Adaptation, Cellular Injury, Inflmmation, and Healing Flashcards
Cellular Adaptation
Allows stressed tissue to survive or maintain function
Atrophy
decreased or shrinkage in cellular size due to decrease in work demand or adverse conditions
It can be physiological or pathological
Hyperplasia
increase in # of cells
Hypertrophy
Increase in cell size
Metaplasia
reversible change of one cell type for another in response to hostile environment
When does metaplasia occur?
in response to chronic irritation and inflammation
Dysplasia
Deranged cell growth
What is Dysplasia a precursor to?
cancer, does not guarantee but a strong implicator
Name the two Pathologic calcification
Dystrophic calcification
Metastatic Calcification
Dystrophic Calcification
occurs in dead or dying tissue
Metastatic Calcification
occurs in healthy tissue
two patterns of reversible cell injury
Cellular swelling
Fatty change
Hypoxic injury
deprives cell of oxygen and interrupts oxidative metabolism and the generation of ATP
Causes acute cellular swelling
Free radical cell injury
highly reactive chemical species
Immune cells called macrophages produce free radicals while fighting off invading germs. These free radicals can damage healthy cells, leading to inflammation
Impaired Calcium Homeostasis
Inappropriate release activates enzyme
regulates calcium flow to and from the bones
Programmed cell death
apoptosis ; pathological
Necrotic cell death
unregulated death caused by injuries to cell
Dry Gangrene
caused by lack of arterial blood supply but venous flow can carry fluid out of tissue
Wet Gangrene
lack of venous flow lets fluid accumulate in tissue
What is inflammation?
an innate , automatic response to cell injury that
- neutralizes harmful agents
- removes damaged and dead tissue
- generates new tissue
- promotes healing
3 types of imflammation
acute inflammation
chronic inflammation
systemic manifestations
5 cardinal signs of inflammation
redness swelling warmth pain loss of function
Cellular Stage of inflammation
vasoconstriction - last only a few seconds
vasodilation - increases blood flow to injury
capillary permeability - allows exudate to escape into the tissue
pain
phagocytosis
systemic effects
coagulation
systemic effects
fever, TNF, prostaglandins
Local signs of inflammation
Exudate ,ulceration
Serous exudate
watery fluid
common with inflammation process
hemorrhagic exudate
associated with severe tissue injury that causes damage blood vessels
or
when there is significant leakage of RBC from capillaries
Fibrinous exudate
large amt of fibrinogen and forms from a thick and steak meshwork
Membrandous or pseudomembranous exudate
necrotic cells enmeshed in a fibropurulent exudate
Purulent / suppurative exudate
pus consists of WBC, proteins, and tissue debrie
Chronic inflammation
longer duration (lasting for weeks to years)
body attempts to repair connective tissue involving proliferation of blood vessels , tissue necrosis, and fibrosis (scarring)
Granuloma formation occurs in chronic inflammation
the immune system is treating the chronic inflammation as “out of sight, out of mind”
Long term management of irritant
Systemic Manifestations of Inflammation 1st mechanism
Acute Phase (released by liver)
- fever, lethargy
- increased ESR and hsCRP
Systemic Manifestations of Inflammation 2st mechanism
White Blood Cell Response
- Leukocytosis : increased in WBCs
- Immature neutrophils released into blood
Systemic Manifestations of Inflammation 3rd mechanism
Enlarged lymph nodes
Bacterial infections
= increase in neutrophils
parasitic and allergic responses
= increase in eosinophilis
viral infections
= decrease in neutrophils and increase
Fever mechanism
Controlled by hypothalamus
increases metabolism
Fever types:
Neurological fever - hypothalamus is damaged/ thermostat is broken. Results from damage/trauma to CNS
Drug Fever - a drug inadvertently leads to a hypermetabolic fever inducing state
Heat Loss
- Conduction - lying on cold surfaces
- Radiation - loss of head from a distant cold objects like windows or walls
- Evaporation - sweating
- Convection - use of fans or effect of cold drafts
Proliferative Capacity:
Continuously dividing cells
readily regenerate
uterus, GI tract, bone marrow, skin
Proliferative Capacity:
Stable tissue cells
normal quiet cells, but when given correct stimulus, they will reconstitute
smooth muscle, fibroblasts,
Proliferative Capacity:
Permanent tissue
Do not proliferate and terminally differentiated
nerve cells, skeletal muscle cells
Connective tissue healing : Phase 1
acute inflammation : platelet activation and immune mobilization
Clot formation
phagoytosis
neutrophils - stimulate release of growth hormone
Connective tissue healing : Phase 2
proliferation : cells multiplication and matrix deposition
filling in the gap / rebuilding
epithelization
Connective tissue healing : Phase 3
Remodeling : scar formation and tissue restoration
remodeled due to fibroblast / collagenase
Wound healing
Primary intention : no skin tissue lost, will not have granulation, can turn into secondary
Secondary : will have granulation
Dysfunctional Wound Healing
- Keloids
- Contractures - shrinkage of wound tissue that pulls wound edges
- Strictures - narrowing of tubular structures from the formation of scar tissue
- Fistula
- Adhesions - abnormal bands of internal scar tissue that can form , they can develop an obstruction from tihs
gas gangrene
clostridium infection
hydrogen sulfide bubbles in muscle
Acute inflammation
the early (appearing within minutes to hrs) host protective response of local tissues and their blood vessels to injury and is critical for restoration of tissue homeostasis
occurs before adaptive immunity and is aimed at removing the injurious agent and limiting the extend of tissue damage
Factors involved in wound healing
Nutrition - Individuals most be in a state of positive nitrogen balance (protein best source in diet)
Immune Strength-conditions that contribute to immunocompromised states delay wound healing
Blood Flow and Oxygen delivery - adequate blood flow to bring O2 and remove waste
Liquenfaction
necrotic cell death
release of enzymes following cell death
coagulation necrotic cell death
acidosis develops and denatures proteins
characteristics of hypoxic injury
Caseous necrotic cell death
soft- cheese life debris
commonly found in the center of TB granulomas
Leukotrienes
Key cell-derived Mediator
slow reacting substances of anaphylaxis’s, (SRS-A)
causes slow and sustained constriction of the bronchioles
Prostaglandins
Key cell-derived Mediator
induces vasodilation and bronchoconstriction
inhibits inflammatory cell function
PGI2 / PGF2a
Thromboxane
Key cell-derived Mediator
Causes :
Vasoconstriction
Bronchoconstriction
Promotes platelet function
TxA2
