Pathophysiology test 1

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Purpose of immune system

protect us from microbial agents and cancer cells

antigen

reacts with products of immune response (T cells receptors and antibodies)

antibody

glycoprotein which specifically binds to an antigen and carries out immune functions such as activating the complement pathway

innate immunity

acts within minutes, born with this defense, not specific, response does not improve with 2nd exposure

Adaptive/aquired immunity

takes days to become effective, highly specific,memory cells produced. Includes hemoral and cellular immuinity

Cellular immunity

mediated by T cells. Most active reponse to intracellular infections (viruses, fungi, tb) and cancer cells

humoral immunity

mediated by B cells, antibody mediated immune defense, most active to extracellular infection

Components of innate immunity

I-interferons
N-Neutrophils
N-natural killer cells
A-acids (stomach acids)
T- tears (have lysozyme to degrade bacterial cell wall)
E-Englufment ( of microbes by neutrophils and macrophages)

natural barriers

skin, cilia, mucus in respiratory tract, mucus in GI, gastic acid

neutrophils and macrophages

phagocytic cells engulf and intracellularly kill microbial organism

complement activation

by contact with microbial surfaces they:
1. form MAC and drill holes in invaders
2. help phagocytic cells recognize and engulf invaders
3.attract neutrophils to invader site to kill invader

natural killer cells

Directly kill virus-infected cells and cancer cells by perforating membrane of invader. None specific, killing is activated by failure of NK cells to recognize a sureface protein that is present on normal human cells but significantly reduced or absent on infected cells.

Interferons

Virally infected cells release interferons to protect the surrounding uninfected cells from virus. Type of cytokine.Stimulate production of proteins which prevent replication and formation of virus within surrounding uninfected cells

Cells of adaptive immunity

Macrophages, B lymphocytes, Cytotoxic T cells, Helper T cells

Macrophages

present antigen to T lymphocytes

B lymphocytes

transform into plasma cells and make antibodies.
Each B cell expresses a specific antibody on its surface with binds a specific antigen of invader. Once B cell is activated it transfrms into plasma cells and makes many identical antibodies to the same invader.

Cytotoxic T cells

directly kill infected cells and cancer cells

Helper T cells

"generals of the immune response" direct actions of cytotoxic T cells and B cells ( enable B cells to become plasma cells and make antibodies); activate macrophages

B lymphocytes

B lymphocytes: orgiinate and mature in bone marrow (since develpment is bone marrow dependent, and bone marrow begins with B are called B cells) Millions of B ells made each with unique sureface receptor recognizing unique antigen

T lymphocytes

originate in bone marrow and mature in the thymus; millions of T cells are made, each with a unique receptor recognizing a unique antigen

Primary Lymphoid Organs

1. B lymphocytes
2. T lymphocytes

Secondary lymphoid tissue

tissues in which lymphocytes come into active contact with antigens of invaders, and immune response is activated; killing of invaders occurs in these tissues and products of immune response (ex. antibodies) are developed to fight the same invaders infecting other body tissues.

Lymph nodes

lymphatic channels bring invaders in lymph fluid to lymph node. B cells and helper T cells recognize and bind to specific antigens of an invader and are activated. Helper T cells realease cytokine allowing B cells to transform into plasma cells and make large # of antibodies. Antibodies leavie lymp node and go into circulate to other tissue the invader may be infecting. Cytotoxic T cells are stimulated by helper T cells. Memorey B cells, helper T cells and cyto toxic T cells are made so that future exposure to same invader will be faster and more effective.

Spleen

blood born invaders brough to spleen by blood vessels. Similar response as lymph node

Mucosal associated lymphoid tissue (MALT)

B and T lymphocytes distributed in epithelial lining of Respiratory, GI, and genitourinary tracts. Protects these areas from invaders

Antibodies Structure

monomer is a single Y for and composed of 2 heavy chains and 2 light chains; there are 2 antigen binding sites at "V" end and functions of antibody are carried out at the opposite "I" end

Functions of antibodies

a. activation of complement
b. connect microbial organizm to neutrophil/macrophage, there fore aiding in phagocytosis called "opsonization"
c. antibody binds to toxin to block its action
d. antibodies block viral infection by bonding to viral attachment sites on virus
e. antibodies bind bacterial attachment sites on the bacterial cell thereby blocking bacterial invasion
f. Antibodies DO NOT directly kill bacteria

5 classes of antibodies

1. IgG
2: IgA
3. IgM
4. IgD
5. IgE

IgG

Structure: monomer. a. activation of complement
b. connect microbial organizm to neutrophil/macrophage, there fore aiding in phagocytosis called "opsonization"
c. antibody binds to toxin to block its action
d. antibodies block viral infection by bonding to viral attachment sites on virus
e. antibodies bind bacterial attachment sites on the bacterial cell thereby blocking bacterial invasion
f. Antibodies DO NOT directly kill bacteria. Only antibody call wich crosses the Placenta

IgA

Structure: monomer in blood; structure in GI/Respiratory/GU tract is dimer. Protects mucose from entrance of invaders by binding to and blocking attackment sites on invaders

IgM

sites on B cells as monomer (single "Y"). Very important in binding antigens. Is pentamer in blood (largest immunogloblin). Activates complement because has 10 antigen binding sites, and multiple sites to bind to complement.

IgD

least well characterized

IgE

important in the allergic reponse (type 1 hypersensitivity reaction) and parasitic infections.

Primary Humoral Response

1. IgM is first antibody made and detected in the blood (7-10 days).
2. IgG is then made
3. Memory B cells are made with an increased # of receptors to recognize and bind the same antigen of invader; live a long time.

Difference between cell mediated immunity and antibody mediated immunity

Cellular immunity- mediated by T lymphocytes. Does not involve any antibodies. Just activation of Macrophages, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines (chemical messengers) in response to an antigen. Mostly related to specific cells.
Humoral Immunity- mediated by B cells. B cells transform to plasma and produce antibodies. Mostly related to bodily fluids and blood

Second humoral response

Anti-body response upon second exposure. Is faster, more effective, and long lasting because memory cells made during primary.
1. IgG typically predominates (not IgM)
2. Antibody response occurs in 1-3 days

Describe the immune response against viral infection

Innate immune resonse: within minutes
1. virus-infected cell realease interferons which protect surrounding cells.
2. Natural killer cells kill virus infected cells
Adaptive response takes a few days
1. Macrophages present viral antigen to helper T cell after engulfing virus and chopping it up into peptides. Helper T cell becomes activated and helps activate B cells and cytotoxic T cells,
2. B cell binds to same virus and becomes activated. Make antibodies.
Antibodies will bind virus to macrophage and block viral attachment sites on virus.
3. Cytotoxic T cells can directly kill virus-infected cells.

Which cells in the immune response produce memory cells

Memory cells are produced by B cells, T helper cells, and cytotoxic T cells.

Type I hypersensitivity reaction initial exposure

B cells and helper T cells expose to allergen result in transformation of B cells to plasma cells which make IgE. IgE binds to mast cell surface.

Type 1 hypersensitivity reaction second exposure

Immediate response. Allergen binds to IgE antibodies on mast cell surface, cross-linking them. Mast cells immediately release histamine from blue granules in mast cell.

Effects of Histamine

Vasodilation, increase in vascular permeability, itchiness.

Urticaria

swollen, red, itchy hives. Type 1 hypersensitivity reaction. Due to food or drugs

Allergic rhinitis

Type 1 hyperactivity reaction. clear nasal discharge, itchy nose and eyes due to pollens, grasses, dander and dust

Anaphylaxis

Anaphylaxis: life threatening because severe low BP and bronchiole constriction due to histamine effects. Causes are drugs, foods, latex and insect venom.

Immune components bring about Hypersensitivity rxn II

Complement Mediated! Antibodies(IgG and IgM) attach to antigen on invading cells and the MAC complex is formed on cell --> punctures the invading cell's membrane and it dies.

Examples of Hypersensitivity type II rxn

Red blood transfusion. Patient has antibody to antigen on donor red blood cell surface. Antibody binds to red blood cell antigen and activates complement which causes membrane attack complex to form on the donor red blood cells and make the red blood cells come apart.

Type III Hypersensitivity reaction

Antibody involved. Antibody binds to bacterial or tissue antigen and forms antibody-antigen complex. Complex travels in blood and gets deposited in another tissue. Circulating antigen-antibody complexes are deposited in tissues such as the kidneys, and then wreak havoc on that organ by activating compliment which attracts neutrophiles. An example is post-streptococcal glomerulonephritis.

post-streptococcal glomerulonephritis.

antibody-antigen complex from strep throat gets deposited in the kidney.Complement activated and neutrophiles release destructive chemicals causing kidney damage.

Type IV sensitivity reaction

antibodies not involved at all. T cell mediated!
Prior sensitization required: Antigen presenting cell (macrophage or dendritic cells) present to T cell, which makes memory cells
Re-exposure: Helper T cell release cytokines--> reactivating macrophages --> release chemical mediators ( which causes tissue damage, vasodilation, increased premeability) Tissue becomes red and swollen.
-Delayed reaction (1-2 days) with the second exposure unlike type I because it takes time for Helper T cells to come and be presented with the antigen from the macrophage.

Example of type 4: allergic contact dermatitis

Autoimmune diseases

• Autoimmune diseases are caused when autoantibodies bind to self tissue and activate complement, which forms MAC on self tissue cells and destroys them.

Contact Demititis

chemical irritants, poison ivy, poison oak, jewelry, cosmetics, adhesive tape, antimicrobial agents. T cell mediated!!!!
protein altered in skin and taken up by antigen presenting cells in skin (dendritic cells) which present antigen to helper T cells. Helper Tcells become activated and make memory cells.
Re-exposure: helper T cells activated and activate macrophages. Macrophages release chemical mediators into skin and skins reaction is red swollen and itchy.

Systemic lupus erthematosus

Multi-system autoimmune disease. Involves multiple organs due to very well characterized auto antibodies that cause tissue destruction in serveral organs. significant female predominance. Presents in young females with a butterfly rash, chest pain, fever, and pain and swelling of joints. Involves skin, kidney, blood vessels, joints, membranes covering lungs and heart.

IgA deficiency

most common immunodeficiency disease. IgA antibody is severly deficient which protects mucosal surfaces. Patients get repeated respiratory infections and diarrheal illness

Bruton Disease

(x-linked agammaglobulinemia) occurs when there is a lack of ALL classes of immunoglobulins. Patients have reccurent significant bacterial infections

diGeorge Syndrome

partial or complete lack of thymus developement. T-cell deficient. Patients have microbial infections in which T cells are important. ( viral, fungal, protozoan infections, TB). Infants extreamly vulnerable to microbial infections

Acquired Immunodeficiency-Secondary

1. Immunodeficiency acquired from drug treatment with surpresses the immune system.
2. AIDS- caused by infection of helper T cells by HIV, results in depletion of helper T cells. Helper T cells direct actions of B cells, cytotoxic T cells and macrophages. W/o helper T cells patient are vulnerable to many infections and cancers.

Inflammation

Reaction to injurious agents (microbes and trauma, damage, necrotic cells) . Consists of vascular responses, migration, and activation of leukocytes and systemic reactions ( like fever)

Desirable Effects of Inflammation

A. inactivation and elimination of offending agents
B. demolition of necrotic tissues
C. establishing conditions for repair and restoration

Undesirable effects of inflammation

A. Acute inflammation: asthma (inflammation of the airways)
B. Chronic inflammation
-Rheumatoid arthritis
-Atherosclerosis- inflammation is a factor causing chronic injury to arterial walls resulting in wall thickening.

Role of Granulocytes in inflammation

Granulocytes:
-neutrophils: (smiley face nuclei) first to arrive to acute inflammation and they phagocytose.
-eosinophils:(red) important in allergic responses and parasitic infections.
-basophils: (blue) have histamine.
Mast cells similar to basophiles but more important in acute response.

Monocytes: in inflammation

Monocytes:
-macrophages: phagocytose invaders intracellulary, stimulate T lymphocytes, "clean up" areas of inflammation, long lasting--> used in repair of inflamed tissue.

Lymphocytes

Lymphocytes:
-important in chronic inflammation and only important with certain infectious agents. Only important in the acute infections epstein bar virus, mono, and pertussis

Roles of Different WBCs

Granulocytes:
-neutrophils: (smiley face nuclei) first to arrive to acute inflammation and they phagocytose.
-eosinophils:(red) important in allergic responses and parasitic infections.
-basophils: (blue) have histamine.
Mast cells similar to basophiles but more important in acute response.
Monocytes:
-Monocytes transform into macrophages: phagocytose invaders intracellulary, stimulate lymphocytes, "clean up" areas of inflammation, long lasting--> used in repair of inflamed tissue. Dominate chronic inflammation

Lymphocytes:
-important in chronic inflammation and only important with certain infectious agents.

Vascular events acute inflammation

1.Vasodilation
2. Incrased vascular permeability: protiens can now pass through vessel
3. Outflow of fluid into extravascular space

Outflow of fluid into extravascular space

Results from:
a. increased vascular permeability
b.decreased intravascular oncotic pressure ( water leaves vessels bc of increased vascular permeability)
c. Increased hydrostatic pressure (pushes water out)

Cellular events acute inflammation

WBC line up along vascular walls and adhere to the endothelial cells there--> WBC can leak through into extravascular space and migrate to injury site (chemotaxis).
- Exudate forms
Neutrophiles precominated injury site during first 24 hours and then macrophages arrive.

Exudate

fluid which is high in protein and while blood cell content

5 Clinical signs of inflammation

1. rubor-redness by vasodilation and congestion
2. calor- heat cause by increase in blood flow
3. tumor- swelling by outflow of fluid in extravascular space
4. dolar- painby local pressure from swelling in chemical mediatiors
5. functio laesa- loss of function

Cell Derived Mediators in Acute Inflammation

1. Histamine: vasodilates and increases permeability
2. Arachidonic acid metabolites (newly synthsized)
-Prostoglandins (newly synthesize): vasodilate, produce pain and fever. Are inhibited by NSAIDS and aspirin which inhibit cyclooxygenase.
-Leukotrienes (newly synthesized): increase vascular permeability, constrict bronchials, leukocyte chemotaxis. Inhibitors used to treat asthma.
3. Cytokines (newly synthsized)-produced by lymphocytes and macrophages. cause sleepiness, decreased appetite, stimulate repair, recruit leukocytes to injury site.

Plasma Derived Mediators in Acute Inflammation

In order
1. Complement system-vasodilation, increased vascular permeability, promotes phagocytosis, MAC directly kills, recruit WBC
2. Kinin system- bradykinin, increases cascular permeability, vasidilation, pain
3. Clotting system-activation of clotting factors, fibrin clot thrombin
4. Fibrinolytic System-plasmin recruits WBC

Lymphangitis

secondary inflammation of lymphatic channels draining infectious organisms...See red streaks! ex. infection of hand speads up arm and visible red streak on arm

Lymphadenitis

secondary inflammation and infection of lymph nodes draining on site of bacteria...swelling at lymph node! ex. bacterial infection of tonsils can spead to tonsillar lymph node

Possible outcomes of acute inflammation

1. Complete Resolution-lymphatics and macrophages clean up. Injured tissue capable of regeneration
2. Abscess Formation
3. Healing by scarring
4. Progression to Chronic Inflammation

Chronic inflammation

Inflammation of prolonged duration in which active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously.ex. syphilis, silicosis, chronic autoimmune disease (rheumatoid arthritis, systemic lupus)

Macrophages and Lymphocytes' Role in Chronic

Macrophages: Helper T cells release cytokines--> activate macrophages--> recruit leukocytes, destruct tissue or repair Lymphocytes: Kill invaders. B cells make plasma cells--> antibodies. Cytotoxic T cells directly kill infected cells. Lympocytes can adi in killing of invaders. B lymphocytes produce antibodies. T lymphocytes -(helper T and cytotoxic T)

Granulomatous Inflammation:

specific type of chronic inflammatory response when activated macrophages are fused and surrounded by a "collar" of Helper T cells.
-only occurs when foreign bodies can't be phagocytized (sutures) or when microbials can't be degraded and killed (tuberculosis, syphilis, cat scratch).

Serous inflammation

thin fluid with low protein and low cell content which is derived form serum. Ex skin blister. usually results from a mild injury like a burn

Fibrinous inflammation

Outpouring of a protein rich fluid to cause increase in vascular permeability allowing large proteins out of vessels. Usually from severe injury. Ex Pericarditus from necrosis of lung tissue after infarct (TB pneumonia, lung abcess)

Purulent Inflammation

Puss filled. Neutrophiles (living, dying, degraded) necrotic tissue cells, protein, and bacteria.
Abcess- pocket of pus in tissue. Necrotic tissue and neutrophils in a fibrous capsule.

Causes of Purulent inflammation

Pyogenic bacteria like staph. Examples. acute appendicitis, acute bacterial meningitis.

Ulcer

Local defect on the surface of a tissue or organ caused by sloughing off of necrotic inflammatory tissue

Systemic affects of Inflammation

1. Fever- 1-4 increase in temperature, helps leukocytes with killing. Inhibit prostoglandin prod. with tylenol
2. Chills- Shivering, paleness caused by increase in core body temp
3. Rigors- shaking chills (more serious)
4. others: sleepiness (somnolence), decrease in appetite, malaise

C Reactive Protein

Marker of inflammation. Indicator for
1. Heart Attack- Arterosclerosis
2, Rheumatoid Arthritis-
3. Other inflammatory diseases

Leukocytosis

Elevation of Leukocytes. Common with bacterial infections esp. neutrophiles.

Regeneration

Replacement of lost cells with cells similar in function and structure

Repair

Proliferation of connective tissue formation of collagenous scar

Labile cells

undifferentiated cells continuously dividing and replicating. Ex Epithelium (surface and columnar in GI) and Bone Marrow. Regenerate Well

Stable Cells

Normally low level replication, Rapidly divide in response to stimuli. Regenerate well if tissue outlines (extracellular matrix) maintained during inflammatory process. ExGlandular cells, liver paraenchymal cells, mesenchymal cells (supportive) fibroblasts, smooth muscle, vascular endothelial cells, bone cells

Permanent Cells

Non-dividing, regenerative capacity is very limited. Ex Cardiac Muscle and Skelatal Muscle

Phases of Wound Healing

1. Inflammation: clot(platelets and fibrin messwork) , acute inflammation (neutrophiles phag, of bacteria pervent infection), macrophage infliltration( phagacytosis stimulates fibroblast to lay collagen)
2. Proliferation Phase- Development of granulation Tissue (new vessesls and proliferating fibroblasts, red soft appearance. Fibrin and Fibronectin pass through and serve as scaffold for scar. Epidermis begins to regenerate
3. Maturation Phase- Mylofibroblasts help wound edges to close. 80% of original strength.

Primary Wound Healing Vs Secondary

Primary: "First Intention" surgical incision, uninfected. Simplest type of wound healing. Incision immediately fills with clotted blood. Compact dermal scar 80% strength of original skin
Secondary: ex. large surface wound, infected wound, inflammatory ulveration, infarction, or very small laceration. Much slower, wound is left to heal by itself, not bringing edges together.
MORE INFLAMMATION, GRANDULATION TISSUE, EPITHELIAL REGENERATION, WOUND CONTRACTION

Systemic Factors Impairing Wound Healing

1. Nutritional Deficiency
2. Inadequate Blood Supple (atherosclerosis or peripheral artery dieases
3. Diabetes Mellitus- impaired blood supple, decreased sensation, impaired immune function
4. Steroid Hormones- inhibit inflammatory process and collagen synthesis
5. Immunocompromised patients ( HIV pos)

Local Factors Impairing Wound Healing

1. Infection- most important cause
2. Early Motion of Wounds
3. Foreign bodies
4. Debris and Necrotic Tissue- form physical barrier to growth of new tissue and provide a medium for bacteria growth

1. Inadequate Formation of Granulation Tissueor assembly of scar

1. Inadequate Formation of Granulation Tissueor assembly of scar
a. wound dehiscense- wound opens. Common of abdominal surgery, poor suturing, malutrition
b. Ulceration- predisposing conditions of inadequite blood supply from atherosclerosis and impaired sensation in extreamities (peripheral neuropathy)
c. Incision Herniation- bulding sac within healing or healed abdominal incision due to abdominal pressure

Complications of Wound Healing

W-wound contraction
A-adhesions
G-Granulation tissue does not form
E-excessive scar
S-suture complications

2. Excessive Formation of Components of Repair Process

a. Hypertrophic Scar- raised scar caused by excessive collagen within boundaries of original wound
b. keloid- excessive collagenous protrusion at scar site beyond boundaries of original wound. ex. ear piercing, lacerations from surgery

3. Formation of Wound Contractures

a. excessive contraction may result in deformities of an area as well as limitation of motion at a joint, commonly seen after burns

4. Formation of Adhesions

a. Inflamed serosal surfaces(ex. outside intestinal surfaces) bind together. ex collagenous adhesions b/w inflamed loops of bowel.

5. Suture Therapy Complications

a. Sutures may be a source of infection
b. Premature suture removal prolongs healing process

Different Pathways of Reparative Response after injury or acute inflammation

STUDY CHART
Based on:
1. Whether injurious stimulus is promptly destroyed
2. Presence and extent of cell necrosis
3. Intactness of supporting framwork
4. Regenerative capacity of injured cells.

Non-neoplastic disturbances in cell growth

1. Hypertrophy- increase in mass due to cell size- ex. left ventricle due to increased work load
2. Atrophy- shrinkage of tissue- testes of elderly men
3. Hyperplasia- increase in mass due to cell number- ex. prostate or adrenal cortical hyperplasia.
4. Aplasia- no development. ex 1 kidney
5. Hypoplasia- underdeveloped- left ventricle
6. Metaplasia- cell transforms into another cell type- Barrett's Esophagus GERD. can progress to dysplasia
7.Dysplasia- abnormal organization and growth of cells. May progress to cancer such as with cervical epithelial cells. nuclei gets larger

Neoplasm

Neoplasm- an abnormal growth that is self-perpetuated.

Tumor

abnormal mass of tissue growing autonomously. interchangeable with neoplasm

Cancer

malignant neoplasm

Metastasis

cancer than migrates from primary site

Neoplasm differentiation

Degree that neoplasm is similar to comparable normal cells in appearance and function
1. Well differentiated- close resemblence, good prognosis
2. Moderately differentiated- intermediate
3. Poorly differentiated-poor resemblence
4. Anaplasia-lack of differentiation. Worst

Sarcoma

Sarcoma- a malignant tumor originating in mesenchyme tissue

Oma

Oma- a benign tumor of epithelial tissue

Adenoma

Adenoma- a benign tumor originating from glandular epithelium

Carcinoma

- a malignant tumor of epithelial tissue

Adenocarcinoma

- a malignant tumor of glandular epithelial tissue

Squamous Cell Carcinoma-

malignant tumor of squamous cell epithelia and/or well differentiated to squamous cell epithelia.

Differences between Benign and Malignant

Differences between Benign and Malignant
- Benign tumors: well differentiated. Contained with clear borders. Don't metastasize.
- Malignant tumors: poorly differentiated. No clear borders (crablike). Metastasize.

Naming Tumors

Names:
Smooth Muscle Benign Tumor: leiomyoma
Smooth Muscle Malignant Tumor: leiomyosarcoma
Lipid Benign Tumor: lipoma
Lipid Malignant Tumor: Liposarcoma
Fibroblast Benign Tumor: fibroma
Fibroblast Malignant Tumor: fibrosarcoma

Routes of Metastases

1. Hematogenous Spread of Tumor: tumor cells separate and some travel via the venous blood. Cells set up camp in new tissue. Ex) colon cancer to the portal vein to liver.
2.Lymphatic Spread of Tumor: tumor cells separate and some travel via the lymphatic
system and set up camp in lymph nodes. Ex). Breast cancer travels to axillary lymphatic ducts.
3. Metastasis by Seeding Body Cavities: tumor travels through surface of organ and spreads to the body cavity it's in and can spread to other organs in the same

Four Categories of Genes Altered Cancer

1. Protooncogenes: promote regulated cell growth/cell division-oncogene-uncontrolled growth. Ras and MYC gene
2. Tumor suppressor genes: inhibit cell growth- damaged on hereditary basis. NF1, NF2 RB p16
3. Genes promoting repair of damaged DNA. BRCA
4. Genes promoting apoptosis of cells with damaged DNA- most common gene mutated in human tumors. p53 most common damaged gene

Phases of Carcinogenesis

Initiation Phase: causes permanent damage to DNA. Irreversible. Ex) polycyclic hydrocarbons (combustion of tobacco-bladdar, kidney, lung, and oral cavity cancer), asbestos, alcohol, smoke.
-Promotion Phase: sustained or enhanced proliferation of cells damaged by initiation agents resulting in increased successive mutations leading to cancer Ex). when given estrogen for a long period of time, the high levels of estrogen may initiate(1st) and promote(2nd) cell modification bc of such exposure. Without being given progesterone to balance it, endometrial cancer can result.
---Cell changes caused by promotor are reversible, no tumor if promoting agent is applied before initatior or time between application of the promoter is successfully extended

. Viruses and Bacterial Carcinogens

- HPV- cervical cancer type 16 and 18
- Epstein Barr- lymphoma
- Hepatitis B- liver cancer
- Helicobacter pyloric BACTERIA- gastric carcinoma. treating h pylori can regress cancer

Cancers linked to radiation

1. UV- sunlight- skin cancer (squamous cell carcinoma, basal cell carcinoma, melanoma
2. Ionizing radiation- electromagnetic and particulate. ex. atomic bomb surivers (thyroid, breast, colon, and lung cancer)
nuclear powerplant accident chernobly- thyroid cancer of children
Miners of radioactive elements- lung cancer

Inherited alterations of tumor suppressor proteins

Rb- retinoblastoma
NF 1 and 2- neurofibromatosis. In brain like meniginoma
p16- malignant malanoma
APC- familial adenomatous polposis syndrome- patients develop 500-2500premalignant colon tumors , develop colon cancer by 50

Inherited genes allow repair of damaged DNA

BRCA1 BRCA2 breast cancer
xeroderma pigmentation- cannot repair mutations by UVB
heredity nonpolyposis colon cancer syndrome- mutation for DNA repair cause colon cancer, tested in patient that get cancer before 50.

Inherited muation to gene Preventing propagation of DNA muations

mutation to gene that causes apoptosis in mutated cells. P53

In situ vs invasive

- In Situ Cancer: cancer has not broken through the basal membrane of tissue.
- Invasive Cancer: cancer has broken through the basal membrane (basement) of the tissue.

Chronic Vs Acute Pain

Acute Pain- less than 6 months
Chronic- greater than 6 months

Pain threshold

point at which stimulus is perceived as pain. minimum varies between people. Tolerance- max intensity of duration endured

Processes (physiological events)

-Pain transduction-conversion of noxious stimulus to electrical activity at receptor
-pain transmission- transmission of that impulse from an afferent receptor to the CNS
-pain modulation- influences on the transmission
-pain perception-subjective experience of pain in the brain

Afferent Pathways

transmit impulses to dorsal root
A delta-small diameter, thinly mylenated, fast pain characterized as sharp or prickling, localized, located on skin surface
C Fibers- slow pain- small diameter, unmylenated, less localized, do not trigger withdrawl reflex, associated with increased tissue damage
-Substaintia gelantinosa- lamina II of dorsal horn, pain modulation, gated mechanism.
-(anteriolateral) Contralateral tract- pain travels on opposite side of body.Pain crosses at midline at spinal cord level. Any damage to tract will result in contralateral loss of sensation.
-Dorsal-Column-medial lemniscus- conveys touch, pressure and corsses at midline of medulla. Contralateral sensation.

Activation of nociceptors

*Activation of nociceptors- pain producing chemicals are realized in the area of tissue damage. If prolonged, hyperalgesia and lowered pain threshold.
Released chemicals depend on type of tissue or cells that are damaged

Synthesized Chemicals

-Prostaglandins- Inhibited by NSAIDS pain and fever
-Leukotrines- vasoconstriction, bronchiospasms, increased vascular permiablity. important in asthma.
-Arachidonic acid metabolites- vasodilation and permeability
-Substance P- edema, vasodilation, bradykinin release, histamine and seratonin release

Cutaneous Pain

If only skin, Tingling, sharp, burning, cutting possible along a dermatone. Caused by burning, freezing, cutting, pricking. Generally if something is tender to touch then injury localized at the area.

Deep Somatic Pain

Muscles Joints, Tendons Periostium. Poorly localized because of fewer receptors

Visceral Pain

Renal, Gallbladdar, appendix. Insensitive to some stimiul (cutting). Usually secondary to stretching, distention- swollen internal pressure, ischemia, inflammation.
True Visceral Pathway-small unmylenated pain fibers travel with axon of the autonomic nervous system. Poorly localized with classic symptoms

Referred Pain

MEMORIZE CHART!!!!!!
Percieved at a site different from its origin. Visceral pain is often referred
-Convergence Projection Theory- brain incorrectly projects visceral pain to somatic dermatone
ex. Heart pain- substernal radiatingto the back and inner arm.

Dysfunctional Pain

Not associated with noxious pain or nerves. No damage going to tissue or inflammation but still in pain Fibromyaligia, tension headache, migraine, IBS

Neuropathic Pain

Both Peripheral and Central Causes.Due to damage or diseased nerves. Ex. Shingles- pain comes days before rash
Hyperalgia- excessive response to normal pain
Allodynia- response to no pain

Descending Pathway

-Control and influence over painful stimuli- frontal cortex
-Interpretation and response- efferent pathway
Cerebral cortex to spinal cord- periaqueductal gray matter.

Modulation

THE PROCESS OF DAMPENING PAIN AND RELATED NEURAL SIGNALS
- can be activated by systemic or neuraxial injection of opiods, electrical stimulation, stress, suggestion, pain, serotonin neuromodulator
-Segmental inhibition- hammer to thumb
-Diffuse noxious inhibitory control- acupuncture
-Neurotransmitters- excitatory, inhibitory, inflammation
-Inhibitory transmitters- GABA, norepinephrine receptors, endogenous opiods

Dermatones

Innervation from dorsal root
Neck- C3
Nipples- T4
Umbilicus- T10

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