Bio 2302 Unit 1 Exam Study Guide PDF

Topic 1: Homeostasis & Disease: - Know and understand the definitions of the following terms: o Acute ▪ Short and Strong o Anaplasia ▪ Cells begin to form backwards o Apoptosis ▪ Programmed cell suicide o Atrophy...

Topic 1: Homeostasis & Disease: - Know and understand the definitions of the following terms: o Acute ▪ Short and Strong o Anaplasia ▪ Cells begin to form backwards o Apoptosis ▪ Programmed cell suicide o Atrophy ▪ Cells decrease in size / also decrease size in an organ o Calor ▪ Heat o Chronic ▪ Long and not strong o Congenital ▪ Occurs during gestation, you’re born with it o Disease ▪ Abnormal condition that affects structure or function o Dolor ▪ Pain o Dysplasia ▪ Chronic irritation causes BAD changes in cells, disordered growth and maturation of cells and these cells do NOT look like normal cells ▪ Always precancerous o Epidemiology ▪ The study of disease occurrence in different human populations o Etiology ▪ The cause of a disease; what sets a disease in motion Biological Forces Physical forces Chemical agents Nutritional excesses or deficits o Focal ▪ Local and specific o Genetic/Hereditary/Familial ▪ Passed on genetically ▪ Ex) Cystic Fibrosis and Cardiovascular disease o Hyperplasia ▪ Increase number of cells in organ or tissue o Hypertrophy ▪ Enlargement of cells / produces increase in size of organ o Hypoxia ▪ Deficiency of oxygen o Iatrogenic ▪ Medical Environment ▪ Ex) Surgery o Idiopathic ▪ Doctors aren’t sure why it happened, but something happened o Infarction ▪ Death of tissue due to lack of blood o Inflammation ▪ Reaction of Vascularized (vessels) Tissues to cell injury or death ▪ Goal is to: Minimize injury and effects Remove damaged tissue Generate new tissue o Metabolic ▪ More than one system/organ is involved o Metaplasia ▪ Replace one normal adult cell type with another o Morbidity ▪ Relative incidence of disease and effect of illness on quality of life o Morphology ▪ Fundamental structure or form of cells/tissue. Changes with disease o Mortality ▪ Causes of death and death rate in a population o Necrosis ▪ Injury causes massive cell death o Neoplasia ▪ Abnormal new growth of cells not responsive to normal controls Benign vs. Malignant o Nosocomial ▪ Medical Environment ▪ Ex) Infection o Pathogenesis ▪ How the disease process evolves o Predisposition ▪ Potential to develop a certain disease in the presence of specific environmental stimuli  o Psychosomatic ▪ Psychological origin o Pyrogen ▪ Resetting thermostatic (Hypothalamus) set point o Risk factors ▪ Environmental factors or chemical/psychological/genetic elements that predispose someone to a disease o Rubor ▪ Redness / indicates vasodilation and hyperemia o Sign ▪ Noted by an observer: visual o Stress ▪ Non-Specific response of the body to any demand placed upon it o Symptom ▪ Noted by person with a disorder:spoken (my tummy hurts) o Systemic ▪ Affects the entire body rather than one specific area o Tumor/Turgor ▪ Swelling / Vasodilation, hyperemia, edema - Recall the differences between primary, secondary, and tertiary prevention. o Primary: Keep disease from ever occurring ▪ Ex) Seatbelts, helmets, shots o Secondary: Early detection of disease ▪ Ex) Pap smears, colonoscopy’s o Tertiary: Prevent damage and complications from disease ▪ Ex) Change diet, rehab, medication - Describe the endocrine pathway involved with the normal stress response. o 2 of them ▪ Hypothalamus → Pituitary (ACTH) → Adrenal Gland → Cortisol (Stress Hormone) ACTH: Adrenocorticotropic Hormone: Corticotropin o Stimulates synthesis and release of cortisol from adrenal cortex ▪ Hypothalamus → CRF → Anterior Pituitary → ACTH → Adrenal cortex → cortisol CRF : Corticotropin Releasing Factor/Hormone  o Stimulates ACTH release from anterior pituitary - Discuss the effects of cortisol on the body. o Decreased inflammatory and immune responses ▪ Atrophy of thymus ▪ Decreased # of leukocytes ▪ Decreased immunoglobins and antibodies ▪ Ex) finals = stress (high cortisol levels) = lower immune system = sick! o Elevated plasma glucose ▪ Elevated amino acid concentrations and lipolysis ▪ Gluconeogenesis and Glycogenolysis ▪ Needs energy to operate!!!! o Increase plasma volume o Basically it’s here to provide energy for the body, increase transport through body, and regain homeostasis when sick - Describe the sympathetic response to stress. o Fight or Flight , Nervous response o Autonomic Nervous System realizes something is wrong and activates the hypothalamus which activates the Sympathetic Nervous System. The SNS then activates the Arenal Medulla who releases hormones (Epinephrine and Norepinephrine) directly into the bloodstream. These hormones then amplify and prolong the fight-or-flight response - Recall the causes of cell injury. o Physical Agents o Radiation o Chemicals o Biologic Agents o Nutritional imbalances - Explain how cellular hypoxia, free radicals, and impaired calcium homoeostasis can lead to cell death. o Free Radicals: molecules with unpaired electrons in the outer shell (makes them super reactive/unstable and want to pair up)  o Cellular Hypoxia: most common form/ interferes with oxygen delivery which then causes ATP deletion. Less ATP means Na+/K+ pump can’t run fast enough. Cells lysate and burse o Impaired Calcium homeostasis: cell typically maintains low calcium. When calcium is released into the cell, it acts as a second messenger inside the cell which then turns on enzymes and can lead to a calcium problem ▪ Opens calcium gates and causes calcium to rush in - Compare and contrast liquefaction necrosis, coagulation necrosis, and caseous necrosis. o Liquefaction necrosis: Cells die, enzymes release, and enzymes break down surrounding tissue, which results in a fluid mess left over. Hint: LIQUIDFACTION o Coagulation necrosis: Tissue death due to lack of blood flow where dead cells are digested by enzymes, resulting in area of dead mass but the cells maintain their outline and don’t move. o Caseous necrosis: Only in Tuberculosis. Mixture of Coagulation and Liquefaction. You end up with an area that looks like crumbly cottage cheese. - Describe the etiology, locations, and manifestations of: o Dry gangrene: Lack of blood from arterial blood supply due to lack of arteries, but venous flow is still happening and fluid is being carried out. o Wet gangrene: Lack of venous Flow lets fluid accumulate in tissue which then makes the tissue liquefy and infection is more likely. Swollen, smelly, sucks! o Gas gangrene: Clostridium (dirt/debri causes that ) infection produced toxins. The infection starts in the muscle tissue and the patient needs immediate surgery to prevent spreading - Describe the acute inflammatory process, specifically recalling the vascular and cellular phases. o Acute inflammatory process: Body’s immediate response to injury or infection o Vascular: Vasodilation (hyperemia, rubor, calor) o Cellular Phase: white blood cells leaving the bloodstream and attacking the threat - Explain how the inflammatory process contributes to the cardinal signs of acute inflammation. o SHARP  ▪ S: Tumor (swelling) ▪ H: Calor (Heat) ▪ A: Loss of Function (Absence of Function) ▪ R: Rubor (Redness) ▪ P: Dolor (Pain) - Know the mechanism of fever and the purpose of this response. o Hypothalamus → Pyrogen → Fever → A. Cryogen → B. End the inflammatory rxn ▪ Hypothalamus (thermostat in brain) ▪ Pyrogen (resets thermostat) ▪ Fever (increases higher temperature) ▪ Cryogen (Tylenol, Advil) o Fevers happen due to wanting to make an inhospitable environment for invaders (disease). They don’t like the heat, they can’t multiply as quickly, the rising fever uses up the nutrients in our bodies, and heat helps inflammatory response go better with the blood cells and helps enzymes work more efficiently - Recall the proposed basis of cellular aging. o Genetic and Environmental ▪ As you get older, Telomeres become too short meaning cells can no longer divide and replace themselves. As a result, older cells have more DNA damage and they have more free radicals. Topic 2: Genetic Disorders - Know and understand the definitions of the following terms: o Aneuploid ▪ Organism that has abnormal number of chromosomes o Carrier: ▪ Individual who carries can can poss on a specific gene for a recessive genetic disorder but does not exhibit symptoms themselves o Monosomy ▪ Individual has one less chromosome than normal. Has 45 total chromosomes o Teratogen ▪ Environmental agent that produces abnormalities during embryonic or fetal development o Trisomy  ▪ One extra chromosome than normal. Has 46 chromosomes. - Identify teratogenic agents and explain how they are able to cause birth defects. o So many agents: ▪ Radiation ▪ Drugs and Chemical Substances ▪ Infections Agents: Viruses Nonviral factors: Syphilis, Toxoplasmosis (cat litter) o Cause of birth defects: ▪ Direct exposure to pregnant woman and embryo Radiation ▪ Exposure of soon-to-be pregnant woman that has a slow rate so that teratogenic agent is retained during early pregnancy Like when women drink/smoke and they don’t know they’re pregnant ▪ Mutagenic effects of agent permanently damaging reproductive cells - Recall the time period during development when the fetus is most susceptible to teratogens. o MOST SUSCEPTIBLE: 2-6 weeks ▪ CNS ▪ Heart ▪ Extremities ▪ Eyes - Describe the etiology, pathogenesis, and manifestations for the following diseases: o Achondroplasia ▪ Etiology: Mutation in Fibroblast Growth Factor Receptor ▪ Pathogenesis: Impaired cartilage formation ▪ Manifestations: Dwarfism (Torso normal, limbs shortened) o Marfan Syndrome ▪ Etiology: Mutation on chromosome 15 alters fibrillin I production ▪ Pathogenesis: Defective elastin and collagen formation ▪ Manifestations: Skeletal, cardiovascular and eye problems o Neurofibromatosis (type 1) ▪ Etiology: Type 1 from defect of tumor suppressor gene on chromosome 17 ▪ Pathogenesis: Neurogenic tumors from Schewann cells and other parts of PNS  ▪ Manifestations: Numerous pigmented skin lesions, pigmented nodules in iris o Von Willebrand disease ▪ Etiology: Lack of or defective von Willebrand factor ▪ Pathogenesis: Prolonged bleeding time ▪ Manifestations: Frequent nosebleeds, bleeding gums post brushing, heavy menstrual periods o Huntington’s chorea ▪ Etiology: Chromosome 4 ▪ Pathogenesis: Progressive degeneration of basal ganglia and frontal lobe ▪ Manifestations: Loss of short term memory, loss of reasoning and decision making, FATAL o Phenylketonuria ▪ Etiology: Deficiency of phenylalanine hydroxylase ▪ Pathogenesis: Can damage nervous system ▪ Manifestations: Mental retardation o Tay-Sachs disease ▪ Etiology: Lysosomal storage disease (can’t break down GM2 ganglioside of cell membranes) ▪ Pathogenesis: Accumulates in lysosomes of neurons causing their destruction ▪ Manifestations: Progresses within 1st year, hypotonic reflexes, seizures, excessive startle response. Child dies before 5 years old o Sickle-cell Anemia ▪ Etiology: Heterozygotes = have the trait. ▪ Pathogenesis: Normal hemoglobin turns to hemoglobin S ▪ Manifestations: Hemolytic anemia, sickle-cell crisis, infections. Treatments but no cure o Cystic Fibrosis ▪ Etiology: Defect on chromosome 7; cystic fibrosis transmembrane regulator protein (CFTR protein) ▪ Pathogenesis: Problem with chloride transport across cell membranes ▪ Manifestations: Frequent lung infections, sinus problems, trouble breathing, trouble digesting food - X-Linked Recessive Disorders o Fragile X syndrome ▪ Etiology: FMR1 gene contains triplet repeat ▪ Pathogenesis: Broad forehead, elongated face, large ears, siezures, etc. ▪ Manifestations: Mental retardation o Hemophilia A  ▪ Etiology: Lack clotting factor VIII ▪ Pathogenesis: Blood is slow to clot and causes excessive bleeding Can bleed into joints and cause damage ▪ Manifestations: Can treat by giving factor VIII o Duchenne Muscular Dystrophy ▪ Etiology: Dystrophin gene mutated ▪ Pathogenesis: Muscle cells poorly anchored to connective tissue ▪ Manifestations: Signs around 3 years old. Wheelchair bound by age 7, death by age 20 - Chromosomal Abnormalities o Down’s Syndrome ▪ Etiology: Trisomy 21 ▪ Pathogenesis: Characteristic facial appearance ▪ Manifestations: mental retardation, congenital heart defects o Turner’s Syndrome ▪ Etiology: Monosomy X (45, XO), Phenotypically female ▪ Pathogenesis: Short with webbed neck and underdeveloped breasts ▪ Manifestations: Developmental delays o Klinefelter’s Syndrome ▪ Etiology: Trisomy XXY (47, XXY), Phenotypically male ▪ Pathogenesis: Female fat deposition, hair growth, voice ▪ Manifestations: Tall and lanky Topic 3: Neoplasia and Cancer: - Know and understand the definitions of the following terms: o Anemia ▪ Lack of healthy red blood cells resulting in insufficient oxygen delivery o Angiogenesis ▪ Process where new blood vessels form from existing blood vessels o Anorexia ▪ Loss of appetite or reduction in desire to eat o Cachexia ▪ “wasting” syndrome, severe lean bone mass loss o Cancer ▪ Disorder of altered cell differention and growth o Carcinogen ▪ A substance that has the ability to cause cancer o Leukopenia ▪ Lower-than-normal number of white blood cells o Metastasis  ▪ Process where cancer cells spread from primary tumor to other parts of the body creating secondary tumors o Monoclonal ▪ Population of identical cells that derive from a clone o Oncogene ▪ Stimulates protein synthesis of growth factors, GF receptors, cytoplasmic signal transducers, transcription factors o Telomere ▪ Protective cap at the end of a chromosome to protect important genetic information during cell division and from degradation o Thrombocytopenia ▪ Low platelet count in the blood, leads to impaired blood clotting and increased risk of bleeding o Tumor suppressor gene ▪ Normally prevent runaway cell division, counteracts oncogenes - Compare benign and malignant tumors. o Benign tumor: Normal function and cells are found where they could be. Only seem different because they grow in clusters, but they are not harmful o Malignant tumor: Extremely fast growing and not necessarily where they should be. They divide and conquer to invade and metastasize. - Identify common carcinogens and how they can contribute to carcinogenesis. Describe how behaviors can cause these carcinogens to become risk factors for cancer. o Chemicals: o Radiation: UV o Microorganisms: HPV, Epstein bar virus o Genetic/Familial: o Congenital: damage to fetus triggering tumor o Anticancer drugs: cause cancer lol o Animal fat in broiled and smoked meats o Insecticides and fungicides o Lunch meet and processed meats - Describe the initiation phase of carcinogenesis. Explain how genetic changes contribute to this process. o Oncogenesis: starts with ONE cell  ▪ Initiation: initial mutation occurs ▪ Promotion: mutated cells are stimulated to divide ▪ Progression: Tumor cells compete with one another so they develop more mutations which makes them more aggressive o Initiation: Exposure to factors causing irreversible DNA damage to ONE cell ▪ Mutations: spontaneous and/or induced genetic changes ▪ Carcinogens: agent capable of causing cancer - Explain how cancer cells become immortal. o Telomeres shorten with cell division and undergo apoptosis when they recognize that the next cell division will cause damage to the DNA. Telomerase, an enzyme that repairs Telomeres, is typically turned off when danger is present and relies on Telomeres to know what is and isn't a threat. For cells to become immortal, Telomeres attempt to undergo apoptosis, but tumors turn Telomerase back on to let the Telomeres know that there is "no danger" present and that the cancerous cells should and can replicate. By doing this, the Telomeres listen and do not undergo apoptosis, letting the cancerous cells continue to multiple, making the individual sicker with more tumors that reproduce, thus by essentially becoming immortal. - Describe the promotion phase of carcinogenesis. o Second stage after the initiation phase where damage first occurs. During this phase, cells are exposed to promoting agents that enhance their growth and increase their potential for further mutations. - Describe the progression phase of carcinogenesis. o Final stage in cancer development. Mutated cells acquire additional genetic changes that allow them to become fully cancerous. Here is where they invade surrounding tissues, metastasize and become resistant to normal growth control. - Understand the process of metastasis and the changes in tumor cells that contribute to this process. o Metastasis is how cancer spreads from their primary tumor to the other parts of the body to form secondary tumors. The tumor cells break away from the primary site, travel through the blood stream, and latch on to new parts of the body to establish growth in new tissues. - Recount how tumors are staged (concentrate on the summary in the notes).  o Staging determined how far the tumor has spread ▪ May not have spread at all ▪ May have spread to only local lymph nodes ▪ Or has spread far o Staging is more important than grading!!! o Staging Cancers (TMN): ▪ T = Tumor TX = tumor cannot be evaluated T0 = no evidence of primary tumor Tis = preinvasive cancer (one step away from cancer) T1,T2,T3,T4 = size / extent of primary tumor (higher the number, worst off it is) ▪ N = Nodes NX = cannot be evaluated N0 = no lymph node involvement (good!) N1,N2,N3 = # of nodes / how far it’s extended , look at the chain of lymph nodes and cut one open for N1, N3 means everything is getting taken ▪ M = Metastasis Mx = can’t figure it out M0 = no distant metastasis M1 = Metastasis are present, SUPER bad - Discuss the effects of cancer on the body. o Hormones: ▪ Endocrine tumors: excess ▪ Damaged organs: loss o Hematology: ▪ Excess procoagulation factors ▪ Anemia ▪ Leukopenia ▪ Thrombocytopenia o Dermatology ▪ Thin, dry, rough ▪ Slow wound healing o Musculoskeletal ▪ Cachexia: loss of lean body mass ▪ Weak and immobile : fatigue o Neurological  ▪ Pain – bones, organs, treatment ▪ Loss of function ▪ Anxiety and Depression - Explain the following cancer therapies and note common side effects of each: o Surgery: Removal of the tumor for Diagnosis or staging ▪ Side effects: Scarring, Lymphedema (swelling), Problems with mvmt or activity, nutritional problems, cognitive problems, sexual problems, pain may by acute or chronic, emotional effects o Radiation: mostly local treatment, damages DNA, injures all cells (normal and tumor) ▪ Side effects: cataracts, hair loss, dental decay, loss of tears and ability to produce saliva, problems with thyroid and adrenal glands, slowed bone growth in children, effects on the pituitary gland and multiple hormonal effects, decreased range of motion, skin sensitivity, bowl problems, secondary cancers, infertility o Chemotherapy: systemic treatment often combined with surgery and radiation ▪ Side effects: fatigue, early menopause, infertility, changes to the heart, reduced lung capacity, kidney and urinary problems, neuropathy, muscle weakness, cognitive problems, osteoporosis, changes in texture and appearance of hair and nails, secondary cancers o Hormonal Therapy: negatively alter hormonal environment of cancer cell. Become dependent upon presence of specific receptors in tumor, tumor might become resistant o Immunotherapy: Get immune system to target tumors. Stimulate entire immune system and introduce activated immune cells sensitized toward tumor. - Describe the etiology, pathogenesis, and manifestations for the following diseases: o Basal Cell Carcinoma: ▪ Etiology: UV light, neoplasm of nonkeratinizing cells of basal layer ▪ Pathogenesis: Small, white to pink lesions on face, neck, chest or back ▪ Manifestations: new growth or sore that will not heal, waxy/smooth/red/pale/flat/lumpy, may or may not bleed Highly curable if detected and treated early o Squamous Cell Carcinoma: ▪ Etiology: UV damage to keratinized layers of epidermis. Pro-apoptotic gene p53 damaged ▪ Pathogenesis: Same symptoms as Basal Cell. Ulcerated in center ▪ Manifestations: Can recur and metastasize o Malignant Melanoma:  ▪ Etiology: UV damage to melanocytes (light skinned people with history of sunburns, non-sun exposed areas of dark skin people, family history) ▪ Pathogenesis: appear on trunk, head, neck of men. Arms and legs of women. Itches or bleeds ▪ Manifestations: surgery and biopsy, removal of lymph nodes, chemotherapy and radiation therapy, immunotherapy. Rapidly progresses and frequent metastasis Topic 4: Musculoskeletal Disorders (Independent study): - If you have taken the topic quiz and feel comfortable with those questions, you will not have any problem with the 2 questions on the Unit 1 exam about this topic. I didn’t want to do an elaborate list of topics to study because it would put too much emphasis on the least important part of your exam. Focus on the other topics.