Clinical Topics Conference: Chapter 2, Inflammation
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- Acute inflammation -- vascular phase
- Acute inflammation -- cellular phase
- Chronic inflammation
- Granulomatous inflammation
Case 1: Acute Inflammation - Vascular Phase:Clinical vignette:
A twenty five year-old woman is bitten on her right index finger bya cat. The cat's canine tooth punctures the joint between her first andsecond phalanges. Within 24 hours, the skin around the puncture wound reddens,the tissue surrounding the site swells, the joint becomes extremely painful,and she loses the ability to flex the finger. At this point, she presentsherself at an emergency room, where you examine her. She has a slight feverand the skin at the site of the puncture wound is warmer to touch thanskin at the same site on the opposite hand. Lymph nodes in her right axillaare slightly enlarged and somewhat painful.
Discussion topics:
- Discuss how you used knowledge of the cardinalsigns of inflammation to distinguish this as an acute inflammatorylesion. Why is it not a chronic inflammatory lesion?
- Acute inflammation is a vascular phenomenon. What vascular changeshave occurred to produce the signs (objective evidence of a pathologicprocess) and symptoms (subjective evidence) described above?
- Were you to order a hemogram, what would you expect to find with respectto her leukocytes, both in terms of absolute numbers and kinds? How wouldthese findings relate to the process of acute inflammation?
- What are the origins of the proinflammatory mediators that cause thevascular changes that have resulted in the clinical presentation describedabove?
- Inflammation is a dynamic process. What are the possible outcomes thatyou can predict for the inflammatory lesion described above?
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Case 2: Acute Inflammation - Cellular Phase:Clinical vignette:
A thirty year-old man is planning to be married in two months. He hashad an unsightly nevus on his right cheek, which he decides to have removedprior to his wedding. The surgical site begins to heal normally, but thenthe surrounding tissue suddenly becomes red, swollen, painful, and a clear-to-slightlyturbid, viscous fluid begins to ooze from the incision site. He cannotsleep with the lesion against his pillow, because of the pain, and it hurtsto open his mouth widely. Unfortunately, he is without insurance and shortof cash, so he tries to treat the problem himself, using hot epsom saltcompresses and aspirin. The pain begins to subside, the redness beginsto diminish, and the oozing fluid becomes thicker, opaque, and reddishwhite. He misses application of the compresses several times and the drainingincision seals. The site then begins to swell rapidly until, after twodays, it ruptures and discharges a thick, fetid, yellow-white exudate,leaving a distinct cavity or pocket beneath the incision site.
Discussion topics:
- Discuss the stages of inflammation that are evident in this time course,i.e., acute, subacute, and chronic (not all may be present).
- Why did the redness and pain begin to subside? Where would aspirin have had its effect(s)?
- Why did the oozing, clear fluid become, first, turbid and then opaque?Discuss the succession of events, at the level of the postcapillaryvenule, that allowed these changes in turbidity to develop.
- Discuss the pathogenesis of an abscess. What is it that causes a cavityto develop in an abscess? What is the difference between a purulent exudate,
a purulent effusion, and
a suppurative inflammatory
process?
- Assume that the cause of this man's problem was postoperative infectionwith a pyogenic bacterium. What killing mechanisms will be employed bythe man's leukocytes as they attempt to eliminate the invading microorganisms?
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Case 3: Chronic Inflammation:Clinical vignette:
An eighty year-old, rural woman presents with the signs and symptomsof chronic renal failure. She had experienced several episodes of acutebacterial cystitis during the prior twenty years, which were thought tohave been treated successfully with antibiotics, i.e., until no bacteriacould be detected in her urine. Otherwise, she had had no urinary tracksigns or symptoms, and several hemograms and urinalyses performed at intervalsduring routine physical examinations had been normal. Clinical assessmentat the time of this presentation indicates that she has no renal reserveand is in end-stage renal failure. The severity of her condition is explainedto her and she is told that, without entering a dialysis program, she willdie. In spite of this bleak prognosis, she elects, on the basis of qualityof life issues, not to enter such a program. Prior to her death, she asksthat a postmortem examination be made, in the hope that it will be possibleto determine what caused the loss of her renal reserve, thereby hopefullyallowing the process to be recognized and treated in others who might besuffering from the same condition. The primary postmortem diagnosis ischronic-active pyelonephritis. Small numbers of Escherichia coliare cultured from tissue samples removed aseptically from her kidneys.
Discussion topics:
- The kidneys can be visualized radiographically, especially by performingan intravenous pyelogram. This test was undoubtedly performed here. Whatwould you expect this woman's kidneys to have looked like radiographically? Why?
- What was the most likely underlying cause of the chronic pyelonephritis?
- Why wasn't this woman's condition picked up when routine hemogramsand urinalyses were performed during the course of the preceding twentyyears?
- What is the meaning of chronic-active in describing her pyelonephritis?What destructive process caused the loss of this woman's renal reserve?What was the process actually trying to accomplish?
- What were the principal inflammatory cell types that were involvedin the destructive process?
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Case 4: Granulomatous InflammationClinical vignette:
A twenty-eight year-old, male, homeless, intravenous drug user is referredby the director of a Salvation Army mission, because he is coughing andoccasionally spitting up bloody sputum. He has a low grade fever and testsPPD (Purified Protein Derivative)-positive. Radiographicstudies of his lungs reveal scattered focal densities, some with areasof calcification. He is HIV-negative. Your diagnosis is pulmonary tuberculosis,a disease that is being seen again with increasing frequency, especiallyin patients with a background similar to this man's.
Discussion topics:
- What are the areas of radiographic density that are seen in his lung?Why are there occasional areas of calicification?
- What cell types would be seen in the radiodense areas if they weresampled for histologic analysis? Would there be any kind of organizationwithin the lesions, with respect to the locations of these cell types?What is the functional role of each cell type?
- Why is this man's sputum occasionally bloody?
- What is the process in this man's lungs trying to accomplish? Whatsequellae are potentially associated with this process?
- How might this process differ if the man had full-blown AIDS? Why?
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