Patho CH. 4: Altered Immunity Flashcards
SPECIFIC immune defense
Involves:
adaptive immunity
inflammatory response
NONSPECIFIC immune defense
Involves:
innate immunity
T and B lymphocytes
two types of humoral immunity
active and passive
development of antibodies to an antigen
How?
active immunity
specific disease or vaccine
immunity transfer from host to recipient
How?
passive immunity
From mother to infant transfer or injection of antibody
histames cause
bronchodilation
humoral immunity includes B lymphocyte which include these cells
antibodies from plasma cells
memory cells
primary adaptive immune response
activation with first recognition of specific antigen
secondary adaptive immune response
reactivation with later recognition of the same antigen
immunoglobulin concentrated in bodily secretion
IgA
breast milk, tears, saliva
most common immunoglobulin
second response
IgG
passive immunity
First immunoglobulin
IgM
cell mediated immunity has
cytotoxic T lymphocytes: CD4 - class 2 MHC
helper T lymphocytes: CD8 - class 1 MHC
Major histocompatibility complex (MHC) only in what immunity
cell mediated
Processes of altering immune function
host defense failure
hypersensitivity
autoimmunity
alloimmunity
host defense failure examples
antigenic variation
viral latency
immunodeficiency
ex of antigenic variation
cold
flu
ex of viral latency
herpes zoster (shingles)
TB
they hide
Type 1 hypersensitivity type
immediate
Type 2 hypersensitivity type
antibody-mediated
Type 3 hypersensitivity type
immune complex-mediated
Type 4 hypersensitivity type
cytotoxic T lymphocyte-mediated
Type 1 hypersensitivity reaction ex and etiology
anaphylaxis
IgE mediated
Type 2 hypersensitivity reaction ex
reaction against normal “self” antigens
Type 4 hypersensitivity reaction ex
cell lysis
delayed reaction
failure to distinguish self
autoimmunity
alloimmunity examples
graft rejection
graft versus host disease
organ rejection
immunosuppression treatment leads to
opportunistic infection
using the immune response for disease management
use pt own immune system to combat disease
develop drugs to distinguish self from cancer
AIDS comes from
HIV infection
loss of CD4 T lymphocytes means
loss of cell mediated and humoral immunity
CD4 count diagnostic of AIDS
below 200 - AIDS and high risk for opportunistic infection
above 500 - asymptomatic
Below 350 - substantial immune suppression
AIDS CM
HA
high fever
white patches on tongue
swollen lymph nodes
heavy night sweats
loss of appetite
severe weight loss
chronic diarrhea
fatigue
AIDS opportunistic infections
oral candidiasis
pneumocystis
kaposi sarcoma
AIDS DC
H and P
Labs
labs for diagnosing AIDS
detection of antibodies
HIV viral load
CD4 count
test reveals just antigens and no antibodies means
newly exposed
has not yet made antibodies
AIDS treatment
antiretroviral therapy
antiretroviral therapy
suppress viral load
restore immune function
reduce morbidity and mortality
change in medications for AIDS over time
More medications made into less pill to reduce drug resistance
anaphylaxis patho
exaggerated SYSTEMIC immune response
anaphylaxis due to
type 1 hypersensitivity reaction
triggers for anaphylaxis
insect stings
food allergies
drug allergies
response stimulated by antigen exposure in anaphylaxis
IgE mediated response
open and lets out
degranulation
degranulation of mast cells and basophils causes
dilation of vascular smooth muscle
constriction of bronchial smooth muscle
increase in vascular permeability
anaphylaxis phase 1 manifestations
difficulty breathing
skin flushing and itching
angioedema (vessels swell)
uticaria - hives
anaphylaxis phase 2 CM
difficulty breathing - wheezing
severe hypotension - shock (vasodilation = expansions of vessels = decreased pressure
severe edema
anaphylaxis DC
H and P
allergy testing
symptomatic anaphylaxis treatment
drugs to relax bronchial smooth muscle ( first is epinephrine second is steroids)
drugs to constrict vascular smooth muscle
limit inflammation
preventative anaphylaxis treatment
desensitization to allergen - allergy shots
SLE patho
autoimmune response
response from innate and adaptive immune systems
SLE hypersensitivity
Type 3
SLE is chronic due to what persistent antigen
your own body
B cells produce
antibodies
T cells promote
inflammation
potential cause of SLE
virus
hormones
genetic predisposition
drugs
SLE clinical manifestations
specific to organ injured by inflammation and complex deposition
local SLE CM areas
skin
musculoskeletal
pulmonary
kidney
systemic SLE CM areas
neurologic
pulmonary
hematologic
cardiac disease
conditions caused by SLE
pleuritis (lungs)
myocarditis
hemolytic anemia (RBC)
leukopenia (increase WBC)
thrombocytopenia (decreased platelets)
glomerulonephritis
lymphadenopathy
arthritis
SLE DC
H and P
labs
SLE lab
ANA - antinuclear antibodies - antibody against cell components and DNA
SLE treatment
Pharmacologic - antiinflammatory - antimalarial - immunosuppressants
Rh immunization patho
antibodies against Rh antigen attack RBCs causing hemolysis
Rh negative mothers exposed to fetal Rh positive antigen
Rh isoimmunization hypersensitivity
type 2 cytotoxic antibody-mediated reaction
Rh isoimmunization CM - fetal and infant
fetal effects - anemia, edema, death
infants - kernicterus, lethargy, hearing loss, cerebral palsy, learning problems
Rh isoimmunization DC
H and P
Screening (antigen and antibody)
Diagnostic testing
diagnostic testing for Rh
amniocentesis to measure bilirubin
fetal blood sampling to determine anemia
Rh isoimmunization treatment
risk reduction
prevention (Rh immunoglobulin)
exchange transfusion to replace damaged RBC to healthy ones
