ch 2 - repair, regeneration, inflammation

injury

result of an alteration in environment causing TISSUE DAMAGE

necrosis

severe injury

hyperplasia, hypertrophy, atrophy

less severe injury

inflammation allows body to

• eliminate injurious agents

• contain injuries

• heal defects

inflammation is SEQUENTIAL RESPONSE TO

cell injury

physical barrier (innate defenses protecting from injury)

intact skin or mucosa

mechanical defense (innate defenses protecting from injury)

respiratory system’s cilia and mucus

antibacterial activity (innate defenses protecting from injury)

enzymes in saliva and tears

removal of foreign substances (innate defenses protecting from injury)

flushing action of tears, saliva, urine, diarrhea

inflammation process (innate defenses protecting from injury)

white blood cells

repair

restoration of damaged or diseased tissue

regeneration

process by which injured tissue is replaced with tissue identical to that present before injury

hyperplasia (healing)

increase in NUMBER of cells

hypertrophy (healing)

increase in SIZE of cells (same #)

atrophy (healing)

decrease in size or function of a cell

soft tissue repair

• primary intention healing

• secondary intention healing

• tertiary intention healing

primary healing

• mechanical apposition of wound edges (sutures, staples, etc)

• little loss of tissue

• margins close tg

• very little granulation tissue forms

secondary intention healing

• edges of injury CANNOT be joined during healing — too far apart

• allowed to heal on its own — basal layer outwards

• large CLOT FORMS - increased granulation tissue

• may cause scar tissue — cicatrix, keloid

cicatrix

scar

keloid

scar larger than expected from wound size, result of too much collagen

tertiary intention healing

• primary intention healing than infection

• “delayed primary”

• infected would left open until controlled

• suture at later date

types of bone

• compact/ cortical

• cancellous/ spongey/ trabecular

compact/ cortical bone

• dense done forming external surface

• provides strength for protection, support chemical storage

cancellous/ spongey/ trabecular

• honeycombed internal surface

• houses bone marrow

woven bone

immature bone

lamellar bone

mature bone

cells invloved with bone repair

• osteoclasts

• osteoblasts

• osteocytes

osteoclasts

breaks down bone

osteoblasts

new bone growth

osteocytes

• mature osteoblasts

• act as SENSOR (detect damage)

osteogenic cells

stem cells that turn into osteoblasts

suffix for blood condition

-emia

low cell count suffix

-penia

high cell count suffix

-cytosis

during EMBRYONIC PERIOD blood is formed in the

LIVER

after birth, blood is made in the

BONE MARROW

bone marrow makes

stem cells and progenitor cells

Haemopoiesis

process of creating a wide variety of blood and bone marrow cells

Hematopoietic stem cells differentiate into

• Red blood cells (RBC)

• Erythrocytes

• White blood cells (WBC)

• Leukocytes

• Platelets (Thrombocytes)

blood composition

• fluid — serum

  • plasma, contains and transports nutrients, proteins, hormones, byproducts

• cellular — solid

  • RBCs, WBCs, platelets

Erythroblasts (RBC)

• Formed from the hematopoietic stem cell

• Has a nucleus

Reticulocyte or immature red blood cell

• Develops from the erythroblast

• Has granulated or reticular appearance to the cytoplasm (instead of a nucleus)

Erythrocyte or mature red blood cell

• Has no nucleus

• Transports oxygen from lungs to body tissues

• Transports carbon dioxide waste from body back to lungs to be exhaled

• Biconcave shape characteristic, enhances oxygen and carbon dioxide exchange and repeated cycles of high flow

types of leukocytes (WBCs)

• granulocytes

  • Neutrophils

  • Eosinophils

  • Basophils

• Agranulocytes

  • Lymphocytes (T-cells and B-cells)

  • Monocytes (differentiate into macrophages

Neutrophils – (polymorphonuclear leukocytes or PMNs)

• 1st type of WBC to the area of injury

• Constitute 60% to 70% of WBC population

• Phagocytic

Eosinophils

active in allergic reactions and parasitic infections

Basophils

instrumental in allergic reactions and produce histamines

Lymphocytes (T-cells and B-cells)

Coordinate immune response, antigens/antibodies, kills infected cells

Monocytes (differentiate into macrophages)

• 2nd type of WBC to the area of injury

• Constitute 3% to 8% of WBC population

• Phagocytic

platelets (thrombocytes)

• Involved in blood clotting

• Attach to the wall of damaged tissue to halt bleeding

Clotting process

• Thromboplastin – released from the platelets

• Prothrombin – produced by liver – changed into thrombin by the action of thromboplastin and calcium

• Thrombin then acts upon fibrinogens to produce fibrin

• Fibrin – a red strand – then attaches to the platelets at the wound site to form the clot

Microscopic Events: Day of Injury

• Blood flows into injured tissue to produce a clot

• The clot contains fibrin, clumped red blood cells (RBCs), and platelets

Microscopic Events: Two Days After Injury

• Monocytes change to macrophages

• Macrophages continue phagocytosis and secrete growth factors that stimulate growth of new blood vessels (angiogenesis)

• Neutrophils are reduced in #

• Fibroblasts increase in # and produce new collagen fibers (fibroplasia)

• Granulation tissue (CT) is formed

• Epithelialization occurs — new surface tissue is created

• Blood clot acts as a scaffold for new connective tissue

• Lymphocytes and plasma cells migrate to the area as chronic inflammation

• immune response begins

FIVE CARDINAL SIGNS OF INFLAMMATION

• Rubor – Redness (vasodilation caused by histamine)

• Calor – Heat (increased vascularity as a result of

• histamine and serotonin release)

• Dolor – Pain (bradykinin and kallikrein)

• Tumor – Swelling (increased vascular permeability due to histamine and serotonin)

• Functio Laesa – Loss of function (decreased cell functioning)

inflammtion

• “-itis”

• nonspecific response

• extend duration of inflamm response

• local or systemic

• acute, subacute chronic

• primary objective = return tissue to original state

CAUSES of INFLAMMATION

• Mechanical trauma

• Microbes

• Chemical agents

• Sun or radiation exposure

• Imbalances in the body

• Allergies

• Arthritis

Acute inflammation

Immediate reaction to the stimulus lasting a few days to a few weeks

Sub-acute inflammation

Intermediate duration (3-4 weeks)

chronic inflammation

Persists for several weeks, months, or years. May begin acutely or so gradually that it may go unnoticed

Exudates

• Increased blood plasma and proteins in injured tissue

• Helps dilute injurious agents

• BUT results in excess fluid in tissues: Edema

Serous exudates

• thin/watery/clear

• Mainly plasma fluids and proteins, a few WBC

Purulent exudates

• contains pus – suppuration (process)

• Contains plasma fluids and proteins, tissue debris, and many WBCs

Sanguineous exudates

• blood - deeper wound - thicker layers of tissue – thicker red blood

• if it continues —> hemorrhagic

hemorrhagic

Sanguineous that continues to flow – bright red – hemorrhage — possible damage to artery or vein

Fluid Dynamics

Axial flow refers to how fluid flows through a pipe

Emigration* (inflammation)

WBCs escape from blood vessels through gaps in endothelial cells

Diapedesis* (inflammation)

• WBC that is under firm adhesion at the wall, starts to physically make its way through a blood vessel/capillary walls into tissues

• LEAVING THE CAPILLARY WALLS INTO TISSUES

Chemotaxis (inflammation)

Directed movement of WBCs toward the site of injury – TRAVELING TO INJURY SITE (margination and pavementing)

Phagocytosis (inflammation)

• WBCs ingest and then digest foreign substances

• May include pathogenic organisms and tissue debris

explain Diapedesis

• axial flow

• WBCs out of the circulatory system (through capillary walls) and into the tissues, towards the site of tissue damage or infection

• WBC physically making way thru blood vessel wall:

  • Margination - WBC move to the periphery

  • Pavementation - WBC line the wall

  • Emigration - WBC go through the wall and into the tissue thru gaps in endothelial cells

injury to tissue releases

histamine from mast cells

inflammatory response

• injury to tissue — histamine released

• vasoconstriction

• vasodilation —> hyperemia —> erythema and heat

• increased blood viscosity and decreased blood flow

• Increase in permeability by histamines and prostaglandins

• Margination and pavementing of WBCs and proteins —> chemotaxis

• WBC eneter tissue —> emigration —> exudate and edema

• WBC ingest foreign material (phagocytosis)

Systemic Clinical Signs of Inflammation

• Fever

• Leukocytosis

• Elevated C-reactive protein

• Lymphadenopathy

Leukocytosis

• WBC # increases to 10,000 - 30,000/ mm³ of blood

• Body’s attempt to provide more cells for phagocytosis

normal WBC count per mm³ of blood

4,000 to 10,000 mm³

The ___ of WBC that is increasing in number can aid in differential diagnosis

type

Viral infection leads to increase in

lymphocytes

Bacterial infection lead to increase in

neutrophils

Allergic reaction leads to increase in

eosinophils

Lymphadenopathy

• Enlarged and palpable superficial lymph nodes

• occurs because of changes in lymphocytes

Elevated Levels of C-Reactive Protein

• Produced in liver

• Levels used to help assess rheumatoid arthritis and systemic lupus erythematosus

• Used to monitor tissue healing

• Used as early infection detection system

• Chronically increased level associated with an increased risk for cardiovascular disease

• Possible marker for periodontal disease