Injury and Inflammation

Cell injury that is characterized by:

Swelling

Less efficient mitochondria

Reduced protein synthesis

Undamaged nucleus

Chronic injury with the following adaptations:

Atrophy

Hypertrophy

Hyperplasia

Metaplasia

Dysplasia

Reduction in cell/organ size

Increase in cell/organ size

Increase in # of cells

Change in cell structure/function

Increase in cell #s with structural change

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

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

Abnormal apoptosis result

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

Ex: early pressure sores

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

Ex: Miliary tuberculosis, mycobacterioum tuberculosis

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

Ex: late pressure sores

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

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

Ex: organ transplant rejection

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

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

Cell injury, examples are chromosomal abnormalities and gene mutations

Examples of genetic factors that can result in cellular injury

Malnutrition and obesity causing reduced protein synthesis and amino acid deficiencies

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

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

Unpaired electrons latching onto things and disrupting cells

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

Chemical factors of cellular injury that neutralize free radials by binding

Endogenous : enzymatic and nonenzymatic defense systems within cells

Exogenous: Vitamin C and E

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

Chemical factors of cellular injury that increase NO production.

Improved antioxidant defense and regulation or repair systems

___________ can lead to reduced ability to fight infection

Our response to restore tissue to the injury state

Inflammation ends when when the ____________ _________ is removed

To be a protective response

To get rid of the cause and consequences of an injury

Initiate healing

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

Vasodilation

Increased capillary permeability

Loss of fluid

Increased fibrinogen

Migration of leukocytes

Increases blood flow → causing heat and redness (erythema)

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

Causes fluid loss

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

Increases swelling of cells, as leukocytes move into cell

Clotting of fluid

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

Exudation

Transudation

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

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

Exudate or discharge that is blood tinged yellow or pink

Exudate or discharge that is thin clear yellow

Ex: blisters

Exudate or discharge that is viscous cloudy pus

Exudate or discharge that is thin clear mucus

Occurs when fluid leaks into a space

1st step of leukocyte accumulations

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

2nd step of leukocyte accumulations

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

3rd step of leukocyte accumulations

Occurs when chemostatic agents pull leukocytes closer to inflammation site

4th step of leukocyte accumulations

Occurs when macrophages clean up debris IF inflammatory stimulus subsides

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

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

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.

Ingesting microorganisms, killing, or deactivating them

1st step of Phagocytosis

“Harpoon gun”

Leukocytes attaching identifying signals to cell/agent

2nd step of Phagocytosis

3rd step of Phagocytosis

Engulfing of the cell/agent

4th and final step of Phagocytosis

May manifest or leave the body as pus