Practice your knowledge of the concepts raised in the small group discussions dealing with inflammation, healing and repair.
In the multiple choice answers [ square check boxes ] click on whichever answer you feel is the most appropriate. In some questions there may be more than one appropriate answer. When finished, submit your quiz for marking and your result will be returned to you within a few minutes.
THESE TESTS ARE ONLY TO HELP YOU LEARN THE MATERIAL AND THE "GRADE" IS NOT RECORDED.
Please e-mail feedback to Dr. Bertha Garcia delivery: simultaneous question: The "tumor" of inflammation is due predominantly to: ans: arteriolar dilation ans: venous dilation ans: capillary dilation ans: increased intracellular fluid ans: increased extracellular fluid fbk: Yes - Increased permeability leads to accumulation of fluid in the extracellular tissues. Accumulation of neutrophils also plays a role. correct_answer: 5
question: The warmth of an acutely inflamed skin lesion is due to ans: exudation fbk: No - try again. ans: fever fbk: No - Although this may be a systemic response to infection and inflammation. Looking for the local factor. ans: increased blood flow fbk: Yes - Owing to dilatation of arterioles there is increased blood flow through the skin. ans: proteolytic enzymes fbk: No - try again. ans: increased extracellular fluid fbk: No - causes the swelling seen in inflammation. See answer to previous question. correct_answer: 3
question: If these following events were put in sequence as they occur in an inflammatory reaction, which would occur fourth? ans: emigration of leukocytes fbk: Yes - The development of acute inflammation leads to the sequence of vascular dilatation and increased permeability followed by slowing of the blood flow and concentration of red cells. Adhesion and then emigration of leukocytes follows. ans: phagocytosis and enzymatic digestion fbk: No - this is a relatively late event in the inflammatory process. ans: slowing of blood flow and red cell concentration fbk: No - in this series this would be the second event, following vascular dilation and increased permeability. ans: adhesion of leukocytes fbk: No - in this series this would be the third event, prior to their emigration. WBCs become "sticky" and adhere because of alterations on the cell surface and the interaction of cell adhesion molecules with endothelial cell surfaces. ans: vascular dilation and increased permeability fbk: No - in this series this would be the first event followed by a slowing of blood flow and the adhesion and emigration of leukocytes. correct_answer: 1
question: The first cells of an acute inflammatory response to emigrate into an injured area are ans: red blood cells fbk: No - they are already present. ans: mast cells fbk: No - they are important in the early stages of inflammation, but the key word here is "emigration" to the injured area - that is the neutrophils. ans: monocytes fbk: No - they appear later in the inflammatory reaction. ans: neutrophils fbk: Yes - The neutrophil is the characteristic cell of the acute inflammatory response and emigrate to the injured area in response to chemotactic factors. ans: lymphocytes fbk: No - these cells appear late in inflammation and are mainly associated with immunologically mediated inflammation correct_answer: 4
question: Each of the following is true of neutrophils EXCEPT ans: They phagocytose injurious agents. fbk: True - they are capable of changing shape and pseudopod formation. Their granules have powerful proteases, lipases, myeloperoxidases and other enzymes. ans: They reproduce and maintain a relatively constant number in foci of inflammation. fbk: False - Neutrophils are formed in the bone marrow and reach an inflammatory focus via the blood stream and do not proliferate locally. ans: They usually degenerate rapidly in inflammation and their cell membrane ruptures releasing their enzymes. fbk: True - they have a short half-life (about 7 hours). They are also very sensitive to the acidic environment in inflammation. ans: They can cause tissue damage and thereby provoke further inflammation. fbk: True - the enzymes they release may provoke further tissue damage and/or inflammation. correct_answer: 2
question: Migration of leukocytes directly toward a foreign substance of an injured tissue is called ans: diapedesis fbk: No - this refers to the outward "passive" passage of blood cells (e.g. RBCs) through blood vessel wall. ans: exudation fbk: No - this refers to the leakage of large plasma proteins and leukocytes from blood vessels as a result of increased vascular permeability in inflammation. ans: emigration fbk: No - this refers to the escape of leukocytes through the blood vessel walls. ans: anaphylaxis fbk: No - a manifestation of immediate hypersensitivity. ans: chemotaxis fbk: Yes - by definition! The movement of a cell along a concentration gradient toward the greater concentration of the substance. Chemoattractants include lymphokines, bacterial products, C5a (or other activated complement components). correct_answer: 5
question: Substances which are chemotactic to neutrophils and/or monocytes include ans: C3a fbk: No - C3a is involved in the increase of capillary permeability. ans: C5a fbk: Yes - but both 2 and 4 are correct. The C5a component of complement is a potent chemotactic agent. ans: prostaglandins fbk: No, not directly - PGs are involved in vasodilation and increased capillary permeability, the production of fever and pain. Think about how acetylsalicylic acid (aspirin) acts in the arachidonic acid pathway! ans: leukotriene B4 fbk: Yes - but both 2 and 4 are correct. PMNs and monocytes respond. Leukotriene is a metabolite of arachidonic acid. mult_ans: 2 4
question: A mediator of acute inflammation that causes increases in both vascular permeability and pain is ans: endotoxin ans: complement ans: histamine ans: bradykinin fbk: Correct! ans: endogenous pyrogen correct_answer: 4
question: Histamine is thought to be the direct cause of: ans: leucocytosis fbk: No - the increase of numbers of WBCs is due to the release of chemotactic factors. ans: emigration fbk: No - the migration of cells is due to chemotactic factors. ans: phagocytosis fbk: No - this is related to the action of PMNs and their proteolytic enzymes. ans: increased vascular permeability fbk: Yes - Histamine released from mast cells is the initial chemical mediator that increases vascular permeability. correct_answer: 4
question: The newly formed, highly vascularized connective tissue with a component of acute inflammatory exudation is known as: ans: angioma ans: scar ans: granulation tissue fbk: Yes - by definition! ans: granuloma ans: purulent exudate correct_answer: 3
question: As a scar becomes older the: ans: connective tissue becomes more cellular. fbk: No - usually becomes less cellular as more collagen is laid down. ans: amount of collagen decreases. fbk: No - the amount of collagen usually increases. ans: fibroblasts increase. fbk: No - usually becomes less cellular (fewer fibroblasts) as more collagen is laid down. ans: number of blood vessels decreases. fbk: Yes - many of the capillaries that formed in the granulation tissue are resorbed. ans: older areas remodel. correct_answer: 4
question: The principal cells of granulation tissue are: ans: fibroblasts and endothelial cells fbk: Yes - these cells proliferate to provide new capillaries and blood vessels and fibroblasts deposit collagen and fibronectin. ans: macrophages and giant cells fbk: No - macrophages may be present but these are not the principal cells of granulation tissue. ans: lymphocytes and plasma cells fbk: No - lymphocytes may be present but these are not the principal cells of granulation tissue. ans: osteocytes and chondrocytes fbk: No - these are mature cells that form bone and collagen. ans: neutrophils and macrophages fbk: No - neutrophils are a component of acute inflammation and are usually not present during repair. Macrophages may be present in small numbers. correct_answer: 1
question: If nonfatal, a massive myocardial infarct would be expected to: ans: heal by resolution fbk: No - cardiac myocytes do not divide so healing is by scar formation. ans: heal by regeneration fbk: No - cardiac myocytes do not divide so healing is by scar formation. ans: heal by scarring fbk: Yes - the dead tissue is removed by an inflammatory process and cardiac tissue is replaced by collagen. ans: form a chronic abscess fbk: No - cardiac myocytes do not divide so healing is by scar formation. ans: form a fluid-filled cyst fbk: No - cardiac myocytes do not divide so healing is by scar formation. correct_answer: 3
question: When is the tensile strength of a healing skin wound restored to pre-wounding strength? ans: by the 3rd day, when tissue debris is cleared. fbk: trick question! Although the time sequence of the above answers is correct most wounds never regain the initial strength of the original tissue. Seventy to 80% of tensile strength is achieved at 3 months. ans: by 1 week, when the gap is bridged by granulation tissue. fbk: trick question! Although the time sequence of the above answers is correct most wounds never regain the initial strength of the original tissue. Seventy to 80% of tensile strength is achieved at 3 months. ans: by 2 months, after scar remodelling has begun. fbk: trick question! Although the time sequence of the above answers is correct most wounds never regain the initial strength of the original tissue. Seventy to 80% of tensile strength is achieved at 3 months. ans: from 6 months to 1 year, after collagen cross-linking. fbk: trick question! Although the time sequence of the above answers is correct most wounds never regain the initial strength of the original tissue. Seventy to 80% of tensile strength is achieved at 3 months. ans: never, scars are always weaker than intact issue. fbk: Yes - trick question! Although the time sequence of the above answers is correct most wounds never regain the initial strength of the original tissue. Seventy to 80% of tensile strength is achieved at 3 months. correct_answer: 5
question: Factors which tend to interfere with wound healing include ans: vitamin C deficiency fbk: Yes - partially, all are correct. Vitamin C is a cofactor in collagen biosynthesis. ans: foreign body in the wound fbk: Yes - partially, all are correct. ans: protein deficiency fbk: Yes -partially. All are correct. Severe protein deficiency can affect several steps - initial inflammatory response and the adequacy of repair (impaired collagen synthesis). ans: infection fbk: Yes - partially. All are correct. ans: corticosteroid therapy fbk: Yes - partially. All are correct. mult_ans: 1 2 3 4 5