nr 324 wk 3

antirejection transcription inhibitor

tacrolimus and cyclosporine

antirejection nucleotide synthesis inhibitor

mycophenolate

antirejection growth factor signal transduction inhibitor

sacrolimus

antirejection DNA alkylating agent

cyclophosphamide

antirejection immunosuppressant s/s

myelosuppression, infxn reactivatino, new infxn, cancer, n/s, teratogenic, alopecia, skin rash, anaphylaxis, hyperglycemia, irregular periods

hyperacute transplant rejection

<24 hr post op

pre-existing antibodies attack organ

remove organ

acute transplant rejection

1-6 months post op

cell mediated or humoral

lymphocytes activate against organ

reversible

chronic transplant rejection

t and b cells → organ → fibrosis

supportive tx for life

antirejection immunosuppressant education

do not rinse syringe

dry/replace cover

no grapefruit

autoimmunity

immune system attacks own cells instead of fighting infxn

pt has less effective central/peripheral tolerance or less functional regulatory t cells

systemic autoimmunity

RA

lupus

organ- specific autoimmunity

hemolytic anemia

hashimoto thyroiditis

graves dz

central tolerance

thymus and bone marrow

immature lymphocyte binds to self peptide strongly → apoptosis

peripheral tolerance

self-reactive lymphocytes that escaped central tolerance → apoptosis or anergy

assisted by regulatory t cell

apheresis

separation of blood components via removal

autoimmune dz tx

immunity

body’s ability to resist dz

immune system main fxns

defend from pathogens

homeostasis to remove damaged cells

surveillance to detect abnormal cells

innate immunity

present at birth

1st line of defence

fast and nonspecific

wbc and neutrophils

acquired immunity

develops over time

specific response

active immunity

make your own antibodies

artificial active immunity

vaccination

natural active immunity

infection

passive immunity

you receive antibodies

natural passive immuity

mom → baby via placenta or breastmilk

artificial active immunity

antibody (gamma globulin) injection

primary lymphoid organs

thymus: matures t cells and shrinks w age

bone marrow: produces all blood cells

secondary lymphoid organs

lymph nodes

tonsils

spleen

mucosa

lymphocyte

made into bone marrow

turns into b and t cellsb

b cell

antibodies

t cell

helper cd4 and cytotoxic cd8

dendrite immune cell

captures antigens and presents them to t cells → immune response

macrophage/monocyte

phagocytosis

presents antigens

cytokines

released by wbc

immune system boss

IL

IFN

TNF

colony-stimulating factors

IL-1 and IL-6 cytokines

inflammation and fever

IL-2 cytokine

activates T cell

IFN cytokine

fight virus

TNF cytokine

kill tumor cells → wt loss and inflammation

humoral immunity

made by plasma cells

b cell

immunoglobulins

IgG

most common

long term

remembers pathogen

crosses placentaIg

IgA

mucosal (saliva and breast milk)

immune fxn in mucous membrane

IgM

1st to respond

fight current pathogen

IgD

b cell fxn

activated basophil and mast cells as well for inflamm/immune response

anaphylaxis s/s

stridor, SOB, Ha, abdominal pain, decreased bp, increased hr, anxiety, triggers

anaphylaxis tx

epinephrine

latex allergy rxn

contact dermatitis: dry and pruritis

allergic rxn: red, conjunctivitis, rhinitis

foods to avoid w latex allergy (→ latex good syndrome)

banana, grape, chestnut, peach, apricot, avocado, kiwi, potato, hazelnut, tomato, guava

wound healing types

regeneration: same cells replaced. perfect healing

repair: scar tissue forms

inflammatory phase of wound healing

first

3-5 days

blood clot forms

wbc arrive

red and swollen

granulation phase of wound healing

second

fibroblast → collagen

new tissue

pink, moist wound

maturation phase of wound healing

scar strengthens

lasts months to years

primary wound healing

clean, closed edges

minimal scar

secondary wound healing

large, open wound

drainage and scarring

tertiary wound healing

delayed closure

for contaminated wound

acute inflammation

first

neutrophils at site

heals in 2-3 weeks

no residual damage

swelling at site

subacute inflammation

second

heals in 2-6 wk

infectious endocarditis

chronic inflammation

third

lymphocyte and macrophage at site

residual damage at site

RA, obesity, allergies

inflammation s/s

red, heat, swelling, pain, loss of fxn (NO fever bc that is infection)

inflammatory biomarkers

CRP and cytokines (IL 6)

pressure ulcer braden scale 19-23

no risk

pressure ulcer braden scale 15-18

mild risk

pressure ulcer braden scale 13-14

moderate risk

pressure ulcer braden scale 10-12

high risk

pressure ulcer braden scale <9

severe risk

stage 1 pressure ulcer

non blanchable redness

stage 2 pressure ulcer

partial-thickness skin loss

shallow/open w pink and red wound bed

stage 3 pressure ulcer

full-thickness skin loss

SQ fat seen

tunneling

stage 4 pressure ulcer

muscle/tendon/bone seen

slough and eschar

undermining and tunneling

unstageable pressure ulcer

slough and eschar cover wound

DTI

blood-filled blisters

soft tissue damage

how does HIV work

1. virus enters body

2. attacks cd4 cells

3. replicated inside

4. destroys cd4 cells

5. immune system weakens over time

acute HIV

2-4 wk

flu-like (fever, sore throat, rash, lymphademopathy)

chronic/latent HIV

can be asymptomatic

virus active

AIDS

severe immune damage

opportunistic infxn

cd4 <200 (normal is 500-1500)

HIV PrEP

reduces HIV risk

Truvada, Descovy, Cabotegravir

HIV PEP

post exposure within 72 hr

raltegravir and Truvada

take for 28 days

HIV s/s

fever, swollen lymph nodes, sore throatm Ha, malaise, nausea, muscle/joint pain, diarrhea, rash

HIV can lead to…

aseptic meningitis, peripheral neuropathy, facial palsy, Guillian-Barre

opportunistic infections

PJP, TB, candidiasis, Kaposi’s sarcoma, cytomegalovirus

opportunisitic infxn diagnosis

HIV antibody/antigen test

cd4 <200

viral load

opportunistic infxn tx

ART for entire life to decrease viral load and increase cd4 count