Injury and Inflammation

Acute Reversible Injury

Cell injury that is characterized by:

Swelling

Less efficient mitochondria

Reduced protein synthesis

Undamaged nucleus

Chronic Reversible Injury

Chronic injury with the following adaptations:

Atrophy

Hypertrophy

Hyperplasia

Metaplasia

Dysplasia

Atrophy

Reduction in cell/organ size

Hypertrophy

Increase in cell/organ size

Hyperplasia

Increase in # of cells

Metaplasia

Change in cell structure/function

Dysplasia

Increase in cell #s with structural change

Necrosis

Irreversible cell injury, that is a rapid process that includes swelling and the release of intracellular contents, causing inflammation

Apoptosis

Irreversible cell injury that is intentional/programmed cell death. Involves cells shrinking and cellular fragmentation.

Syndactyly

Abnormal apoptosis result

Coagulative necrosis

Necrosis causes by ischemia, in which cell membrane remains intact but organelles dissolve. Found in solid organs (heart, kidney, live)

Ex: early pressure sores

Caseous necrosis

"Cheesy” necrosis found in lungs, bone, and lymph nodes. Cells die, disintegrate and then clump together.

Ex: Miliary tuberculosis, mycobacterioum tuberculosis

Liqufactive necrosis

Necrosis with abscess formation of tissue by lysosomal enzymes due to infection. Found in brain tissue, skin, wound, joint infections

Ex: late pressure sores

Fatty necrosis

“Chalky” necrosis caused by acute pancreatitis and abdominal trauma, in which tissue is replaced by fat.

Fibrinoid necrosis

Necrosis caused by trauma in blood vessel walls, where the boy attacks blood vessels through autoimmune response.

Ex: organ transplant rejection

Ischemia

Cell injury characterized by the lack of blood flow leading to oxygen deprivations

Infectious agents

Cell injury that invades tissue and releases toxins leading to cell death and lysis. Spreads infection

Genetic factors

Cell injury, examples are chromosomal abnormalities and gene mutations

Down syndrome, Huntington’s chorea, sickle cell anemia

Examples of genetic factors that can result in cellular injury

Nutritional factors

Malnutrition and obesity causing reduced protein synthesis and amino acid deficiencies

Physical factors

Trauma, such as motor vehicle accident, gunshot wounds, extreme temperatures (burns), radiation

Chemical factors

Factors that include heavy metals and medications that can cause cellular damage.

Free radicals

Unpaired electrons latching onto things and disrupting cells

Reactive oxygen species (ROS)

Chemical factors that fight inflammation, kill bacteria, regulate autonomic nervous system

Caused by prolonged exercise, irradiation, ultraviolet/fluorescent light, pollutants, tobacco, and pesticides.

Create oxidative stresses that lead to diseases/conditions

Antioxidants

Chemical factors of cellular injury that neutralize free radials by binding

Endogenous : enzymatic and nonenzymatic defense systems within cells

Exogenous: Vitamin C and E

Nitric Oxide

Chemical factors of cellular injury that relax blood vessels and decreased levels are associated with cardiovascular disease

Exercise & Free Radicals

Chemical factors of cellular injury that increase NO production.

Improved antioxidant defense and regulation or repair systems

Overtraining

___________ can lead to reduced ability to fight infection

Inflammation

Our response to restore tissue to the injury state

Injurious agent

Inflammation ends when when the ____________ _________ is removed

Purpose of inflammation

To be a protective response

To get rid of the cause and consequences of an injury

Initiate healing

Signs/Symptoms

Redness, swelling, increased temperature, pain, decreased function of affected site

Vasodilation

Increased capillary permeability

Loss of fluid

Increased fibrinogen

Migration of leukocytes

Effects of vasodilation in inflammation

Increases blood flow → causing heat and redness (erythema)

Effects of increased capillary permeability in inflammation

Movement of plasma proteins and leukocytes which causing swelling (edema)

Causes fluid loss

Effects of fluid loss in inflammation

Slows blood flow, increase red blood cell concentration, and increases blood viscosityE

Effects of leukocyte migration in inflammation

Increases swelling of cells, as leukocytes move into cell

Effects of increased fibrinogen in inflammation

Clotting of fluid

Role of vascular changes during inflammation

Movement of plasma/cells from intracellular space to the injury site

Exudation

Transudation

Exudation

Escape of fluid, protein, and blood from vasculature system into tissue/body cavities (pu

Hemorrhagic/Sanguineous exudate

Exudate or discharge that is bright red or bloody, presence of RBCs

Serosanguineous exudate

Exudate or discharge that is blood tinged yellow or pink

Serous exudate

Exudate or discharge that is thin clear yellow

Ex: blisters

Purulent exudate

Exudate or discharge that is viscous cloudy pus

Catarrhal exudate

Exudate or discharge that is thin clear mucus

Transudation

Occurs when fluid leaks into a space

Binding (LA)

1st step of leukocyte accumulations

Occurs when leukocytes bind to endothelial cells at the site of inflammation

Migration

2nd step of leukocyte accumulations

Occurs when leukocytes move out of the vessels and into the problem area (process called diapedesis)

Attraction

3rd step of leukocyte accumulations

Occurs when chemostatic agents pull leukocytes closer to inflammation site

Clean up

4th step of leukocyte accumulations

Occurs when macrophages clean up debris IF inflammatory stimulus subsides

Acetylated Lysophospholipid

Type of acid arachidonic acid derivative and chemical mediator that acts as a platelet activating factor

Cyclooxygenase Pathway

Type of acid arachidonic acid derivative that involves prostaglandins modulating vasomotor tone and platelets; helps with restructuring and stopping the bleeding

Lipooxygenase Pathway

Type of acid arachidonic acid derivative and chemical mediator that involves the creation of leukotrienes that produce smooth muscle contraction, increased vascular permeability, migrations of leukocytes.

Phagocytosis

Ingesting microorganisms, killing, or deactivating them

Coating

1st step of Phagocytosis

“Harpoon gun”

Leukocytes attaching identifying signals to cell/agent

Binding (P)

2nd step of Phagocytosis

Enfolding

3rd step of Phagocytosis

Engulfing of the cell/agent

Infusion of lysosome to kill/degrade

4th and final step of Phagocytosis

May manifest or leave the body as pus