Chapter 16- Altered Cellular and Tissue Biology and Biology of Cancer
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cdixon0104 on January 2, 2011
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chapter 16- altered cellular and tissue biology and biology of cancer
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93 terms
Terms | Definitions |
|---|---|
 Can be physiologic | good |
| Can be Pathologic | bad |
| Stop using a muscle it will get smaller | Atrophy/Disuse |
| Atrophy ccan affect any organ, but most common are the | skeletal, heart, secondary sex organs and brain. |
| Cardiomyopathy is considered | Atrophy pathologic |
| Exercising is considered | Atrophy physiologic |
| When women are pregnant, uterus will get bigger, breasts will get bigger | Hyperplasia physiologic During a pap test, will have more cells: Hyperplasia pathologic |
| Precursor to cancer | Metaplasia |
| Epithelial cells are exposed to chronic cigarette smoke convert to squamous cells, do not have the cillia, will develop smokers cough | Metaplasia |
| Precursor to cancer, women that are perimenopausal | Dysplasia |
| Reversible cell injury | cellular swelling and fatty changes |
| In Cellular swelling with cell injury what happens? | Na + enters cell, Na+/K+ pump malfunctions, impaired synthesis of ATP |
| In Cellular swelling there is an Inflammatory processes this causes? How can we stop it? | Ischemia, if we take away the inflammatory process and reduce inflammation, the swelling will go down |
| Fatty changes in cell injury do what? | Increased fat load or unable to metabolize fat appropriately |
| Fatty changes take place where in the body? | Liver, heart... |
| What medications can you take to reduce the fatty cells? | Lipitor, Zocor |
| In cell injury what happens to Ca and what does this change in Ca cause? | Ischemia can cause increased ICF concentrations of Ca++, Plasma membrane becomes damaged, Enzymes become activated, Cell work becomes disrupted |
| What happens to ATP in cell injury? | ATP depletion- Loss of stores, cannot make new ATP- cells cannot run without ATP, not going to have the energy to run, Cellular swelling, Decreased protein synthesis, Membrane transport disrupted so ICF and ECF concentrations abnormal |
| Byproduct of cellular reactions | Free radicals, are pointed and can cause damage to cell membrane |
| Most free radicals are "mopped up" by | antioxidants, take care of free radicals, may have too many free radicals or not enough antioxidants then the free radicals will cause damage |
| Free Radicals can Cause damage to cells | DNA |
| Single most common cause of cell injury | hypoxia |
| S/S of hypoxia | Decreased O2 in air, decreased blood flow to cell, respiratory causes, circulatory causes, anemia |
| When the pH falls in the cell | lactic acid accumulates and death occurs in various time for different cell |
| You can have reperfusion in the cell when the | blood restores as cells swell and free radicals are produced |
| The Most common cause of hypoxia is? | ischemia |
| What affects nervous system, blood, kidneys, inhibits enzymes necessary for Hgb synthesis (problems with oxygenation), induces hemolysis, neurological effects (attention deficit, convulsions) | Lead |
| What causes hypoxia d/t increase binding with Hgb, displaces O2, HA, tinnitus, N/V | CO |
| What causes liver damage from acetylaldehyde, genetic abilities to metabolize ETOH, also contributes to nutritional deficits | Alcohol |
| What can cause or worsen degenerative disease like AD, MS, PD | Mercury |
| What causes viruses enter cell and incorporate DNA into theirs, can replicate and produce continued injury after the initial exposure, bacteria produce toxins that interfere with ATP production | Biologic agents |
| What causes ionizing breaks chemical bonds to kill cells, injury depends on dose, time of exposure and sensitivity of tissue, cancer treatment (dividing cells more susceptible to damage), blood vessel dilation (erythema of skin), repeated exposure leads to scarring and fibrosis, UV (damage to melanin producing cells), damages DNA | Radiation |
| What has an entry and exit wound, disrupts brain and cardiac impulses, burns from impedence of electrical flow, heat generated (when electricity stopped), worse burn in tissue that are resistant to current | Electricity |
| Water | ECF moves to ICF, ATP loss impairs Na/K pump, increased Na inside cell pulls H2O, is reversible |
| Tay Sachs disease | glycolipids in the brain and other tissues, motor and mental deterioration |
| Fatty liver | as result of ETOH use and increased intake and subsequent deposit |
| Glycogen | accumulation results in excessive vacuolation of cytoplasm, most common cause is diabetes |
| Protein | excess accumulates primarily in epithelial cells of renal convoluted tubule and in antibody-forming plasma cells, usuall little or no protein in urine and presence in significant amounts indicates cellular injury and altered cellular function |
| Melanin | absorbs UV rays, stimulated by UV exposure, traps free radicals produced by UV exposure, overexposure can lead to melanoma |
| Hemoproteins | hemosiderosis (excess iron stored in cells, risk in those with repeated blood transfusions, can lead to liver damage), bilirubin (leads to jaundice) |
| Dystrophic calcification | comes from dead or dying tissues, atherosclerosis, heart valves, coronary arteries, center of cancer growths |
| Metastatic calcification | calcium from blood deposits in otherwise healthy tissues, hyperparathyroidism, renal failure |
| What is gangrene? | Large area of tissue necrosis |
| What are the three types of gangrene? | Dry, Wet, Gas |
| What are defining characteristics of Dry Gangrene? | shrinking away from tissue, Obvious, Usually definitive line of demarcation from healthy tissue, Not enough arterial blood and cause hypoxia, Develops more slowly, Arterial circulation compromised but venous circulation non-impaired |
| What are defining characteristics of Wet Gangrene? | smells, hard to treat, No definitive line of demarcation, Part cold, swollen, pulseless, smelly, black, Can affect any organ, tissue, Neutrophils invade the area, Venous circulation impaired (waste sitting there) |
| What are defining characteristics of gas Gangrene? | Caused by clostridium bacteria (anaerobic), found in soil, Toxins dissolve cell membrane, bubbles of gas form in muscle cells, Leads to cell death, hemolyticanemia, hemoglobinuria, renal failure |
| What is apoptosis? | Normal elimination of "worn out" cells or those programmed for removal, Genes called suicide cells become activated to stop life saving functions of cell |
| Physiologic apoptosis | lose the webbing in fingers during embryonic life |
| Pathologic apoptosis | blood cells during chemo, produces free radicals |
| Benign tumors | Well encapsulated and well differentiated, contain some normal tissue structure and do not invade the capsule and regional lymph or distant locations, Can progress to cancer |
| Malignant tumors | Rapid growth and specific microscopic alterations (loss of differentiation), absence of normal tissue organization, lack of capsule, invasion into blood vessels, lymphatics, and surrounding structures and distant spread (metastasis) |
| Hallmark of a malignant melanoma | anaplasia (loss of differentiation, nuclear irregularities and loss of normal tissue structure |
| Stage 1 of cancer | Cancer confined to organ of origin |
| Stage 2 or B of Cancer | Locally invasive |
| Stage 3 or C | Spread to regional structures such as lymph nodes |
| Stage 4 or D | Spread to distant sites such as liver spreading to the lungs or prostate spreading to bone |
| Autonomy | Cancer cells independence from normal cell controls |
| Anaplasia | "Without form", Loss of differentiation (developing specialized functions and organization) Normal cells have uniform size and shape, cancer cells variable in size and shape, or pleomorphic |
| As cells become more differentiated they? | loses its ability to replicate |
| Cancer cells act like | embryonic or precursor cells b/c thay are less differentiated and divide more frequently |
| What are tumor markers? | Substance produced by cancer cells that are found on tumor plasma membranes or in blood, spinal fluid, or urine. |
| AFP are found in the | Liver and germ cell |
| PSA are found in the | Prostate |
| Tumor Markers are used in 3 ways | Screen and ID people at high risk, Help diagnose specific type of tumor in people with clinical manifestations relating to cancer, Follow clinical course of cancer |
| As a result of a mutation, a cell acquires characteristics that allow it to have selective advantage over normal cells meaning an | Increased growth rate or decreased apoptosis (cell death) |
| Multiple mutations are required before | cancer can develop |
| What are the six hallmarks of cancer? | Self-sufficienty in growth signals, Insensitivity to antigrowth signals, Evading apoptosis, Limitless replicative potential, Sustained angiogenesis, and Tissue invasion and metastasis. |
| How does angiogenesis supports cancer development? | As cancer grows they need their own blood supply to deliver oxygen and nutrients. Small cancers can lack the ability to grow new blood vessels. But more advanced cancers can secrete factors that stimulate new blood vessel growth. |
| What are telomeres? | Telomeres are specialized multicopy repeat DNA sequence that protects and maintains the ends of the chromosomes. |
| What is the role of telomeres in cancer development? | The telomeres are maintained bya specialized enzyme call Telomerase. Cancer cells when reach a critical age, somehow activate telomerease in order to restore and maintain their telomeres, they protect their chromosomes and accordingly retain he ability to divide over and over again. |
| What is the role of oncogenes? | Oncogenes are mutant genes that in their normal nonmutant state direct synthesis of proteins that positively regulate (accelerate) proliferation. |
| What is the role of tumor suppressor genes in cancer development? | Tumor-suppressor genes encode proteins that in their normal state negatively regulate (Put the brakes on) proliferation. Hence they also have been referred to as antioncogenes. |
| Explain the first stages for transformation of normal cells into cancer cells | 1st their has to be initiation:Exposure to carcinogenic agent or toxin (only have to have 1 exposure) like cigarettes, Single or multiple exposures |
| Explain the second stages for transformation of normal cells into cancer cells | 2nd Promotion-Unregulated growth in initiated cells, Can be long latency period, Complete carcinogens cause initiation and promotion |
| Explain the second stages for transformation of normal cells into cancer cells | 3rd Progression, Malignate phenotype, invasion, ability to metastasize, autonomous growth, cell instability. |
| Time between divisions | different cell cycles |
| Movement through phases controlled by proteins | cyclins, cyclin-dependent kinases and CDK inhibitors |
| Phases | GI, S, G2, M |
| G1 | Post-mitotic, RNA, protein synthesis, cell growth |
| S | DNA synthesis |
| G2 | Pre-mitotic, RNA, protein synthesis |
| M | Mitosis |
| What factors contribute to tumor growth? | Number of cells dividing, Cell cycle time, Number of cells dying compared to new cells |
| What is the role of DNA repair genes in cancer development? | The integrity of genetic information can be compromised at several points: during each round of DNA synthesis, during each mitosis when chromosomes are segregated to daughter cells, and when external mutagens alter or disrupt DNA. |
| Multiple mechanisms have evolved to protect and repair the genome.These repair mechanisms are | directed by caretaker genes, genes that are responsible for the maintenance of genome integrity. |
| Caretaker genes | encode proteins that are involved in repairing damaged DNA, such as occurs with errors in DNA replication, mutations caused by UV or ionizing radiation, and mutations resulting from chemicals and drugs. |
| What makes certain families more prone to cancer development? | Exposure to mutagens, Can have defects in tumor suppressor genes, If the mutation occurs in somatic cells, it is not passed to children, If the mutation occurs in germ line cells, it can be passed to future generations, BRCA 1, If we identify can help us initiate earlier or more rigorous screening |
| What are the ways cancers metastasize? | Direct Invasion, Seeding, Blood/lymph |
| Direct Invasion (Local spread) | lack contact inhibition so continue to grow and invade surrounding tissues. |
| Mechanisms important in local invasion include | cellular proliferation, angiogenesis and perhaps lymphatogenesis, digestion of capsules and other structural barriers, changes in cell-to-cell adhesion, and increased motility of individual tumor cells. |
| Seeding | Erosion into cavities (Peritoneal, pleural, pericardial) |
| Blood/lymph | Multi-step process with strong primary tumor cells, Multiple steps, including invasion, survival in the circulation, attachment, and growth, and induction of angiogenesis at a favorable distant site are required. |
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