Chapter 1-4 Study Guide and answers

BIOL 131Week 1 CHPTS 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.

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The internal environment

• 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:

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o Intracellular compartment: Fluid inside the cell & 25L

o Extracellular compartment: 15 L & 2 Subdivisions: Blood plasma

3L & Interstitial fluid 12L

Extracellular fluid:

15L

2 Subdivision:

Blood plasma 3L

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.

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• 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

• 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

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• 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.

Minerals

• Small quantity with the exception of Ca2+

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

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• 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.

Fluid Exchange

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• 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-

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25=10mmHg filtration

• At the venular end the osmotic force exceeds the filtration force

→25-15=10mmHg reabsorption

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

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• 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

• Adaptation / cell death

Response to Injury

• Adaptations (reversible)

– Hydropic degeneration

– Hypertrophy

– Hyperplasia

– Atrophy

– Accumulations - hyaline, fat, etc.

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• 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

“Progressive time related loss of structural and functional capacity of cells leading to death”

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http://www.medterms.com/script/main/art.asp?articlekey=4514

http://health.howstuffworks.com/adam-200096.htm


• 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.

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http://faculty.plattsburgh.edu/donald.slish/Telomerase.html


• Loss of Lens elasticity opacity vision

• Lipofuscin pigment deposition – Brown atrophy in vital organs.

Factors affecting ageing

• 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

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http://www.nlm.nih.gov/medlineplus/ency/article/002242.htm


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

Injury Mechanism

• Depends persons perspective

• Mechanism often acts in combination

• Establish cause and effect relationship

Mechanical Loading

• Loads greater than physiological lead to injuries

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• 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

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

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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)

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Tissue Injury

• vasodilatory phase– flow of fluid/plasma proteins into tissue

• Plasma proteins– 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

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http://www.nlm.nih.gov/medlineplus/ency/article/003650.htm


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

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

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http://www.nlm.nih.gov/medlineplus/fractures.html

http://books.google.com/books?id=lF9FWFZbGN8C&lpg=PA117&ots=pl3asoH2VF&dq=Osteoporosis%20Clinical%20conditions&pg=PA117

http://www.mayoclinic.com/health/osteoporosis/ds00128

http://www.nlm.nih.gov/medlineplus/osteonecrosis.html


• 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)

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

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• 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

• Force transfer

• Injuries

– direct (cuts)

– indirect (excessive loads applied to unit)

• Musculotendinous injuries: strain

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– 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

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http://www.caringmedical.com/conditions/Tendinosis.htm


• lack organization

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

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• Injuries

• chemical

• thermal

• ischemic

• mechanical

• 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

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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).

– 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 matrix is a mixture of collagen elastin fibers creates by fibrolasts, it creates a structural meshwork t o support cell growth.

Cell Migration into the Wound

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• 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

• 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

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• 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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Chapter 1-4 Study Guide and answers