1
Q
natural immunity
A
exists before any exposure to an infectious agent
ie. skin, phagocytes
2
Q
acquired imunity
A
occurs after exposure to an antigen, response becomes faster each time we are exposed to the antigen
3
Q
cell-mediated immunity
A
target cells are attacked by cells of the immune system
4
Q
humoral immunity
A
immune response is driven by antibodies
5
Q
b cells
A
- make antibodies
- antibody specificity is dependent on receptors on b cell surface
6
Q
cytolytic t cells (CD8)
A
- directly attack and kill target cells
- specificity depends on antigen molecules on target cells and receptors for tjose antigens on the surface of t cells
7
Q
helper t cells (CD4)
A
- help with antibody production
- help with delayed hypersensitivity reactions
- help to activate cytolytic t cells
- ability to attack specific antigens from receptors on the surface of the t cell
8
Q
macrophage
A
- primary role is phagocytosis of cells with antibodies
- scavengers of the body
- help to activate t cells (antigen presenting cell)
8
Q
A
9
Q
dendritic cells
A
role in activation of t cells (same as macrophages)
10
Q
mast cells and basophils
A
- primary role in hypersensitivity
- triggered when antigen binds to antibody on cell surface
11
Q
neutrophils
A
- phagocytize bacteria and foreign particles
- roles in inflammation
- important in humoral immunity
12
Q
antibodies
A
- glycoproteins that are responsible for humoral immunity
- bind to specific antigens, produced by b cells
- most ab are secreted from the b cell and bind to their antigen
- some antigens are retained on the surface of the b cell
13
Q
antigens
A
- molecules that cause an immune response
- trigger the production of antibodies and t cells, which attack the antigen
- antigens are large molecules, ab only bind to portions of the antigen (antigenic determinants)
- each antigen has many antigenic determinants that more than one ab can bind to
14
Q
phases of the immune response
A
recognition, activation, effector
15
Q
recognition phase
A
- a mature lymphocyte matches its antigen
- the ability for the lymphocyte to recognize its antigen is from antigen-specific receptors on the cell’s surface
16
Q
activation phase
A
lymphocytes proliferate and differentiate into immune response cells and memory cells
17
Q
effector phase
A
- immune system tries to eliminate the antigen that caused the response
a) cell-mediated: antigen cells are lysed by cytolytic t cells or ingested by macrophages
b) antibody mediated: target cells are primed for attack by phagocytes or the complement system
18
Q
features of the immune response
A
a) specificity: ability to target/mount an IR against specific anitgens
b) diversity: many diff b/t cells
c) memory: allows for faster activation of IR, contributes to severe allergic reactions
d) time limited: amount of antigen dec overtime as its targeted by immune cells
e) recognition of self and non-self: uses MHC complexes to differentiate, can contribute to organ rejection
19
Q
major histocompatability complex
A
- important for immunity (activates t cells, guides t cells toward target cells, differentiates b/w self and non-self)
- nobody has the same MHC molecules (recognized as foreign in other people, important for organ transplant)
20
Q
immunosuppressant
A
- prevent or stop an immune response
- used to treat autoimmune disorders or prevent organ rejection
21
Q
cyclosporine: MOA
A
- drug of choice to prevent rejection of allograft (from others)
- binds to cyclophilin (present in t cells and lymphocytes)
- once bound, binds to and inhibits calcineurin
- leads to a reduction in IL-2 production (needed for t cell actovation and proliferation)
- suppresses immune response
22
Q
cyclosporine: PK
A
- given oral or IV
- low BA, narrow TI
- trough levels assessed at regular intervals
- widely distributed to all tisues, crosses BBB
- metabolized by CYP3A4, mainly hepatic excretion
23
Q
cyclosporine: AE
A
a) nephrotoxicity: occurs in up to 75%, dose-dependent
- monitor BUN and creatinine
b) hepatotoxicity: monitor billirubin and liver function at regular intervals, improves w dec dose
c) lymphoma: inc risk when combined with other immunosuppressants
d) infection: inc risk from iunosuppression, inform patient of early signs of infection
24
cyclosporine: drug interactions
a) drugs that inc cyclosporine levels: azole antifungals, macrolide antibiotics, amphotericin B
- all inhibit CYP3A4, which slows metabolism
b) drugs that dec cyclosporine levels: phenytoin, phenobarbital, rifampin, sulpha
- these drugs express CYP3A4, inc metabolism
c) nephrotoxic drugs
d) grapefruit juice
e) repaglinide (oral antihyperglycemic): at risk for hypoglycemic
25
tacrolimus
- used to prevent allograft rejection
- more effective than cyclosporine
- often given with glucocorticoids
- narrow TI
26
tacrolimus: MOA
- similar to cyclosporine
- binds to FKBP-12 instead of cyclophilin
27
tacrolimus: AE
a) nephrotoxicity (33-40%)
b) neurotoxicity: headaches, tremor, insomnia
c) GI symptoms: N/V, diarrhea
d) HT
e) hyperkalemia
f) hirutism
g) gum hyperplasia
28
corticosteroids
- produced by adrenal glands
- glucocorticoids influence carb metabolis, so it's important to measure glucose levels
- role is to maintain normal physiology and suppress inflammation/cancer/IR
- cortisol is the primary endogenous GC
29
physiology of endogenous GC
a) metabolism effects: creates glucose from aa/lipids, suppresses protein metabolism, breaks down lipids
b) vascular and hematologic effects: inc capillary permeability (fluid leaves bv, dec BV/edema)
c) CNS effects: wide range of effects from depression to excitability
d) stress effects: inc epi and GC release from adrenals, no GC release can lead to hypotensions and hypoglycemia
f) fluid and electrolyte effects: similar to aldosterone, Na/water retention
30
glucocorticoid: MOA
- glucocorticoids penertrate the cell surface and bind to receptors in the cytoplasm
- the receptor-GC complex moves to the nucleus, binds to chromatin on DNA and alters gene activity
- activates the transcription of anti-inflammatory genes, decreases the transcription of pro-inflammatory genes and enzymes
31
glucocorticoid: pharmacologic effects (antiinflam/immunosupp)
- signs and symptoms mediated by prostaglandins and histamine (swelling, redness, pain through VD and bv permeability) & neutrophils and macrophages (inc inflammation from lysosomal enzymes that cause injury)
- inibit prostaglandins, leukotrienes, histamine
- suppress phagocytes
- dec proliferation of lymphocytes
32
glucocorticoid: pharmacologic effects (altered metab/electrolytes)
- inc glucose, dec protein synthesis, altered fat deposits
- can impact Na/H2O reabsorption
- dec absorption of calciu from the GI tract
33
glucocorticoid: PK
- oral, IV, IM, intra-atricular, topical, inhalation admin
- high/systemic absorption from oral/IV/IM/SC, high/local absorption from others
- crosses BBB and placenta
- hepatic metablism (CYP3A4), renal excretion
34
glucocorticoid: therapeutic uses
rheumatoid arthritis, systemic lupus erythmatosus, IBD, dematologic conditions, asthma, allergies, hemotologic malignancies, allograft rejection, acute respiratory distress syndrome in premature infants
35
glucocorticoid: AE
a) adrenal insufficiency: inc dosing of GC dec adrenal excretion
b) osteoporosis: suppresses osteoblast formation, inc osteoclast activity, dec GI calciu abs
- PTH is increased and moves more ca from bone to blood
- measure bone density and give supplements
c) infection: risk of new and latent infections, infections can occur without typical manifestations
d) hyperglycemia: periodic evaluation of glucose
36
glucocorticoid: AE pt.2
e) myopathy: improves with dose reduction
f) fluid and electrolyte abnormalities: retention of water/sodium (HT, edema), pt education on signs/symptoms of fluid retention and heart failure
g) growth delay: measure height, weight and consider every other day dosing
h) psychological changes: mild reaction (insomnia, agitation, anxiety), severe reaction (depression, euphoria, hallucinations, mania, suicide)
- improves when drug is stopped
37
glucocorticoid: AE pt.3
i) cataracts/glaucoma: regular eye exams
j) peptic ulcer disease: altering prostaglandins can inhibit cytoprotective mucous and can inc gastric acid secretion
- inc risk for peptic ulcers, dec pain response
- check stool for blood
k) iatrogenic cushing syndrome: muscle weakness, electrolyte imbalance
38
glucocorticoid: drug interactions
a) thiazide/loop diuretics: inc K loss, monitor K levels
b) NSAIDs: inc risk of GI ulcers
c) insulin/oral antihypertensives: glucocorticoids can inc glucose
d) vaccines: dec ab response from immunosuppression, repsonse to vaccine is less
39
glucocorticoid dosing
- goal is to reduce symptoms to an acceptable level, always give the smallest effective dose
- discontinuing drug should be gradual
- alternate day dosing can minimize impact on growth, dec adrenal insufficiency and dec toxicity
- give early morning to mimic endogenous GC
- can cause flare-ups of symptoms
40
discontinuation of GC
- done slowly, use a taper schedule to prevent adrenal insufficiency
- signs and symptoms include hypotension, hypoglycemia, myalgia, athralgia, fatigue
41
example of tapering schedule
1. taper to physiologic dose over 7 days
2. go from multiple doses per day to once in the AM
3. taper dose to 50% of physiologic dosing over one month
4. monitor endogenous cortisol and stop drug when it is normal
nurs 3550 final exam
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