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39 Cards in this Set
- Front
- Back
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Normal cell cycle: what 4 things to cells normally do?
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1) develop
2) grow 3) differentiate 4) die |
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What three ways do cells die? Describe
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1) Necrosis
-tissue injury -release cytoplasmic content --> inflammatory process 2) Apoptosis-programmed cell death -regulated intracellular physiological process 3) spontaneously..97% of new cells |
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what is the balance of cellular process?
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Number of cells produced = number of cells dying
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How do cells communicate?
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1) gap junctions: adjacent cells via cytoplasm (electric and chemical signaling)
2) contact-dependent: binding of surface molecules from one cell to another 3) paracrine and autocrine: chemical secretion acting on nearby (paracrine) or self (autocrine) |
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*******What is CA?
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abnormal and uncontrolled cell division
-a neoplasm (neoplasm) that has the ability to invade locally and metastacize -potentially can occur in nearly every cell in body |
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******CA formation: what are the 3 steps (just list)
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Initiating Factors
Promoting factors Progression -CA cells acquire ability to invade and metasticize |
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CA formation- what is the first step in more detail?
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Initiating factors-mutation in a single cell
-genetic predisposition -carcinogens: chemicals/toxins; radiation -these cause DNA mutation |
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******CA formation-what are promoting factors in more detail?
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Promoting factors-proliferation of mutated cells
-hormones and growth factors-growth promoting signals promoting abnormal cell growth --tumor growth factor --angiogenesis |
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******CA formation-closer look at third step?
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Progression
-mutated cells proliferate independent of carcinogen |
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*****characteristics of CA cells of malignant tumor growth
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CA cells
-circumvent signals that regulate cell growth, differentiation, and death ****CA cells NEVER stop dividing or mitosis |
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What does growth rate of CA depend on?
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growth fraction (higher in malignant cells)
-number of cycling cells -ratio of dividing cells to resting cells Cell cylce time: long/short Ratio of living cells to dying cells CA cell proliferation |
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What is doubling time? What does it have to do with CA?
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doubling time is the amt of time it takes for the total mass of cells in a tumor to double in size
-as growth fraction increases, doubling time decreases -malignant cells continue to undergo mitosis until they have used all available nutrients and blood supply |
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*********What is angiogenesis? What does it have to do with CA?
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Angiogenesis is growth of a new network of blood vessels
-is the blood supply for tumor -density of capillaries correlate w/ metastasis and death -occurs in non-neoplastic tissue -allows tumors to grow |
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Components of mutations?
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Multiple mutations needed to create CA
Components: -self sufficient in growth signals/proliferate in the absence of external signals -insensitive to antigrowth signals -evade apoptosis -limitless potential to replicate -sustained angiogenesis -tissue invasion and metastasis |
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******What classes of genes are involved in genetic mutation?
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Mutated genes that regulate cell development, growth, and differentiation
Classes of genes involved: *****Proto-oncogenes-code for proteins that help regulate cell growth and differentiation; overexpression can lead to mutated oncogenes and cause CA ***tumor suppressor genes (anti-oncogenes)-when mutated/inactivated, CA can proliferate mutator genes-DNA repair genes, mutations in mutator genes allows mutations to occur in cells |
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***********What are oncogenes?
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mutated/over expressed proto-oncogenes
-lead to gain of function -accelerate cellular growth and/or accelerate proliferation and /or facilitate abnormal cell division -avoid apoptosis |
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*****What is tumor suppressor genes?
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inhibit abnormal cell proliferation
-pRB-inhibits transcription (master brake of cell cycle) -p53-suicide gene, induces cellular apoptosis in abnormal cells -deactivation can occur from mutations/chromosomal deletions |
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What are etiologies of genetic mutations?
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heredity factors
environmental factors physical injury oncogenic viruses normal cellular metabolism |
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What are viral causes of CA?
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mutated DNA sequences
invade host cell and incorporate into its DNA associated with certain cancers often have cofacter associated, i.e. Hep B + smoking leads to hepatocellular carcinoma |
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************Cell differentiation and CA
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*****-the more highly specialized (differentiated) a cell becomes, the less likely it will undergo mitosis
-highly differentiated cells cannot be replaced when they are damaged -less differentiated cells undergo continuous replacement ******-CA cells lack differentiation |
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What is the progression from dysplasia to neoplasm?
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dysplasia
in situ neoplasm invasive neoplasm |
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What is metaplasia?
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differentiated cell replaced by another differentiated cell (not in normal location)
-cell function may vary -can lead to dysplasia --> CA |
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What is anaplasia?
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loss of cell differentiation --> loss of function
morphologic changes |
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What is carcinogenesis?
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healthy cells proliferate into abnormal cells
abnormal cells circumvent detection and thrive (theory of CA immune surveillience) |
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Inflammation and CA
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proinflammatory cytokines (protein molecules secreted by cells of the immune system) - when chronically expressed can
-suppress apoptosis -promote proliferation -promote angiogenesis -promote invasion and metastisis |
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****Solid tumors: benign vs. Malignant
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B vs. M
slow growth vs rapid growth low mitotic index (ratio of cells in mitosis compared to total number of cells) well differentiated vs poorly differentiated/anaplatic localized vs invasive to nearby tissues encapsulated vs non encapsulated defined, demarcated borders vs undefined borders non-metastatic vs metastatic to other areas of the body thru blood and lymph vessels |
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How do malagnancies disupt normal homeostasis?
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-compress blood vessels
-obstruct tissues and organs -outgrow their own blood supply -take essential nutrients away from healthy tissue -liberate enzymes that destroy malignant and healthy tissue |
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MOA in local tumor invasion?
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-cellular expansion
-mechanical pressure -release of lytic enzymes -decrease cell-to-cell adhesion -increase motility of individual tumor cells |
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MOA of metastatic (distant) tumor spread?
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-penetration of basement membrane
-movement through extracellular matrix -penetration of vascular or lymphatic channels -release into blood and lymph vessels -transport to secondary sites -entry and proliferation in secondary sites -some metastasize early, others late -some may be far advanced before detection or primary tumro |
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Problems with sx and metastatic tumors?
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no clear demarcated boundaries b/w malignant and health tissue
-one cell left behind can progress the disease |
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How does CA metastasize and move around?
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theory-anatomical selection by blood and lymph vessels
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**********What is cachexia?
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most severe form of malnutrition associated with CA: altered carb, fat, protein metabolism
-wasting -extensive loss of adipose tissue -emaciation -decreased quality of life Anorexia (loss of appetite) -cachexia syndrome -involves hormones, neuropeptides, and proinflammatory cytokines -act on HTO-creates loss of appetite |
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********Hematological malignancies-what is the pathology?
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*******CBC-elevated WBC
anemia-suppressed RBC production |
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*******what are s/sx of hematological malignancies?
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joint pain
bone pain/tenderness coagulopathy fever fatigue infection pallor palpitations lymphadenopathy weight loss |
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What is lymphoma?
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aberrant proliferation of cells within tissues of the lymphatic system
-lymph nodes -spleen -other organs containing lymph tissue (i.e. intestines) Predominant hematological malignancy |
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What is Hodgkin's Lymphoma (HL)?
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-Reed-Sternberg cells
-begins in one lymph node and spreads to contagious lymph nodes |
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****Hodgkin's Lymphoma-clinical signs and symptoms
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****Remember starts in one lymph node and spreads to contiguous lymph node
enlarged painless lymph nodes -***cervical -mediastinal -problems tolerate-itching and lymph node pain-after alcohol -night sweats, enlarged lymph nodes, cough, chest pain, SOB, fever |
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******Non-Hodgkin's Lymphoma what is it?
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patho
-cell injury and mutation -malignant transformation of T or B cells during differentiation in the ***peripheral lymph nodes |
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Difference between HL and NHL
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HL vs NHL
spread: orderly contiguous vs noncontiguous sensitive to etoh: yes vs no extent of disease: often localized vs rarely localized |
