Download General Principles of Pathophysiology

GENERAL PRINCIPLES
OF
PATHOPHYSIOLOGY
“Cellular Physiology”
Ray Taylor
Valencia Community College
Department of Emergency Medical Services
Topics
Introduction
The Cell
Types of Tissue
Disease Causes
Disease Pathophysiology
The Cell and the Cellular
Environment
Introduction
Correlation of pathophysiology with
disease process
Cells appear similar to multicellular “social”
organism
 Cells communicate electrochemically


When interrupted disease processes can
initiate and advance
Introduction
Knowledge of coordination of specific bodily functions
leads to better understanding of the disease process



Endocrine
Exocrine
Other coordinating receptors
Chemoreceptors
 Baroreceptors
 Adrenergic
 Others: Neurotransmission

Introduction
Understanding disease process is important for
paramedics to better anticipate, correct, and
provide appropriate care


Once knowledge of physical laws and principles
have been gained paramedics can apply these to
the mechanisms and complications of disease
Cells of the immune system and inflammatory
responses are found with every type of trauma or
disease process
The Normal Cell
The cell is the
fundamental
unit of the
human body.
Cells contain
all the
necessary
components
for life
functions.
Cell Structure
Small self sustaining
city
Normal balanced
environment
Three main
elements



Cell membrane
Cytoplasm
Organelles
Cell
Major classes of cells

Living cells are divided
into two major divisions

Prokaryotes


Eukaryotes


Cells of lower plants
and animals
Cells of higher
plants and animals
Composed chiefly of
water
Cell
Chief cellular functions



Cells become specialized
through processes of
differentiation or
maturation
Eventually perform one
function or act in concert
with other cells to
perform a more complex
task
Conversion of nutrients
into



Energy
Waste
Heat
Cell Structure
The cell membrane is
the outer covering that
encircles and protects
the cell.
Cytoplasm is the thick,
viscous fluid that fills and
gives shape to the cell.
Organelles are structures
that perform specific
functions
within a cell.
Organelles
Nucleus
Endoplasmic reticulum
Golgi apparatus
Mitochondria
Lysosomes
Peroxisomes
Nucleus
Largest organelle known
as control center of cell
Contains genetic material
which governs all
activities of cell including
cellular reproduction
Composed of DNA and
proteins
Endoplasmic Reticulum
Network of small
channels that has
both rough and
smooth portions


Rough endoplasmic
reticulum functions in
synthesis of proteins
Smooth endoplasmic
reticulum funcitons in
the synthesis of
lipids
Golgi Apparatus
Synthesis and
packaging of
secretions such as
mucus and enzymes
Layers of
membranes
Mitochondria
Energy factories of the
cell
Powerhouse of the cell
Responsible for
provision of cellular
energy
 Converts nutrients
into energy sources
 In the form of
adenosine
triphosphate (ATP)
Lysosomes and Perozisomes
Lysosomes

Contain digestive
enzymes



Protect against disease
Production of nutrients
Breaking down bacteria
and organic debris
entering cell and
releasing unstable
substances
Perozisomes

Absorb and neutralize
toxins
Cilia and Flagella
Cilia


Short hair like projections
from cell
Create fluid movement
around cell
Flagella


Long whip like
projections from cell
Moves cell through
extracellular fluid
Cell Function
All human cells have the same
general structure and genetic
material.
Differentiation causes cells to
become specialized.
There are seven major
functions of cells.
Major Functions of Cells
Movement
Conductivity
Metabolic
absorption
Secretion
Excretion
Respiration
Reproduction
Tissues
Tissue refers to a group of cells that
perform a similar function.
Tissue Types
Epithelial Tissue
Lines internal and external body
surfaces and protects the body.
Some forms perform specialized
functions:




Secretion
Absorption
Diffusion
Filtration
Skin, mucous membranes, lining
of intestinal tract.
The Three Types of Muscle:
Skeletal muscle, also called
voluntary muscle, is found
throughout the body.
Cardiac muscle is limited to
the heart.
Smooth muscle, occasionally
called involuntary muscle, is
found within the intestines
and surrounding blood
vessels.
Muscle Tissue
Has the capability of contraction
when stimulated.

Cardiac tissue is found only within the heart.


Smooth muscle is found within the intestines,
bronchial tubes and encircling blood vessels.


Has the unique capability of spontaneous stimulation without
external stimulation.
Generally under control of the autonomic nervous system.
Skeletal muscle allows movement and is
generally under voluntary control.

Most abundant type.
Connective Tissue
Most abundant tissue in
the body.
Provides support,
connection, and
insulation.
Examples include bone,
cartilage, and fat.
Blood is classified as
connective tissue.
Nerve Tissue
Specialized tissue
that transmits
electrical impulses
throughout the body.
Examples include
the brain, spinal
cord, and peripheral
nerves.
Organs, Organ Systems, and
the Organism
An organ is a group of tissues
functioning together.
A group of organs working
together is an organ system.
The sum of all cells, tissues,
organs, and organ systems
makes up an organism.
Organ Systems
Cardiovascular
Respiratory
Gastrointestinal
Genitourinary
Reproductive
Nervous
Endocrine
Lymphatic
Muscular
Skeletal
System
Integration
Homeostasis
Homeostasis is the term for the body’s
natural tendency to keep the internal
environment and metabolism steady
and normal.
A significant amount of energy
is required to maintain the
anatomy and physiology of
the body.
Metabolism
Metabolism is the term used
to refer to the building up (anabolism) and
breaking down (catabolism) of biochemical
substances to produce energy.
The body’s cells interact
and intercommunicate with
substances secreted by various
body glands.
Endocrine Glands
Sometimes called
ductless glands.
Secrete hormones
directly into the
circulatory system.
Some endocrine glands
include: pituitary,
thyroid, parathyroid,
adrenal glands, Islets of
Langerhans in the
pancreas, testes, and
ovaries.
Exocrine Glands
Secrete
substances such
as sweat, saliva,
tears, mucus,
and digestive
juices onto the
epithelial surfaces
via ducts
Signaling
Endocrine signaling—hormones distributed
throughout the body.
Paracrine signaling—secretion of chemical mediators
by certain cells that act only upon nearby cells.
Autocrine signaling—cells secrete substances that act
upon themselves.
Synaptic signaling—cells secrete neurotransmitters
that transmit signals across synapses.
Hormones and neurotransmitters are
received by various receptors:
Nerve endings
Sensory organs
Proteins that interact with, and then
respond to the chemical signals and
other stimuli
Many medications act upon
these receptors…
Chemoreceptors respond to
chemical stimuli.
Baroreceptors respond to
pressure changes.
Alpha and beta receptors
respond to neurotransmitters
and medications.
When normal intercellular
communication and normal
metabolism are disturbed, the body
will respond in various ways to
compensate and attempt to restore
normal metabolism,
a.k.a. — homeostasis.
Stressors on a body system are
inputs.
The portion of the system creating
the input is an effector.
A negative feedback loop exists
when body mechanisms work to
reverse an input.
Decompensation occurs when the
system cannot compensate and
restore homeostasis.
Negative Feedback Loop
Body mechanisms that function to reverse or
compensate for a pathophysiological process (or to
reverse any physiological process, whether
pathological or nonpathological
Output of a system corrects the situation that created
the input
Feedback negates the input caused by the original
stressor
Feedback must be orchestrated and synchronized to
maintain homeostasis
Pathology and Pathophysiology
Pathology

Study of diseases and its cause
Pathophysiology
The study of how diseases alter
the normal physiological
processes of the human body
 Disease may include illness or injury
 From the root “patho” meaning
disease.

How Cells Respond to
Change and Injury
Cellular and Tissue Alteration
Body tends to maintain a constantly
balanced environment and to adapt
(correct or compensate) for any change
that disturbs the balance
Cellular adaptation


Cells adapt to their environment to avoid and
protect themselves from injury
Adapted cells are neither normal or injured (they
are somewhere between these two states)
Cellular Adaptation
Cells, tissues, organs, and organ
systems can adapt to both normal
and injurious conditions.
Adaptation to external stressors
results in alteration of structure
and function.
Examples:

Growth of the uterus during pregnancy,
dilation of the left ventricle after an MI.
Types of Cellular Adaptations
Atrophy—decreased
size resulting from a
decreased
workload.
Hypertrophy—an
increase in cell size
resulting from an
increased workload.
Types of Cellular Adaptations
Hyperplasia—An increase in the number of
cells resulting from an increased workload.
Metaplasia—Replacement of one type of
cell by another type of cell that is not
normal for that tissue.
Dysplasia—A change in cell size, shape, or
appearance caused by an external
stressor.
Cellular Injury
Hypoxic
Chemical
Infectious
Immunologic/ Inflammatory
Physical agents
Nutritional balances
Genetic factors
Cellular Injury
Hypoxic injury


Most common cause of
cellular injury
May result from:





Decreased amounts of
oxygen in the air
Loss of hemoglobin or
hemoglobin function
Decreased number of
red blood cells
Disease of respiratory
or cardiovascular
system
Loss of cytochromes

Iron containing protein in
the mitochondra (electron
transport system)
Cellular Injury

Chemical agents causing cellular injury
 Poisons
 Lead
 Carbon
monoxide
 Ethanol
 Pharmacological
Cellular Injury
Infectious injury
 Disease causing agents (Pathogens)
 Virulence or pathogenicity of microorganisms
depends on their ability to survive and reproduce
in the human body, where they injure cells and
tissues
 Disease producing potential depends upon its
ability to
 Invade and destroy cells
 Produce toxins
 Produce hypersensitivity reactions
Infectious Injury
Possible outcomes
 Pathogen
wins
 Pathogen and body battle to a draw
 Body defeats pathogen
Bacteria
Survival and growth depend upon the effectiveness of
the body’s defense mechanisms and the bacteria’s
ability to resist the mechanisms
 Coating protects the bacterium from ingestion and
destruction by phagocytes and capsules may also
function as exotoxins (outside poisonous substance)
 Not all virulent extracellular pathogens are
encapsulated mycobacterium tuberculosis can
survive and be transported by phagocytes
Bacteria
Bacteria also produce substances such as enzymes or toxins
which can injure or destroy cells
 Toxins are produced by many microorganisms
 Exotoxins (staph, strep, psuedomonas)
 Endotoxins (lipopolysaccharide that is part of the
cell wall of gram-negative bacteria)
 Fever is caused by the release of endogenous
pyrogens from macrophages or circulating WBC’s
 Inflammation is one of the body’s responses
 Hypersensitivity reactions is an important pathogenic
mechanism
 Bacteremia or septicemia is proliferation of
microorganisms in the blood
Viruses
Viral diseases are among the most common afflictions seen in
humans
Intracellular parasites take over the control of metabolic
machinery of host cells for use to replicate the virus
Protein coat (capsid) encapsulating most viruses allows them to
resist phagocytosis
Viral replication occurs within host cell
Having no organelles, viruses are incapable of metabolism
Viruses do not produce exotoxins or endotoxins
Viruses can evoke a strong immune response but can rapidly
produce irreversible and lethal injury in highly susceptible cells
(as in AIDS)
Immunologic and Inflammatory Injury
Cellular membranes are injured by direct contact with
cellular and chemical components of the immune or
inflammatory process as in phagocytes and others
such as histamine, antibodies, lymphokines
Membrane alterations are associated with rapid
leakage of potassium out of the cell and an influx of
water
Can result in


Hypersensitivity: exaggerated immune response
Anaphylactic: life threatening
Injurious Physical Agents
Cellular damage can be caused by physical agents
Physical agents causing injury

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
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Temperature extremes
Burns
Atmospheric pressure changes (blast injury, deep sea
diving accident)
Ionizing radiation
Illumination (eye strain from lighting)
Skin cancer
Noise
Mechanical stressors (trauma)
Injurious Nutritional Imbalances
Improper nutrition contributes to one of
the most widely publicized forms of
cellular injury
Examples
Atherosclerosis
 Vitamin deficiency
 Malnutrition
 Starvation

Injurious Genetic Factors
Some cellular dysfunctions are caused by genetic
predispostion, either defective genes or altered
chromosomes that a person is born with
Genetic injuries involve
 Alterations to the nucleus or cell membrane
 Alterations to the shape of cell or receptors of cell
membrane
 Alteration to transport mechanism that carries
substances across cell membrane
Manifestation of
Cellular Injury
When cells are injured metabolism is
changed, causing substances to
infiltrate or accumulate to an abnormal
degree in cells.
Cellular Swelling
Results from a permeable or
damaged cellular membrane.
Caused by an inability to
maintain stable intra-and
extracellular fluid and
electrolyte levels.
Fatty Change
Lipids invade the area
of injury.
Occurs most commonly
in vascular organs,
most frequently the
liver.
Causes a disruption of
the cellular membrane
and metabolism and
interferes with the vital
functions of the organ.
Signs and Symptoms of
Cellular Change
Fatigue and malaise
Altered appetite
Fever
Increased heart rate
associated with fever
Pain
Cell Death
Apoptosis



Injured cell releases enzymes
that engulf and destroy the cell.
Cells shrink.
Eliminating damaged and
dead cells allows tissues to
repair and possibly regenerate.
Cellular Necrosis
Cell death; a pathological cell change
Four forms of necrotic cell change
Coagulative
 Liquefactive
 Caseous
 Fatty

Cellular Necrosis
Coagulative necrosis
 Generally results from hypoxia and commonly occurs in
kidneys, heart, and adrenal glands
 Transparent viscous albumin of the cell becomes firm
Liquefactive necrosis
 Cells become liquid and contained in walled cysts
 Common in ischemic death of neurons and brain cells
Caseous necrosis
 Common in TB
 Cells become infected and look like fried cheese
Fatty necrosis
 Fatty acids combine with calcium, sodium, and
magnesium ions
Gangrenous Necrosis
Tissue death over a wide area
Types
Dry gangrene: results from coagulative
necrosis
 Wet gangrene: results from liquefactive
necrosis
 Gas gangrene: results from bacterial
infection in tissue generating gas bubbles
in cells

Dispatch
You, a paramedic, and your EMT partner
are dispatched to an MVC with injuries.
Dispatch reports that another unit is on
scene and has requested a second
ambulance.
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Arrival
After you notify dispatch of your arrival,
the EMT from the other unit tells you that
they “are bringing the patient over to you
now.”
You and your partner pull the stretcher
out of the back of your rig.
The patient is placed on the stretcher.
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Initial Impression
Patient presents as
Fully immobilized
 Alert and oriented
 Complaining of rib
pain

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Discussion
• What is your initial impression of the
patient’s status?
• What concerns do you have about the
mechanism of injury (MOI)?
• What are your next, most immediate
actions?
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Initial Assessment
You ask your partner to begin an initial
assessment in the back of the
ambulance while you go and look at the
car the patient was in.
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Initial Assessment
On the way to the vehicle, one of the
firefighters tells you that
Your patient was the restrained driver of
vehicle T-boned on the driver’s side
 Vehicle then hit tree
 Patient self-extricated and was ambulatory
when fire services arrived



Standing takedown was performed onto
backboard
Passenger required extrication and is in
critical condition
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Discussion
• Is it necessary to inspect the vehicle?
•
Why or why not?
• What does the damage to the vehicle tell
you about the
•
•
MOI?
Potential for injury to your patient?
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Initial Assessment
You note
Significant front-end and passenger-side
damage
 One foot of intrusion into driver’s
compartment
 Windshield on driver’s side intact
 Glass on driver’s door shattered

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Initial Assessment
You return to the ambulance where your
partner has performed an initial assessment.
He reports
Airway open, patient describes slight difficulty
breathing
 Bruising to the left lateral rib cage
 Possible decreased lung sounds on the injured
side
 No bleeding noted
 No neurological deficits noted

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Initial Assessment
Vital signs
HR = 104 regular
 RR = 20 regular
 BP = 136/80
 SaO2 = 96% on room air

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Discussion
• What are your immediate concerns?
• What are your next, most immediate
actions?
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Assessment
Oxygen administered via nonrebreather mask
You confirm your partner’s initial assessment
findings and perform a chest exam.
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Assessment
When asked, the patient states
He did not hit his head or lose
consciousness.
 He was able to get out of the car and walk
around without neck or back pain.
 His only complaint is left-sided chest pain.



Worse pain with deep inspiration
“I can’t catch my breath.”
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Assessment
Your assessment reveals

Bruise to lateral/anterior chest wall

Crepitus with palpation
Lung sounds slightly diminished on injured
side, clear bilaterally
 Head, neck, abdomen, pelvis, and
extremities all atraumatic
 Skin slightly pale, warm, dry

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Discussion
• What injuries might the patient have
suffered?
• What are your immediate concerns?
• What are your next, most immediate
actions?
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Ongoing Assessment
You ask your partner to begin the 15minute response to the trauma center.
Repeat vital signs
HR = 110 regular
 RR = 22 regular
 BP = 134/80
 SaO2 = 99% on 15 Lpm

Breath sounds still diminished on left
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Assessment
You place the patient on the cardiac
monitor.
Interpretation?
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Treatment/Assessment
As you are preparing for large-bore IV
access with a 16-gauge, 1-1/4 inch
catheter, the patient says that he is
having trouble breathing.
You note
He is becoming restless and diaphoretic
 RR = 28 shallow, labored
 HR = 128 regular
 Skin pale, diaphoretic

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Discussion
• What do you think is responsible for these
sudden changes?
• What are your immediate concerns?
• What are your next, most immediate
actions?
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Treatment/Assessment
You immediately prepare a prepackaged
needle thorocostomy kit.
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Treatment
A 12-gauge
thorocostomy
needle is affixed to
a 10 cc syringe
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Ongoing Assessment
You now note
HR = 134 regular
 RR = 34 shallow
 SaO2 = 84% on 15 Lpm
 Very weak radial pulse
 Skin pale, cold, diaphoretic
 Jugular vein distention (JVD)
 Absent lung sounds on left side

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Discussion
• Is this patient in shock?
•
•
What classification of shock?
Compensated or decompensated?
• What is your next, most immediate action?
•
•
•
Assist BVM ventilations?
Intubation?
Needle decompression?
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Treatment
You identify the
midclavicular line
in the second
intercostal
space.
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Treatment
You prepare the
area with an iodine
swab and insert the
catheter.
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Treatment
You feel a “pop” as
the catheter passes
into the pleural
space.
The syringe plunger
pulls back easily
and air is aspirated.
The needle is
removed.
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Discussion
• What suggests that the needle
decompression was successful?
• What assessment findings will confirm that
the needle decompression was
successful?
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Treatment
Heimlich valve
attached
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Ongoing Assessment
You reassess the patient.
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Ongoing Assessment
Reassessment reveals:
Lung sounds increased on left
 Color returning to skin
 Decreased patient anxiety
 SaO2 increasing steadily

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Ongoing Assessment
Vital signs
HR = 108 regular
 RR = 22 regular
 BP = 130/76
 SaO2 = 97% on 15 Lpm

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Discussion
• Do the assessment findings suggest that
the needle decompression was
successful?
• What are your next, most immediate
actions?
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Treatment
You initiate large-bore IV access.

1000 cc normal saline with large-bore
tubing hung, rate KVO
Patient tells you he is feeling better but
still feels he cannot catch his breath.
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Treatment
You contact medical
control and give a
report.
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Discussion
• Is the fact that the patient is experiencing
shortness of breath a concern?
• What are your next, most immediate
actions?
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Ongoing Assessment
Ongoing assessment reveals
Patient alert and oriented
 Lung sounds still slightly diminished on left
 No JVD or tracheal deviation
 Skin slightly pale, warm, dry
 Head, neck, abdomen, pelvis, and
extremities still appear atraumatic

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Ongoing Assessment
Vital signs
HR = 102 regular
 RR = 20 regular
 BP = 126/76
 SaO2 = 98% on 15 Lpm

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Discussion
• How do you explain the patient’s
shortness of breath?
• What are your next, most immediate
actions?
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Treatment
You prepare the patient for arrival and
transfer to the ED.
Patient's only complaint at time of
arrival is chest pain and shortness of
breath.
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ED Treatment and Beyond
ABCs assessed

Oxygen administration continued
Central venous access obtained
Imaging studies
Trauma radiograph series obtained
 Left-sided pneumothorax and pulmonary
contusion identified
 No other injuries noted

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ED Treatment and Beyond
Laboratory studies
Complete blood count (CBC), type and
cross, coagulation profiles
 Arterial blood gas (ABG)

Chest tube placed
Patient sent to CT

No additional injuries noted
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ED Treatment and Beyond
Admitted to the trauma service for
observation
Lung reexpands without complication
Patient discharged 3 days later
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Thank you!