General Principles of Pathophysiologyfd.valenciacollege.edu/file/rholborn1/Cellular...
Transcript of General Principles of Pathophysiologyfd.valenciacollege.edu/file/rholborn1/Cellular...
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
Cells of lower plants
and animals
Eukaryotes
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.
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.
The Three Types of Muscle:
Muscle Tissue
Has the capability of contraction
when stimulated.
Cardiac tissue is found only within the heart.
Has the unique capability of spontaneous stimulation without
external stimulation.
Smooth muscle is found within the intestines,
bronchial tubes and encircling blood vessels.
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
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 15-minute 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!