Pathopart6

Copyright © 2017, 2013, 2009 Pearson
Education, Inc. All Rights Reserved.
Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Paramedic Care: Principles & Practice
Volume 1, 5e
Pathophysiology
Part 6

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Part 6
The Body's Defenses Against Disease and Injury

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
Against Disease and Injury
• Self-Defense Mechanisms
– Infectious Agents
 Bacteria
 Viruses
 Fungi
 Parasites
 Prions

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Infectious Agents
– Bacteria
 Single-cell organisms.
 Can reproduce independently; need host to supply food and
other support.
 Can be cultured and identified in hospital laboratories.
 Categorized according to appearance; after staining with dyes
(Gram stains).

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Bacteria
 Cause many common infections.
 Antibiotics kill or inhibit growth of bacteria.
 Many bacteria release poisonous chemicals (toxins).
 Exotoxins: proteins secreted and released by bacterial cell
during growth.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Bacteria
 Endotoxins: trigger inflammatory process and produce fever.
 Septicemia (sepsis): systemic spread of toxins through
bloodstream.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Viruses
 Cause most infections.
 Much smaller than bacteria; only seen with electron
microscope.
 Cannot grow without assistance of another organism.
 Incapable of metabolism.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Viruses
 If does not find host cell, virus will die.
 Do not produce toxins.
 Very difficult to treat.
 Cannot be treated with more than symptomatic care.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Fungi (yeasts and molds): more like plants than
animals.
 Rarely cause human disease other than minor skin infections.
 Mycoses: fungus infections.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Parasites
 Protozoa to large intestinal worms.
 Treatment depends on organism and location.
– Prions
 Differ from viruses.
 Smaller; made entirely of proteins; do not have protective
capsids.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Three Lines of Defense
– Anatomic barriers
– Inflammatory response
– Immune response

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-14 Three Lines of Defense against Infection and Injury
External Internal Nonspecific Specific
Anatomic barriers External Nonspecific
Inflammatory
response
Internal Nonspecific
Immune response Internal Specific

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-15 Characteristics of the Inflammatory and Immune Responses
Inflammatory
Response
Immune Response
Speed Fast Slow
Specificity Nonspecific Specific
Duration (memory) Transient (no memory) Long-term (memory)
Involving which
plasma systems
Multiple plasma protein
(complement, coagulation,
kinin systems)
One plasma protein
(immunoglobulin)
Involving which cell
type
Multiple cell types
(granulocytes,monocytes,
macrophages)
One blood cell type
(lymphocytes)

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• The Immune Response
– Detects antigens as foreign.
– Produces antibodies that combine with antigens to
control or destroy them.
– Immunity: long-term protection against specific foreign
substances.
– Natural immunity: not generated by immune response.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Natural immunity: inborn; part of genetic makeup of
individual or species.
– Acquired immunity: develops as outcome of immune
response.
– Active acquired immunity: generated by host's immune
system after exposure to antigen; long-lasting.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Passive acquired immunity: transferred to person from
outside source; temporary.
– Immunoglobulins: antibodies.
– Primary immune response (initial): first exposure to
antigen.
– Secondary immune response (anamnestic): second
exposure.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Lymphocytes responsible for recognizing foreign
antigens, producing antibodies, developing memory.
– B lymphocytes: do not attack antigens directly.
– Humoral immunity: long-term immunity to specific
antigens.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– T lymphocytes: do not produce antibodies.
– Cell-mediated immunity: recognize presence of foreign
antigen; attack it directly.
– Lymphocytes: circulated through body as part of
lymphatic system.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Induction of the Immune Response
– Immunogens: antigens that trigger immune response.
– Not every antigen is immunogen.
 Sufficient foreignness
 Sufficient size
 Sufficient complexity
 Presence in sufficient amounts

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– HLA antigens: body recognizes as self or foreign.
– Major histocompatibility complex (MHC): chromosome
6.
– Determines suitability (compatibility) of tissues and
organs grafted or transplanted from donor.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Rh factor: Rh antigen D.
– Incompatibility between Rh positive and Rh negative
blood can cause harmful immune responses.
– ABO blood groups: two types of antigens may be
present on surface of red blood cells; A and B.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Blood type A carries only A antigens.
– Blood type B carries only B antigens.
– Blood type AB carries both; universal recipient.
– Blood type O carries neither; universal donor.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-16 Blood Groups—ABO System
Blood Type
Antigen Present
on Erythrocyte
Antibody Present
in Serum
O None Anti-A, Anti-B
AB A and B None
B B Anti-A
A A Anti-B

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-17 Compatibility among ABO Blood Groups
Reaction with Serum of Recipient
Cells of Donor AB B A O
O  + + +
AB   + +
B  +  +
A    

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Humoral Immune Response
– Lymphocytes generated from stem cells in bone
marrow.
– T lymphocytes: cell-mediated immunity.
– B lymphocytes: humoral immunity.
– Specialization of B cells: processes of clonal diversity
and clonal selection.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Mature B cells produce memory cells.
– All antibodies are immunoglobulins.
– Structure of immunoglobulin molecules: Y-shaped
chains.
– Antibody: direct or indirect effect on target antigen;
inactivation or destruction of antigen.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Direct Effects of Antibodies on Antigens
 Agglutination
 Precipitation
 Neutralization
– Indirect Effects of Antibodies on Antigens
 Enhancement of phagocytosis
 Activation of plasma proteins

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Antibodies serve four main functions:
 Neutralization of bacterial toxins.
 Neutralization of viruses.
 Opsonization of bacteria.
 Activation of inflammatory processes.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Classes of Immunoglobulins
 IgM: largest immunoglobulin.
 IgG: "memory"; recognizes repeated invasions of antigen.
 IgA: present in mucous membranes.
 IgE: least-concentrated immunoglobulin.
 IgD: very low concentrations.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Antigenic Determinants
 Isotypic antigens: species-specific.
 Allotypic antigens: can differ between members of same
species.
 Idiotypic antigenic: can differ within same individual.
– Monoclonal antibody: produced in laboratory; pure and
specific to single antigen.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Secretory immune system (external or mucosal
immune system): lymphoid tissues beneath mucosal
endothelium.
 Protect body from pathogens inhaled or ingested.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Cell-Mediated Immune Response
– T cells do not produce antibodies.
– Attack pathogens directly and create temporary
immunity.
– Travel through thymus gland.
– T cells become specialized: clonal diversity and clonal
selection.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Cell-Mediated Immune Response
– Mature T Cells
 Memory cells: secondary immune responses.
 Td cells: transfer delayed hypersensitivity.
 Tc cells: cytotoxic.
 Th cells: helper cells.
 Ts cells: suppressor cells.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Cellular Interactions in Immune Response
– Immune and inflammatory responses are interacting,
not separate.
– Antigen-presenting cells (macrophages) interact with
Th (helper) cells.
– Th (helper) cells interact with B cells.
– Th (helper) cells interact with Tc (cytotoxic) cells.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Cytokines: proteins produced by white blood cells;
"messengers" of immune response.
– Monokine: cytokine released by macrophage.
– Lymphokine: cytokine released by a lymphocyte (T cell
or B cell).

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Sequence of processes necessary before immune
response can begin:
 Antigen processing (by macrophages)
 Antigen presentation (by macrophages)
 Antigen recognition (by T cells or B cells)

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Antigen processing: ingestion of invading organism;
breakdown of its antigens.
– Antigen-presenting cells (APCs).
 T cell receptor (TCR): antigen-specific.
 CD4 or CD8 receptors: respond no matter what antigen
presented.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– T cells and B cells not differentiated until antigens in
system react with appropriate receptors on cell
surfaces.
– Ts (suppressor) cells help suppress immune
responses.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Fetal and Neonatal Immune Function
– To protect child in utero and during first months after
birth, maternal antibodies cross placenta into fetal
circulation.
– As immune system matures, levels of immunoglobulin
begin to rise.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Aging and the Immune Response
– As human body ages, immune function begins to
deteriorate.
– Primary assault on T cell function.
– Men and women over age 60 have decreased
hypersensitivity responses; decreased T cell response
to infections.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Inflammation
– Body's response to cellular injury.
– Immune response develops slowly; inflammation
develops swiftly.
– Immune response specific; inflammation nonspecific.
– Immune response long-lasting; inflammation
temporary.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Inflammation
– Immune response: one type of white blood cell
(lymphocytes); inflammation: platelets and white blood
cells.
– Immune response: one type of plasma protein
(antibodies); inflammation: several plasma protein
systems.
– Immune response and inflammation interdependent.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Inflammation
– Inflammation and immune response both considered
part of immune system.
– Phases of inflammation:
 Phase 1: Acute inflammation
 Phase 2: Chronic inflammation
 Phase 3: Granuloma formation
 Phase 4: Healing

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Inflammation
– Four Functions of Inflammation
 Destroy and remove unwanted substances
 Wall off infected and inflamed area
 Stimulate immune response
 Promote healing

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Inflammation
– Acute inflammation: triggered by any injury
(lethal/nonlethal) to body's cells.
– Blood vessels contract and dilate.
– Vascular permeability increases.
– White cells and plasma proteins destroy invader and
heal injury site.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Inflammation
– Mast cells activate inflammatory response through
degranulation and synthesis.
– Degranulation: mast cells empty granules from their
interior into extracellular environment.
 Physical injury, chemical agents, immunologic and direct
processes.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Figure 12-99 The inflammatory response.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Inflammation
– Histamine: vasoactive amine (organic compound)
released during degranulation of mast cells.
– Chemotactic factors: chemicals that attract white cells
to site of inflammation.
– Chemotaxis: attraction of white cells.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Figure 12-101 Mast cell degranulation and synthesis.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Inflammation
– When stimulated, mast cells synthesize: leukotrienes
and prostaglandins.
– Leukotrienes: slow-reacting substances of anaphylaxis
(SRS-A); actions similar to histamines.
– Prostaglandins: increased vasodilation, vascular
permeability, chemotaxis; cause pain.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Plasma Protein Systems
– Plasma proteins: proteins present in blood.
– Immunoglobulins (antibodies): key factors in immune
response.
– Plasma protein systems critical to inflammation:
complement system, coagulation system, kinin system.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Cascade: first action stimulated; that action causes
next action, which causes next action until final action
completed.
– Complement proteins lie inactive in blood until
activated.
– Take part in almost all events of inflammatory
response.
– Classic and alternative pathways.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Classic pathway: activated by formation of antigen-
antibody complex during immune response.
– Alternative pathway: begins without development of
antigen-antibody complex.
 Much faster than classic pathway; acts as part of first line of
inflammatory defense.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Coagulation system (clotting): forms network at site of
inflammation.
 Composed of protein called fibrin.
 Fibrinous network stops spread of infectious agents and
products of inflammation.
 Forms clot that stops bleeding.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Extrinsic pathway of coagulation: injury to vascular wall
or surrounding tissues.
– Intrinsic pathway of coagulation: exposure to elements
in blood itself.
– Continue toward same end product: fibrin.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Kinin system: chief product, bradykinin.
– Vasodilation, extravascular smooth muscle contraction,
increased permeability, chemotaxis.
– Plasma kinin cascade: triggered by factors associated
with coagulation cascade.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Control of plasma protein systems:
 Inflammatory response essential for protection of body from
unwanted invaders.
– Functioning must be guaranteed.
 Inflammatory processes powerful; potentially very damaging to
body.
– Must be controlled and confined to site of injury or infection.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Most inflammatory processes interact.
– Substance or action that activates one element tends
to activate others.
– Inflammatory processes have to be both reliably
started and stopped.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Cellular Components of Inflammation
– Exudate: collective term for all helpful substances.
– Sequence of events in inflammation
 Vascular response
 Increased permeability
 Exudation of white cells

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Granulocytes: appearance of bag of granules;
polymorphonuclear cells (multiple nuclei).
 Neutrophils, eosinophils, basophils.
– Monocytes: single nucleus; change and mature when
involved in inflammation.
 Become macrophages.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-18 Types of White Blood Cells (Leukocytes)
Lymphocytes (25–30 percent of all white blood cells)*
T cells
B cells
Granulocytes**
Neutrophils (55–70 percent of all white blood cells)
Basophils
Eosinophils
Monocytes**
Monocytes (immature) become macrophages (mature)**

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– All granulocytes and monocytes are phagocytes; blood
cells that ingest other cells and substances.
– Neutrophils: first phagocytes to reach inflamed site.
– Eosinophils: primary defense against parasites.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Basophils: function within blood as mast cells do
outside blood.
 Release histamines and chemicals that control constriction and
dilation of vessels.
– Platelets: act with components of coagulation cascade
to promote blood clotting.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Cellular Products
– Lymphokines: cytokines produced by lymphocytes.
 Stimulate monocytes to develop into macrophages; critical
phase of inflammatory response.
– Monokines: cytokines produced by macrophages and
monocytes.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Cellular Products
– Interleukins (ILs): important group of cytokines.
– Interleukin-1: lymphocyte-stimulating factor.
– Interferon: cytokine critical in body's defense against
viral infection.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Systemic Responses of Acute Inflammation
– Fever, leukocytosis, increase in circulating plasma
proteins.
– Fever: increase in temperature can create environment
inhospitable to invading microorganisms.
– Fever: increases susceptibility of infected person to
effects of endotoxins.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Chronic Inflammatory Responses
– Chronic inflammation: inflammation that lasts longer
than two weeks.
– Caused by foreign object or substance that persists in
wound.
– May accompany persistent bacterial infection.
– Prolonged by presence of chemicals and other irritants.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Chronic Inflammatory Responses
– Large numbers of neutrophils degranulate and die.
– Infiltrate tissues; sometimes forming cavity that
contains dead cells, dead tissue, tissue fluid (pus).
– Granuloma: walls off infection.
– Tissue repair and scar formation final stages of
inflammation.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Local Inflammatory Responses
– Vascular changes and exudation.
– Exudate has three functions:
 To dilute toxins released by bacteria and toxic products of
dying cells
 To bring plasma proteins and leukocytes to site to attack
invaders
 To carry away products of inflammation

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Resolution and Repair
– Resolution: complete restoration of normal structure
and function.
– Regeneration: proliferation of remaining cells.
– If resolution not possible, repair takes place, with
scarring being end result.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Debridement: phagocytosis of dead cells and debris;
dissolution of fibrin cells (scabs).
– Primary intention: minor wounds.
– Secondary intention: extensive wounds.
– Reconstruction: initial wound response, granulation,
epithelialization, contraction.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– First step of healing: sealing off of wound by clot
(scab).
– Repair begins with granulation.
– Epithelial cells move in under scab, separating it from
wound surface.
 Provides protective covering for healing wound.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Six to twelve days after injury, contraction begins as
wound edges begin to move inward.
– Maturation: scar tissue remodeled; blood vessels
disappear, leaving avascular scar; scar tissue becomes
stronger.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Dysfunctional healing: insufficient repair, excessive
repair, new infection.
 Causes: diabetes, hypoxemia, nutritional deficiencies, certain
drugs.
 Positioning, exercises, surgery, drugs can sometimes help to
prevent or correct dysfunctional wound healing.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Age and Mechanisms of Self-Defense
– Newborns and elderly particularly susceptible to
problems of insufficient immune and inflammatory
responses.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Variances in Immunity and Inflammation
– Hypersensitivity: exaggerated and harmful immune
response.
 Allergy: exaggerated immune response to environmental
antigen.
 Autoimmunity: disturbance in body's normal tolerance for self-
antigens.
 Isoimmunity (alloimmunity): immune reaction between
members of same species.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Original insult (exposure to antigen).
– Genetic makeup; determines susceptibility to insult.
– Immunologic process that boosts response beyond
normal bounds.
– Immediate hypersensitivity reactions.
– Delayed hypersensitivity reactions.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Mechanisms of Hypersensitivity Reaction
 Type I: IgE-mediated allergen reactions
 Type II: tissue-specific reactions
 Type III: immune-complex-mediated reactions
 Type IV: cell-mediated reactions

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– H1 receptors on target cells promote inflammation
when contacted by histamine.
– H2 receptors inhibit inflammation when contacted by
histamine.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Clinical Indications of IgE-Mediated Responses
– Skin: flushing, itching, urticaria, edema
– Respiratory system: breathing difficulty, laryngeal
edema, laryngospasm, bronchospasm
– Cardiovascular system: vasodilation and permeability,
increased heart rate, increased blood pressure

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Clinical Indications of IgE-Mediated Responses
– Gastrointestinal system: nausea, vomiting, cramping,
diarrhea
– Nervous system: dizziness, headache, convulsions,
tearing

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Anaphylactic reactions are life threatening.
– Tissue-specific antigens: exist on the cells of only some
body tissues.
– Four mechanisms by which Type II tissue-specific
reactions attack cells.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Type III immune-complex-mediated reactions: antigen-
antibody formed when antibody in blood or suspended
in body secretions meets and binds to specific antigen.
– Systemic and/or localized.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Type IV cell-mediated tissue reactions: activated
directly by T cells; do not involve antibody.
– Lymphokine-producing T cells (Td cells); cytotoxic T
cells (Tc cells).

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Hypersensitivity/Targeted Antigen
 Allergy/environmental antigens
 Autoimmunity/self-antigens
 Isoimmunity/other person's antigens
– Allergens: antigens that are targets of allergic reaction.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Autoimmunity: breakdown in body's tolerance for self-
antigens; immune system attacks body's own cells.
– Isoimmunity: one member of species has immune
reaction to cells from another member of the same
species.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Autoimmune and Isoimmune Diseases
– Graves' disease
– Rheumatoid arthritis
– Myasthenia gravis
– Immune thrombocytopenic purpura (ITP)
– Isoimmune neutropenia
– Systemic lupus erythematosus (SLE); lupus
– Rh and ABO isoimmunization

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Deficiencies: Immunity and Inflammation
– Congenital (primary) immune deficiency develops if
development of lymphocytes in fetus or embryo is
impaired or halted.
– Acquired (secondary) immune deficiencies develop
after birth; do not result from genetic factors.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Nutritional deficiencies
– Iatrogenic deficiencies
– Deficiencies caused by trauma
– Deficiencies caused by stress
– Acquired immunodeficiency syndrome (AIDS)
– Human immunodeficiency virus (HIV)

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Replacement Therapies
 Gamma globulin therapy
 Transplantation and transfusion
 Gene therapy

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Stress and Disease
– Stress: state of physical and/or psychological arousal
to a stimulus.
– Stressor: stimulus/cause.
– General adaptation syndrome (GAS)
 Stage I: Alarm
 Stage II: Resistance, or adaptation
 Stage III: Exhaustion

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Physiologic stress: chemical or physical disturbance in
cells or tissue fluid produced by a change; requires
response to counteract disturbance.
 Stressor that initiates disturbance.
 Chemical or physical disturbance stressor produces.
 Body's counteracting response.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– No direct correlation between stressor and response.
– Total body response to different stressors must be
specific.
– Homeostasis: dynamic steady state.
– Turnover: continual synthesis and breakdown of all
body substances.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Stress Responses
– Stress response: initiated by a stressor.
– Hormones released in response to stress
 Catecholamines (norepinephrine and epinephrine)
 Cortisol
 Beta endorphins
 Growth hormone
 Prolactin

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Figure 12-104 The stress response: effects on the sympathetic nervous, endocrine, and immune
systems.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Effects of catecholamines prepare body for "fight-or-
flight" in response to stressor.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-19 Physiologic Effects of Catecholamines (1 of 2)
Organ Effects
Brain Increased blood flow
Increased glucose metabolism
Cardiovascular system Increased contractile force and rate
Peripheral vasoconstriction
Pulmonary system Increased ventilation
Bronchodilation
Increased oxygen supply
Liver Increased glucose production
Increased gluconeogenesis
Increased glycogenolysis
Decreased glycogen synthesis
Gastrointestinal and
genitourinary tracts
Decreased protein synthesis
Muscle Increased glycogenolysis
Increased contraction
Increased dilation of skeletal muscle vasculature

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-19 (continued) Physiologic Effects of Catecholamines (2 of 2)
Organ Effects
Skeleton Decreased glucose uptake and utilization
(insulin release decreased)
Adipose (fatty) tissue Increased lipolysis
Increased fatty acids and glycerol
Skin Decreased blood flow
Lymphoid tissue Increased protein breakdown (shrinkage of
lymphoid tissue)

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-20 Physiologic Effects of Cortisol (1 of 2)
Function Effects
Carbohydrate metabolism Diminished peripheral uptake/use of glucose;
promotes gluconeogenesis; elevates blood glucose
levels
Protein metabolism Increases protein synthesis in liver; depresses
protein synthesis in other tissues; depresses
immunoglobulin production
Inflammatory effects Decreases blood levels of lymphocytes,
macrophages, eosinophils; decreases leukocytes at
inflammation site; delays healing/promotes wound
infection
Lipid metabolism Increases lipolysis in extremities, lipogenesis in
face and trunk
Immune reserves Decreases lymphoid tissue mass; decreases
circulation white cells; inhibits production of
interleukin-1 and interleukin-2; blocks cell-mediated
immunity and generation of fever

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-20 (continued) Physiologic Effects of Cortisol (2 of 2)
Function Effects
Digestive function Promotes gastric secretions; at high levels,
causes ulceration
Urinary function Enhances production of urine
Connective tissue
function
Decreases proliferation of fibroblasts (delays
healing)
Muscle function Maintains normal contractility and work output
for skeletal and cardiac muscle
Bone function Decreases bone formation
Cardiovascular function Maintains normal blood pressure; assists
arteriole constriction; supports myocardial
function
Central nervous system
function
Modulates perceptual/emotional functioning
and daytime arousal

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
– Complex interaction among nervous, endocrine, and
immune systems.

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-21 Stress- and Immune-Related Diseases and Conditions (1 of 2)
Target Organ Diseases and Conditions
Cardiovascular system Coronary artery disease
Hypertension
Stroke
Arrhythmias
Muscles Tension headaches
Muscle-related backaches
Connective tissues Rheumatoid arthritis
Pulmonary system Asthma
Hay fever
Immune system Immunosuppression or immune deficiency
Gastrointestinal system Ulcer
Irritable bowel syndrome
Ulcerative colitis

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
Table 12-21 (continued) Stress- and Immune-Related Diseases and Conditions (2 of 2)
Target Organ Diseases and Conditions
Genitourinary system Diuresis
Impotence
Skin Eczema
Acne
Endocrine system Diabetes mellitus
Central nervous system Fatigue
Depression
Insomnia

Bryan E. Bledsoe
Richard A. Cherry
Robert S. Porter
The Body's Defenses
• Stress, Coping, and Illness Interrelationships
– Physiologic stress: caused by events that directly affect
body.
– Psychological stress: unpleasant emotions caused by
life events.
– Those who cope positively with stress have reduced
chance of becoming ill; those who don't have greater
chance of becoming ill.

Pathopart6

Recommended

Recommended

More Related Content

Viewers also liked

Viewers also liked (19)

Similar to Pathopart6

Similar to Pathopart6 (20)

More from djorgenmorris

More from djorgenmorris (20)

Recently uploaded

Recently uploaded (20)

Pathopart6

Editor's Notes