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- Unmyelinated fibers - Existing, chemical

- Paleospinothalamic Stress response:
tract  Long-term, Disabling, Fatigue, Depression, Irritability
Emotion: Loss of hope, anger

Pain – Chapter 13 (continued)

Two main classes of pain medication act at different locations:

Non-steroidal Inflammatory Drugs (NSAIDs)  Act at the peripheral level

Opioids  Act at the central nervous system (CNS) level

Causes  Pain may be felt d/t inflammation, infection, ischemia, tissue necrosis, stretching of tissue,
chemicals or burns.
 Skeletal muscle  Pain may result from ischemia or hemorrhage

Somatic Pain  May arise from the skin (cutaneous) or deeper structures – such as bones or muscles –
 Conducted my sensory nerves
Visceral Pain  Originates from the organs
 Travels by sympathetic fibres.

*Transmission of pain senses

 The peripheral nerves transmit the afferent pain impulses to the Dorsal root ganglia  then
into the spinal cord  through the dorsal horn or substantia gelantinosa

Inflammation & Healing – Chapter 2

Inflammation  The body’s nonspecific response to tissue injury resulting in:
 redness
 warmth
 edema
 pain
 *loss of function

General signs and symptoms serve as a warning

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 Inflammation is not the same as infection – although, infection is one of the causes of
inflammation.

With infection  microorganisms such as: Bacteria, viruses, and fungi – are always present at the site –
causing inflammation,
 When inflammation is caused by an allergy or a burn  no microbes are present

Normal:
1) Blood flow  Normal fluid shift  protein remains in blood & water electrolytes, glucose
into interstitial fluid  Cells remain in blood
Inflammation:
1) Injury  Cells release chemical mediators  Vasodilation – increases blood flow  Increased
capillary permeability  Leukocytes move to the site of injury  Macrophages - Phagocytosis
– removal of debris in preparation for healing

Acute Inflammation
Pathophysiology

Inflammation may develop immediately and last only a short period of time  may have a delayed
onset. (e.g. sunburn)  or it may be more severe and ongoing
 The severity is based on the cause and the amount of exposure

Chemical Source Major Action

Histamine Mast cell granules Immediate vasodilation and
increased capillary permeability to

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form exudate
Chemotactic factors Mast cell granules Attract neutrophils to the site
Platelet-activating factor (PAF) Cell membranes of platelets Activate neutrophils
Platelet aggregation

Cytokines T-lymphocytes Increase plasma proteins

ESR
Macrophages Induce fever, chemotaxis,
leukocytosis
Leukotrienes Synthesis from arachidonic acid in Later response: Vasodilation &
mast cells increased capillary permeability
chemotaxis
Prostaglandins (PGs) Synthesis from arachidonic acid in Vasodilation and increased capillary
mast cells permeability, pain, fever,
potentiate histamine effect
Kinins (e.g. bradykinin) Activation of plasma protein Vasodilation and increased capillary
(e.g. kinogen) permeability, pain, chemotaxis
Complement System Activation of plasma protein Vasodilation and increased capillary
cascade permeability, chemotaxis, increase
histamine release

Chemical mediators  include: histamine, serotonin, prostaglandins, and leukotrienes into the
interstitial fluid and blood
 These chemicals affect blood vessels and nerves in the damaged area
 Cytokines serve as communicators in the tissue fluids  sending messages to lymphocytes and
macrophages, the immune system, or the hypothalamus  to induce fever
 Local vasodilation: relaxation of smooth muscle  causing an increase in the diameter of
arterioles  which causes hyperemia (increased blood flow in the area)
 Capillary permeability also increases  allowing plasma proteins to move into the interstitial
space along with more fluid
- The increased fluid dilutes any toxic material at the site  while globulins serve as antibodies
- Fibrinogen attempts to localize the site by providing a fibrin mesh

Function of Cellular Elements in the Inflammatory Response

Leukocytes Activity
1) Neutrophils Phagocytosis of microorganisms
2) Basophils Release of histamine leading to inflammation
3) Eosinophils Numbers are increased in allergic responses

Lymphocytes Activity
1) T-Lymphocytes Active in cell-mediated immune response
2) B-Lymphocytes Produces antibodies
3) Monocytes Phagocytosis
4) Macrophages Active in phagocytosis. These are mature
monocytes that have migrated into tissues from
the blood

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Cardinal Signs of Inflammation Causes/Effects

Redness and warmth Increased blood flow to the area (hyperemia)
Swelling (edema) Shift of protein and fluid into the interstitial
space
Pain Increased pressure from fluids exerted onto the
nerve endings (e.g. bradykinins)
*Loss of function Lack of nutrition or swelling interferes
mechanically with function – restricts joint
movement

Exudate  refers to a collection of interstitial fluid formed in the inflamed area

Type of exudate Description Example
Serous Watery – consist primarily of fluid with small Allergic reactions and burns
amounts of proteins and WBCs
Fibrinous Thick and sticky – have a high cell and fibrin Class Notes:
content
- Increases the risk of scar tissue in the area
Purulent Thick, yellow-greenish in color Indicates bacterial infection
Contains more leukocytes, cell debris, and
microorganisms
Referred to “pus”
Abscess Localized pocket of purulent exudate or pus in Around the tooth or the brain
solid tissue

Hemorrhagic Present in damaged blood

vessels

Systemic Effects of Inflammation Class Notes

Mild fever (pyrexia)
Malaise (feeling unwell)
Fatigue
Headache
Anorexia (Loss of appetite)
Leukocytosis

Inflammation & Healing – Chapter 2 (continued)

Changes in the blood with Inflammation Description
Leukocytosis Increased numbers of WBCs  especially,
neutrophils
Differential count Proportion of each type of WBC altered 
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depending on the cause

Plasma proteins Increased fibrinogen and prothrombin
C-reactive protein A protein not normally in the blood  appears w/
acute inflammation and necrosis within 24-48hrs
Increased Erythrocyte Sedimentation Rate (ESR) Elevated plasma proteins  increase the rate at
which RBCs settle in a sample
Cell enzymes Released from necrotic cells and enter tissue fluids
and blood  may indicate site of inflammation

A granuloma  a small mass of cells with a necrotic center and covered by connective tissue  may
develop around a foreign object (e.g. splinter)  or part of the immune response in some infections
such as tuberculosis

Healing
Types of Healing Description Example/Class Notes
Resolution The process that occurs when there is After a mild burn
minimal tissue damage.
The damaged cells recover, the tissues
return to normal within a short period of
time
Regeneration Healing process that occurs in damaged Some type of cells – epithelial –
tissue in which the cells are capable of are constantly replicating
mitosis
Replacement Replaced by connective tissue (scar or Brain tissue or myocardium
fibrous tissue formation)
Takes place when there is extensive tissue
damage or the cells are incapable of mitosis
*Healing by first intention Refers to the process involved when the This type of healing is seen in
wound is clean, free of foreign material and some surgical incisions
necrotic tissue, and the edges of it are held
close together  creating a minimal gap
between the edges
*Healing by second intention Refers to a situation in which there is a A compound fracture would
large break in the tissue and consequently heal in this manner
more inflammation  a longer healing
process and formation of more scar tissue

Inflammation & Healing – Chapter 2 (continued)

The Healing Process
The process of tissue repair  begins following injury when a blood clot forms and seals the area
- After 3 to 4 days  foreign material and cell debris have been removed by phagocytes,
monocytes, and macrophages
- Granulation tissue grows into the gap from nearby connective tissue  granulation tissue is
highly vascular and appears moist and pink or red in color  it contains many new capillary
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buds from the surrounding tissue  very fragile and is easily broken down by microorganisms or
stress on the tissue
- Wound cavity is being filled in, nearby epithelial cells undergo mitosis, extending across the
wound from the outside edges inward
- Collagen  a protein that is the basic component of scar tissue and provides strength for the
new repair

Factors Affecting Healing

A small gap in the tissue results in complete healing within a short period of time with minimal scar
tissue formation
- A large or deep area of tissue damage requires a prolonged healing time  results in a larger
scar
Complications of healing by scar formation
Loss of function
Loss of function results from the loss of normal cells and the lack of specialized structures or normal
organization in scar tissue
- For example  if scar tissue replaces normal skin, that area will lack hair follicles, glands, and
sensory nerve endings.
Contractures or Obstructions
Scar tissue is nonelastic and tends to shrink over time
Fixation and deformity of the joint  a conditional referred to as contracture

Adhesions
Bands of scar tissue joining two surfaces that are normally separated

Hypertrophic Scar Tissue

Overgrowth of fibrous tissue  consisting of excessive collage deposits may develop  leading to hard
ridges of scar tissue or keloid formation

Ulceration
Blood supply may be impaired around the scar  resulting in further tissue breakdown and ulceration

Types of microorganisms
Bacteria
Bacteria are unicellular (single cell) organisms that do not require living tissue to survive

The major groups of bacteria are:

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