechanism, clinical manifestations)
IGE mediated, increases mast cells= increased histamine= increased inflammation
Mechanism: increased histamine act thru H1 receptors and cause bronchial constriction, edema, increased blood flow
Clinical manifestations: large numbers of mast cells and histamine in blood, vomiting, anaphylaxis, death, urticaria- hives, conjunctivitis
Describe hypersensitivity reaction type 2 (what is this rxn mediated by, what antibodies are involved, what does it react to, mechanism, ways antibody attacks the cell) ex?
Tissue specific rxn
Reactss to: Specific antigen on cells or tissues
Antibodies: IgG, IgM
Mechanism: Cell may be destroyed by IgG or IgM antibodies, complement cascade is activated = cell lysis
Ways: antibodies destroy by recruiting macrophages that phagocytize because complement deposited c3b on cell surface = more macrophages
Tissue damage due to neutrophils releasing toxic content which activates complement =more neutrophil damage
ADCC: NK release toxins that kill target cell directly
Cell malfunction: replaces a ligand on attaches onto receptor site causing the receptor to be abnormally stimulated
Example: hyper acute graft rejection, graves, myasthenia gravis, rheumatic fever
Describe type III hypersensitivity rxn (what is this rxn mediated by, antibody involved, mechanism of how it occurs, examples )
Immune Complement mediated rxn
Antibody: IgM IgG
Mechanism: free circulating antigen in blood binds onto antibody = antigen antibody complex that is later embedded into tissue, cell, or blood vessels, triggering complement cascade
Examples: Rh. Arthritis, systemic lupus, post strep glomerulonephritis
Describe type four hypersensitivity (what is is mediated by, mechanisms, examples)
T cell mediated rxn, does not involve antibody, delayed type
Mechanism: t cytotoxic cells directly kills or lymphokine producing cells TH1 or TH17 release cytokines that chemotaxis phagocytic cells (macrophages)
Examples: autoimmune disorders, direct killing ex. Hepatitis, delayed killing = Mantoux test, contact dermatitis
What is the major underlying mechanism that underlies all hypersensitivities
Sensitization against certain antigen resulting in immune response that is delayed or immediate
What types of symptoms indicates anaphylaxis
-Increased release of histamine causes activation of platelets, Eosinophils and neutrophils, increase in blood flow which causes swelling redness, bronchoconstriction, bronchospasm, mucosal Edema , inflammation increase capillary permeability
What should the nurses initial response be to a client with anaphylaxis
Administer oxygen immediately
Assess signs and symptoms of anaphylaxis: airway, breathing patterns, vital signs, edema, increase respiratory distress, notify provider, rapid initiate emergency procedures such as intubation oxygen, give IV epinephrine if indicated
How do antihistamines reduce anaphylaxis
Prevent vascular permeability, prevents vasodilation, prevents urticaria, Prevent smooth muscle contraction, Increase muscle secretions 
How do beta adrenergics affect the airway and how does it help during anaphylaxis 
Vasoconstriction of mucosal vessels (reduces mucous)
Adrenergic nasal decongestants work along the alpha receptor sites on smooth muscle of nasal mucosal blood vessels, reducing blood flow, reducing fluid exudation, reducing mucosal edema.
Use of these during anaphylaxis event can cause dilation of airway, reduced mucous, prevents suffocation
What is an anticholinergic agent and how does it treat anaphylaxis, why would it be treated for allergies that are not relate to anaphylaxis
- blocks increased pns activity which would cause a reciprocal increase sympathetic response causing bronchodilation.
Blocking pns stimulates alpha and beta receptors more easily, as a result alpha 1 receptors causes arterial constriction in nose which decreases mucous production, stimulation of beta 2 receptor = bronchodilation by vasoconstriction mucous production
Why are glucocorticoids use for an anaphylactic reaction as well as allergic reaction
Because they suppress the inflammatory response by suppressing the immune system
Suppressed immune system = no mast cell degranulation = no histamine= no inflammation
Glucocorticoids are used to treat acute therapy but may be used in long run to treat allergic rxn 
What are the five stages of viral infection
Attachment
Penetration
Synthesis of nucleic acid and protein
Assembly and packaging
Release/lysis
What happens in the attachment stage a viral infection
Protein on virus attaches to protein receptor sites on host cells
What happens in Penetration stage of viral infection
-Virus contents of genes and enzymes are injected into the host cell
What happens in the synthesis of nucleic acid and protein stage of viral infection
Immediately after penetration if you viral proteins are made immediately which assist in the duplication of DNA and RNA
One of two things can occur, Virus can start replicating itself by making viral capcids proteins or viral enzymes to then assemble to make more viruses or viral protein can enter the nucleus and insert into the chromosome and remain for a long period of time
What happens in assembly and packaging stage of viral infection
All viral components, structural protein, enzymes, and nucleic acids are packaged and ready to leave cell
What happens in Release/lysis stage of viral infection
Number of virus so large is has to it causes cell to burst, it leaves all at once the host cell is killed
Or
Leaves in smaller amounts and buds off which does not result in cell death
What is the action of antiviral drugs and when does it work
Ability to enter cells infected with the virus and interfere with viral nucleic acid synthesis, interfere with ability of virus to bind to cells, stimulate body’s immune system
Only works effectively when viral replication is occuring
Which susceptible to viruses are killed by anti-virals (her cunt has increased reproduction)
Herpes simplex virus HSV
Cytomegalovirus CMV
Human immunodeficiency virus HIV
Influenza A (the flu)
Respiratory syncytial virus RSV)
