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IgM
first to increase in immune response
bound to T cells
largest antibody
IgG
most common
crosses placenta
creates neonatal passive natural immunity
IgA
tears and saliva
protects mucous membranes from toxins
local immunity
IgE
allergies
releases histamines that result in inflammation
IgD
activates B-cells
delivers signals to B cells
contact-dependent
membrane to membrane contact
parocrine
secrete local mediations that are quickly taken up, destroyed or immobilized (sends everywhere)
autocrine
signals to themselves
hormonal signaling
involves specialized endocrine cells that secrete chemicals
travel through the blood stream to produce a response in other sets of cells
neurohormonal
released into blood by neurohormone secretory neurons
neurotransmitter
nerve cell directly communicates to cell
atrophy
decrease in size
hypertrophy
increase in cell size
hyperplasia
increase in cell number
metaplasia
change in cell phenotype
dysplasia
abnormal/deranged cellular growth
physiologic atrophy
thymus change in childhood
decrease in uterine size after childbirth
pathological atrophy
atrophy or denervation
atrophy of disuse
ischemia
malnutrition
pressure
ischemia
lack of blood
reperfusion
damage of reoxygenation
oxidative stress
increase indifferent reactive species, depletion of antioxidant defense
injury caused by ROS
coagulative
heart
protein denaturation
opaque appearance
liquefactive
brain tissue
enzymes eating themselves
soft, runny appearance
fatty
primarily in breasts, pancreas
breakdown triglycerides
opaque appearance
caseous
lungs
primarily intuberculosis infection
combo of coagulative and liquefactive
necrosis
enlarged cell size
swelling
may leak out of cell
apoptosis
fragmentation of nucleosome-size fragments
often physiologic
pathologic: cell injuries
autophagy
recycling
C3B
opsonins
coats like glue
C5A
leukocyte chemotaxis
attracting and activating WBCs
C3A-C5A
anaphylatoxins
rapid and release histamines
leaky capillaries
C6-C9
cellysis/MAC attack
drilling holes to allow water in cell membrane
complement system
intensifies the capacity of antibodies and phagocytes to clear pathogens, activate inflammation
clotting system
forms a blood clot
fibrin/fibrinogen
kinin system
interacts with the clotting system, bradykinin
TNF-a
tumor necroting factor alpha
muscle wasting
respond to virtually an injury
IL-1
fever-causing
IL-6
stimulate growth
protein production
repair
IL-10
anti-inflammatory
SIGNS of inflammation
redness
heat
edema
pain
loss of function
adherence
1st step
enhanced by opsonization
margination
roll against vessel
increased adhesion
diapedesis
emigration of cells
chemotaxis
movement against chemical gradient
vasodilation
increased diameter of blood vessels that increase the volume of blood delivered to the injured site
result in erythema and warmth in the area
increased capillary permeability
proteins and large molecules are last into interstitial fluid
prulent
foul odor
white, yellow, green
indicates infection
serous
blister
watery fluid
normal
fibrinous
thick and clotted
normal
hemorrhagic
full of RBCs
thick and STICKY
indicates infection
hemorraging = BAD
cytokines
intercellular signaling molecules
secreted by many different types of cells
bind to specific cell membrane receptors
chemokines
chemotaxis
stimulate migration of cells
phase 1: inflammation
coagulation (hemostasis)
damage to blood vessels causes immediate vasoconstriction followed by vasodilation
infiltration of platelets, neutrophils, macrophages
phase 2: proliferation and new tissue formation
macrophages
dissolve clot (hemostasis)
granulation tissue = invasive cells (red beefy appearance)
epithelialization (moist wound improves process)
phase 3: remodeling and maturation
cell differentiation
scar formation
scar remodeling
primary intention
clean-approximate wound
surgical cut
paper cut
secondary intention
open wound, requires extensive epithelialization
dog bite
pressure ulcer
done without intention
clinically important normal flora
candida albicans
clastridium difficile
lactobacillus
opportunistic infections
illnesses that occur when the bodies immune system is down and affected
people with HIV are more at risk
viral infection
acellular, capsid
dependent on host cells
influenza, covid-19
viral hepatitis, HIV, AIDS
binding, penetration, uncoating, replication, budding
cell-mediated
bacterial infections
humoral
single-celled prokaryotes
tuberculosis, UTI, C-diff, staph.
DOES NOT require an enriched environment to survive
most common cause of SEPSIS
bacterial resistance to antibiotics
produce surface coats that inhibit phagocytosis and toxins
generate a large surface capsule to block off access of antibiotics
exotoxin
staphylococcus aureus
polypeptide
both gram NEGATIVE and gram POSITIVE
can be used for a vaccine
endotoxin
only gram NEGATIVE
integral part of cell wall
heat-tolerable
E. coli
lipopolysaccharide complex
Sustained proliferative aging
Foremost hallmark of cancer: uncontrolled cellular proliferation
Proto-oncogenes
genes that direct normal cellular proliferation
Oncogenes
mutated or overexpressed proto-oncogenes
Evading growth suppression
Tumor-suppressor genes (anti-oncogenes)
Regulate cell cycle (stop mitosis)
◦ Inhibit proliferation
◦ Stop cell divisions if cell is damaged ◦ Prevent mutations
hypertrophic cardiomyopathy (HCM)
condition where the heart muscle (myocardium) becomes abnormally thick
acromegaly
excessive production of growth hormone (GH) by the pituitary gland
cervical dysplasia
abnormal cells grows on the surface of the cervix
systemic lupus erythematosus (SLE)
chronic autoimmune disease where the body’s immune system mistakenly attacks its own healthy tissues and organs
hyperthyroidism (Grave’s disease)
the thyroid gland produces excessive amounts of thyroid hormones
hypothyroidism (Hashimoto’s thyroiditis)
the body’s immune system attacks the thyroid gland, leading to inflammation and damage
rheumatoid arthritis
chronic autoimmune disease that primarily affects the joints, causing inflammation, pain, and stiffness
inflammatory bowel disease (IBD)
group of chronic conditions that cause inflammation in the digestive tract
keloid scarring
abnormal overgrowth of scar tissue that extends beyond the original wound boundaries
wound contractures
a condition where the edges of a healed wound pull together, resulting in a tight, inflexible scar
genomic instability
increased tendency for genetic mutations
increased risk of cancer
replicative immortality
normal body cells are not immortal
cancer cells are able to have limitless replicative potential
angiogenesis
growth of new blood vessels
essential in tissue undergoing repair
reprogramming energy metabolism
warburg effect and reverse warburg effect
deregulate proliferation
resistance to apoptotic cell death
apoptosis is programmed cell death
tumor-promoting inflammation
chronic inflammation is an important factor in the development of cancer
tumor-associated macrophage (TAM)
avoiding immune destruction
normal immune system protects against cancer
tumor associated antigens
activating invasion and metastasis
invasion: local spread, pre-req for metastasis
metastasis: spread of cancer from a primary site of origin to a different site
benign tumors
grow slowly, encapsulated, not invasive, cane become LARGE
lipoma (fat cells)
leiomyoma (smooth muscle of uterus)
meningioma (meninges)
malignant tumors
grow rapidly, not encapsulated, invasive
carcinoma (epithelial tissue)
adenocarcinoma (ducal or glandular tissue)
sarcoma (mesenchymal tissue, connective tissue)
lymphoma (lymohatic tissue)
leukemia (blood-forming cells)
type 1: immediate hypersensitivity
IgE antibodies, allergies
insect bites, food allergies, certain drugs
type 2: cytotoxic antibod hypersensitivity (specific)
IgG antibody activation of complement cascade
autoimmune disease, fetal Rh incompatibility
specifically targeted at a particular tissue
Grave’s disease
involves IgM
type 3: immune complex disease
immediate development
SLE
serum sickness, glomerular nephritis
deposition of IgG and IgM
type IV: cell-mediated hypersensitivity
delayed
T cells/macrophages destroy antigen-coated host cells
contact dermatitis, granuloma, poison ivy
primary immune response
occurs at 1st exposure
produces IgM and IgG
secondary immune response
occurs at the next exposure
more rapid production
memory cells
can eliminate the antigen
IgG is the main player
CD8 killer T cells
kill virus infected host cells through cytolysis
CD4 inflammatory T cells
enhance activities of phagocytes
dendritic cells
antigen presenting cells (APCs) to T cells