Unit I Exam
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
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| Atrophy | a wasting or decrease in size of a body organ, tissue, or part owing to disease, injury, or lack of use
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| Hypertrophy | a non-tumorous enlargement of an organ or a tissue as a result of an increas in size rather than the number of constituent cells
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| Hyperplasia | an abnormal increase in the number of cells in an organ or a tissue with consequent enlargement
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| Metaplasia | normal transformation of tissue from one type to another, as in the ossification of cartilage to form bone; transformation of cells from a normal to an abnormal state
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| Dysplasia | abnormal development or growth of tissues, organs, or cells
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| Neoplasia | formation of new tissue; formation of a neoplasm
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| Anaplasia | reversion of cells to an immature or a less differentiated form, as occurs in most malignant tumors
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| Which cellular adaptation is considered to be the most dangerous? Explain why. | Dysplasia is the most dangerous because it is the forerunner of neoplasia.
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| Define anaplasia. Explain the significance of anaplasia. | Failure of cells to differentiate or develop specialized features; term applied to grading malignant tumors
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| What is the difference between dysplasia and anaplasia? | Dysplasia leads to the development of neoplasia. Anaplasia is characteristic of malignant neoplasia.
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| List seven causes of cellular damage | 1. ischemia; 2. physical agents (e.g., excessive temperature, radiation); 3. mechanical damage; 4. chemical toxins or foreign substances; 5. pathogens; 6. abnormal metabolites; 7. nutritional deficits or fluid or electrolyte imbalances
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| Symptom | a subjective indication of disease that can be known with certainty only by the affected person, such as blurry vision or headache
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| Exacerbation | an increase in the severity of disease
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| Precipitation | the triggering of an acute episode of a disease
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| Incidence | the number of new cases of a disease that appear in a population over a given time period
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| Acute | a short-term illness that develops very quickly with marked signs such as high fever or severe pain
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| Idiopathic | a disease that is of uncertain or unknown origin or cause
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| Mortality | the rate of death from a particular disease in a population
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| Necrosis | When a group of cells die; the process of cell death varies with the cause of the damage
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| Sign | an objective indication of disease that can be seen by any trained observer, such as a fever or skin lesion
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| Exogenous | originating from outside the body
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| Etiology | the study of disease; the cause of any specific disease
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| Lesion | an abnormality involving any tissue or organ due to a disease or injury
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| Chronic | often milder condition than an acute disease state; develops more gradually, but persists for a long time and usually causes more permanent tissue damage; often marked by intermittent acute episodes
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| Endogenous | originating from inside the body
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| Communicable | infections that can be spread from one person to another, some of which are notifiable
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| Precipitating factor | a condition that triggers an acute episode of disease; differs from a predisposing factor
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| Hypoxia | reduced oxygen in a tissue
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| Pathogenesis | the development of a diseased or morbid condition
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| What is the body's first "line of defense"? | Mechanical barrier such as intact skin and mucous membrane
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| Identify the body's second and third "lines of defense." | Second: processes of phagocytosis and inflammation; Third: the immune system
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| Which line of defense is specific? | The immune system
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| What is meant by the term "specific"? | It provides protection by stimulating a unique response following exposure to foreign substances
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| Phagocytosis | Process by which neutrophils and macrophages engulf and destroy bacteria, cellular debris, or foreign material.
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| Identify types of cells that are phagocytic and where these cells are located within the body | Neutrophils and monocytes are circulating in the blood and enter the interstitial fluid when inflammation occurs. Macrophages are located (fixed) in tissues such as the alvioli, liver, and spleen.
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| Identify the events of the "vascular response" that occur during an inflammatory response. Explain why each change occurs, as well as the consequences of each event. | Transient vasoconstriction is followed by vasodilatin, hyperemia, and increased capillary permeability in response to a chemical mediator (e.g., histamine, serotonin, etc.) released at the site of injury. This allows for the accumulation in the area of fl
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| Identify the five cardinal signs of an inflammatory response and the cause of each. | 1. redness due to vasodilation in the injured area; 2. warmth due to hyperemia or increased blood flow to the area; 3. swelling or edema due to the shift of protein and fluid into the interstitial space; 4. pain resulting from increased fluid pressure on
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| Outline the events of the cellular response of an inflammationn in the correct chronological order. | 1. chemotaxis; 2. margination; 3. emigration (diapedesis); 4. phagocytosis and subsequent release of lysosomal enzymes
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| Neutrophils | the first cells to emigrate to an injured area; phagocytic microorganisms
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| Basophils | Secrete histamine
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| Eosinophils | Elevated during allergic responses
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| Macrophages | Phagocytic microorganisms
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| Mast cells | Secrete histamine
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| Monocytes | elevated during chronic inflammation; a source of macrophages; phagocytic microorganisms
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| T lymphocytes | Involved in cell-mediated immunity; Involved in antibody production
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| B lymphocytes | Involved in antibody production
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| List the systemic effects of inflammation identifying the reason that each of these manifestations occurs | Fever due to the release of pyrogens by leukocytes and macrophages; malaise, fatigue, headache, and anorexia
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| Causative agents of acute inflammation | Direct damage 9trauma); chemicals; ischemia; cell necrosis or infarction; allergic reactions; physical agents (burns); foreign bodies (splinters or dirt); infection
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| What is the causative agent of chronic inflammation | when the cause persists and is not removed or eradicated
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| Differentiate the onset of symptoms of acute and chronic inflammation | Acute: immediate or delayed (e.g., sunburn)Chronic: delayed
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| Intensity of symptoms of acute inflammation | Severity varies with the situation or cause
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| Intensity of symptoms of chronic inflammation | Varies depending on the cause and pathophysiology and duration
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| Duration of acute inflammation | usually of short duration, but may be prolonged
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| Duration of chronic inflammation | Prolonged duration
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| Cells involved in acute inflammation | Neutrophils and macrophages; lymphocytes if an immune response is involved
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| Cells involved in chronic inflammation | Lymphocytes, macrophages, and fibroblasts
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| Outcome of acute inflammation | Healing, unless it becomes chronic due to persistence of causative agent; regeneration; or resolution
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| Outcome of chronic inflammation | scarring and / or granuloma
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| Define RICE and explain the rationale for each of these interventions | R = rest: allows time for healing, minimizing further pain and irritation to the injured areaI = ice: early application of cold causes vasoconstriction, decreasing pain and edemaC = compression: compression to facilitate blood clotting, prevent or minimiz
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| Identify nonpharmacologic interventions that could be used to treat inflammation, particularly conditions that are chronic, such as arthritis | Heat, physiotherapy, adequate nutrition and hydration, mild to moderate exercise, elastic stockings to reduce fluid accumulation
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| State five differences between NSAIDs and glucocorticoids or steroidal anti-inflammatory drugs | NSAIDs are analgesic and antipyretic. They may cause allergic reactions, slow blood clotting, and cause nausea and / or stomach ulceration.Steroids decrease immune responses and increase the risk of infection, high BP, and edema. They may also cause osteo
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| Identify differences between NSAIDs and acetaminophen | NSAIDs are anti-inflammatory, They may cause allergic reactions and slow blood clotting.Acetaminophen has no anti-inflammatory action. High doses may cause kidney and liver damage.
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| Resolution | Occurs when there is minimal tissue damage, the damage is repaired, and cells recover and resume normal function in a short time.
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| Regeneration | the healing process that occurs in tissues whose cells are capable of mitosis (e.g., epithelial cells of the skin, GI tract). The damaged cells are replaced by the proliferation of nearby undamaged cells.
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| How could the nature of the tissue / location of the wound influence tissue healing? | an inoperable bullet wound to the brain may be inaccessible without further tissue damage and loss of function
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| How could the nutritional status of the injured individual influence tissue healing? | Malnutrition, especially deficiencies in vitamins such as C, E, and K, would impair the blood-clotting capability of the individual, impairing wound closure and repair of damaged tissues
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| How could the size and shape of the wound influence tissue healing? | Large, deep cuts, for example, especially if untreated, or presenting difficult suture closure would facilitate extensive scar formation; e.g., cuts due to broken glass or power tools
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| How could the drugs that the injured individual is taking influence tissue healing? | Anticlotting medications would limit or impair clotting and hence wound closure; e.g., aspirin and other anti-platelet drugs prior to surgery
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| How could the age of the individual influence tissue healing? | Nutritional status is often inadequate in the elderly, and the aging process itself slows down normal healing responses at many levels.
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| How could the presence of foreign material in the wound influence tissue healing? | foreing bodies, if not removed, impair wound closure and promote scarring as well as predispose to infection; e.g., a large splinter
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| How could the blood supply of the injured tissue influence tissue healing? | If the blood supply is limited or cut off from the damaged tissuue, then most of the cellular and blood factors necessary for healing would not reach the affected area; e.g., a thrombus or an embolus.
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| How could the presence of infections in the damaged tissue influence tissue healing? | Infection requires iits own cure, before healing can occur; removal of the infectious agent, if impaired or delayed, would prolong the healing process, leading to more extensive scarring and, if untreated, perhaps systemic infection. A puncture to the dam
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| How could the degree of immobilization of the injured tissue influence tissue healing? | Broken bones, if not immobilized, do not heal properly
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| How could pre-existing disease states that exist in the injured individual influence tissue healing? | Disease, if chronic and with systemic effects, could impair immune and other normal healing tissue responses. Diabetes, for example, may result in impaired circulation to the damaged area.
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| Identify potential complications that may occur during and inflammatory process and subsequent healing. | Loss of function; contractures and obstructions; adhesions; hypertrophic scar tissue; ulceration
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| Describe the classification of burns based on body surface area | the % of BSA burned, using the "rule of nines" for calculation to determine the extent of injury and fluid replacement needs
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| Describe the classification of burns based on the depth of tissue damage | Partial-thickness burns involve the 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 subcutaneous
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| Explain why full-thickenss burns initially may be painless | Nerves in the burned area have been destroyed
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| Keloid | hypertrophic scar formation due to excess collagen deposits leading to hard, often elevated, ridges of scar tissue
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| Eschar | A thick coagulated crust that develops following a full-thickness burn
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| Stenosis | Narrowing of structures
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| Adhesion | Bands of scar tissue joining two surfaces that are normally separate
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| Ulcer | A surface lesion due to breakdown of surface tissue
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| Exudates | Interstitial fluid accumulation in an area of inflammation
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| Contracture | Fixation and deformity of a joint as a result of scar formation and shrinkage.
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| Inflammation | a nonspecific body defense response to any tissue injury, which may be casued by chemical, physical agents, trauma, ets.; it involves neutrophils and macrophages as part of the cellular response and chemical mediators like histamine and prostaglandins wi
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| Immunity | a specific host defense response to "foreing" antigens; it involves specific cellular (T & B lymphocytes) and humoral (antibodies) components and mediators (e.g., complement); and it varies depending on the nature of the antigentic stimulus (immediate and
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| What is a cell surface antigen and why is it important? | a unique protein or glycoprotein configuration that is a distinctive marker for the recognition of a cell by the immune system. They provide the means by which the immune system distinguishes self from nonself. Important because it provides for the detect
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| What are HLAs? What is the MHC? | HLAs = Human Leukocyte Antigens; they are the Major Histocompatibility Complex cell membrane antigens on human leukocytes that determine "self" and serve as the basis for IDing histocompatible cells and tissues for transplantation, including blood transfu
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| Source and effects of Histamine | Mast cells and basophilsVasodilation and increased vascular permeability, contraction of bronchiolar smooth muscle; pruritis
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| Source and effects of Prostaglandins | Group of lipids synthesized in mast cellsVarious effects from causing inflammation, vasodilation, increased capillary permeability, and pain
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| Source and effects of Cytokines (lymphokines, monokines, interleukins, interferon) | T-lymphocytes and macrophagesIncrease in plasma proteins, ESR; stimulate activation and proliferation of B and T cells and communication between cells (messengers); induce fever, leukocytosis, and chemotaxis
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| Source and effects of Leukotrienes | Group of lipids derived from mast cells and basophilsContraction of bronchiolar smooth muscle; vasodilation and increased capillary permeability; chemotaxis
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| Source and effects of Kinins (bradykinin) | Activation of plasma protein (kinogen; e.g., bradykinin)Vasodilation, edema, and pain
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| Source and effects of Complement | Group of proteins circulating in the bloodstream; activated by antigen-antibody reactions on cell surfaceRelease of chemical mediators promoting inflammation, chemotaxis, phagocytosis, cell membrane damage (e.g., hemolysis)
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| Which chemical mediators are responsible for vasodilation? | histamine, prostaglandins, kinins, leukotrienes
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| Which chemical mediators are responsible for increased capillary permeability? | histamine, prostaglandins, leukotrienes
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| Which chemical mediators are responsible for chemotaxis? | cytokines, leukotrienes, complement
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| Which chemical mediators are responsible for pain? | prostaglandins, kinins
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| Which chemical mediators are responsible for contraction of bronchiolar walls / bronchospasm? | histamine, leukotrienes
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| Which chemical mediators are responsible for proliferation of leukocytes | cytokines
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| Which chemical mediators are responsible for pruritus? | histamine
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| Which chemical mediators are responsible for fever? | TNF, cytokines
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| What is the roll of macrophages? | phagocytosis, foreign antigen recognition
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| What is the roll of natural killer (NK) cells | destroy foreign cells, virus-infected cells, and cancer cells
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| What is the roll of cytotoxic or killer T cells? | destroy antigens and cancer and virus-infected cells
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| What is the roll of helper T cells (T4 and CD4) | activate B and T cells; limit immune cells
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| What is the roll of memory T cells | remember antigen and stimulate immune response upon subsequent exposure (secondary response)
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| What is the roll of suppressor T cells (T8) | limit immune response
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| What is the roll of B-lymphocytes | plasma cells: produce specific antibodiesB memory cells: secondary antibody response
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| Which types of cells play a role in both inflammation and immunity? | monocytes, macrophages, basophils
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| Which cells participate in both cellular and humoral immunity? | helper T cells
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| List the five classes of antibodies or immunoglobulins | IgG, IgM, IgA, IgE, IgD
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| Function of IgG | primary and secondary antibody responses; activates complement; includes antibacterial, antivirals, and antitoxins; crosses placenta, creates passive immunity in newborns
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| Function of IgM | primary antibody responses; activates complement; forms natural antibodies; involved in blood ABO incompatibility reactions
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| Function of IgA | found in secretions such as tears and saliva, in mucous membranes, and in colostrums to provide protection for newborns
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| Function of IgE | binds to mast cells in skin and mucous membranes; when linked to allergen, causes release of histamine and other chemicals, resulting in inflammation
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| Function of IgD | attached to B cells; activates B cells
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| Explain how antibodies exert their effects | by binding to the specific antigen that elicited their production, usually on a cell or bacterial surface, resulting in antigen destruction, cell membrane damage (especially in the presence of complement), and, in the case of RBCs, cell lysis. Some antige
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| What is the time frame between exposure to an antigen and the appearance of immunoglobulins in the serum? | Primary response on initial antigen exposure may range from days to weeks.Secondary response is almost immediate.
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| What is the average length of time required to acquire an effective antibody titer following exposure to an antigen? | Primary response is approximately 3 to 4 weeks. Secondary response is quicker with much higher titer within a week or two.
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| Explain the rationale for "boosters"? | To promote a stronger, faster secondary immune response
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| Explain why individuals may contract infections such as colds, influenza, and sexually transmitted diseases (STDs) repeatedly. | There are many strains of a virus or bacteria that cause new strains, then, because the immune response is specific, infection with one strain does not create immunity to subsequent exposures to new, different strains.
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| Identify measures taken in an attempt to prevent organ rejection after transplantation. | A close match of HLAs between donor and host tissues reduces risk of rejection. The common treatment involves immunosuppressive drugs such as cyclosporine, azanthioprine (Imuran), and prednisone
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| What is meant by the term "opportunistic" and why does this complication occur? | Describes microorganisms that are usually harmless in healthy individuals; however, patients taking immunosuppressant drugs have limited body defenses.
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| What medications are often prescribed prophylactically for an individual taking immunosuppressant drugs? Explain the rationale. | preventative antibiotics are usually administered because opportunistic infections are common and can be difficult to treat. They are best prevented.
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| List the types of medications that might be prescribed in the treatment of allergic conditions. | Antihistamine drugs for early signs and symptoms; glucocorticoids for severe or prolonged reactions
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| State the underlying mechanism responsible for autoimmune disorders | When individuals develop antibodies to their own cells or cellular material
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| What type of medications might be prescribed in the treatment of autoimmune disorders? Explain the rationale for each drug group. | Prednisone (glucocorticoid) to reduce the immune response and subsequent inflammation; dydroxychloroquine (antimalarial) may be used to reduce exacerbations
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| How is systemic lupus erthematosus diagnosed? | Diagnosed by the presence of numerous ANAs, especially anti-DNA, as well as other antibodies.
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| What are Lupus erythematous (LE) cells? | Mature neutrophils containing nuclear material found in the circulating blood; a positive sign of SLE
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| SLE effect on skin | butterfly rash
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| SLE effect on joints | polyarthritis
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| SLE effect on heart | carditis and pericarditis
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| SLE effect on blood vessels | Reynaud's phenomenon
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| SLE effect on blood | anemia, leukopenia, thrombocytopenia
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| SLE effect on kidneys | glomerulonephritis, with marked proteinurea and progressive damage
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| SLE effect on lungs | pleurisy
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| SLE effect on CNS | psychosis, depression, mood changes, seizures
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| Outline therapeutic interventions used in the treatment of lupus erythematosus | usually treated by a rheumatologist with predinisone, NSAIDs, and hydroxychloroquine for exacerbations
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| List common causes of primary immunodeficiency | hypogammaglobulinemia, thymic aplasia, DiGeorge's syndrome, CIDS, inherited deficits in any one or more of the components
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| List common causes of secondary immunodeficiency | kidney disease, Hodgkin's Disease, AIDS, radiation, immunosuppressive drugs, immunosuppression, malnutrition
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| Identify the general effects of immunodeficiency | Predisposition to opportunistic infections and an increased risk of cancer
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| Identify the types of medication that are often prescribed for the immunodeficient individual or immunocompromised host, and explain the rationale for each drug group. | Prophylactic antimicrobials to reduce incidence of opportunistic infections; gamma globulin replacement therapy
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| What is the causative agent responsible for HIV and AIDS? Describe its properties | Human immunodeficiency virus is the causative agent for AIDS. I is a "slow-acting" retrovirus containing two strands of RNA and the enzyme reverse transcriptase. ts envelope is characterized by spokes of glycoprotein. The virus is inactivated by many disi
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| List the routes of transmission of HIV | Must enter the bloodstream of the recipient through transmission of body fluids such as blood, semen, and vaginal secretions. Transmission most often occur through unprotected sexual intercourse with an HIV-positive partner, intravenous injection with con
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| Identify individuals who are at high risk for contracting HIV. | At the highest risk are IV drug users, people with multiple sexual partners, and the unborn fetuses of HIV-positive mothers
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| What is the usual incubation period for HIV? State the possible range. | Infected individuals usually become HIV positive within 2 to 10 weeks, but the "window" may be as long as 6 months. full-blown AIDS may not occur for many years. After an initial infection, mild "flue-like" symptoms appear in 3 to 6 weeks, followed by an
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| How is a diagnosis of HIV infection confirmed? What is meant by the "window period"? | A blood tes is performed for HIV antibodies. A positive test is followed by the Western blot test. The "window period" refers to the time from infections to the presence of HIV antibodies. This may be anywhere from 2 weeks to 6 months depending on the mod
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| What is the average length of time between infection with HIV and development of full-blown AIDS? | average of 6 - 7 years
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| How is a diagnosis of AIDS confirmed? | AIDS is diagnosed by a major decrease in the CD4 T-helper lymphocyte count and a change in the CD4+ to CD8+ ratio in the presence of opportunistic infection or certain cancers.
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| Which cells are targeted by HIV? Indentify the consequences of this. | Helper T4 lymphocytes are the major target and, when destroyed, eliminate the immune surveillance and detection function of these cells, thereby interfering with their critical function in the initiation of both humoral and cellular immunity.
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| Identify possible manifestations of the initial phase of HIV infection | Mild, self-limited nonspecific "flu-like" symptoms; low fever, fatigue, joint pain, and sore throat.
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| Advanced HIV general effects | lymphadenopathy, fatigue and weakness, headache, and arthralgia
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| Advanced HIV opportunistic infections | Pneumocystis carinii in the lungs, causing severe pneumonia; herpes simplex, causing cold sore; and Candida, a fungus infection of the mouth and esophagus
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| Advanced HIV GI manifestations | including parasitic infections; chronic severe diarrhea, vomiting, and ulcers; necrotizing periodontal disease weight loss, malnutrition and wasting
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| Advanced HIV oral manifestations | cold sores (herpes simplex) and Candida
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| Advanced HIV respiratory manifestations | Pneumocystis carinii causing pneumonia
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| Advanced HIV nervous system manifestations | HIV encephalopathy (AIDS dementia), aggravated by lymphomas, causing confusion, progressive cognitive impairment, memory loss, loss of coordination and balance, and depression; seizures.
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| Advanced HIV malignancies | Kaposi’s sarcoma and non-Hodgkin’s lymphoma
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| Identify medications that are used in the treatment of an individual with HIV and AIDS | drugs such as AZT, protease inhibitors; viral integrase inhibitors such as saquinavir and ritonavir; reverse transcriptase inhibitors such as zidovudine and lamivudine; various drug combinations known as “cocktails”; fungal, and antituberculosis drugs; ot
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| What is the prognosis for an individual infected with HIV? | Prognosis is much improved due to earlier detection and newer drug and nutritional therapies. Without treatment, death occurs within several years of diagnosis.
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| Explain the difference between an inflammation and an infection | Inflammation is a normal body response. It is the second line of defense caused by anything that results in tissue damage. Infection is caused by pathogenic microorganisms.
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| Identify the three major groups of bacteria, including examples of each | bacilli: Clostridium tetanicocci: Staphylococcus aureusspirals: Treponema pallidum
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| Describe the basic structure of a bacterium | An outer rigid cell wall, a cell membrane, a DNA strand, and cytoplasm. In addition, some species contain an external capsule or slime layer, specialized structures such as flagellae, and pili or fimbriae.
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| What is the difference between exotoxins and endotoxins? | Exotoxins are produced / secreted by gram-positive bacteria. Endotoxins are components of the cell wall of gram-negative organisms.
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| What is an endospore or bacterial spore? Describe the process of spore formation. Identify bacteria that produce spores. | Endospores are latent forms of some bacterial species with an outer coat that is resistant to heat and other environmental conditions. The process of spore formation is illustrated in Figure 4-4, p. 82. Examples of spore-producing bacteria include tetanus
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| Describe the process of binary fission | A simple division in half, forming two daughter cells identical to the parent bacterium.
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| Compare and contrast bacterial cells and human cells with regard to the presence of a cell wall | Bacteria: presentHuman: not present
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| Compare and contrast bacterial cells and human cells with regard to the presence of a cell membrane | Bacteria: present - selectively permeable; site of metabolic processesHuman: present - selectively permeable
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| Compare and contrast bacterial cells and human cells with regard to the presence of a capsule or slime coat | Bacteria: present in someHuman: not present
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| Compare and contrast bacterial cells and human cells with regard to the presence of a flagella | Bacteria: present in someHuman: sperm only
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| Compare and contrast bacterial cells and human cells with regard to the presence of a pili or fimbriae | Bacteria: present in someHuman: not present
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| Compare and contrast bacterial cells and human cells with regard to the presence of cilia | Bacteria: not presentHuman: present in some
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| Compare and contrast bacterial cells and human cells with regard to the presence of membrane-bound organelles (mitochondria, lysosomes, ER) | Bacteria: not presentHuman: present
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| Compare and contrast bacterial cells and human cells with regard to the presence of ribosomes | Bacteria: presentHuman: present - larger
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| Compare and contrast bacterial cells and human cells with regard to the presence of a nucleus | Bacteria: not presentHuman: present
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| Compare and contrast bacterial cells and human cells with regard to the number of chromosomes | Bacteria: single; circularHuman: 46; paired (except sex cells)
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| Compare and contrast bacterial cells and human cells with regard to the method of reproduction | Bacteria: binary fissionHuman: mitosis
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| Why are viruses said to be "obligate intracellular parasites"? | They require a living host cell for replication
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| Describe the structure of a viral particle or virion | Consists of a protein coat or capsid and a DNA or RNA nucleic acid core
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| Outline the process of viral replication | Virus attaches to the host cell and penetrates. It uncoats and takes over the host cell DNA. The host cell synthesizes viral components. The components assemble and are released by host cell lysis.
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| Describe the structure of a fungus | Classified as eukaryotic. Consist of cells or chains of cells and may have long filaments called hyphae that intertwine to form a mass called the mycelium, which is large enough to be visible.
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| List pathological conditions caused by chlamydiae | pelvic inflammatory disease; eye infections in newborn of infected mothers
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| List pathological conditions caused by rickettsiae | typhus; Rocky Mountain spotted fever
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| List pathological conditions caused by mycoplasmas | pneumonia
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| List pathological conditions caused by protozoa | Trichomonas vaginalis; malaria; amebic dysentery
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| What is a helminth? | A worm
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| Normal or resident flora | Microorganisms that normally inhabit various areas of the body such as the skin and GI tract
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| Areas of the body that lack resident flora and therefore should be sterile | Lungs, bladder, stomach
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| Virulence | The degree of pathogenicity of a microbe or pathogen. It can be enhanced by production of exotoxins or endotoxins, destructive enzymes, spore formation, and presence of bacterial capsule
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| Pathogenicity | The capacity of a microbe to cause disease. Immunodeficiency or immunodepression can result in opportunistic infections; relocation of normal flora to another body site can also result in their production of disease.
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes pneumocystis carinii pneumonia? | Fungus
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes candidiasis? | fungus
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes syphilis? | Bacteria
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes trichomoniasis? | Protozoa
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes tuberculosis? | bacteria
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes pneumonia? | bacteria; viruses; fungi; mycoplasma
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes tetanus? | bacteria
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes Rocky Mountain spotted fever? | rickettsia
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes tinea pedis? | fungus
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes herpes simplex? | virus
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes influenza? | virus
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| Bacteria, Virus, Fungus, Rickettsia, Chlamydia, ProtozoaWhich causes botulism? | bacteria
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| What is meant by the "infection cycle"? Identify its components and ways in which the cycle can be broken. | The sequence or chain of events that lead to infection and disease by a pathogen. (a) locating and removing the reservoir or sources of infection(b) blocking the exit from the source; providing or cleaning barriers(c) maintaining immunizations(d) treating
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| What is meant by the term "culture and sensitivity"? | To take a tissue culture of a specimen that is placed in a medium containing various antimicrobials to determine the nature and drug sensitivity or the microbe
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| How do manifestations of an infection differ from those of an inflammation? | Microbes are present at the source of infection. With infection due to bacteria, purulent exudate and tissue necrosis usually develop at the site. Lymphadenopathy, high temp, and leukocytosis are often present. Inflammation results in a serous exudate and
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| Antibacterial spectrum | The range of bacteria for with the drug is effective:narrow: either gram positive or negativebroad: both gram-positive and gram-negative bacteria
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| Bacterial resistance | Bacteria that develop or adapt in order to lose their sensitivity to a drug such as altering their metabolism to block the drug's effects, producing enzymes that inactivate the drug, altering their cell membranes
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| Bactericidal | Drugs that destroy microorganisms
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| Bacteriostatic | Drugs that reduce the rate of bacterial reproduction
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| Why has it been difficult to develop antiviral drugs? | Because viruses are obligate intracellular parasites, a drug that destroys viruses would also destroy the host cell.
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| What is probably the most serious adverse effect associated with antibacterial drugs | Allergic reaction - anaphylaxis
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| Superinfection | A secondary infection by pathogens that results from disruption or reduction of the normal resident flora by antimicrobial drugs
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| What is the difference between a superinfection and an opportunistic infection? | A superinfection occurs only during treatment with antimicrobial agents. An opportunistic infection occurs in an individual with decreased immunity. Both are usually caused by fungi that are part of the normal resident flora.
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| When is it appropriate for a physician to prescribe a narrow spectrum antibacterial drug? | When the identity of the bacterium is known; after culture and sensitivity have been completed
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| How can a bacteriostatic drug help one eliminate the infecting microorganism? | the drug prevents replication of the bacteria, thereby keeping the number of bacteria constant - the body's own defensive cells will destroy the organism.
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| When would the prescription of a bacteriostatic drug not be advisable? | If the individual was immunosuppressed (e.g., organ transplant recipient) or immunodeficient (e.g., someone with AIDS)
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| Explain how the misuse or overuse of antibacterial agents could lead to the development of bacterial resistance. | Bacteria adapt and / or mutate to develop various means of losing drug sensitivity; excessive or unnecessary use of drugs provides a stimulus for such adaptation.
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| If antibacterial drugs are not effective in the treatment of viral infections, why are they often prescribed for individuals with chronic viral infections such as hep B, hep C, or HIV? | Because they may reduce the risk of secondary bacterial infection
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| Identify guidelines that an individual should follow to maximize the effects of antibacterial medications. | Drugs should be taken according to the prescription. Drug should be taken until the prescription is completely used. Follow instructions regarding food or fluid intake. provide a good medical history including known drug allergies.
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| Apoptosis | A form of cell death in which a programmed sequence of events leads to the elimination of cells without releasing harmful substances into the surrounding area.
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| Which adaptive change is considered to be the most dangerous? | Dysplasia
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| Anaplasia | failure of cells to develop specialized features
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| Give 2 examples of hyperplasia | development of a callus on a laborer's hands; enlargement of the prostate gland with age
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| What change will occur in response to prolonged hypoxia? | Atrophy
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| What disorder would cause liquefactive necrosis? | Stroke
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| Name 3 tissues that enlarge by hypertrophy after birth. | Skeletal muscle, urinary bladder, brain
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| Which cells secrete histamine? | Basophils, Mast cells
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| Which cells are phagocytic? | neutrophils, Monocytes, Macrophages
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| Name 2 effects of NSAIDs that are not effects of acetaminophen | Anti-inflammatory, platelet inhibition
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| Diapedesis | Movement of leukocytes into the interstitial spaces
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| What type of exudate is found inside a blister? | Serous
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| Adhesions | Bands of scar tissue between two normally separate surfaces
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| Name a tissue where you would expect healing to be slow to occur | cartilage
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| Which cells are the first to migrate into the interstitial spaces after an injury? | neutrophils
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| What type of cell becomes a macrophage once it migrates into the tissue? | monocyte
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| What type of cell is prevalent in allergic responses? | eosinophil
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| What is the term for a hypertrophic scar? | keloid
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|
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| What cells are prevalent in chronic inflammations? | Fibroblasts, macrophages, lymphocytes
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| What is the 2nd event in the vascular response of inflammation? | Vasodilation
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|
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| What would be elevated during an acute inflammation involving a large area? | neutrophils, erythrocyte sedimentation rate, body temperature, c-reative protein level
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|
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| What type of burn involves destruction of all of the epidermis and part of the dermis? | Deep partial thickness
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|
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| How do NSAIDs decrease inflammation? | They decrease production of prostaglandins
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| Inflammation | The body's local response to tissue injury
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|
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| Which cells are involved in the production of antibodies? | helper T cells, B lymphocytes
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|
||||
| Which cells are the antigen-capturing cells? | macrophages
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| Which cells process and present antigen? | macrophages
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|
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| Which immunoglobulin is involved in allergic responses? | IgE
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|
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| Which immunoglobulin is found in body secretions such as saliva? | IgA
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| Which immunoglobulin is responsible for passive immunity? | IgG
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|
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| Which cell regulates the activity of all the other immune cells? | T-helper (CD4)
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|
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| Which chemical mediators stimulate the proliferation of B and T cells? | Cytokines
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|
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| What does seroconversion mean in relation to HIV and AIDS? | HIV antibodies have been identified in the blood
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|
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| What is true of the period between seroconversion but before the development of AIDS? | The individual is contagious and capable of spreading the virus, a pregnant woman may pass the virus to her unborn child
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|
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| What organism commonly causes severe respiratory problems and often death in patients with AIDS? | Pneumocystis carinii
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|
||||
| What is the etiology of SLE? | It is an autoimmune disorder
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|
||||
| What is the criterion for changing the diagnosis from HIV-positive to one of AIDS? | When the helper T (CD4) cell count falls below a certain level
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|
||||
| How could passive immunity be acquired? | An injection of antivenom following a snakebite; an injection of hep B immunoglobulin
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|
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| What is the mechanism by which bacteria reproduce? | Spore formation
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|
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| Name two structures found in human cells but not in bacterial cells | cell membrane, nucleus
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|
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| Name 3 structures found in bacterial cells but not in human cells | cell wall, capsule, fimbriae
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|
||||
| What type of orgainsms may produce spores? | bacteria, fungi
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|
||||
| Superinfection | An infection caused by an alteration of normal body flora during treatment with an antibiotic
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|
||||
| Name the causative agent(s) of Pneumocystis carinii pneumonia | fungi
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|
||||
| Name the causative agent(s) of candidiasis | fungi
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|
||||
| Name the causative agent(s) of gonorrhea | bacteria
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|
||||
| Name the causative agent(s) of trichomoniasis | protozoa
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|
||||
| Name the causative agent(s) of tuberculosis | bacteria
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|
||||
| Name the causative agent(s) of pneumonia | bacteria, viruses, fungi, chlamydia
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|
||||
| Name the causative agent(s) of tetanus | bacteria
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|
||||
| Name the causative agent(s) of malaria | protozoa
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|
||||
| Name the causative agent(s) of athlete's foot | fungi
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|
||||
| Name the causative agent(s) of herpes zoster | viruses
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|
||||
| Name the causative agent(s) of influenza | viruses
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|
||||
| Name the causative agent(s) of botulism | bacteria
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|
||||
| How could a diagnosis of malignancy be positively confirmed? | biopsy
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|
||||
| Is measles an oncogen? | no
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|
||||
| What is often a dose-limiting factor for chemotherapy? | bone marrow suppression
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|
||||
| What kind of tumor is an osteosarcoma | malignant tumor of bone
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|
||||
| Transformation | conversion of normal cell to cancerous cell
🗑
|
||||
| What conditions may predispose an individual to neoplasia? | Immunosuppression, prolonged hormone replacement therapy, chromosomal abnormalities, exposure to radiation, dysplastic tissue changes
🗑
|
||||
| True or false? Benign tumors are usually encapsulated? | True
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|
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