 Using examples, explain five ways in which our bodies are
physiologically protected from injury (defense mechanisms).
1. Physical barriers- skin, mucous membrane, hair.
2. Chemical barriers- mucous secreted by mucous membranes, saliva, gastric juice
in stomach, tears, urine, sweat.
3. Inflammation.
4. Fever.
5. Immune system.
 Define and contrast inflammation and infection.
An infection is the invasion of an organism's body tissues by disease-causing
agents, their multiplication, and the reaction of host tissues to the infectious agents
and the toxins they produce. Inflammation is a response of vascularized tissues to
infections and tissue damage that brings cells and molecules of host defense from
the circulation to the sites where they are needed, to eliminate the offending agents.
 Define and contrast exudation and transudation.
The escape of fluid, proteins, and blood cells from the vascular system into
interstitial tissues or body cavities is known as exudation. The process of passing
through membrane pore or interstice known as transudation.
 List and explain the mechanism of production of the cardinal signs of
inflammation.
Heat (calor): Vasodilation leads to increase blood flow, more blood arrives, blood
is warm.
Redness(rubor): Vasodilation leads to increase blood flow, more blood arrives,
blood is red.
Swelling(tumor): increase vascular permeability lead to leakage of fluid, proteins
and blood cells from vascular system to interstitial tissues lead to edema or
swelling.
Pain(dolor): direct damage to the nerve fibers, pressure of swelling on nerve
endings, chemical irritants: histamine, bradykinin and prostaglandin.
Loss of function (function laesa): increased pain and swelling.
 Using an example, explain the series of steps that take place in the
capillary bed during an acute inflammatory process.
1- Alterations in vessel caliber resulting in increased blood flow (vasodilation)
and changes in the vessel wall that permit plasma proteins to leave the
circulation (increased vascular permeability).
2- The microvasculature becomes more permeable, and protein-rich fluid
moves into the extravascular tissues. This causes the red cells in the flowing
blood to become more concentrated, thereby increasing blood viscosity and
slowing the circulation. These changes are reflected microscopically by
numerous dilated small vessels packed with red blood cells, called stasis.
3- In addition, endothelial cells are activated, resulting in increased adhesion of
leukocytes and migration of the leukocytes through the vessel wall.
 Using an example define normal and abnormal permeability at the
microcirculation during inflammation.
According to timing and severity:
Immediate transient vascular permeability 15-30 minutes>normal
Abnormal- such as a Burn- prolonged leakage and tissue damage, delayed
prolonged leakage-2-12 or more hours, like a burn or radiation or bacterial toxin
Severity- Endothelial damage also abnormal-high thermal injuries
 List and contrast the three common patterns of increased vascular
permeability.
1. Retraction of endothelial cells resulting in opening of inter-endothelial spaces is
the most common mechanism of vascular leakage. (Induced by histamine, other
mediators. Rapid and short-lived (minutes).
2. Endothelial injury, resulting in endothelial cell necrosis and detachment. Caused
by burns, some microbial toxins. Rapid; may be long-lived (hours to days).
3. Lysis of the basement membrane by collagenase released from injured
endothelial cells.
 Describe the cellular events of inflammation.
1. Margination and rolling. 2. Adhesion.
3. Diapedesis(transmigration). 4. Chemotaxis. 5. Phagocytosis.
 Define chemotaxis and list four common chemotactic factors.
After exiting the circulation, leukocytes move in the tissues toward the site of
injury by a process called chemotaxis, which is defined as locomotion along a
chemical gradient.
Chemotactic factors:
1234-
IL-8.
C5a.
Leukotriene B4.
Platelet activating factor.
 Using an example, describe the steps involved in phagocytosis. Defining
what is opsonization. (biochemical formulas are not required).
Phagocytosis consists of three steps:
(1) recognition and attachment of the particle to the ingesting leukocyte;
(2) engulfment, with subsequent formation of a phagocytic vacuole;
(3) killing and degradation of the ingested material.
Some of these receptors recognize components of the microbes and dead cells
and other receptors recognize host proteins, called opsonins, that coat microbes
and target them for phagocytosis (the process called opsonization). Coating of
bacteria with antibodies or the complement protein C3b (opsonization) elicits
phagocytosis of bacteria by macrophages.
 List and explain the three possible mechanisms of release of leukocyte
products during phagocytosis and inflammation.
 Reactive oxygen species- oxidative burst
 Nitric oxide
 Lysosomal products
 Enzymes
 Formation of neutrophil extracellular traps
 Define chemical mediation in inflammation. Explain the mechanisms
of action and effects of: vasoactive amines, and plasma proteases
(biochemical formulas are not required).
The two vasoactive amines, histamine and serotonin, are stored as preformed
molecules in mast cells and other cells and are among the first mediators to be
released in acute inflammatory reactions. In humans, histamine causes arteriolar
dilation and rapidly increases vascular permeability by inducing venular
endothelial contraction and formation of inter-endothelial gaps. Soon after its
release, histamine is inactivated by histaminase. Serotonin induces
vasoconstriction during clotting. It is produced mainly in some neurons and
enterochromaffin cells, and is a neurotransmitter and regulates intestinal
motility.
 Define arachidonic acid metabolites. Give examples describing some of
their actions.
Conversion of arachidonic acid into prostaglandins by the enzyme
cyclooxygenase-2 (COX-2).
 PGI2, a vasodilator and a potent inhibitor of platelet aggregation
 PGE2 augments pain sensitivity to a variety of other stimuli and interacts
with cytokines to cause fever.
Conversion of arachidonic acid to leukotrienes by lipoxygenase.


1.
2.
3.
4.
Increased vascular permeability Leukotrienes C4, D4, E4
Classify inflammatory exudates. Give examples.
Serous- ↓protein ↑fluid →skin bruises
Fibrinous→ fibrinous pericardis
Catarrhal- mucus →common cold
Suppurative (Purulent)- pus →skin boils (dead neutrophils, organisms,
necrotizing cells)
5. Hemorrhagic
 Define cytokines. Give examples including their effects.
TNF and IL-1 stimulate the expression of adhesion molecules on endothelial cells,
resulting in increased leukocyte binding and recruitment, and enhance the
production of additional cytokines (notably chemokines) and eicosanoids.
 Mention in details the possible outcomes of acute inflammation.
1. Complete resolution:




Neutralize chemicals- elimination of offending agent
Mediators disappear- normalization of permeability
Apoptosis of neutrophils
Lymphatic draining
[Healing – labile cells regenerate all the time while stable cells regenerate when
needed]
2. Abscess: (if not drained)
Sinus fistula – chronic abscess
Lymphangitis- vessles, lymphadenitis- lymph nodes
Toxemia, septicemia, bacteremia
Septic thrombophlebitis
Septic emboli
3. Healing by scaring:
Need ↓blood/ function less cell
4. Spread
5. Chronic inflammation
 Define: abscess, empyema and two other special forms of inflammation.
Abscesses are focal collections of pus that may be caused by seeding of pyogenic
organisms into a tissue or by secondary infections of necrotic foci.
Empyema; suppurative material may accumulate in the pleural cavity.
 Describe different morphological patterns of acute inflammation.
1- Serous inflammation- characterized by the outpouring of a watery,
relatively protein-poor fluid that, depending on the site of injury, derives
either from the plasma or from the secretions of mesothelial cells lining the
peritoneal, pleural, and pericardial cavities. Example: the skin blister
resulting from a burn or viral infection.
2- Fibrinous inflammation- occurs as a consequence of more severe injuries,
resulting in greater vascular permeability that allows large molecules (such
as fibrinogen) to pass the endothelial barrier.
3- Suppurative (purulent) inflammation and abscess formation. These
are manifested by the collection of large amounts of purulent exudate (pus)
consisting of neutrophils, necrotic cells, and edema fluid. Abscesses are
focal collections of pus that may be caused by seeding of pyogenic
organisms into a tissue or by secondary infections of necrotic foci.
 Certain organisms (e.g., staphylococci) are more likely to induce such
localized suppuration and are therefore referred to as pyogenic (pusforming).
4- An ulcer is a local defect, or excavation, of the surface of an organ or tissue
that is produced by necrosis of cells and sloughing (shedding) of necrotic
and inflammatory tissue
 Define and contrast: bacteremia, septicemia, toxemia.
Bacteremia: Presence of bacteria in blood stream.
Septicemia: blood poisoning by bacteria.
Toxemia: Presence of toxic substance in the blood.
 List three common possible defects in leukocyte function that may affect
the Inflammatory response (use examples).
Defect in adhesion (Leukocyte Adhesion Deficiency)
Chronic granulomatous disease (defective in phagocytosis)
Chediac Higashi syndrome (problem in trafficking inside the cells)
MPO deficiency which will effect the inflammatory response
 Describe the role of lymphatics in inflammation.
Lymphatics drain the small amount of extravascular fluid that seeps out of
capillaries under normal circumstances. In inflammation, lymph flow is
increased to help drain edema fluid that accumulates because of increased
vascular permeability. In addition to fluid, leukocytes and cell debris, as well as
microbes, may find their way into lymph. Lymphatic vessels, like blood
vessels, proliferate during inflammatory reactions to handle the increased load.

123-
List three systemic effects of inflammation.
Increased blood pressure
Fever
Sepsis