Acute vs chronic inflammation
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- Acute vs chronic inflammation
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Acute vs chronic inflammation
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[post_content] => Practice Passage (Question 1-6)
*This passage is the property of Khan Academy and has been reformatted into an AAMC-style interface in their entirety by MedLife Mastery. MedLife Mastery does not endorse and is not an affiliate of Khan Academy.
Acute inflammation is induced by tissue damage due to trauma, noxious compounds, or microbial invasion. The process of acute inflammation is mediated by immune cells, important cell-signaling proteins called cytokines, and other small molecules. Anaphylatoxins, small immune-mediating molecules released at the site of inflammation, stimulate mast cells to release histamine, serotonin and prostaglandins, which bind specific receptors on endothelial cells and smooth muscle cells, promoting endothelial permeability and smooth muscle relaxation. This response allows immune cells such as neutrophils to migrate into affected tissue through the capillary wall (diapedesis) and respond to the offending agent, as shown in Figure 1; neutrophils are thus the major component of pus. Additional clinical signs of acute inflammation include swelling, redness, pain and heat at the site of the insult.
Figure 1 Neutrophil Diapedesis; adapted from Kantari et al. The role of neutrophils and monocytes in innate immunity. Contrib Microbiol. 2008;15:118-46
Chronic inflammation, in contrast, may be the only inflammatory response seen in certain viral infections and hypersensitivity reactions, particularly if the cause of inflammation is persistent. In chronic inflammation, the primary immune cells are macrophages and T lymphocytes, which produce cytokines and enzymes that cause more lasting damage to cells. Acute inflammation caused by infection or injury will also transition to chronic inflammation over a period of days to weeks.
Table 1 shows the main cell types, mediators, and symptoms observed in acute and chronic inflammation.
Table 1 Characteristics of Acute versus Chronic Inflammation
General treatments used for both types of inflammation include nonsteroidal anti-inflammatory drugs (NSAIDs), which are commonly used to reduce pain, swelling, and body temperature/fever associated with inflammation; and corticosteroids, which are potent anti-inflammatory medications that can rapidly suppress inflammation. Other treatments that can address specific types of both chronic and acute inflammation include rilonacept, a monoclonal antibody against interleukin-1, and colchicine, which interferes with microtubules and disrupts the normal cellular processes involved in inflammation.
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[question] => Which of the following best describes the effect of anaphylatoxins in acute inflammation?
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[answer] => 2
[description] => Reason for Correct Answer:
Macrophages and T cells drive chronic, not acute, inflammation.
Granulomas are seen in chronic inflammation, whereas abscesses are a sign of acute inflammation.
The first paragraph states that anaphylatoxins stimulate the release of “histamine, serotonin and prostaglandins, which bind specific receptors on endothelial cells and smooth muscle cells, promoting endothelial permeability and smooth muscle relaxation.” And that this allows “neutrophils to migrate into affected tissue through the capillary wall (diapedesis).”
Endothelial cells are present in blood vessels, and the relaxation of smooth muscle cells in blood vessels causes vasodilation. Therefore, the binding of anaphylatoxin-stimulated mediators causes vasodilation, in addition to increased vascular permeability. Other things, like cytokines, likely attract neutrophils to the area, but the passage makes it clear that the role of anaphylatoxin is to cause vasodilation and permeability to allow neutrophils to reach and enter the area.
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[answers] => Array
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[each_answer] => A. Release of acute-phase cytokines to attract neutrophils
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[each_answer] => B. Stimulation of vasoactive compounds and vasodilation
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[each_answer] => C. Induction of localized vasoconstriction
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[each_answer] => D. Recruitment of macrophages and T cells
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[1] => Array
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[quiz_unique_key] => 1403770772
[question] => A 3-year-old previously healthy child presents to the emergency room with a painless lump on the bottom of her foot that, according to her mother, has been present for several weeks. She has not had a fever and the lump is not red. A biopsy of the lump demonstrates fibrosis. Other biopsy findings most likely include:
[value] => Array
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[answer] => 4
[description] => Reason for Correct Answer:
Paragraph 2 states that “acute inflammation caused by infection or injury will also transition to chronic infection over a period of days to weeks.”
Table 1 also shows that fibrosis, as seen in this patient, is characteristic of chronic inflammation.
Paragraph 2, as well as Table 1, state that macrophages and lymphocytes are the prevalent cell types seen in chronic inflammation.
In this case, given the location of the lump and the fact that it is not red or accompanied by fevers, it is more likely a small foreign object than an infection.
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[answers] => Array
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[0] => Array
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[each_answer] => A. neutrophilic infiltrates and bacteria.
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[each_answer] => B. neutrophilic infiltrates and a small foreign body.
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[each_answer] => C. T lymphocytes and bacteria.
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[each_answer] => D. macrophages and a small foreign body.
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[2] => Array
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[quiz_unique_key] => 1403770772
[question] => In patients with cystic fibrosis (CF), bronchoalveolar lavage (BAL), otherwise known as lung washout, can help diagnose causes of symptom exacerbations. In a 15-year-old patient hospitalized for a CF exacerbation, BAL demonstrates neutrophils, macrophages and large numbers of bacteria. Results of BAL are consistent with all of the following EXCEPT:
[value] => Array
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[answer] => 3
[description] => Reason for Correct Answer:
Neutrophils support acute inflammation, and macrophages support chronic inflammation, according to Table 1.
Large numbers of bacteria are suggestive of infection.
Although patients with CF can experience allergic symptoms, we would expect to see eosinophils present in this case, as delineated in the table. This is therefore not supported by the BAL.
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[answers] => Array
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[0] => Array
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[each_answer] => A. signs of chronic inflammation.
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[each_answer] => B. acute inflammatory responses.
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[each_answer] => C. an allergic reaction.
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[each_answer] => D. a lung infection.
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[quiz_unique_key] => 1403770772
[question] => What is a likely side effect of prolonged corticosteroid use in patients with chronic inflammation?
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[answer] => 1
[description] => Reason for Correct Answer:
Normally, the hypothalamus secretes corticotropin-releasing hormone (CRH), which stimulates adrenocorticotropic hormone (ACTH) release from the pituitary, which in turn stimulates corticosteroid (cortisol) release from the adrenal glands. Elevated cortisol in the blood then decreases the amount of CRH and ACTH released, via negative feedback on the hypothalamus and pituitary, thus keeping the balance in check.
Prolonged use of corticosteroid medications can lead to suppression of the body’s natural production of ACTH and CRH. When corticosteroids are taken externally, the body’s feedback mechanism senses the elevated levels of these synthetic steroids and reduces the production of these hormones.
This reduction in CRH/ACTH signals to the adrenal glands to produce less cortisol over time. If the corticosteroid medication is suddenly stopped or reduced, the adrenal glands might not be able to produce enough cortisol to meet the body’s needs, leading to adrenal insufficiency. This is why careful management and gradual tapering of corticosteroid doses are important to prevent this potential complication.
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[answers] => Array
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[0] => Array
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[each_answer] => A. Adrenal insufficiency resulting from adrenocorticotropic hormone (ACTH) suppression
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[each_answer] => B. Adrenal insufficiency resulting from excess ACTH stimulation
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[2] => Array
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[each_answer] => C. Enhanced adrenal output from corticotropin-releasing hormone (CRH) suppression
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[each_answer] => D. Enhanced adrenal output from excess CRH stimulation
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[question] => A patient with gout is initially treated with Medication 1 before being placed on a combination course with Medication 2. Medication 1 inhibits the production of prostaglandins, which typically modulate the activity of the hypothalamus during inflammation and infection; Medication 2 inhibits immune cell activity by blocking intracellular transport.
What is the most likely identity of Medication 1 and Medication 2, respectively?
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[answer] => 2
[description] => Reason for Correct Answer:
The hypothalamus is the part of the brain that regulates body temperature.
The last paragraph states that NSAIDs help to decrease body temperature/fever during inflammation. Given this information, an NSAID is likely the medication mediating the effect of inflammation on the hypothalamus (Medication 1).
Microtubules are very important for processes such as intracellular transport.
The last paragraph states that colchicine interferes with microtubules. Given this information, colchicine is likely the medication blocking intracellular transport (Medication 2).
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[each_answer] => A. An NSAID and rilonacept
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[each_answer] => B. An NSAID and colchicine
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[each_answer] => C. A corticosteroid and rilonacept
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[each_answer] => D. Rilonacept and colchicine
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[quiz_unique_key] => 1997864699
[question] => Which molecules are primarily responsible for mediating the process of neutrophil diapedesis during inflammation?
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[answer] => 3
[description] => Reason for Correct Answer:
Neutrophil diapedesis is the movement of neutrophils across blood vessel walls (endothelial barriers) in response to inflammatory signals. This allows them to exit the bloodstream and reach areas of infection or tissue damage. Figure 1 shows neutrophils attaching to endothelial cells and transmigrating into the tissue.
While G-protein coupled receptors (GPCRs) and cytokines do play roles in various aspects of immune response and cell signaling, they are not the primary molecules responsible for the initial capture, rolling, and adhesion of neutrophils to endothelial cells during diapedesis.
Toll-like receptors (TLRs) are involved in recognizing microbial components and initiating immune responses, but they are not directly responsible for the capture, rolling, and adhesion of neutrophils to endothelial cells during diapedesis. Histone proteins are involved in DNA packaging and gene regulation, and they are not directly related to neutrophil diapedesis.
Leptin and adiponectin are hormones primarily associated with metabolism and energy regulation, and they do not have direct roles in neutrophil diapedesis.
Selectins and integrins, on the other hand, are the only cell adhesion molecules listed. In neutrophil diapedesis, selectins initiate the process by causing neutrophils to “roll” along the endothelial surface. Integrins then allow firm adhesion of neutrophils to endothelial cells, facilitating their migration through the vessel wall.
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[each_answer] => A. G-protein coupled receptors and cytokines
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[each_answer] => B. Toll-like receptors and histone proteins
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[each_answer] => C. Integrins and selectins
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[each_answer] => D. Leptin and adiponectin
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Figure 1