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Pathophys U1

Unit 1 Terms - Pathophysiology - Glass

QuestionAnswer
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.
Created by: michellerogers
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