BIOL 131

Week 1 CHPTS 1-4 Study Guide

CHAPTER 1-4 Study Guide

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Chapter 1: The Nature of Disease: How to Think about Illness

Introduction to Human Physiology

What is physiology?

Physiology: The study of the normal functioning of a living organism and its
component parts.

Pathology is the science that deals with the function of organs and systems and
the way they do this functions.

Man and the environment

External environment

• The environment man lives in, interacts with (benefits and hazards)

Major environmental factors are: oxygen, water, food, physical factors, social
factors, micro organisms and parasites.

The internal environment

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The human body consists of organs& tissues that are formed of cells.

The cell is the smallest unit of life.

The cell is surrounded by tissue fluid (Internal Environment).

The composition of the internal environment should remain constant within

narrow limits.

Internal environment
Claude Bernard stated that all the life processes have only one goal, that is to
keep the internal environment constant, and this fixity of the internal
environment is necessary condition for life

Homeostasis
Cells live a fairly constant environment

The cells in turn constitute the tissues which provide the environment

Body-Fluid Compartments
60% of total body weight H20

In a 65kg man, there is 40 liters, distributed as:

Intracellular compartment: Fluid inside the cell & 25L

Extracellular compartment: 15 L & 2 Subdivisions: Blood plasma 3L & Interstitial

fluid 12L

Extracellular fluid:
15L

2 Subdivision:

Blood plasma 3L

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Interstitial Fluid 12L

It is the internal environment that immediately surround the units of life of the
whole body

Intravascular     : within the vascular system

Interstitial     : lies between the cells

Transcellular      : secreted by epithelial lining e.g., CSF, pleural fluid

,peritoneal fluid, joint fluid,….

Large volumes are present in disease states, pleural effusion , ascites.

Large losses in diarrhea and vomiting leads to dehydration and electrolyte

disturbances.

Homeostasis:
It is all the physological processes that are carried out by all body systems.

It is to insure that chemical and physical structure of the internal environment is

kept constant in spite of external (e.g.: temp, oxygen tension, pressure) or
internal

(e.g.: increased muscular activity) changes.

It deals with all automatic reactions which take place to correct all deviations
from normal

It is a necessary condition for the existence

Failure of homeostasis often leads to diseases and death.

Homeostasis

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This is the name for the process which keeps the condition and environment of
the tissues in the proper condition to sustain life

Composition of the human body

Water: 60%

Protein: 18%

Fats: 18%

Minerals: 4%

Body water
60%

Varies with age (newborn 82, old age 52).

Varies with fat content (males have more water than females)

Body protein
It is the second largest components

It is found in the structure of all tissues

The largest amount is found in the skeletal muscle.

Body fat
Triglycerides in adipose tissues: found in the subcutaneous tissue and
surrounding the abdominal viscera, energy stores, in females, it is one of the
secondary sex characters

Phospholipids: in the cell membrane

In the structure of CNS.

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Minerals
Small quantity with the exception of Ca2+

Ca2+ is about 1.2 kg in young adult, found in bones

Ca2+ is functionally significant in tissue fluids.

Iron 3-4gm: in heme, stores,

transport forms, and in enzymes.

Other minerals are closely regulated to maintain the composition of the internal
environment

Minerals
The concentration of the minerals in the intracellular fluid is different from the
concentration of them in the extra cellular fluid.

This difference depends on :

Active transport

Passive diffusion according to concentration gradient and electrical charges

distribution.

Fluid exchange
The intravascular fluid and the interstitial fluid are in continuous exchange.
Estimated to be 100L/ h.

Aim: to renew tissue fluid and maintain its constancy (Homeostasis) by

supplying materials needed by the cells, and removing wastes produced by
cell metabolism.

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Fluid Exchange
i) hydrostatic pressure: filtration force, it moves the fluid out of the capillaries

ii) colloid osmotic pressure: osmosis (suction) force, it draws the fluid back into
the capillaries

These two forces act in opposite directions.

The colloid osmotic is uniform throughout the capillary length.

The hydrostatic pressure

Forces
Fluid exchange between the plasma & ISF is governed by algebric sum of
hydrostatic & osmotic forces on either sides of the capillaries

Pcap is due to pumping action of the heart

High hydrostatic in the arterial end of the capillary P=35mmHg

Low hydrostatic pressure in the venous side of the capillary P=15mmHg

Opposed by osmotic pressure of plasma proteins: пcap= 25mmHg

Mainly opposed by пcap, without opposing forces the plasma would rapidly
transferred into the interstitium

The osmotic pressure is uniform throughout the capillary length

The hydrostatic pressure falls from the arteriolar end to the venular end

At arterial end the filtration force exceeds the osmotic force→35-25=10mmHg

filtration

At the venular end the osmotic force exceeds the filtration force →25-
15=10mmHg reabsorption

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Chapter 2: Cell Injury, Adaptation, and Death

Concept of Injury and Cellular Response to Injury

Cells are constantly exposed to a variety of stresses.
When stress is too severe, injury results.
Injury alters the preceding normal steady state of the cell.

What hurts cells?

Causes of Cell Injury/Lesions

oxygen deprivation (anoxia)

physical agents
chemical agents
infections agents
immunologic reactions
genetic defects
Nutritional imbalances
Aging

Disease
Dis + Ease = Disease.
“Discomfort due to Structural or functional abnormality”
Disease is caused by an agent.
Causes (etiology) can be
External / Environmental. E.g.. Heat, Bacteria.
Internal E.g. stress, genes, ageing.

Cellular Injury & Adaptation

Normal cell is in a steady state “Homeostasis”
Change in Homeostasis due to stimuli - Injury
Injury - Reversible / Irreversible

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Adaptation / cell death

Response to Injury
Adaptations (reversible)
Hydropic degeneration
Hypertrophy
Hyperplasia
Atrophy
Accumulations - hyaline, fat, etc.
Necrosis (irreversible) – cell death.

Terminology
Necrosis: Morphologic changes seen in dead cells within living tissue.
Autolysis: Dissolution of dead cells by the cells own digestive enzymes. (not
seen)
Apoptosis: Programmed cell death. Physiological, for cell regulation.

Types of Necrosis
Coagulative – Eg. Infarction
Liquifactive - Brain, abscess
Caseous - Bacterial / Tuberculosis
Gangrene - With infection

Sequels of Necrosis
Cell Death
Necrosis
Autolysis
Phagocytosis
Organization & fibrous repair.

Aging

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“Progressive time related loss of structural and functional capacity of cells

leading to death”

Senescence, Senility, Senile changes.

Ageing of a person is intimately related to cellular ageing.

Factors affecting Ageing

• Genetic – Clock genes, (fibroblasts)

• Diet – malnutrition, obesity etc.

• Social conditions -

• Diseases – Atherosclerosis, diabetes      etc.

Cellular mechanisms of aging

Cross linking proteins & DNA     .
Accumulation of toxic by-products.
Aging genes.
Loss of repair mechanism.
Free radical injury
Telomerase shortening.

Ageing –changes
Gradual atrophy of tissues and organs.
Dementia
Loss of skin elasticity
Graying and Loss of hair
BV damage – atherosclerosis/bruising.
Loss of Lens elasticity  opacity  vision
Lipofuscin pigment deposition – Brown atrophy in vital organs.

Factors affecting ageing

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Stress
Infections
Diseases
Malnutrition
Accidents
Diminished stress response
Good health

Conclusions
Cellular Injury - Various causes
Reversible Injury  Adaptations
Hypertrophy, Hyperplasia, Atrophy
Accumulations - Hydropic, hyaline, fat..
Irreversible Injury - Necrosis
Coagulative, Liquifactive, Caseous
Ageing - Causes, Changes, Factors

Chapter 3: Inflammation: The Reaction to Injury

Why is it necessary to determine the mechanism of injuries? Important for the

diagnosis, rehabilitation and prevention of injuries.

Distant Effects of Inflammation

Systemic effects
Involvement of the lymphatic system
Production of reactant proteins

The Consequences of Acute Inflammation

Complete resolution
Scarring
Abscess
Chronic inflammation

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Injury Mechanism
Depends persons perspective
Mechanism often acts in combination
Establish cause and effect relationship

Mechanical Loading
Loads greater than physiological lead to injuries
Chronic injuries
Cumulative trauma
Repetitive stress
Acute injuries

Principles of Injuries
Catch-all terms
shinsplints
tennis elbow
jumper’s knee
Level of dysfunction
catastrophic injuries
Progression
untreated or lack to time to heal lead to more severe injuries

Assessment of Severity
Clinical classifications
• help assign common characteristics to injuries

Severity linked to amount of tissue      damage

Mild & moderate: partial disruption, tissue is able to accept loads
Ligaments
• grade 1 mild: negligible       structural & minimal time loss     

• grade 2 moderate: partial rupture & swelling tenderness & up to 6

wk time

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• grade 3 severe: complete, gross swelling & 8 wk min

Injury Principles
Micro vs macrotrauma
Primary: direct consequence of trauma
Secondary
injury surface after original trauma
accommodation to primary injury (adaptation of loads)
Tissue structure

Contributing factors
Age
acute injuries: young
chronic: older
Gender
Genetics
Fitness level
nutrition     
Psychological
Human interaction
Fatigue
physical & mental
Environment

Tissue Injury
Inflammation: pathological process
vascular response
increase capillary permeability (swelling)
Pain: swelling related pressure on nerve endings (more in confined spaces)

Tissue Injury
vasodilatory phase
flow of fluid/plasma proteins into tissue
Plasma proteins

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fibrinogen
Functions
dilutes & inactivates toxins
nutrients to inflammatory cells
antibodies, proteins
Control of inflammation

Chemicals Mediators
– histamines, serotonin, bradykin, prostagladins, plasmin etc.
Other Cells
– phagocytes (fungal and bacterial infection)

– lymphocytes (antigens)

Why inflam0mation?
Body’s first line of defense against injuries

The Inflammatory Response to Infection

Infection and inflammation

Bacteria
Parasites
Viruses

Bone
Any conditions that affects osteocyte performance
Osteonecrosis: cessation of blood flow
vessel disruption
occlussion
injury or pressure to arterial walls
↓ matrix, bone strength likelihood of fracture

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Bone
Osteoporosis
Major public health issue
Affect mostly trabercular bone
Bone of axial skeleton
Multifactor
Clinical conditions

Bone
Fracture (break): applied loads exceeds bone’s ability
Resistance
material properties
geometry
anisotropic effects
porosity
Type of loading
acute vs chronic

Fractures
Indirect or direct
Risk and type of bone
Diagnosis
site
extent of injury
configuration
fragments (displaced)
environmental (open closed)
complications
etiological

Fractures

Healing phases:
inflammation
union of bony ends (3wk)
callus remodeling (6 wks)

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Articular Cartilage
Excessive loading
loss of cartilage matrix
chondral fractures
osteochondral fracture
Inability to repair

Articular Cartilage

AO
non inflammatory
weight bearing joints
deterioration of AC
osteophytes formation
cartilage fibrillation
Artificial Joints
cemented or non

Joint Injuries
Excessive loading
Dislocation (luxation)
Partial dislocation (subluxation)
Synovitis
Arthritis
OA
RA
Gouty

Fibrocartilage
Distributes forces at joints
Shock absorber
Improve joint fit
menisci
intervertebral disks

Tendon

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Force transfer
Injuries
direct (cuts)
indirect (excessive loads applied to unit)
Musculotendinous injuries: strain
Mild, moderate, severe
severe: precede by microdamage

Tendon
Repetitive overloading: inflammatory response or tendinitis     
Also could affect tendon sheath, peritenon etc.
Healing
inflamation
Synthesis of collagen and GAG (matrix)
Cyclic loading (2-3 wk)
Progressive stress
• Peritenonitis

• Tendinosis (intratendinous degeneration dut ot atrophy)

• Tendinitis (Symptomatic degeneration vascular disruption and

inflammation

Ligaments
Ligament injuries
sprain
partial tears
complete tears
Healing
bleeding& inflamation (fibrin, fibroblas scar cells)
proliferation of building material (scar tissue)
matrix remodeling
smaller fibers
lack organization

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Muscle
Injuries
acute muscular strain
Over stretching or overloading
force, rate, application
moderate: partial tear
severe: complete tear, hemorrhage,swelling
contusions
intramuscular bleeding
myositis ossificans
exercise induced injury
DOMS 24-72 hr after exercise
Eccentric

Skin

Abrasions
Contusions
Penetrating wounds
obscure deeper damage
Lacerations
Infection
Excessive bleeding

Nervous tissue
Not musculoskeletal

Greatest potential for dysfunction

Injuries

chemical

thermal

ischemic

mechanical

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entrapment

trauma: compressive or tensile

Temporary or complete axonal discontinuity

Motor impairment can lead to secondary injuries

Nervous Tissue
Compartment or entrapments of nerves or vessels
increase pressure transmitted
Enclosed spacing
Symptoms
numbness, tingling & pain
decreased vessel perfusion
Inflammation: positive feedback loop

Chapter 4: Repair: Recovery from Injury

Chapter 4
      is the body’s collective attempt to restore normal structure and function to
the injured site.
      is one type of repair and is the complete or nearly complete restoration of
normal anatomy and function by the regrowth of normal parenchymal cells and
supporting tissue; little or no scarring is present.
      is another type of repair that occurs when regeneration is partial or not
possible; some scarring is always present.

The Repair Process

In tissues capable of regeneration (those with stem cells), repair of mild injury
takes place by means of regeneration of new functional (parenchymal) cells
and the restoration of normal anatomy.
Repair of severe injury occurs by means of regeneration of new functional
cells and partly by scarring (fibrous repair).

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In tissues not capable of regeneration (without stem cells), repair of injury

takes place only by scarring.

Types of cells according to their ability to regenerate

Labile cells, which divide continuously from a pool of stem cells
Stable cells, which have a reserve of stem cells, and which divide very slowly
until stimulated by injury, after which they divide rapidly
Permanent Cells, which are highly specialized and have no reserve of stem
cells, and which are incapable of division and regeneration

The Scaffolding for Cell Regeneration

Basement membranes is a thin, filmy membrane under the epithelium, it
provides the surface upon which epithelial cells grow.
Extracellular matrixis a mixture of collagen elastin fibers creates by fibrolasts, it
creates a structural meshwork t o support cell growth.

Cell Migration into the Wound

Wound     : A wound is the injury resulting from short term injury at a discrete
site
Steps in fibrous repair (scarring)
Fibrocyte migration: raw material for repair
Angioneogensis: growth of new blood cells
Scar development: synthesis of excellular matrix proteins and deposition of
collagen followed by contraction, reshaping and strengthening

Scar Development
Scar development follows angioneogenesis and occurs in several overlapping
steps
Granulation tissue is a mixture of new blood vessels, fibrous tissue, and residual
edema and leukocytes that is at its peak a few days into wound healing.

Healing by First intention vs Second intention

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First intentions     :
Wounds with closely approximated edges; surgical incisions are an example.
Healing by first intention: inflammation first, followed by macrophage clean-
up, neovascularization, and scarring.

Second intentions:
Wounds with widely separated margins heal by; for example, skin or intestinal
ulcers.
Healing by second intention is much the same as healing by first intention:
inflammation first, followed by macrophage clean-up, neovascularization,
and scarring. However, the volume of necrotic tissue to be removed is
greater, and reepithelialization of the surface is slower because the wound
is wider.

Host Factors Interfering with Wound Healing

Infection is the most common obstacle to normal repair
Other obstacles
Poor nutrition
Steroid drugs
Diabetes
Poor vascular supply
Foreign objects
Mechanical forces

Pathologic Wound Repair

A keloid is a hyperplastic scar that is prominent, raised, or nodular and that
contains excess collagen.
Pyogenic granuloma is a localized, highly vascular collection of persistent
granulation tissue.

Recaps
Distinguish between repairs, regeneration and healing
Name the types of cells according to their ability to regenerate
List the component steps in fibrous repair
What is meant by “healing by first and second intention”
What are ostavles to normal repair

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