immunity

what is the bodys first line of defense

skin/mucus membrane

urticaria

hives

raised bumps

puritis

itching

innate immunity

in your body since birth

adaptive/aquired immuity

something we’ve been exposed to

active immunity

actively fighting

passive immunity ex

breast feeding

immune system is

self-regulated

must be able to distinguish self from non-self so immune system can work normally!

antigens

foreign agents

things that are presenting on cells

major actions for the immune system

defending and attacking

two types of defenses

innate and adaptive

innate

neutrophils (1st responder)

mast cells- release histamine (connective tissue)

macrophages- eating invaders

adaptive

b cells - memory, antibody

t cells include

• t helper (CD4)

• t killer (CD8)

t helper cell

CD4

t killer cell

CD8

order that cells work for immune system in adaptive

t helper (CD4)

b cells

t killer (CD8)

innate defense barrier

from birth

has immediate response distinguish self from non-self

external defense/barrier for innate defense is primary

not completely impenetrable

surface- skin, mucous membrane

chemical- saliva, sweat, vaginal bacteria/pH

bloodborne innate defenses for innate defense is secondary

WBCs!

imflammatory response

pyrogens (adjusts body temp)

complete proteins (relates to inflammatory response)

what manifestations may we expect with an inflammatory response

swelling, erythema (redness), warm to touch

inflammatory response s triggered by

mast cells- histamine (causes inflammation and capillary permeability) and prostaglandins

vasodilation

sends blood to site to dilute/send immune cells like neutrophils, monocytes/macrophages nutrients and o2

pyrogens

fever producing molecules

produced by bacteria exposed macrophages

fever creates bad environment for bacterial growth and improves healing

macrophages are

WBC

severe/life threatening temperature

105

can change with age

interferons

do not protect infected cells, they stop the spread of the virus to new cells

proteins released from virus-infected cells

complement proteins

is a plasma protein that enhance antibodies

is activated by antigens

has to do with inflammatory process

plays an enhancement role

adaptive/acquired defenses

specific

developed over time after exposure to disease (vaccine/get it)

uses memory system (body can response faster 2nd time exposed)

distinguishes self from non-self AND between pathogens

2 approaches to adaptive defenses

cellular immunity

humoral immunity

cellular immunity

job: destroy antigen

t cells

humoral immunity

job- produce antibodies against again

B cells

cellular immuniy

mediated by T CELLS on recognition of antigen

T Cells in cellular immunity

T cells are produced in bone marrow & mature in thymus

protect against viruses and cancer

responsible for hypersensivity reactions and transplant rejections

two types of t cells in cellular immunity

regulatory- t helper, t suppressor

effector/killer

cells in order for crime

1) t helper (CD4)- identify (detective)

2) B cells- antibodies (officer)

3) Killer T (swat team)

more info about what T cells do

recognize the antigen (t helper)

bind t the antigen

trigger a response by the immune system

helper t cells activate and call up b cells to produce antibodies

humoral immuiy

mediated by b cells

antibodies take longer to produce after initial antigen exposure compared to innate immunity

b cells in humoral immunity

mature in bone marrow

2 types of b cells in humoral immunity

memory cells

immunoglobulin-secreting cells

memory cells in humoral immunity

recall the trigger and quickly triggers a response leading to acquired immunity

2 types of acquired immunity

active immunity

passive immunity

active immunity (type of acquired immunity)

acquired by having the disease and/or by taking vaccination

long lasting but takes a few days to become effective

passive immunity (type of acquired immunity)

passed down

short lasting

receiving antibodies from external sources (material fetal transfer/breastfeeding

hypersesitivity

exaggerated immune response to a feign substance

leads to inflammation

can be immediate or delayed

autoimmune

mistakes self as non-self

immunodeficiency

inadequate immune reaction

four types of hypersensitivty

type I: IgE mediated

type II: cyototoxic hypersensitivity reaction

type III: immune complex-mediated

type IV: delayed hypersensitivity reaction

to remember hypersensitivities

A- allergies= IgE

C- cytotoxic= IgG or IgM

I- immune complex

D- delayed hypersensitivity reaction

Type I, IgE mediated

produces an immediate response (2-30 min)

local or system (anaphylaxis)

IgE coats mast cells and basophils, sensitizing them to the allergen (when you’re exposed to an allergy you have a bad reaction, get worse)

ex- seafood allergy, hay fever

anaphylaxis

priority concern

can affect airway

treatment for type I, IgE mediated

includes epinephrine, antihistamines, corticosteroids, and desensitizing injections

type II hypersensitivity, cytotoxic

IgG or IgM antibodies bind to antigen on individuals own cells

causes cell lysis (cell destruction) and phagocytosis (clean up)

reaction takes 5-8 hours to develop

type II, cytotoxic example

mom and baby: mom is A blood type and baby is A+, 1st pregnancy is fine but 2nd causes issues

reason: blood transfusion reaction and erythroblastosis fetalis (hemolytic disease of the newborn)

type III hypersensitivity, immune complex-mediated hypersensitivity reaction

circulating antigen- antibody complexes accumulate and are deposited in the tissue (tissues include kidney, joints, skin, blood vessels)

triggers the complement system, causing inflammation

takes 2-8 hours to develop

examples of type III hypersensitivity, immune complex-mediated hypersensitivity reactions

autoimmune conditions (systemic lupus eruthematosus)

causes glomerulonephritis

type IV hypersensitivity, delayed hypersensitivity reaction

cell-mediated rather than antibody-mediated (only T cell mediated/ran) involving the T helper cells and killer cells

leads to inflammation causing severe tissue injury and fibrosis (scaring) (usually involves skin)

reactions occur 1-3 days after exposure

examples of type IV, delayed hypersensitivity reaction

tuberculin skin testing

transplant reactin

contact dermatitis (nickel- only at ONE site)

type I- allergies picture

•Whole body reacts

•Sudden itchiness

•Puffy face, itchy eyes/nose

•Difficulty breathing, wheezing

•Anxiety

asthma

allergies

N/V/D

type IV- delayed hypersensitivity reaction picture

type II- cytotoxic picture

type III- immune complex

autoimmune disorder

self doesn’t recognize self, attacks self

defenses are directed against host

can affect any tissue

could be triggered by stressor or chronic stress

known characteristics of autoimmune disorders

genetics play a role (received from immediate family)

more prevalent in females

onset is associated with abnormal stressor, physical or pschological

has periods of sx getting worse and then sx getting better

Systemic (whole body) lupus erythematosus (SLE)

chronic inflammatory autoimmune condition

stressors influence severity

remission and exacerbations

may affect connective tissue of any body organ

more common in women (estrogen), asians, and african americans

SLE is thought to be caused by

B cells are activated→ produce autoantibodies + autoantigens tha combine to form immune complexes, which attack the body’s own tissues

manifestations of SLE

S erositis (lining of organs)

O ral ulcers

A rthritis

P hotosensitiity (body is sensitive to UV radiation) (gets rash)

B lood disorders (decreased counts)

R enal inflammation (reduces function, leaks protein through urine)

A ntinuclear antibody

I mmunological phenomena

N eurological disorders (seizures/psychosis)

M alar rash (butterfly rash over cheeks)

D iscoid rash (patchy redness that can cause scarring-scaly)

when is lupus normally diagnosed

20s-30s

not kids!

diagnosing SLE

abdominal/chest xray

elevated sedimentation rate from inflammation

C-reactive protein from inflammation

urinalysis (kidneys inflamed, protein in urine)

echocardiogram (inflammation in heart)

skin biopsy (not definitive by itself) (caused by photosensitivity)

blood test complications

treatment for SLE

no sure

sx management

stress management and health promotion behaviors

immunosuppressants

prognosis for SLE

improves with early diagnosis and treatment

discoid rash

mallor rash

A female client asks the nurse if there are any conditions that can exacerbate systemic lupus erythematosus (SLE). Which is the best nurse response?

pregnancy is often associate with an SLE exacerbation (estrogen)