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184 Cards in this Set
- Front
- Back
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Primary Healing
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First Intention
-damage is minimal and edges are closely opposed -sterile, no jagged edges -minimal scarring - quick healing ex. papercut, incision - best case scenario |
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Secondary Healing
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Second Intention
- wound edges are far apart and don't reattach - takes longer and scaring is likely ex. big gash, scrape knee on bike - infection complicated the healing |
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Gliosis
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proliferation of nonconducting neuroglia
repair of nervous tissue |
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Tissue Repair in CNS
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If soma is intact, some regeneration may occur
However, after 14 days, glial cells form scar tissue that blocks further regeneration No function is restored |
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Tissue Repair in PNS
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If soma is intact AND if schwann cells remain, regeneration may occur
1. Process distal to injury degenerates; macrophages clear debris; Schwann cells regenerate at injury site 2. Buds emerge from remaining stump 3. Buds follow tube; other buds degenerate 4. Myelination of new process = reinnervation |
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How likely is tissue repair in PNS?
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Very conditional; not likely to happen
If surrounding connective tissues are lost, guidance of bud growth is lacking so they grow in all directions and no function is regenerated |
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What inhibits neurons in the CNS from regenerating?
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Oligodendrocytes
They secrete growth factors that stop the axon |
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Acquired Immunity
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AKA: Adaptive/Specific Immunity
- Second line of defense - Responds less rapidly than innate immunity; takes days/weeks - It is specific to each microbe and antigen |
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What are the three characteristics of Acquired Immunity?
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1. Specificity
2. Memory 3. Tolerance |
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What is specificity?
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It reacts to a specific substance and is specific to each antigen it encounters
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Immune System Memory
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Long-term retention
Immune system remembers what we've been attacked by On second exposure the immune system is more rapid and efficient at killing |
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Immune System Tolerance
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Ability to distinguish between self and foreign antigens
Builds defenses against only appropriate antigens Self-recognition |
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What is an antigen?
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Molecule that elicits an immune response by causing an antibody to be formed
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What is the epitope?
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Binding site for the antigen
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Pathogen
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disease causing antigen
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Tolerance largely depends on which cell surface proteins?
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MHC antigens
Major Histocompatability Complex also called Human Leukocyte Antigen (HLA) |
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Where are MHCs coded?
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On chromosome 6
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MHC Class I
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- Molecules found on the surface of all nucleated cells
- Their function is to display fragments of proteins from within the cell to T cells; healthy cells will be ignored while cells containing foreign proteins will be attacked by the immune system - Like an ID tag or billboard - Looked at my CTLs or Killer T cells |
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MHC Class II
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- Molecules made by antigen processing cells
- Found on macrophages, dendritic cells and B cells - Examined by Helper T cells |
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Who created the first vaccination?
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Edward Jenner
small pox vaccine |
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What are the different types of lymphocytes?
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B lymphocytes and T lymphocytes
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Which type of lymphocyte is responsible for Humoral Immuity?
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B lymphocytes
aka: Antibody Mediated Immunity create a specific antibodie |
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What are the different types of B lymphocytes?
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PLASMA CELL
- antibody factory MEMORY B - Long lived immunity - if infected a second time, it mounts a fierce attack |
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What type of immunity are T lymphocytes responsible for?
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Cell Mediated Immunity
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What are the different types of T lymphocytes?
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HELPER T CELLS
- recognize MHC IIs - aka CD4 lymphocytes MEMORY T CELLS - long term retention CYTOTOXIC T CELLS - recognize MHC I - aka CD8 lymphocytes - Search and destrory; activate cell to kill itself - Produce and release peforin |
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What does perforin do?
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Perforates cell membrane
Causes cell to commit apoptosis |
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Where do B lymphocytes mature?
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In the red bone marrow
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Which part of the antibody is specific to an antigen?
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FAB binding site
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Where does the FAB portion attach?
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to the epitope
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Which region is constant for all antibodies?
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Fc Region
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How do antibodies destroy?
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1. Atrracting IS cells
- Opsinization - Attracts phagocytes and makes it easier to eat - "Puts ketchup on them" 2. Agglutination - Clumping - Antibodies hook to them and clump them all together - Prevents it from getting in the cell - Allow phagocytes to engulf more at a time 3. Activate Complement - Membrane Attack Complex (MAC attack) - Activated in cascade - Antibody binds to antigen, and 20 proteins follow suit till we get MAC attack - Come together, insert into membrane, destroys cell |
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What are the five types of anitbodies?
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GAMDE
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IgG antibodies
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- MAIN TYPE IN BLOOD
- Only one to cross placenta - Binds to macrophages * SECONDARY RESPONSE ANTIBODY |
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IgA antibodies
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- Secreted in saliva, breat milk, respiratory, and urogentical tract
- Protects mucous membranes |
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IgM antibodies
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- In plasma
- Star shaped * PRIMARY/FIRST ANTIBODY PRODUCED |
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IgD antibodies
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- Found on B lymphocytes
- Needed for B cell activation - Function unknown |
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IgE antibodies
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- Found on MAST CELLS in allergic response
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What are the body's primary lymph tissues?
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Bone marrow and the thymus
Produces B and T cells |
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What are secondary lymph tissues?
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Lymph nodes, tonsils, spleen, lymphatics
Then re-enters the circulatory system through the right lymph duct and the thoracic duct |
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Thoracic Duct
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Drains majority of body
Left upper head, extremeity, chest, and lower limbs |
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Right lymphatic duct
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Drains right upper head, extremity, and thorax
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First antibody response takes how long?
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About a week
Peaks at about 12 days and then tapers off |
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Second exposure to antigen produces what?
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Faster rise in antibody production
Quick, fierce attack is mounted |
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Autoimmunities
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Loss of tolerance
Attacking self cells |
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Hypersensitivities
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Over reaction of immune system
It attacks things that it should ignore |
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Immunodeficiencies
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Insufficient immune response
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Autoimmune Diseases
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"Friendly Fire"
- Result from breakdown in the integrity of immune tolerance such that humoral (B cell) and cellular (T cell) immune response is mounted that attacks host cells or antigens |
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Etiology of Autoimmune Diseases
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Idiopathic - Unknown
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Which proteins are responsible for the immune system being able to distinguish between foreign and self antigens?
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MHC/HLA complex
(genes on chromosome 6) Something is wrong with the ID tages on MHC's |
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Theories for autoimmune disease causes
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1. Genetics - defective chromosome 6 where MHCs are made
2. Hormones - estrogen 3. Environment |
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What is the most common autoimmune disease?
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Grave's Disease
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Grave's Disease
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- Autoantibodies bind to TSH receptors
- Attach and overstimulate Thyroid hormones (hypersecretion) - Enlarged thryoid = GOITER - anxiety, weight loss, expothalmus (eye bulging) |
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Insulin Dependant Diabetes Mellitus
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Type 1 Diabetes
- beta cells are destroyed so no insulin is produced at all |
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Myasthenia Gravis
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- autoantibodies produced against ACH receptors
- block ACH receptors from binding at NMJ, and destory them as well - stops muscle from contracting |
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Rheumatoid Arthritis
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- target synovial membrane and cartilage
- chronic inflammation leads to scarring and joint deformation |
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SLE
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Systemic Lupus Erythematosis
" The Great Imitator" |
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Statistics of Lupus
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More prominent in females
Younger girls (20-40) get it More prominent in black females |
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Etiology of Lupus
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Idiopathic
Thought to be genetic (chromosome 6), environment (common in twins) |
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What are the 4 areas Lupus targets?
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1. Skin (malor rash)
2. Joints 3. Kidneys 4. Heart (pericardial and valve damage) |
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Pathogenesis of Lupus
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- Autoantibodies are produced against a variety of targets
- Its a multisystem disease that affects DNA, ribosomes, etc - Ag/Ab complexes deposit in bone marrow of tissues |
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Signs and Symptoms of Lupus
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Vary widely depending on target
* characterized by remission and exacerbation Sunlight exposure and stress can cause it to flare up |
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How is Lupus diagnosed?
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Anti-nuclear antibodies (ANA) test
they are produced against DNA, RNA, etc and are common in those with Lupus |
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How is Lupus treated?
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Palliative = reduce pain, but no cure
- Corticosteroids and anti-inflammatory drugs Ex. ibuprofin |
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In severe cases how is Lupus treated?
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With immunosuppressants
- give them because the immune system is responding too much, so we weaken it - wait till life or death because of the severe side effects - they put you at an increased risk for infections |
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What are the #1 and #2 causes of death in Lupus?
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#1: Immunosuppresants
#2: Kidney failure |
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What happens in Multiple Sclerosis?
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- Demyelination of axons in the CNS
* PNS nerves are left untouched |
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Etiology of MS
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Idiopathic
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Contributing Factors to MS
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GENETICS
- chromosome 6 variations HORMONES - estrogen - peak diagnosis is 20-40 years old MOLECULAR MIMICRY THEORY - ID tag on herpes and mono (epstein bar) is similar to myelin sheath ID tags, so its a mistaken identity problem ENVIRONMENT - colder environment increases chances of getting MS - Increased Vitamin D decreases MS chances |
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Pathogenesis of MS
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Characterized by remission and exacerbation
Autoimmune destruction of the myelin sheath Dymelination triggers inflammation |
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Signs and Symptoms
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(Vary depending on area of demyelination)
Common ones: - Visual impairment - Muscle weakness - Ataxia (loss of coordination) - Speech - Mental impairment |
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Diagnosis of MS
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Evoked potentials: EEG, shown different light patterns and watch brain activity
MRI: show plaque and scars |
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Prognosis
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Palliative
- corticosteroids, interferon Prognosis varies widely |
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Immune Hypersensitivity Reactions
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An abnormal response to a relatively harmless environmental agent, an allergen (exogenous antigen)
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Describe Type 1 Hypersensitivity Reactions
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Anaphylactic-Type Reaction aka Immediate Hypersensitivity Reaction
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Type 1 Hypersensitivity Reactions are mediated by?
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IgE antibodies and mast cells
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Examples of Type 1 Hypersensitivity Reactions
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Hay fever, broncial asthma, anaphylatic shock, food allergies, latex allergies
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Etiology
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Idiopathic
Genetic, Environmental - familial - more common in industrialized countries and urban settings - hygiene hypothesis |
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Hygiene Hypothesis
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- Kids who grow up in antigenically rich environments = less likely to get allergies
- Dirtier is better - Worms = decreased allergies |
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1st Exposure to Type 1 Hypersensitivity Reactions
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- Allergen is processed by the immune system
- Plasma cells produce IgE antibodies against the allegen - IgE become fixed on mast cells and they become "sensitized mast cells" |
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2nd Exposure to Type 1 Hypersensitivity Reactions
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- Allergen binds with IgE causing degranualtion (exploding) of mast cell and release of histamine
- Histamine vasodilates and increases capillary permeability resulting in S&S of allergies |
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Anaphylaxis
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severe life threatening systemic hypersensitivity
ex. penicillin, bee sting, shell fish, peanuts - second exposure results in: systemic vasodilation and bronchospasm |
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Treatment of Anaphylaxis
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- Epipen
- People with severe allergies should wear a med alert bracelet |
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Effects of mast cell degranulation in various places
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1. SKIN
- urticaria (hives) - pruitis (itching) 2. EYES - water - conjunctivitus 3. GI TRACT - nausea, vomiting, diarrhea 4. NOSE - sneezing, runny nose, itchy nose 5. RESPIRATORY TRACT - coughing, wheezing |
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Etiology of AIDS
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Infected by the Human Immunodeficiency Virus (HIV)
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What cells does AIDS destroy?
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Helper T cells
Results in opportunistic infections |
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AIDS was first recognized when and where?
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June 1981 in LA
The HIV virus was first isolated in 1983 |
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General Statistics of AIDS
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- More news infections occur in men then women
- The largest ages infected are 13-29 - Most young people are infected sexually - 44% of infections occur in African Americans; racially disproportionate - Women account for 50% of infections |
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What continent is affected worst?
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Africa (2/3) of cases
Sub-Saharan region is hardest hit |
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What is life expectancy of a person with AIDS?
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Raised from 49 years old in 2003 to 69 years old in 2008
In Africa it remains lower, somewhere around 30-40 years old |
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Describe the structure of the HIV virus
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1. Core of 2 strand or RNA and enzymes
2. Surrounded by core proteins/capsid (p24) 3. Outer coat of glycoprotein (gp120) |
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What do CD4 Helper T cells bind to?
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gp120 glycoprotein
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What are the different types of virus?
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HIV-1: common type = HIV positive
HIV-2: least common; mostly in West Africa; not as easy to be infected; progess much slower Testing accounts for both |
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What role does co-receptor CCR5 play in HIV?
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HIV has to have CCR5 in order for virus to enter cell
People without CCR5 can't get HIV |
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HIV can be considered what type of virus?
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A lentivirus (attacks immune system) and a retrovirus (genetic material carried on RNA)
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RNA is changed to DNA by?
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Reverse transcriptase
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After RNA is converted to DNA, what is the next step?
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DNA is inserted into the host cell's DNA
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After HIV's DNA is inserted into the cell's DNA what happens?
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HIV takes over the cell's machinery and starts replicating, producing viral proteins
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What are the 8 steps of HIV replication?
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1. HIV binds to CD4 (Helper T cell)
2. Uncoating of virus (viral core enters cell) 3. Reverse Transcriptase makes viral DNA 4. Integration into cell's DNA via integrase 5. Transcription of viral DNA to messenger RNA 6. Translation of mRNA to produce HIV polyprotein 7. Protease cleaves viral proteins into individual proteins 8. Assembly and release from host cell |
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What are the host cell functions in HIV?
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- recognize foreign antigens
- stimulate B cell response (antibody mediated) - stimulate CTL - stimulate macrophages |
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Properties of HIV?
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- replication rate (billions per day)
- escapes detection (NEF prevents MHC I's from being displayed) - mutation rate (reverse transcriptase is error prone) - host choice |
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What are the three stages of HIV?
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1. Primary HIV infection
2. Clinically asympotomatic stage 3. Symptomatic HIV/Progression to AIDS |
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Stage 1:
Primary HIV Infection |
- develop mono like symptoms
(fatigue, fever, swollen glands, headache, night sweats, myalgia - muscle pain, sore throat, nausea, vomiting) - Lasts 2 to 4 weeks - During this stage there is a large amount of HIV in the blood and the immune systems responds by producing HIV antibodies - PROCESS CALLED SEROCONVERSION |
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How long does it take for seroconversion to be complete?
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1 to 3 months
If an HIV test is done before seroconversion is complete, then it may be a false negative |
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Stage 2:
Clinically Asymptomatic Stage |
- Lasts an average of 10-12 years
- Free from major symptoms, although lymph nodes may be swollen - Level of HIV in the blood is low, but people remain infectious and antibodies are present - HIV IS NOT DORMANT HERE, and is very active in the lymph nodes - Viral load test can measure the amount of HIV RNA in the body |
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Stage 3:
Symptomatic HIV / Progression to AIDS |
- As the immune system fails, symptoms develop and worsen over time
- Symptomatic HIV is mainly caused by the emergence of opportunistic infections that the immune system would normally prevent |
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What are the three classifications of HIV infection?
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Category 1: More than 500 cells/micro liter
Category 2: 200 - 499 cells/micro liter Category 3: less than 200 cells/micro liter |
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Dying from AIDS is attributed to what?
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Lack of CD4 (Helper T) cells, NOT from the virus itself
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What are some opportunistic infections that arise during AIDS?
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Kaposi's Sarcoma
Pneumocystis Pneumonia Tuberculosis Candidiasis Crytosporidium Wasting Syndrome |
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Kaposi's Sarcoma
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Cancer of endothelial cells that line small lymph vessels
They fill with blood and produce lesions on skin and inside - Associated with herpes (KSHV) - 2000x more common in AIDS |
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Pneumocystis Pneumonia
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aka PCP
* Fungus |
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Tuberculosis
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-attacks lungs, kidneys, brain
- caseous necrosis - caused by bacteria and treated with antibiotics - a lot of people developed MDR (multi-drug resistance) - #1 CAUSE OF AIDS DEATH |
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Candidiasis
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aka THRUSH
fungal; yeast infection |
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Crytosporidium
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Protozoa that causes severe diarrhea (gals/day)
See this when T CD4 levels fall below 200 |
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Wasting Syndrome
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weight loss
muscle mass loss people with AIDS have a higher metabolic rate which constantly burns calories |
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HIV is found in what bodily fluids?
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Blood
Semen Vaginal Fluid CSF Tears Saliva Breast Milk |
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Which body fluids have enough HIV in them to transmit it to someone else?
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Blood
Semen Vaginal Secretions Breast Milk |
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What are the 3 transmission routes for HIV?
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1. BLOOD TO BLOOD
2. SEXUAL 3. PERINATALLY |
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Blood to Blood Transmission
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1. BLOOD TO BLOOD
- needles - IV drug users - accidental needle injection - tattoo needles - blood transfusions * IV drug use is most common |
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Sexual Transmission
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- Male to Male (MSM)
- Male to Female (66%) - Female to Male (11%) * easier for a male to give to a female |
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Perinatal Transmission
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Mom to Baby
- small enough to cross placenta - most common during labor and delivery (do C-section to reduce chances) - Treat with anti-retroviral medicine BEFORE birth |
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Prevention of Transmission of AIDS
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1. If infected, do not have vaginal, oral, or anal intercourse
2. If have intercourse, use condoms with no N-9 3. Donated blood must be tested for HIV 4. Take care when handling needles 5. If infected, females do not get pregnant 6. Circumcision can help cut transmission in 1/2 (only cuts female to male transmission) |
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Testing for HIV
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- Most common test is HIV antibody test
- Also can use EIA (enzyme immunoassay) also known as ELISA (enzyme-linked immunosorbent assay) followed by the confirmatory Western Blot test |
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What does HAART stand for?
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Highly Active Anti-Retroviral Therapy
aka Combination Antiviral Therapy |
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What are the four types of treatment that HAART can combine?
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1. Reverse Transcriptase inhibitors
- prevent RNA from being converted to DNA - most common is AZT 2. Protease Inhibitors - bind to active sites of HIV-1 protease 3. Fusion Inhibitors - Inhibit HIV from binding to Helper T cells 4. Integrase Inhibitors - inhibits DNA from being inserted into cell's DNA |
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When should HAART treatment be started?
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When CD4 levels falls below 350, but before they fall below 200
Should start a 3 drug cocktail |
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When should HAART drugs be switched?
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If the cocktail become too toxic or your body builds up a tolerance to them
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What are the difficulties in finding a vaccine?
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- HIV mutates often
- Antibodies are not very effective against HIV infection (they arent effective in intracellular pathogens. We need CD4s to get them, not vaccines) |
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What does neoplasm mean?
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Tumor
New growth. Abnormal mass growing by uncontrolled proliferation that serves so useful purpose or function |
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Neoplasms can be what two kinds?
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Benign or Malignant
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Normal cell growth
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Depends on the balance on stimulus and inhibition
Promoters and suppressors of growth are balanced |
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Cancer ranks where in causes of death in North America?
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2nd
25% of the population has it, and 15% die as a result |
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They say if you don't usually die from cancer...
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You'll die with it
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Most common of all cancers for men and women is?
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Skin cancer
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Prevalence of cancer deaths for men?
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1. Lung
2. Prostate 3. Colon |
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Prevalence of deaths among women?
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1. Lung
2. Breast 3. Colon |
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What is oncology?
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The study of tumors
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Benign
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"kind"
growth is slow, orderly, and localized NEVER metastasizes |
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Malignant
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"with malice or intent to cause harm"
Characterized by rapid, disordered, unctrolled growth by aggressive invasion into adjacent normal tissues Has the ability to metastasize |
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Malignant neoplasm is?
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Cancer
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Primary Site
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site of origin; where cancer first started
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Secondary Site
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Where the cancer metastasizes to
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What are the 3 modes of metastasis?
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1. Blood
2. Lymph 3. Seeding (spread of cancer through body cavities) ex. ovarian cancer -> pelvic, rectum brain cancer -> vertebral cavity |
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What are common sites of metastasis?
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Bone, brain, liver, lungs
* Places with good blood supply |
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What is Carcinogenesis/Oncogenesis?
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Development of cancer/tumor
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All cancers are thought to be due to?
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Genetic Mutations
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Proto-oncogenes
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Genes that control cell growth
- produce proteins that determine if a cell should divide - make sure they are following directions appropriately Good :) |
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Oncogenes
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Mutated proto-oncogenes that can't control cell division anymore
Bad :( |
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Tumor Suppressor Genes
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TSGs: safeguard against irresponsible growth
- Make sure reproducing cells are the right ones by: 1) Trigger DNA repair (fix mutations) 2) Apoptosis (of cells that are too damaged to fix) |
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What is the p53 gene?
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"The Guardian Angel Gene"
Helps prevent gene mutations that lead to cancer * Over 1/2 of all tumors have a defective p53 gene |
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Neoplasia, or uncontrolled cellular proliferation, can result from?
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- mutations that "turn on" the oncogenes that stimulate disordered growth
- or from mutations that result in loss of TSGs and their products that inhibit cellular growth |
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Mult-Hit Model of Carcinogenesis
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More than one mutational event (hit) is required to cause cancer
- Usually 4-7 hits causes it |
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What are the three steps in Carcinogenesis?
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1. Initiation
2. Promotion 3. Progression |
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Step 1: Initiation
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MUTAGENS that result from exposure of a cell, or cells, to a carcinogen, which permanently alters its genetic material
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Common Mutagens
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Virus, radiation, some chemicals
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Step 2: Promotion
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MITAGENS: A substance that causes intiated cells to turn into tumors.
Tumors result when the promoter is administered after, but not before, inhibition Mitagens tell mutated cells to increase mitosis Usually has to be long-term exposure |
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Common Mitagens
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Hormones, alcohol, most chemical exposures
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Step 3: Progression
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Tumor cells acquire malignant characteristics
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What is a completed carcinogen?
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A substance that is both an initiator and a promoter
Ex. Tobacco Smoke |
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Etiological Factors in Carcinogenesis
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RADIATION
1. Ionizing radiation (x-ray, atomic bombs) 2. UV radiation (low strength radiation) CHEMICAL EXPOSURE - alcohol, coal tar, cigarette smoke, asbestos (leads to lung cancer), etc - alcohol reduces p53 gene activity GENETICS - BRACA 1 and BRACA 2 mutations can lead to breast and ovarian cancer VIRAL - HPV: cervical cancer; inserts where p53 gene is - HBV: hepatitis B virus, liver cancer - KSHV: Kaposi's Sarcoma-Associated Herpes Virus |
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Hyperplasia
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Increased mitosis in response to specific growth stimulus
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Hypertrophy
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Increase in cell size due to increased demands
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Anaplasia
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Undifferentiated; cells lose specialization
Return to a more primitive form |
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Dysplasia
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Disordered cell growth
Cells are variable in size, shape, and structure Usually a precursor to tumor, precancerous lesion/carcinoma in situ |
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The condition of dysplasia is termed?
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Pleomorphism
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Characteristics of a Benign Tumor
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1. CELL STRUCTURE
- near normal - nucleus to cytoplasm ration is normal, 1:4 ratio 2. TISSUE STRUCTURE - organized - resembles tissue it grows in 3. GROWTH RATE - relatively slow but still above normal growth rates - about 3% growth fraction - grows through expansion 4. INVASION - locally invasive 5. METASTASIS - never metastasizes 6. CAPSULE - Connective tissue capsule is common 7. PROGNOSIS - depends on site - can lead to: compression, bleeding, size |
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Characteristics of a Malignant Tumor
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1. CELL STRUCTURE
- bizzare; pleomorphic - N to C ratio is 1:1 - Mitotic figures present - Primitive cell types (anaplysia) 2. TISSUE STRUCTURE - disorganized 3. GROWTH RATE - measure by growth fraction (% of cells dividing) - slow growers = <10% - fast growers = >10% - more mitosis means darker nucleus 4. ANGIOGENESIS - Very agressive tumors sevret a protein, VEGF, that calls vessels to the area to meet its increased blood supply demands 5. INVASION - Collagenase: breaks down CT around tumor and enables the cancer to send out claw-like extensions - Telomerase: allows cancer cells to be immortal - Loss of contact inhibition: overgrow normal boundaries with no regard 6. CAPSULE - rare; if they do it's incomplete 7. METASTASIS - 3 routes: blood, lymph, seeding 8. PROGNOSIS Depends on site of the cnacer, type of cancer, stage, and response to treatment |
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The tendency of cancer cells to overexpress VEGF leads to what two things?
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1. Unlimited growth potential of tumors
2. New vessels are highly permeable, which allows the cancer to easily metastasize |
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What does VEGF stand for?
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Vascular Endothelial Growth Factor
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Why is the liver a common site for metastasis?
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Large blood supply there because
of the hepatic portal circulation (which drains the GI tract) |
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Tumor Effects
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1. Tissue destruction
2. Obstruction/Compression 3. Infection (lack of white blood cells) 4. Anemia - common in cancers of bone marrow, like Leukemia - due to lack of red blood cells 5. Pain - can invade nerve and bone endings 6. Cachexia - wasting syndrome involving general weakness, fever, weight loss, and pallor |
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The best diagnosis of cancer would be?
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An attempt to accurately identify the site of origin and the type of cells involved
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Three ways we diagnose cancer?
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1. Diagnostic Tests / Signs and Symptoms
- use imaging studies and scans 2. Biopsy - removal of tissue for microscopic evaluation 3. Tumor Marker - substances that can be found in abnormal amounts in the blood, urine, or tissues of some patients with cancer - Limited use |
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CA 125
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Ovarian Cancer
(used to monitor treatment) Not detectable until advanced stages , so we cant use it to screen |
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PSA
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Elevated with prostate cancer
> 10ng/mL = abnormal Currently the only screening marker |
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p53 mutations
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colon cancers cells shed in stool
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PSA stands for?
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Prostate Specific Antigen
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HER-2/neu
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An oncogene in breast cancer that indicated aggressive growth likely
- a receptor found on certain breast cancer cells that tells them to undergo mitosis - try to block them to slow breast CA growth |
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Estrogen receptors/ Progesteron receptors
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Determines tx in breast cancer
- estrogen binds to breast cancer cells and tell them to divide |
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Which drug blocks estrogen receptors?
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Tomaxaphin
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What are the 3 stages cancer is based on?
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1. Tumor size and invasion
2. Lymph node involvement 3. Metastasis |
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How does the TNM system work?
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Tumor, Node, Metastasis
a. T is 1-4 - size and invasiveness of primary tumor - 1 is small and localized - 4 is agressive and claw-like b. N is 0-3 - Lymph node involvement - 0 is no involvement - 3 is widespread node involvement c. M is 0-1 - tumor metastasis |
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Grading
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Tumor grade system used to classify cancer cells in terms of how abnormal they look under a microscope and how quickly the tumor is likely to grow and spread
- look at cell characteristics |
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After biopsy, tissue is examined for what 3 things?
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1. Degree of differentiation
- we want it to be more specialized, like the surrounding tissue - more primitive is a worse prognosis 2. Extent of pleomorphism - more it resembles normal cells that better the prognosis - the more bizarre shape = worse 3. Frequency of mitosis - mitotic figures - more GF is worse prognosis |
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What are the four grades?
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G1:
- well differentiated - low grade - low growth so better prognosis - 3% GF G2: - moderately differentiated - intermediate grade - 9% GF G3: - poorly differentiated - high grade - 16% GF G4: - Undifferentiated/Anaplastic - High grade - very primitive - >30% |
