Path INFLammation Dr Johnson

This case is an example of a Type I Hypersensitivity Reaction (Allergic/Anaphylactic). The edema is caused by increased vascular permeability.

Although, altered plasma oncotic pressure, increased arterioloar hydrostatic pressure, lymphatic and venous obstruction can all cause edema, the causes of these alterations are not indicated in this case. For example, changes in oncotic pressure can be caused by a decrease in protein synthesis, mainly albumin (produced by normal hepatocytes) or increased protein loss such as in proteinuria and severe burns.

Edema is due to increased vascular permeability mediated mainly by histamine release.

Altered

Serous exudate is a type of fluid that is typically clear and watery. It is produced in response to inflammation and is often seen in mild or early stages of injury or infection. In this case, the lesion seen in the photomicrograph is likely in the early stages of development, hence the presence of serous exudate.

Soluble bacterial products such as the lipopolysaccharide are chemoattractants for PMNs.

The other answers listed are not soluble bacterial products and do not cause fever, macrophage activation or B cell growth and division.

Pulmonary granulomas heal by scarring and calcification (dystrophic).

Complete resolution is not possible because the lung tissue has been severely damage with destruction of underlying basement membrane. Therefore regeneration and resolution is not possible.

Although TB can spread or disseminate, malignant neoplasms (cancers) usually metastasize or have the capacity to enter the blood supply or lymphatics and spread to distant organs or sites.

Macrophages are involved in granulomatous inflammation but do not replace the granuloma.

Granulomatous inflammation is a distinctive pattern of inflammation. Therefore, it cannot progress to chronic inflammation. Acute inflammation may progress to chronic inflammation.

The correct answer describes an abscess as a small area containing pus made up of apoptotic neutrophils with liquefactive necrosis. This means that the abscess is a localized collection of dead neutrophils (a type of white blood cell) that have undergone programmed cell death, along with pus and tissue debris. Liquefactive necrosis refers to the breakdown of tissue, resulting in a liquid-like consistency. This description accurately explains the composition and characteristics of an abscess in the lung.

Redness (rubor) or erythema is caused by vasodilation of blood vessels in the dermis.

Ischemia is the loss of blood supply and is not suggested in this case.

Edema of the dermis is a result of increased microvascular permeability in the dermis.

Infiltration of neutrophils or PMNs is seen in acute inflammation and is caused by tissue necrosis, C5a, soluble bacterial products, Leukotriene B4, and chemokine family (IL-8)

Bradykinin is a chemical mediator responsible for causing pain and increased microvascular permeability

Suppurative inflammation contains large amounts of purulent exudate (pus) and consist of primarily PMNs (acute inflammation) which is seen around 24 hours. Suppurative inflammation is also seen in an abscess.

Fibrinous inflammation is seen in more severe injuries resulting in greater vascular permeability allowing larger molecules like fibrinogen to escape from the vascular space. If this type of inflammation does not resolve, one can expect to see scarring or organization of the fibrinous exudate which is not completely degraded by fibrinolysis and removed by macrophages. Remember the example of fibrinous pericarditis restricting myocardial function. See Slide 95 (Figure2-24B).

Serous inflammation is seen in association with blisters causes by burn and viral infections. There is a watery protein-poor fluid (effusion) usually seen in serous inflammation.

In fibrino-purulent inflammation one would see both PMNs and fibrin. This type of infllammation may be seen around 48 -72 hours when there may be an overlap between acute and chronic inflammation.

In lymphangitis, red streaks are seen following the course of the lymphatics extending up the arm to the axilla.

Lymphadenitis, inflammatory and reactive lymphadenitis all represent an inflammation or a reaction of the draining lymph nodes characterized by pain and swelling.

Depending upon the location, an abscess (an accumulation of pus) may present as a painful and warm to touch localized area beneath the skin.

An elevated ESR is most likely due to RBCs binding to increased acute phase reactant produced by the liver. The acute phase reactants increase the rate at which RBCs fall to the bottom of the test tube or sediment to the bottom.

Increased numbers of leukocytes (leukocytosis) is usually seen in most patients with infections or inflammation.

Hageman factor activation (XII) initiates 4 plasma mediator systems including the Coagulation, Fibrinolytic, Kinin, and Complement.

Complement is important in opsonization (C3b), chemotaxis (C5a), and cell lysis (C5-9) MAC Attack but does not cause increase in ESR.

Bacteremia or sepsis is the accumulation of blood-borne pyrogens in the blood.

In 2 days one would expect to see the presence of PMNs in the myocardium. PMNs were attracted by dead or necrotic myocardicytes.

In 2 minutes, there will be no changes seen on light or electron microscopy.

In 2 hours, one would not expect to see PMNs. PMNs predominate in the first 6-24 hours of inflammation.

In 2 weeks, one would expect to see the transition of granulation tissue to scar tissue.

In 2 months one would expect to see a well healed collagenous scar.

Vasodilation is the correct answer because it refers to the widening of blood vessels, which allows more blood to flow through them. When a mosquito bites, it injects saliva into the skin, which contains substances that cause the blood vessels in the area to dilate. This increased blood flow leads to erythema, or redness, in the surrounding area.

Hemostasis is the process that occurs first in acute inflammation. It involves the constriction of blood vessels and the formation of a blood clot to prevent excessive bleeding. This initial response helps to limit the damage and prepare the area for the subsequent events in inflammation, such as chemotaxis (migration of immune cells to the site), margination (adhesion of immune cells to blood vessel walls), emigration (movement of immune cells out of blood vessels), and phagocytosis (engulfment and destruction of pathogens by immune cells).

The photomicrograph shows non-caseating granulomas, which are characteristic of sarcoidosis. Sarcoidosis is a systemic disease that can affect multiple organs, including the lungs. It often presents with bilateral hilar adenopathy on chest X-ray, as seen in this case. Brucellosis, Staphylococcus, Streptococcus, and Tuberculosis do not typically present with non-caseating granulomas.

The most likely outcome of a myocardial infarction is repair. Myocardial infarction, also known as a heart attack, occurs when there is a blockage in the blood supply to the heart muscle, leading to tissue death. After the initial injury, the body initiates a healing process to repair the damaged tissue. This involves the formation of scar tissue, which replaces the dead heart muscle cells. Therefore, repair is the expected outcome of a myocardial infarction.

Release of hydrolases from neutrophils is most likely responsible for the necrosis in a suppurative exudate. Hydrolases are enzymes that can break down cellular components, including proteins and nucleic acids. When neutrophils are activated and migrate to the site of infection or inflammation, they release hydrolases as part of their immune response. These hydrolases can cause tissue damage and necrosis, leading to the presence of necrotic debris in the exudate.

The best diagnosis for the specimen submitted to the pathologist from the subcutis of a 32-year-old woman is chronic inflammation. Chronic inflammation is characterized by the presence of immune cells, tissue destruction, and attempts at tissue repair. It is a prolonged inflammatory response that can be caused by persistent infections, autoimmune diseases, or exposure to irritants. Given the information provided, chronic inflammation is the most likely diagnosis for the specimen.

Kinins are a group of inflammatory mediators that are released in response to tissue injury or inflammation. They cause vasodilation, increase vascular permeability, and promote the migration of immune cells to the site of injury. In the given scenario, the friend's sunburn is causing tissue injury and inflammation, leading to the release of kinins. This release of kinins is most likely responsible for the swelling experienced by the friend.

This is the classic description for a caseating granuloma. Granulomatous inflammation is a type of delayed cell mediated hypersensitivity type IV.

Complement fixation is involved in fibrinoid necrosis and not caseous necrosis.

Local histamine release is responsible for the increased vascular permeability and edemia seen in acute inflammation. Granulomatous inflammation is a type of chronic inflammation.

PMNs releasing degradative enzymes is responsible for the liquefactive necrosis seen in an abscess and not in granulomatous inflammation. The enzymes in caseating granulomatous inflammation are released by lymphocytes and macrophages.

In suppurative inflammation, PMNs predominate. This is primarily seen in an abscess.

In an abscess, whether it is acute (short duration) or chronic (longer duration), one will always see PMNs (acute inflammatory infiltrate) and NOT lymphocytes, plasma cells, and macrophages (chronic inflammatory cells).

Caseous necrosis is usually seen in association with some causes of granulomas. Liquefactive necrosis is seen in an abscess.

Coagulative necrosis can be seen in irreversible injury of all types of tissue with the exception of the brain and abscess. Superimposed bacterial infections can cause a liquefactive component.