Pathophysiology chapter 9

National EMS Education
Standard Competencies
Pathophysiology
Integrates comprehensive knowledge of
pathophysiology of major human systems.

Introduction
• The human body is made up of cells,
tissues, and organs.
− Biology: Study of living organisms
− Pathophysiology: Study of organism in the
presence of disease
• To understand disease processes, you must
understand the ways disease alters the structure
and function in cells.

Adaptations in
Cells and Tissues
• When exposed to adverse conditions, cells
undergo a process to protect themselves.
− Atrophy: Decrease in cell size
− Hypertrophy: Increase in cell size
− Hyperplasia: Increase in cell number
− Dysplasia: Alteration in cell size, shape, and
organization
− Metaplasia: Cell type is replaced by another

Disturbances in Fluid Balance
• Human body is composed primarily of water
− All biochemical reactions occur in an
aqueous environment.
− Homeostasis can be upset by excessive
output or input of fluids.
• Sweating
• Salt intake
• Dehydration

• Degree of fluid imbalance required to
compromise homeostasis and cause illness
depends on the patient’s:
− Size
− Age
− Underlying medical conditions

• Edema
− Excessive amount of fluid in the interstitial
space
− Causes include:
• Increased capillary pressure
• Decreased colloidal osmotic pressure
• Lymphatic vessel obstruction

• Edema (cont’d)
− Assessment should include:
• Auscultation of breath sounds
• Evaluation for pedal/sacral edema and jugular
venous distention
• Electrocardiogram (ECG) and vital sounds
− Treatment may include continuous positive
airway pressure (CPAP), supplemental oxygen,
positional therapy, nitrates, and diuretics

• Isotonic fluid deficit
− Decrease in extracellular fluid with proportionate
losses of sodium and water
• Isotonic fluid excess
− Increase in extracellular fluid with proportionate
increases in both sodium and water

Electrolyte Imbalances
• Sodium
− Normal level: 136 to 144 mEq/L
− Hypertonic fluid deficit: Caused by excess water
loss without proportionate loss of sodium
• Results in hypernatremia
− Hypotonic fluid deficit: Caused by excess
sodium loss with less water loss
• Results in hyponatremia

• Potassium
− Normal level: 3.5 to 5.0 mEq/L
− Hypokalemia: Decreased serum potassium
level
− Hyperkalemia: Elevated serum potassium level
• Calcium
− Normal level: 8.2 to 10.2 mg/dL
− Hypocalcemia: Decreased serum calcium level
− Hypercalcemia: Increased serum calcium level

• Phosphate
− Normal level: 2.3 to 4.7 mg/dL
− Hypophosphatemia: Decreased phosphate level
− Hyperphosphatemia: Increased phosphate level
• Magnesium:
− Normal level: 1.3 to 2.1 mEq/L
− Hypomagnesemia: Decreased magnesium level
− Hypermagnesemia: Increased magnesium level

Disturbances of
Acid-Base Balance
• The lower the pH (concentration of
hydrogen ions [H+]), the higher the acidity
• Acids and bases neutralize each other and
must remain balanced.
− Acidosis: Increase in extracellular H+ ions
− Alkalosis: Decrease in extracellular H+ ions
• Disturbances are associated with potassium
balance.

Types of Acid-Base Imbalance
• Fluctuations in pH due to bicarbonate level:
Metabolic acidosis or alkalosis
• Fluctuations in pH due to respiratory
disorders: Respiratory acidosis or alkalosis
• A disorder not correctable by buffers
initiates compensatory mechanisms.

• Respiratory acidosis
− Related to hypoventilation
• Can quickly develop a potentially fatal acidosis
− Chronic obstructive pulmonary disease (COPD)
creates acidosis over time.
− Compensatory mechanism is the renal buffer
system

• Respiratory alkalosis
− Associated with conditions that result in
hyperventilation
− Carbon dioxide levels drop.
− Renal system retains H+
ions.
• Results in hypocalcemia

• Metabolic acidosis: Any acidosis not related
to the respiratory system
− Causes include:
• Lactic acidosis
• Ketoacidosis
• Aspirin overdose
• Alcohol ingestion
• Gastrointestinal (GI) losses

• Metabolic alkalosis: Occurs with excessive
acid loss
− Causes include:
• Upper gastrointestinal losses of acid
• Drinking large amounts of water during exercise
• Excessive intake of alkaline substances
− Compensatory mechanism: Respiratory system

Cellular Injury
• Manifestations depend on how many and
which types of cells are damaged
• Caused by:
− Hypoxia, ischemia, chemical injury, infectious
injury, immunologic injury, physical damage, and
inflammatory injury

Cellular Injury
From An Introduction to Human Disease, 7th edition. Photo courtesy of Leonard V. Crowley, MD, Century College.

Cellular Injury
• Damage in individual cells often affects the
entire organism.
− Entire organ system may fail.
− Repair may occur with proper treatment.
• Irreversible injury will lead to cell death.
• Cell death is followed by necrosis.

Hypoxic Injury
• May result from:
− Decreased O2 in air
− Loss of hemoglobin function
− Decreased number of red blood cells
− Disease of respiratory or cardiovascular system
− Loss of cytochromes

Hypoxic Injury
• Cells that are hypoxic for more than a few
seconds produce mediators.
− Earliest and most dangerous: Free radicals
− Chemical instability causes attacks on other
cells and membranes.

Chemical Injury
• Common poisons: Cyanide and pesticides
• Lead: Chronic ingestion leads to brain injury
and neurologic dysfunction
• Carbon monoxide: Binds to hemoglobin and
prevents adequate oxygenation of tissues

Chemical Injury
• Ethanol: May result in CNS depression,
hypoventilation, and cardiovascular
collapse
• Pharmacologic agents: Produce toxic
products when metabolized in the body

Infectious Injury
• Occurs as a result of an invasion of
bacteria, fungi, or viruses
• Virulence: Measures disease-causing ability
− Pathogenicity: Function of microorganism’s
ability to reproduce and cause disease

Infectious Injury
• Bacteria
− Possess a capsule
that protects them
from phagocytes
− Categorized
depending on Gram
staining
• Gram-positive
• Gram-negative © Jones & Bartlett Learning

Infectious Injury
• Bacteria (cont’d)
− Produce exotoxins or endotoxins
− White blood cells release endogenous pyrogens
(cause a fever).
− Body’s most common reaction is inflammation

Infectious Injury
• Viruses
− Intracellular parasites
− Consists of nucleic acid core of RNA or DNA
− Capsid: Protects from phagocytosis
− Replication occurs inside host cell.
− Symbiotic relationship may be the cause of an
unapparent infection.

Immunologic and
Inflammatory Injury
• Inflammation: Protective response
− Can be triggered by physical, chemical, or
microbiologic agent

Immunologic and
Inflammatory Injury
©Jones&BartlettLearning.

Immunologic and
Inflammatory Injury
• Local effects: Dilation of blood vessels and
increased vascular permeability
• Systemic effects: Temperature elevation
and increased leukocytes
− Outcome depends on amount of tissue damage.
• Cellular membranes may be injured in
process.

Injurious Genetic Factors
• Genetic factors
include:
− Chromosomal
disorders
− Premature
development of
atherosclerosis
− Obesity
• Abnormal gene may
develop:
− If gene mutates
during meiosis
− By heredity
− Due to other
causes later in life

Injurious Nutritional
Imbalances
• Injurious nutritional imbalances include:
− Obesity
− Malnutrition
− Vitamin or mineral excess or deficit
• Can lead to:
− Alterations in physical growth
− Mental and intellectual retardation
− Death

Injurious Physical Agents
or Conditions
• Physical agents include:
− Heat
− Cold
− Radiation
• Degree of cell injury is determined by:
− Strength of agent
− Length of exposure

Apoptosis
• Normal cell death
• During apoptosis:
− Cells exhibit characteristic nuclear changes and
die in clusters.
− Controlled degradation allows their remnants to
be taken up and reused.

Apoptosis
• Can be prematurely activated by pathologic
factors (cell injury)
− Forms of heart failure
− Death of hepatocytes
− Inhibition of normal function

Abnormal Cell Death
• Necrosis: Result of morphologic changes
following cell death
− Simple: Gross and microscopic tissue and cells
are recognizable.
− Derived: Caseation necrosis, dry gangrene, fat
necrosis, liquefaction necrosis

Hypoperfusion
• Perfusion: Delivery of oxygen and nutrients
and removal of wastes
• Hypoperfusion: Level of perfusion drops
below normal
− Compensatory mechanisms set into motion
• Can be enough to stabilize the patient
(compensated shock)
• Can overwhelm compensatory mechanisms
(decompensated shock)

Hypoperfusion
• Response to hypoperfusion:
− Release of catecholamines
− Activation of renin-angiotensin-aldosterone
system (RAAS)
− Release of antidiuretic hormone
− Fluid shifts from interstitial tissues to vascular
compartment.
• Overall response: Increase preload, stroke
volume, and heart rate

Hypoperfusion
• Persistence results in:
− Continued increase in myocardial stress
• Compensatory mechanisms no longer keep up.
• Myocardial function worsens.
• Tissue perfusion decreases.
• Fluid leaks from vessels, causing systemic and
pulmonary edema.

Types of Shock
• Shock: Associated with inadequate oxygen
and nutrient delivery to cell
− Impairment of cell metabolism and inadequate
perfusion of vital organs
− Cells revert to anaerobic metabolism.
− Glucose impairment leads to elevated blood
glucose levels.

Types of Shock
• Shock can occur due to inadequacy of:
− Central circulation
− Peripheral circulation

Central Shock
• Cardiogenic
shock: Heart
cannot circulate
enough blood
• Obstructive
shock: Blood
flow becomes
blocked
Courtesy of Leonard V. Crowley, MD, Century College.

Peripheral Shock
• Hypovolemic shock: Blood is unable to
deliver adequate oxygen and nutrients
− Exogenous: External bleeding
− Endogenous: Fluid loss contained within the
body

Peripheral Shock
• Distributive shock:
Widespread dilation
of vessels
− Common types:
• Anaphylactic:
Exposure to
allergen
• Septic: Result of
widespread infection
• Neurogenic: Results
from spinal cord
injury
© Jones & Bartlett Learning.

Management of Shock
• Clinical determination requires:
− Evaluation of presence and strength or absence
of peripheral pulses
− Assessment of end-organ perfusion and
function
• Signs of shock include:
− Mottling, pallor, peripheral or central cyanosis,
and delayed capillary refill

Management of Shock
• Measuring end-tidal carbon dioxide (ETCO2)
may also be useful.
− Interpret the effectiveness of perfusion.
− Decreasing levels of ETCO2 are an early
indicator of shock.
− Low levels of ETCO2 combined with other
signs/symptoms are ominous clinical findings.

Multiple Organ Dysfunction
Syndrome (MODS)
• Progressive condition that occurs in some
critically ill patients
− Characterized by concurrent failure of two or
more organs or systems
• Types:
− Primary MODS: Direct result of an insult
− Secondary MODS: Progressive organ
dysfunction

Multiple Organ Dysfunction
Syndrome (MODS)
• Occurs when injury or infection triggers
massive systemic immune, inflammatory,
and coagulation response
− Outcome is maldistribution of systemic and
organ blood flow.
− During 14- to 21-day period, renal and liver
failure can develop.

Body’s Self-Defense
Mechanisms
• Immune system: All structures and
processes associated with body’s defense
− Three lines of defense:
• Anatomic barriers
• Inflammatory response
• Immune response

Anatomic Barriers
• Decrease the chances of bodily invasion by
foreign substances
− Skin
− Hairs in upper respiratory tract and lining of
lower respiratory tract
− Acid in stomach

Immune Response
• Body’s defense reaction to any substance
that is recognized as foreign
− Triggered by foreign bodies and even abnormal
growths in the cells
• Involves only one type of white blood cells
(lymphocytes)

Cellular Interaction
in Immune Response
• Basic pattern:
− Bacteria enters body.
• Not encapsulated: Macrophages ingest them
• Encapsulated: Antibodies coat capsule before
ingestion
− Cell wall activates complement system.
− Membrane attack complex is formed.
− Memory B cells or T cells will be activated.

Immune Response

Immune Response
• Characteristics:
− Natural immunity: Nonspecific cellular and
humoral response (first line of defense)
− Acquired immunity: Highly specific method in
which cells respond to a stimulant
• Passively acquired: Preformed antibodies
(mother to infant)

Immune Response
• Primary response takes place during first
exposure to an antigen.
• Secondary response occurs with repeat
exposure to an antigen.

Immune Response
• Antibody: Binds
to antigen so
the complex
can attach itself
to immune cells
that destroy the
complex

Immune System
• Immunogen: Antigen capable of generating
an immune response against itself
− Hapten: Substance that normally does not
stimulate immune response but can be
combined with an antigen and later initiate an
antibody response

Humoral Immune Response

• B-cell lymphocytes produce antibodies.
− Clonal selection theory: Each B cell makes
antibodies that have only one type of antigen-
binding region.
− For B cells to produce antibodies, they must be
activated.

• Activation often occurs via helper T cells.
− Macrophage engulfs antigen, and discarded
particles interact with B cells and helper T cells.
− Antigen binds to B cell and helper T cell.
− Helper T cell stimulates B cell to produce clone.

Immunoglobins
• Immunoglobins:
Antibodies
secreted by B cells
− Consist of
crystallizable
fragment portion
and two antigen-
binding fragment
regions

Immunoglobins
• Three main antigens on antibodies
− Isotypic: Occurs in all subclasses of
immunoglobin class
− Allotypic: Found on some members of a
subclass immunoglobin class
− Idiotypic: Unique structure created on an
immunoglobulin molecule

Immunoglobins
• Antibodies make
antigens more
visible by:
− Opsonization:
Antibody coats
antigen
− Cause antigens to
clump
− Bind to and
inactivate some
toxins

Cell-Mediated Immune
Response
• Characterized by formation of lymphocytes
• Main defense against virus, fungi, parasites,
and some bacteria

Cell-Mediated Immune
Response
• Mechanism by which body rejects
transplanted organs and eliminates
abnormal cells
• T-cell lymphocytes recognize antigens by:
− Secreting cytokines
− Becoming cytotoxic and killing abnormal cells

Cell-Mediated Response
• Five subcategories of T cells:
− Killer T cells: Destroy antigen
− Helper T cells: Activate immune cells
− Suppressor T cells: Suppress activity of other
lymphocytes
− Memory T cells: Remember reaction
− Lymphokine-producing cells: Damage or
destroy infected cells

Inflammatory Response
• Response of the body to irritation or injury
− Characterized by pain, swelling, redness,
and heat
• Most common causes: Injury and illness

• Acute inflammation
− Involves both vascular and cellular components
− Active hyperemia causes blood vessels to
expand.
• Fluid leaks into interstitial spaces.
− When pressure is released, vessel contracts
and outflow slows.
• Leads to stasis of blood in capillaries

• Acute inflammation (cont’d)
− Variety of cells participate:
• White blood cells
• Platelets
• Mast cells
• Plasma cells (B lymphocytes)
− Chemical mediators account for vascular and
cellular events.

• Mast cells: Degranulate and release
substances
− Primary stimuli for degranulation:
• Physical injury
• Chemical agents
• Immunologic substances
− Release vasoactive amines
− Synthesize leukotrienes and prostaglandins

Plasma Protein Systems
• Mediators that modulate the inflammatory
response
• Complement system: Proteins attract white
blood cells to sites of inflammation
− Cells are activated, then destroyed
− Classic or alternate pathway
− Components: C3b, anaphylatoxins, membrane
attack complex

• Coagulation system: Forms blood clots in
blood vessels
− Inflammation triggers fibrin formation.
• Fibrin: Protein that bonds to form the fibrous
component of a blood clot
− Fibrinolysis cascade: Dissolves fibrin and
creates fibrin split products

• Kinin system: Leads to the formation of
bradykinin from kallikrein
− Kallikrein: Enzyme found in blood plasma, urine,
and tissues (normally inactive)
− Bradykinin: Increases vascular permeability,
dilates blood vessels, contracts smooth muscle,
and causes pain when injected
− Hageman factor: Spurs kinin system into action

Cellular Components
of Inflammation
• Goal: Arrive at the sites within tissues
where they are needed
• Two major phases:
− Intravascular phase: Leukocytes move to sides
of blood vessels and attach to endothelial cells
− Extravascular phase: Leukocytes travel to the
site of inflammation and kill organisms

Cellular Components
of Inflammation
• Cellular event sequence:
− Margination: Increase in blood viscosity
− Activation: Mediators trigger the appearance of
selectins and integrins.
− Adhesion: Polymorphonuclear neutrophils
(PMNs) attach to endothelial cells.
− Transmigration: PMNs permeate vessel walls.
− Chemotaxis: PMNs move to site of
inflammation.

Cellular Components
of Inflammation

Cellular Products
of Inflammation
• Cytokines: Products of cells that affect other
cells
− Interleukins: Attract white blood cells to sites of
injury
− Interferon: Protein produced by cells invaded by
viruses

Cellular Products
of Inflammation
• Lymphokines: Stimulate leukocytes
− Macrophage-activating factor stimulates
macrophage to engulf and destroy.
− Migration inhibitory factor keeps white blood
cells at site of infection or injury.

Injury Resolution and Repair
• Normal wound healing involves four steps:
− Repair of damaged tissue
− Removal of inflammatory debris
− Restoration of tissues
− Regeneration of cells

• Healing depends on the type of cells:
− Labile cells: Divide continuously
− Stable cells: Replaced by regeneration
− Permanent cells: Cannot be replaced
• Wounds can be healed by:
− Primary intention: Occurs in clean wounds
− Secondary intention: Occurs in gaping wounds

• Factors that lead to dysfunctional healing:
− Local: Infection, inadequate blood supply,
foreign bodies
− Systemic: Poor nutritional intake and
hematologic abnormalities
• Diabetes and acquired immunodeficiency
syndrome (AIDS)
• Corticosteroids
• Wound separation

Chronic Inflammatory
Responses
• Causes include:
− Unsuccessful acute inflammatory response
− Persistent infection
− Presence of an antigen
• Similar to acute inflammation process
− Also include growth of new blood vessels

Variances in Immunity
and Inflammation
• Hypersensitivity: Response to any
substance to which a patient has increased
sensitivity
− Allergy: Reaction to an agent (allergen)
− Autoimmunity: Antibodies or T cells work
against the tissues
− Isoimmunity: T cells or antibodies are directed
against antigens on other cells

and Inflammation
• Type I: Immediate hypersensitivity reaction
− Acute reaction to a stimulus
− Symptoms depend on mediator release
− Treatment includes:
• Administration of epinephrine
• Subcutaneous injection

and Inflammation
• Type II: Cytotoxic hypersensitivity
− Involves combination of IgG or IgM antibodies
with antigens
− Cells are destroyed by complement fixation or
by other antibodies.
− Example: Transfusion reactions

and Inflammation
• Type III: Tissue injury caused by immune
complexes
− Involves IgG antibodies that form immune
complexes with antigen
− Reactions may be:
• Systemic (serum sickness)
• Localized (Arthus reaction)

and Inflammation
• Type IV: Delayed (cell-mediated)
hypersensitivity
− Mediated by soluble molecules released by
specifically activated T cells
− Subtypes:
• Delayed hypersensitivity
• Cell-mediated cytotoxicity

and Inflammation
• Targets of hypersensitivity reactions:
− Allergic reaction: Antigen or allergen
− Autoimmune: Person’s own tissues
• Graves disease: Caused by thyroid-stimulating or
thyroid-growth immunoglobulins
• Type I diabetes: Body produces autoantibodies
• Rheumatoid arthritis: Chronic systemic disease

and Inflammation
• Targets of hypersensitivity reactions:
− Autoimmune: Person’s own tissue
• Myasthenia gravis: Attack on nerve muscles
• Neutropenia: Decrease in circulating neutrophils
• Idiopathic thrombocytopenia purpura (ITP):
Patient forms antibodies to blood platelets
• Systemic lupus erythematosus (SLE): Immune
system is directed against tissues

Immune Deficiencies
• Immunodeficiency: Abnormal condition in
which part of immune system is inadequate
• Congenital immunodeficiencies:
− Defects include lymphoid stem cells and T and
B cells
− Two types both inherited:
• X-linked agammaglobulinemia
• Isolated deficiency of IgA

Immune Deficiencies
• Acquired immunodeficiencies
− Contributors:
• Nutritional deficiency
• Stress of trauma
• Hypoperfusion or shock
• Mediator production
• Damage to vital organs
• Decreased nutrition occurring during trauma

Immune Deficiencies
• Acquired immunodeficiencies (cont’d)
− Iatrogenic (treatment-induced)
immunodeficiency
− Idiosyncractic reactions
− Physical or mental stress
− AIDS: Caused by RNA retrovirus HIV

Immune Deficiencies
• Treatment of immunodeficiencies:
− Replacement therapy for some types
• Intravenous gamma globulin
• Bone marrow transplantation
• Transfusions

Factors That Cause Disease
• Genetic: Present at birth, passed from one
generation to another
• Environmental: Microorganisms,
immunologic vulnerabilities, habits and
lifestyle, exposure to chemicals and toxins,
physical environment, etc.
• Anatomic: Malrotation of the colon,
degenerative diseases, aortic stenosis

• Immunologic: Agent that triggers an
abnormal response against myelin, leading
to the development of multiple sclerosis

• Uncontrollable:
− Genetics
− Race
• Controllable:
− Smoking
− Drinking alcohol
− Nutrition
− Physical activity
− Stress

• Age-related risk
− Newborns: Immune system not fully developed
− Teenagers: Injury due to trauma, use of drugs,
and alcohol
− Older adults: Increased risk of cancer, heart
disease, and stroke
• Sex-associated factors
− Prevalence more in one sex than the other
− Presentation can differ from men to women

Analysis of Disease Risk
• Causal risk factors: Causes disease
• Noncausal risk factors: Associated with risk
• Consideration should include:
− Incidence: Number of new cases in population
− Prevalence: Number of cases in a period
− Morbidity: Presence of disease
− Mortality: Number of deaths

Analysis of Disease Risk
• Risk factors often interact.

Common Familial Diseases
• Genetic risk: Passes through generations
• Familial tendency: Cluster of diseases in
family groups despite lack of gene evidence
• Autosomal recessive: Must inherit two
copies of a particular gene
• Autosomal dominant: Need to inherit only
one copy of a particular gene

• Immunologic disorders
− Hyper- or hypoactivity of immune system
− Most that exhibit familial tendencies involve an
overactive immune system
− Allergies: Acquired following initial exposure
− Asthma: Chronic inflammatory condition

• Cancer
− Pathology associated with malignant growths
− Prognosis depends on extent of spread and
effectiveness of treatment
− Lung:
• Major risk factor is cigarette smoking.

• Cancer (cont’d)
− Breast:
• Most common type of cancer in women
• Symptoms: Small painless lump, change in
nipple, discharge, pain, and swollen lymph glands
− Colorectal:
• Third most common type of cancer
• Symptoms: Minimal amount of blood in stools

• Endocrine disorders
− Diabetes mellitus: Chronic disorder of
metabolism
• Ketoacidosis (type 1): Insulin dependent
• Non-ketoacidosis (type 2): Non-insulin dependent

• Hematologic disorders
− Hemolytic anemia: Destruction of red blood
cells
− Hemophilia: Excessive bleeding
− Hemochromatosis: Body absorbs more iron
than needed

• Cardiovascular disorders
− Long QT syndrome: Cardiac conduction system
abnormality
− Consider syncope a life threat if:
• Exercise-induced syncope
• Syncope associated with chest pain
• History of syncope
• Syncope associated with startle

• Cardiovascular
disorders (cont’d)
− Cardiomyopathy:
Diseases of the
myocardium
• Leads to heart
failure, acute
myocardial infarction
(AMI), or death

• Cardiovascular disorders (cont’d)
− Mitral valve prolapse: Mitral valve leaflets
balloon into the left atrium during systole
− Coronary heart disease: Caused by impaired
circulation to the heart
− Hypertension: High blood pressure

• Renal disorders
− Gout: Abnormal
accumulation of
uric acid
• Causes
destructive tissue
changes
− Kidney stones:
Masses of uric acid
or calcium salts
• Form in urinary
system
CourtesyofLeonardV.Crowley,MD,CenturyCollege.

• Gastrointestinal disorders
− Malabsorption disorders: Defect in bowel wall
prevents normal absorption of nutrients
• Lactose intolerance: Defect in enzyme lactase
• Ulcerative colitis: Chronic inflammatory disease of
the large intestine and rectum
• Crohn disease: Chronic inflammatory disease
affecting the colon and small intestine

• Gastrointestinal disorders (cont’d)
− Peptic ulcer disease: Circumscribed erosions in
the lining of the gastrointestinal tract
− Gallstones: Stonelike masses in the gallbladder
− Obesity: Unhealthy accumulation of body fat
• Morbid obesity: Body mass index (BMI) greater
than 40 kg/m2
• Overweight: BMI of 25 to 29.9 kg/m2

• Neuromuscular disorders
− Huntington disease: Characterized by
progressive chorea and mental deterioration
− Muscular dystrophy: Group of hereditary
diseases of muscular system
• Duchene muscular dystrophy
− Multiple sclerosis: Myelin sheath surrounding
the nerve fibers of the brain and spinal cord
become damaged

• Neuromuscular
disorders (cont’d)
− Alzheimer disease
results in:
• Cortical atrophy
• Loss of neurons
• Ventricular
enlargement
CourtesyofLeonardV.Crowley,MD,CenturyCollege.

• Psychiatric disorders
− Schizophrenia: Group of mental disorders
• Distortions of reality, withdrawal, and
disturbances of thought, language, perception,
and emotional response
− Bipolar disorder: Characterized by episodes of
mania and depression

Stress and Disease
• Stress
− Range of strong
external stimuli that
can cause a
physiologic
response
• Physiologic stress
− Change that
makes it necessary
for cells to adapt

Stress and Disease
• Physiologic stress (cont’d)
− Three concepts:
• The stressor
• Its effects
• Body’s response
• Usually the response is beneficial.
− Unchecked stress can result in deleterious
outcomes.

General Adaptation Syndrome
• Stage 1: Alarm
− Body reacts by releasing catecholamines.
− Catecholamines activate the sympathetic
nervous system.
− Effects include:
• Increased respiratory rate
• Decreased blood flow to skin
• Smooth-muscle constriction
• Effects on the liver

• Stage 2: Resistance
− Adrenal gland releases two types of hormones
that increase blood glucose level and maintain
blood pressure
• Glucocorticoids and mineralocorticoids

• Stage 2: Resistance (cont’d)
− Hypothalamus stimulates the release of
adrenocorticotropic hormone (ACTH)
− Other hormones released include:
• Endorphins
• Growth hormone

• Stage 3: Exhaustion
− Adrenal glands depleted
− Decreasing levels of glucose
− Results in:
• Decreased stress tolerance
• Progressive mental and physical exhaustion
• Illness
• Collapse

Effects of Chronic Stress
• Hypothalamic-pituitary-adrenal axis: Major
part of the neuroendocrine system
− Controls the reactions to stress
− Triggers a set of interactions among glands,
hormones, and parts of the midbrain
− Continued stress exhausts the normal
mechanisms.

• Stress and depression have a negative
effect on the immune system.
− Body loses ability to fight disease.
− Body releases fat and cholesterol into the blood.
− Related conditions: Depression, headaches,
insomnia, ulcers, acne, diabetes, and asthma

• Coping mechanisms
− Healthy person: Manages stress with very little
impact on immune system
− Ineffective coping mechanisms lead to
deleterious effects on the immune system.
• Treatment includes psychotherapy,
medication, or positive influences.

Pathophysiology chapter 9

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Pathophysiology chapter 9