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Exam 1 class review
1. Benign vs malignant a. What leads to cancer besides genetics? b. Neoplasm is an abnormal growth following uncontrolled proliferation and serving no physiologic purpose. i. Not all tumors of neoplasms are cancer. ii. Malignant tumor is CANCER iii. Benign growths are not consider cancer.
- EX: lipomas or hypertrophy of a organ
- Benign tumors are encapsulated with connective tissue and contain fairly well differentiated cells and well organized stroma.
- They do not invade beyond their capsule nor do they spread to lymph nodes or distant locations.
- VERY RARLY see mitotic cells.
- Name contains “-OMA” a. Leiomyoma -uterus b. Lipoma – fat c. Colon and GI poylps are commonly benign
- Benign tumors can become very large WHICH can then lead to complications or morbidity (depending on location) a. This can happen from ischemia or decreased blood flow do to block caused by tumor size. i. Benign tumors of endocrine organs may lead to overproduction of hormones. iv. Benign tumors that progress to cancer are then called MALIGNANT TUMOS
- Rapid growth
- Microscopic alterations a. Most commonly ANAPLASIA i. Which is “the loss of cellular differentiation”
- Loss of differentiation and absence of normal tissue organization
- Often pleomorphic a. Often large darkly stained nuclei b. Mitotic cells
- Substantial amounts of stroma a. STROMA = “supportive tissue of an epithelial organ or tumor, consisting of connective tissues and blood vessels”
- Lack capsule
- Grow to invade nearby blood vessels, lymphatics and surrounding structures
- Names based on cell time
a. Carcinomas – epithelial tissue b. Adenocarcinoma – duct of glandular structure c. Lymphomas = lymph d. Leukemia = blood forming cells
- Suffix for malignant tumors = “SARCOMA”
- Different trimesters a. What illnesses can affect moms during each trimester 3. Interstitial edema a. An important factor in capillary filtration of fluid is the integrity of the capillary membrane. i. Changes in membrane can lead to plasma proteins escaping into interstitial space. ii. “Osmotic movement of water into the interstitial space, causing tissue edema” iii. Does not indicate fluid excess iv. Common mechanisms:
- Increased capillary hydrostatic pressure a. Venous obstruction or sodium water retention. i. Venous obstruction causes hydrostatic pressure to increase BEHIND obstruction. This pushes fluid into the spaces around obstruction. b. Examples: i. Blood clots ii. Hepatic obstruction iii. Right heart failure iv. Tight clothing v. Prolonged standing c. “volume of interstitial fluid exceeds the capacity of the lymphatics to return fluid to vascular system.”
- Decreased capillary oncotic pressure a. Results from losses or diminished production of plasma albumin. b. Decreased oncotic causes fluid to MOVE INTO the space. c. Common in: i. Liver disease ii. protein malnutrition iii. Glomerular diseases of the kidney iv. Hemorrhage v. Burns vi. Serous open wounds.
i. Aldosterone is from the adrenal cortex and is end product of renin-angiotensin aldosterone system.
- When sodium is low RENIN is secreted.
- Renin stimulates Angiotensin I a. (ACE) Angiotensin-converting enzyme from pulmonary vessels convert Angiotensin I to angiotensin II i. This causes vasoconstriction 1. This increases blood pressure a. THEN aldosterone is secreted!! ii. Aldosterone promotes sodium and water reabsorption by kidney.
- Also cause potassium excretion from kidney a. Aldosterone balances sodium and potassium.
- What are the chromosome numbers for Marfan syndrome a. For the other syndromes in study guide
- How is HPV and HIV contracted? a. HPV b. HIV 8. Booster shots a. How do they work? i. Vaccine-induced immunity does not persist as long as infection- induced immunity; thus booster is necessary b. When do you get them? c. What do they do? i. IF they have to many antibodies can develop “Arthus Reaction”
- Arthus reaction: repeated local exposure to antigen that reacts with antibodies and forms immune complexes in local blood vessel walls d. Examples: e. What immune response comes from a booster i. Localized type 3 hypersensitivity induced by levels of IgG antibodies causing inflammation f. How does the immune system respond to booster verse vaccine i. Memory cells ii. Person previously immunized gets a booster can cause almost immediate rise in antibody to level of sufficient to prevent disease. 9. What test are done for HIV? a. Infects and destroys the T-helper cell. i. T-helper helps maturation of plasma cells and T-cytotoxic cells.
b. Elisa – 1st^ test i. If positive do a second test to confirm ii. Easy to screen huge # of people c. Western blot – 2nd^ test to confirm i. Test is more sensitive than Eliza test d. What is required for a positive diagnosis? e. How is it best treated? i. 1 medications verse 2 medications
- Combination of 2 NRTIs plus a 3rd^ drug f. What is the purpose of the treatment? How is it treated best? i. HAART
- Highly active antiretroviral therapy
- Combination of drugs that attack different portions of the viral replication pathways
- Prevents fusion of HIV with cell membranes 10. HIV states a. Stage 0 : First 180 after infection i. Dendritic and T-cells spread infection. ii. IgM antibody to try and prevent HIV id detected iii. IgG levels rise and remain elevated iv. HIV process has started – MEDIATED DESTRUCTION OF CD CELLS b. Stage 1: > c. Stage 2: 200 -499 CD4 T-cells d. Stage 3: defined as AIDS, CD4 T-cell counts <200, or the development of AIDS-related opportunistic infections, REGARDLESS of CD4 T-cell Count. 11. What does radiation do to a cell? a. Ionizing radiation damages cells by imparting enough energy to cause molecular damage, especially to DNA. i. Level of success:
- Lethal
- Potentially lethal
- Sublethal b. Radiation produces slow changes in most cancers and irreversible changes in normal tissue as well. i. Each tissue has a maximum lifetime dose of radiation it can tolerate. 12. What are different manifestations of inflammation? a. Local inflammation i. Examples:
- Redness
- Heat
- Swelling
- Pain ii. This can lead to loss of function iii. Prostaglandins and bradykinins gather
- Areas with rapidly renewing cells are more radiosensitive.
- MUST have good local delivery of oxygen.
- Well suited to treat localized disease in areas that care hard to reach surgically a. Ex: Brain, pelvis
- Methods: a. “seed” temporially placed into body cavities i. Called brachytherapy 1. Used fro cervical, prostate, head and neck cancers. ii. Chemotherapy agents attack pathways that exist in rapidly dividing normal cells.
- Because of cancer cell growth they are most affected. b. Can they be used together? i. Single chemotherapeutic agents often shrink cancers, but rarely cure.
- Usually given in combinations designed for the cancer. a. “cocktail scheduling” ii. Adjuvant chemotherapy is given AFTER surgical excision of cancer iii. Neoadjuvant chemotherapy is given BEFORE localized treatment
- EX; before surgery or radiation c. What works best? i. Surgery works when it has clear margins = 98% cure
- Can be used for relief of symptoms or decrease chance of developing cancer a. EX: BRAC ½ and mastectomy 14.What effect does apoptosis have on cancer? 15. How does cancer metastasize? a. Neoangiogenic i. When the body makes new blood vessels to supply blood to a tumor and ensures tumor growth
- Driven by hypoxia.
- New vessels are weak and leaky = leads to more routes for cancer to metastasize. b. The spread of cancer cells from the site of the original tumor to distant tissues and organs throughout the body. i. Cells break away from the tumor and enter blood stream/lymph system c. Cells must be able to i. Spread
ii. Survive iii. Proliferate iv. Destination must be receptive to growth of cancers. d. Invasion if prerequisite for metastasis and first step in metastasize.
16. What is the pathology of cancer? a. Cancer cells secrete: Protease i. Breaks down protein and peptides ii. Digests the extracellular matric and basement membranes and create pathways through which cells can move. b. Cancer risk factors i. Behavioral, job’s, areas of living (contamination of environment) 17.QUESTION: a. Epithelial mesenchymal transition (EMT) produces which result? i. Increased resistance to apoptosis 18. Cancer etiology? a. Obesity and alcohol i. Insulin like growth factor axis ii. Sex hormones iii. Adipokines or adipocyte-derived cytokines b. It is liked to metabolic dysregulation of adipose tissue and endocrine and paracine altered signaling of adipose tissue in obesity. i. Metabolic changes in adipose tissue -> insulin resistance, hyperglycemia, dyslipidemia, hypoxia and chronic inflammation ii. Adipose tissue secretes LOT of protein call adipokines
- High adipokines leads to low adiponectin (which induces apoptosis)…. INCREASING cell proliferation 19. What is paraneoplastic syndrome? a. Rare symptom complexes i. Caused by biologically active substances released from a tumor or by an immune response triggered by a tumor ii. Manifested symptoms are directly related to the cancer it self. 20. Define and give examples: a. Dysplasia b. Hypertrophy: i. SWELLS ii. Enlargement in size NOT in number
- Increase in cell size = increased tissue size = increased organ size iii. Physiologic Results from:
- Increased demand
- Stimulation by hormones and growth factors
- Exercise and pregnancy
- Physiological hypertrophy iv. Pathologic results from:
- Adaptive compensatory
- Following a disease
- Chronic hemodynamic overload
- Pulmonary
- Genitourinary tracts 23.What effect does hypoxia have on the body’s pH? a. Increase pH = alkaline b. Decreased pH = acidic 24. What are tumor marker cells? a. They are substances found in cancer cells, blood, SF, or urine. i. Hormones ii. Enzymes iii. Genes iv. Antigens and antibodies b. Biochemical markers of tumors c. “Substances produce by BOTH benign and malignant cells that are either present in or on tumor cells or found in blood, SF, or urine. d. Tumor marker cells is not diagnostic testing. e. How do they work? i. They are used to screen and identify risks for cancer, help with diagnosis, and clinical course of cancer. ii. THEY CAN CREATE PARANEOPLASTIC SYNDROME!!! iii. They can help establish prognosis iv. Detect disease or return of cancer v. Asses treatment response or resistance 25.QUESTION: What factor indicates the return of prostate cancer? a. PSA increased i. Prostate tumor secretes PSA (prostate specific antigen 26. TNM classification a. T = tumor spread b. N = node involvement c. M = Presence of distant metastasis i. Stage 1: confined to the organ of its origin ii. Stage 2: locally invasive iii. Stage 3: has advanced to regional structures iv. Stage 4: has spread to distant sites. 27. What can cause an increase in cells? a. Hypertrophy verse hyperplasia i. ANS: HYPERPLASIA
- Hypertrophy = increase in size b. Can you test to see the difference? 28.RNA
a. Process of it? b. What does it do c. PANAPTOS REVIEW 29.1 chromosome verse 2 chromosomes a. The more chromosomes the better b. Low chromosomes increases chances of miscarriage 30.Chromosomes a. X chromosomes in somatic cells of females is permanently inactivated b. Trisomy 21 is linked to leukemia
31. 1 st^ line of defense? a. Skin b. Linings in GI, RT, an genitourinary c. Mucus membranes d. Earwax 32. 2 nd^ line of defense? a. Inflammation 33. Adaptive immunity – Memory cells a. B-cells (Humoral) i. Primarily protects against bacteria and viruses ii. Produces antibodies iii. Differentiate into antibody producing plasma cells and into long lived memory cells b. T-cells (Cellular) i. Primarily protects against viruses and cancer ii. Matures in thymus iii. Released into the blood and take up residence in the secondary lymph organs to await antigens
c. Where do babies get DNA from? i. Inherited by mom, maternal DNA ii. If there are mutations, its most likely in brain or heart. d. How does it work? i. Mitochondrial DNA contain their own DNA and can encode the central proteins involved in energy production
38. Glycolysis a. Input 1 glucose = 2 pyruvate + NADH + 2ATP i. Pyruvid acid w/ O 1. Krebs cycle ii. Pyruvid acid w/o O
- Lactic acid (reversible b. End products = ATP, carbon dioxide and water AND pyruvate c. Requires ATP to work i. Most of ATP is generated here d. Occurs in cytoplasm e. Transports electron in the mitochondria 39. Osmosis a. Water follows osmotic gradients established by changes in salt concentration. i. Sodium and water must be balanced. 1. Sodium regulated by renal and aldosterone from the adrenal cortex and peptides from the heart. 2. Water balance is regulated by renal response to ADH from posterior pituitary. 40. Passive transport verse active transport i. Chloride transport is generally passive and follows the active transport of sodium. 1. Decrease or increase of chloride are proportional to changes in sodium. b. Active transport: i. Requires energy or ATP 1. 60-70% of ATP is used in this transport system a. Every 1 ATP molecule leads 3 molecules of sodium out of the cell and 2 molecules of POTASSIUM MOVE IN b. This means the inside of the cells is more negative ii. Occurs only across living membranes that flow “uphill”
- Against a concentration gradient c. Who needs a pump? Active transport i. Aka sodium potassium pump 1. Generates voltage across the membrane 2. Moves Sodium out of the cell and potassium into the cell a. Transported by ATPase, adenosine triphosphatase
d. Who needs energy? Active transport e. What happens to solvent verse solute? f. Passive Transport: i. Water and small, electrically unchanged molecules move easily through pores in the plasma membrane’s lipid bilayer. ii. Occurs naturally through any semipermeable barrier. iii. Molecules flow downhill from high to low
- Does not require any energy
- Driven by OSMOSIS, hydrostatic pressure, and diffusion, all of which depend on laws of physics and do not require life. 41. What is filtration? a. Movement of water AND soluts through a membrane because of greater pushing pressure on one side of the membrane than on the other side. i. Hydrostatic pressure
- Mechanical force of water pushing against cellular membrane
- Hydro pressure = BP generated b. Does filtration use energy? YES c. What kind of energy? HYDROSTATIC PRESSURE 42.DYSPLASIA IS ALMOST ALWAYS ABNORMAL 43. Sodium potassium pump a. What happens to the pump in hypoxia? i. Na/K pump fails ii. No Na increases in cell which causes H2) in cell and cell to swell
- Becomes acidic (pH decreased)
- Hypoxia is most common cause of cell injury 44. Lead poisoning a. No level of lead in the blood is safe. b. Untreated can become encephalopathy and is responsible for serious and irreversible neurologic damages. c. Who is most prone? i. Greatest risk are children less than 72 months of age
- Young children are more likely than older children b/c mouthing behavior.
- Young children absorb more easily than older children and adults. ii. A person with Pica iii. Living in lead contaminated environments iv. Highest among
- Non-Hispanic
- Black children
a. X usually inherited from mother b. Females i. Underdeveloped/ sterile ovaries ii. Short iii. Underdeveloped breasts iv. Webbed neck v. Edema vi. High risk of miscarriage c. 1 X chromosome d. NO Barr Bodies
50. Genotype verse phenotype a. Genotype – can’t see b. Phenotype – can see 51. Complement system. a. Classical pathway : i. Activated by proteins of the adaptive immune system (ANTIBODIES) bound to their specific targets (ANTIGENS) 1. “Antibodies bind to antigens” 2. C1 protein activation = activation of C b. Clotting System i. FIBRIN – blood clot 1. Insoluble protein that contains platelets (primary initiator of clotting) 2. Traps other cells – Erythrocytes, phagocytes, microorganisms 3. End product of the coagulation cascade c. Kinin System i. End product I = Bradykinin 52. Brady Kinn a. Causes dilation of blood vessels b. Acts with prostaglandins to stimulate nerve endings and induce pain c. Causes smooth muscle cell contraction d. Increases vascular permeability i. May increase leukocyte chemotaxis e. Responsible for endothelial cell retraction and increased vascular permeability in the later phases of inflammation. f. PANAPTOS 53. Endothelium a. PANAPTOS
b. Function: i. Regulates blood flow and maintains vessel wall permeability ii. Prevents platelet and clotting activation iii. Nitric Oxide maintains vascular tone iv. Acts as a barrier between blood and rest of body. c. Inflammatory response: i. Controls adhesion and migration of proinflammatory mediators ii. Adherence of leukocytes to vessel surface iii. Invasion of leukocytes to the tissue iv. Efflux of plasma from the vessel
54. Cells of inflammation a. Who arrives first? – Neutrophils and leukocytes b. Histamines i. Causes temporary rapid constriction of smooth muscle and dilation of postcapillary venules = increased blood flow into microcirculation. ii. Increases vascular permeability resulting from retraction of endothelial cells lining the capillaries and increased adherence to endothelium iii. H1 = PROinflammatory iv. H2 = ANTIinflammitory (suppress leukocyte function) 55. Leukotrienes (WBC) a. Leukocytes i. Released from mast cell membranes by an intracellular phospholipase that acts on membrane phospholipids ii. Defend the body against microorganisms that cause infection and remove debris, including dead or injured cells. iii. IN tissue, TRANSPORTED in circulation iv. Slow reacting substances of anaphylaxis v. SIMILAR to histamine
- Neutrophil and eosinophil chemotaxis vi. Important in later stages of inflammatory response
- Stimulate slower and more prolonged response than histamines b. Eosinophils i. Large course granules ii. Amoeboid movement and phagocytosis iii. Attack viruses and parasites iv. Helps to CONTROL inflammatory process. v. Type 1 sensitivity reaction and asthma c. Basophils i. Stimulation induces synthesis of vasoactive lipid molecules (leukotrienes) and cytokines
62. SLE patho a. Chronic multisystem inflammatory disease, is one of the most serious of autoimmune disorders. b. Characterized by production of large variety of autoantibodies c. Most autoantibodies are against nucleic acids. i. Single stranded DNA ii. Double Stranded DNA iii. Histones iv. Ribonucleoproteins d. Antibodies against DNA i. Causes inflammatory lesions in the renal tubular basement membrane, brain, heart, spleen, lung, GI tract, Skin & peritoneum. e. Diagnostic findings: i. Butterfly rash ii. Malaise iii. Raynaud’s phenomenon iv. Peripheral neuropathy v. Change in vision and renal status vi. Round lesions on head/ hair loss vii. Arthritis viii. Vasculitis and rash ix. Oral ulcers x. Photosensitivity xi. Hematologic abnormalities f. ASSESSMENT: i. Elisa for SLE specific antibodies ii. CBC with differential iii. Erythrocyte sedimentation rate iv. Kidney function test v. Nonspecific inflammatory studies. 63. Acute graft rejection a. Cell-mediated immune response that occurs within days to months after transplantation. b. Recipient develops an immune response against unmatched HLAs after transplantation. c. Type IV reaction d. Acute antibody-mediated rejection i. 10% of acute rejections ii. Antibodies not present at time of transplantation iii. Takes 2 weeks or longer iv. Accumulation of antibody, complement, neutrophils, and thrombi v. Type II hypersensitivity reaction. 64. Carcinoma in SITU
a. “CIS” b. Preinvasive epithelial tumors of glandular of squamous cell origin. c. Accumulate specific genetic mutations. d. Increased proliferation rate e. Early stage cancer i. Localized to epithelium
- NOT in basement membrane or invaded stroma. f. NOT MALIGNANT i. Often found in:
- Cervix
- Skin
- Oral cavity
- Esophagus
- Bronchus ii. Glandular epithelium SITU lesions found in:
- Stomach
- Breast
- Large bowel. iii. Ductal carcinoma in SITU found in breast g. Different stages? i. Can remain stable for long periods of time ii. They can progress to invade and metastatic cancers iii. They can regress and disappear. h. Either low grade or high grade dysplasia i. High grade have the highest chance of becoming cancer i. MOST COMMON TREATMENT IS REMOVAL 65. Are polyps in colon malignant or benign? BEGIN 66.CML a. Philadelphia chromosome i. Results from a translocation that creates novel protein fusion of the BCR and ABL genes and expression of an unregulated promoter of cell growth. ii. Produces BCR-ABL
- An unregulated protein tyrosine kinase that promotes growth of myeloid cells b. Treatment : Imatinib 67.AML
