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Pathophys U1
Unit 1 Terms - Pathophysiology - Glass
| Question | Answer |
|---|---|
| Pathogenesis | development of the disease or the sequence of events involved in the tissue changes related to the disease process; conclusions that can be made about the pattern of development of a disease by assessing a patient’s signs and symptoms |
| Onset of disease (acute and insidious) | the time when signs and symptoms first appear. |
| Acute Disease | conditions have a rapid onset, develop quickly, and are usually short of duration (< three months) such as colds, flu, and appendicitis. |
| Chronic Disease | conditions are of longer duration (> three months) and can last years. Onset can be abrupt, or can be insidious, and can cause irreversible pathologic changes and permanent alterations of function. |
| Subclinical | exists in some disease states in which pathologic changes occur, but no obvious symptoms are exhibited by the pt. |
| Latent | “silent” stage of disease in which no clinical signs are evident; aka incubation period—time b/t exposure to microorganism and onset of signs/symptoms; agent may be communicable during this time. |
| Prodromal | period in early development of disease when one is aware of a change in the body, but signs are nonspecific; lab tests are negative during this period. |
| Manifestations of disease | clinical evidence or effects, the signs and symptoms, of disease; can be local or systemic |
| Signs | an objective indication of disease that can be seen by any trained observer, such as a fever or skin lesion. |
| Symptoms | a subjective indication of disease that can be known with certainty only by the affected person, such as blurry vision or headache. |
| Lesion | term used to describe a specific local change in tissue; can be microscopic or highly visible. |
| Syndrome | a collection of signs, symptoms, and degenerative processes that occur together in a particular disease |
| Diagnostic tests | lab tests that assist in diagnosis or a specific disease, ordered on basis of pt. manifestation, medical history, clinical exam, and pt interview. |
| Remission | period during which manifestations of disease subside |
| Exacerbation | period during which manifestations of disease increase |
| Precipitating Factor | condition that triggers an acute episode, i.e. seizure in a pt w/ seizure disorder. |
| Complications | new secondary or additional problems that arise after the original disease begins; i.e. after a heart attack, pt may develop CHF |
| Therapy | treatment measures used to promote recovery or slow progression of a disease; can include surgery, drugs, physiotherapy, behavior modification, alternative practices |
| Sequelae | a condition resulting from a disease that comes after the disease (aftermath); potential unwanted outcomes of a primary condition; i.e. paralysis after a stroke |
| Convalescence | period of recovery and return to normal healthy state; can last for days or months |
| Prognosis | prediction of the course and outcome of a disease as a basis for patient care and treatment; defines probability or likelihood for recovery or other outcomes. |
| Morbidity | the incidence or prevalence of a disease in a population. |
| Mortality | the rate of death from a particular disease in a population. |
| Epidemiology | Study of the incidence, distribution, and control of disease in a population |
| Epidemic | occurs when there are a higher than expected number of cases of an infectious disease w/in a given area |
| Occurrence | tracked by recording incidence and prevalence. |
| Incidence | the number of new cases of a disease that appear in a population over a given time period. |
| Communicable | infections that can be spread from one person to another; some must be reported to health authorities |
| Notifiable/reportable | diseases that physicians/health-care providers are required by law to report to certain designated authorities. These are diseases of special public health importance, making it advisable for the government to be aware of their incidence and prevalence. |
| Autopsy | postmortem exam of all or part of the body by a pathologist to determine exact cause of death, or determine course of illness and effectiveness of treatment |
| Diagnosis | identification of the cause of illness through such methods as the patient interview, physical examination, and laboratory tests. |
| Etiology | in the strict sense means the study of the causes of disease; in the broad sense, it also means the cause itself |
| Idiopathic | when etiology is unknown; “disease of one’s own” |
| Iatrogenic | when a treatment, procedure, or an error causes a disease |
| Predisposing factors | tendencies that promote development of a disease in an individual |
| Prevention of disease | closely linked to etiology/predisposing factors; includes vaccinations, dietary/lifestyle modifications, removal of harmful environmental materials, cessation of potentially harmful activities |
| Atrophy | cellular adaptation; decrease in size of cells, resulting in reduced tissue mass; causes—reduced use, insufficient nutrition, decrease neurologic/hormonal stimulation, aging. |
| Hypertrophy | cellular adaptation; increase in size of individual cells, resulting in enlarged tissue mass; causes—additional work by the tissue due to increased demands, excessive hormonal stimulation; example—enlarged heart, bigger muscles from exercise |
| Hyperplasia | cellular adaptation; increased number of cells resulting in enlarged tissue mass; sometimes occurs with hypertrophy; can be compensatory due to increased demands, or pathologic due to hormone imbalance |
| Metaplasia | cellular adaptation; occurs when one mature cell type is replaced by a different mature cell type; change may result from a deficit of vitamin A; sometimes adaptive mechanism that provides a more resistant tissue |
| Dysplasia | cellular adaptation; term applied to tissue in which cells vary in size and shape, large nuclei frequently present, rate of mitosis increased due to chronic irritation/infection, or precancerous change. Most dangerous. |
| Neoplasia | cellular adaptation; “new growth” or tumor |
| Anaplasia | cellular adaption; cells that are undifferentiated w/ variable nuclear and cell structures and numerous mitotic figures |
| Apoptosis | programmed cell death, a normal occurrence in the body, which may increase when cell development is abnormal, cell numbers are excessive, or cells are injured/aged |
| Liquefaction necrosis | process by which dead cells liquefy under the influence of certain cell enzymes; i.e. when brain tissue dies, bacterial infections in which cavity/ulcer develop |
| Coagulative necrosis | occurs when cell proteins are altered/denatured, and cells retain some form for a time after death; typically occurs in a MI |
| Fat necrosis | occurs when fatty tissue is broken down into fatty acids in presence of infection or certain enzymes; may increase inflammation |
| Caseous necrosis | form of coagulation necrosis in which thick, cheesy, yellow substance forms; TB presents this. |
| Infarction | term applied to area of dead cells resulting from lack of oxygen, resulting in functional loss if area is large enough. |
| First line of defense | mechanical barrier of skin/mucous membranes |
| Second line of defense | defense mechanism that includes phagocytosis and inflammation |
| Chemotaxis | movement/change in a cell in response to the presence of a chemical agent; leukocytes attracted via this process to area of inflammation as cells release their contents. |
| Margination | accumulation/adhesion of leukocytes to blood vessel walls at site of injury in inflammatory response |
| Emigration (diapedesis) | movement of cells (leukocytes, monocytes, macrophages) through the capillary wall into the interstitial area during inflammatory response |
| Phagocytosis | process by which neutrophils (a leukocyte) and macrophages (“vulture cells”) randomly engulf and destroy bacteria, cell debris, or foreign matter |
| Interferons | nonspecific agents that protect uninfected cells against viruses |
| Immune system | the third line of defense; specific defense mechanism of the body |
| Inflammation | the body’s nonspecific response to tissue injury, resulting in redness, swelling, warmth, and pain, and perhaps loss of function. |
| Exudate | collection of interstitial fluid formed in inflamed area |
| Serous exudate | water, consist mainly of fluid with small amounts of protein, WBCs; ex. occur w/ allergic reactions or burns. |
| Fibrinous exudate | thick, sticky exudate with a high cell and fibrin content; increases risk of scar tissue |
| Purulent exudate | exudates thick, yellow-green in color, contain more leukocytes and cell debris as well as microorganisms; typically indicates bacterial infection; aka pus. |
| Abscess | localized pocket of purulent exudate/pus in a solid tissue (around tooth/brain) |
| Pyrogens | fever producing substances from WBCs or macrophages that cause the hypothalamus to reset at a higher level |
| Chronic inflammation | may develop following acute episode of inflammation when cause is not eradicated; characteristics include less swelling/exudate, but more lymphocytes, macrophages, and fibroblasts, more tissue destruction, collagen (scar tissue) |
| Granuloma | small mass of cells with a necrotic center and covered by connective tissue |
| Aspirin, ASA, acetylsalicylic acid | anti-inflammatory agent; decreases prostaglandin synthesis at inflammation site, analgesic, antipyretic |
| Acetaminophen (tylenol/paracetamol) | decreases fever and pain, but does not diminish inflammatory response |
| NSAIDS | used extensively to treat inflammatory conditions; anti-inflammatory, analgesic, anti-pyretic, reduce prostaglandins |
| Glucocorticoids/corticosteroids | synthetic chemicals related to naturally occurring glucocorticoids produced by adrenal cortex; significant side-effects, even though extremely effective in treating inflammation |
| RICE approach | rest, ice, compression, elevation |
| Resolution | healing process that occurs when there is minimal tissue damage; damaged cells recover, tissue returns to normal w/in short period of time |
| Regeneration | healing process that occurs in damaged tissue in which cells are capable of mitosis; healing may be limited if organization of a complex tissue is altered |
| Replacement | healing process by connective tissue (scar/fibrous tissue formation) when there is extensive damage or cells are incapable of mitosis; ex. brain, myocardium; wound area must be filled in and covered by some form of tissue |
| Healing by first intention | process of healing involved when wound is clean, free of foreign material and necrotic tissue, and edges are held close together for minimal gap b/t edges, i.e. surgical incisions. |
| Healing by second intention | healing process in which there is a large break in the tissue, consequently more inflammation, longer healing period, and more scar tissue; i.e. compound fracture would heal in this manner. |
| Adhesions | bands of scar tissue joining two surfaces that are normally separate |
| Partial thickness burns | burns involving epidermis and part of the dermis |
| Deep partial thickness burns | involve destruction of the epidermis and part of the dermis |
| Full-thickness burns | result in destruction of all skin layers and often underlying tissues as well |
| Keloid | hypertrophic scar formation due to excess collagen deposits leading to hard, often eleveated, ridges of scar tissue |
| Eschar | a thick coagulated crust that develops following a full-thickness burn |
| Stenosis | narrowing of structures |
| Adhesion | bands of scar tissue joining two surfaces that are normally separate |
| Ulcer | a surface lesion due to breakdown of surface tissue |
| Exudates | interstitial fluid accumulation in an area of inflammation |
| Contracture | fixation and deformity of a joint as a result of scar formation and shrinkage |
| Macrophages | large phagocytic cells that intercept and engulf foreign material and then process and display the antigens from the foreign material on their cell membranes. |
| Antigen | foreign substance or component of cell that stimulates immune response |
| Antibody | specific protein produced in humoral response to bind with an antigen |
| Thymus | gland located in the mediastinum, large in children, decreasing in size in adults; site of maturation and proliferation of T lymphocytes |
| Lymphatic tissue | contains many lymphocytes; filters body fluids, removes foreign matter, immune response |
| Bone marrow | source of stem cells, leukocytes, and maturation of B lymphocytes |
| Neutrophils | WBCs; phagocytic, nonspecific defense, first cells to emigrate to injured area |
| Basophils | WBCs; bind IgE, release histamine in anaphylaxis |
| Eosinophils | WBCs, elevated in allergic responses |
| Monocytes | WBCs, elevated during chronic inflammation, become macrophages, phagocytic |
| Macrophages | phagocytosis; process and present antigens to lymphocytes for the immune response |
| Mast cells | release chemical mediators such as histamine in connective tissue |
| B lymphocytes | humoral immunity-activated cell becomes an antibody-producing plasma cell or B memory cell |
| T lymphocytes | WBCs; cell-mediated immunity, involved in antibody production |
| Cytotoxic/killer T cells | destroy antigens, cancer cells, virus-infected cells |
| Memory T cells | remember antigen and quickly stimulate immune response on reexposure |
| Helper T cells | activate B and T cells; control/limit specific immune response |
| Complement | group of inactive proteins in circulation that, when activated, stimulate the release of other chemical mediators, promoting inflammation, chemotaxis, and phagocytosis |
| Histamine | released from mast cells and basophils, particularly in allergic reactions; causes vasodilation, increased vascular permeability/edema, also contraction of bronchiolar smooth muscle and pruritis |
| Kinins | cause vasodilation, increased permeability (edema) and pain |
| Leukotrienes | group of lipids, derived from mast cells and basophils; cause contraction of bronchiolar smooth muscle and have a role in development of inflammation |
| Cytokines | messengers; includes lymphokines, monokines, interferons, interleukins; made by macrophages and activated T lymphocytes; stimulate activation and proliferation of B and T cells, communication b/t cells; involved in inflammation, fever, leukocytosis |
| Major histocompatibility complex (MHC) | antigen molecules that represent “self” on an individual’s cell membranes |
| IgG, IgM, IgA, IgE, IgD | five classes of antibodies |
| IgG | primary and secondary antibody responses; activates complement; includes antibacterial, antivirals, and antitoxins; crosses placenta, creates passive immunity in newborns |
| IgM | primary antibody responses; activates complement; forms natural antibodies; involved in blood ABO incompatibility reactions |
| IgA | found in secretions such as tears and saliva, in mucous membranes, and in colostrums to provide protection for newborns |
| IgE | binds to mast cells in skin and mucous membranes; when linked to allergen, causes release of histamine and other chemicals, resulting in inflammation |
| IgD | attached to B cells; activates B cells |
| May range from days to weeks | Time frame between exposure to an antigen and the appearance of immunoglobulins in the serum on the first exposure to a specific antigen |
| Almost immediate response | Time frame between exposure to an antigen and the appearance of immunoglobulins in the serum on subsequent exposure to the antigen |
| Active immunity | acquired immunity via exposure to antigen, production of specific antibodies; several wks for primary response; usually lasts for years (memory T cells); ex. polio, measles, diphtheria, vaccines, varicella |
| Passive immunity | acquired immunity via others who have been exposed to the antigen via milk as newborn or injection of pooled IgG fractions; onset immediate, lasts for months, ex. breast milk, rabies, immune globulin and snake anti-venom serum |
| Opportunistic infection | an infection by a microorganism that would normally be harmless in healthy individuals, but pts. Taking immunosuppressant drugs are susceptible due to limited body defenses. |
| Type I hypersensitivity | IgE bound to mast cells; release of histamine and chemical mediators; causes immediate inflammation/pruritus; ex. hay fever, anaphylaxis |
| Type II hypersensitivity | sensitivity; IgG/IgM react w/ antigen; complement activated; causes cell lysis and phagocytosis; ex. ABO blood incompatibility |
| Type III hypersensitivity | sensitivity; antigen-antibody complex deposits in tissue; complement activated; causes inflammation, vasculitis; ex. autoimmune disorders, SLE, glomerulonephritis |
| Type IV hypersensitivity | sensitivity; antigen binds to T lymphocyte, sensitized lymphocyte releases lymphokines; causes delayed inflammation; ex. contact dermatitis, transplant rejection |
| Antibodies developed against an individual’s own cells/cellular material | underlying mechanism for autoimmune disorders |
| Diagnosed by presence of numerous ANAs, esp. anti-DNA, as well as other antibodies. Lupus erythematous (LE) cells are mature neutrophils containing nuclear material, found in the circulating blood and are a positive sign | how is systemic lupus erythematosus diagnosed? |
| Butterfly rash | SLE skin effect |
| Polyarthritis | SLE joint effect |
| Cardiits and pericarditis | SLE heart effect |
| Raynaud’s phenomenom (periodic vasospasm in fingers/toes with pain | SLE blood vessel effect |
| Anemia, leucopenia, thrombocytopenia | SLE blood effects |
| Glomerularnephritis, with marked proteinuria and progressive renal damage | SLE kidney effect |
| Pleurisy—inflammation of pleural membranes | SLE lung effects |
| Psychosis, depression, mood changes, seizures | SLE central nervous system effects |
| Human immunodeficiency virus (HIV) | a “slow-acting” retrovirus containing two strands of RNA and the enzyme reverse transcriptase. Its envelope is characterized by spokes of glycoprotein. The virus is inactivated by many disinfectants and high temperatures. |
| Blood, semen, vaginal secretions via unprotected sex, IV drug use, maternal-fetal transmission, blood transfusion | routes of HIV transmission |
| Blood test for HIV antibodies, positive test followed by Western blot test | how is HIV diagnosed? |
| Time from infection to presence of HIV antibodies; 2 weeks to six months depending on mode of transmission | what is the HIV “window period?” |
| 6 to 7 years on average | average length of time from infection with HIV to development of AIDS |
| Major decrease in CD4 T-helper lymphocyte count and change in CD4 to CD8 ratio in presence of opportunistic infection or certain cancers | |
| Helper T4 lymphocytes; when destroyed, eliminate immune surveillance/detection | which cells are targeted by HIV, and what are the consequences? |
| outer rigid cell wall, cell membrane, DNA strand, cytoplasm; some species contain external capsule/slime layer, specialized structures such as flagellae, pili fimbriae | describe basic structure of a bacterium |
| endospore | latent forms of some bacterial species with an outer coat that is resistant to heat and other environmental conditions; ex. tetanus, botulism |
| protein coat/capsid and a DNA or RNA nucleic acid core | describe the structure of a viral particle/virion |
| virus attaches to host cell & penetrates; uncoats, takes over host cell DNA; host cell synthesizes viral components; components assemble and are release by host cell lysis | describe process of viral infection/replication |
| bacteria | structure includes cell wall, membrane, cytoplasm |
| fungus | structure includes cell wall, hyphae, eukaryotic |
| virus | structure includes capsid, nucleic acid, core of DNA or RNA |
| bacteria | multiplies via binary fission |
| fungus | multiplies via budding, spores, or extending hyphae |
| virus | multiplies via using host cell to replicate and assemble components |
| Normal/resident flora | microorganisms that normally inhabit various areas of the body such as the skin and GI tract |
| Lungs, bladder, stomach | areas of the body that lack resident flora and therefore s/b sterile |
| Culture and sensitivity | tissue culture of specimen is placed in a medium containing various antimicrobials to determine nature and drug sensitivity of the microbe. |
| Superinfection | infection that occurs only during treatment with antimicrobial agents; usually caused by fungi that are part of the normal resident flora |
| Bacteriostatic | antibacterial drug classification; prevents replication of the bacteria, keeping number of bacteria in body constant; body’s own defensive cells will then destroy it. |