Pathology Exam - Know More About INFLammation

The most likely cause of the erythema (redness) on your friend's back is vasodilation of blood vessels in the dermis. Vasodilation refers to the widening of blood vessels, which allows more blood to flow through them. In this case, the blood vessels in the dermis have widened, leading to increased blood flow and causing the redness. This can happen as a result of sun exposure, as the body tries to cool down the skin and regulate body temperature.

The localized swelling and erythema observed after being bitten by a "bug" suggest an inflammatory response. Increased vascular permeability is a characteristic of inflammation, where the blood vessels become more permeable, allowing fluids and immune cells to move from the bloodstream into the affected tissue. This increased permeability leads to the accumulation of fluid in the tissue, causing edema. Therefore, increased vascular permeability is the most likely cause of the observed edema in this case.

The suppurative response of inflammation is the result of the release of hydrolases from neutrophils. Hydrolases are enzymes that break down proteins, and their release from neutrophils helps to break down dead tissue and bacteria at the site of inflammation. This process leads to the formation of pus, which is characteristic of the suppurative response.

Chemotaxis or movement of PMNs towards the necrotic myocardial cells.

Diapedesis or emigration is the movement of WBCs from the vascular space to the interstitium.

Exudation involves the escape of proteins from the microvascular space.

Anaphylaxis is an allergic type I hypersensitivity reaction that does not play a role in MI. Eosinophils are associated with type I hypersensitivity reactions.

Edema is caused by increased vascular permeability.

Venous congestion, lymphatic obstruction, increased arterial flow and pressure can cause edema but do not occur in this case.

An abscess or a collection of pus primarily consists of neutrophils.

Eosinophils are usually increased in parasitic or allergic reactions.
Lymphocytes are usually increased in viral infections unless the infection is so severe that there is a net loss of lymphocytes from the circulating pool.

Macrophages are found in granulomas.

Plasma cells are mature and differentiated B lymphoctyes that secrete immunoglobulins or antbodies.

Necrotic or dead myocardiocytes attract PMNs (acute inflammatory cells). Hence inflammation is immediately followed by inflamation.

Atrophy of heart muscle cells is seen only in the very elderly and associated with lipofuscin (brown atrophy).

Cardiac muscle cells are permanent non-dividing cells that are NOT capable of regeneration. Hence resolution is NOT possible.

Repair of irreversibly injured myocardiocyte occurs via scarring and follows chronic inflammation.

The release of hydrolases from PMNs is responsible for the suppurative response of inflammation.

Activation of eosinophils occurs in type I hypersensitivity reactions or in parasitic infections.

Degranulation of mast cells results in the release of several mediators, but most importantly histamine which caused increase vascular permeability.

Release of bacterial toxins will cause liquefactive necrosis.

Lymphokines are released from lymphocytes and are important for the activation of macrophages in delayed hypersensitivity type IV reactions, particularly granulomatous inflammation.

Histamine causes arteriolar dilation and results in venular endothelial contraction & interendothelial gaps and ultimately increased vascular permeability

Bradykinin is responsible for pain and increased vascular permeability which causes edema.

suppurative refers to "pus" which is caused by Neutrophils.
Neutrophils are the first responders in infection.

After treatment for tuberculosis, the usual outcome of a pulmonary granuloma is scarring and calcification. This occurs as a result of the body's immune response to the infection, leading to the formation of fibrous tissue and deposition of calcium in the affected area. Scarring and calcification help to contain the infection and prevent its spread, but they can also cause long-term damage to the lungs.

Enzymes derived from neutrophils are responsible for the liquefactive necrosis seen in the center of this abscess.

The other answer choices listed do not play a role in abscess or suppurative inflammation. Lymphocytes and macrophages are seen in granulomatous inflammation.

Bradykinin is responsible for pain and increased vascular permeability which causes edema.

Complement system (activation leads to opsonization (C3b), chemotaxis of WBCs, and cell lysis (C5-9).

Endotoxin from bacteria is responsible for vasodilation, particularly in gram negative sepsis and shock.

Histamine causes arteriolar dilation and results in venular endothelial contraction & interendothelial gaps and ultimately increased vascular permeability

Tumor Necrosis Factor (TNF) is an important mediator of acute phase reactions and play a role in the production of Il-1 and fever. TNF is secreted by activated macrophages and other cells.

Vasodilation and its resulting increased blood flow causes the redness (RUBOR)
and increased heat (CALOR).
Increased permeability of the blood vessels results in an EXUDATION (leakage) of plasma proteins and fluid into the tissue (EDEMA),
which manifests itself as swelling (TUMOR).
Some of the released mediators such as bradykinin increase the sensitivity to pain (DOLOR).
The mediator molecules also alter the blood vessels to permit the migration of leukocytes, mainly neutrophils, outside of the blood vessels (EXTRAVASATION)
into the tissue. The neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury. The loss of function (FUNCTIO LAESA)
is probably the result of a neurological reflex in response to pain.

Neutrophils are responsible for killing pyogenic cocci.

Lymphocytes respond to virus (karate kid)
Eosinophils respond to parasitic infections and allergic reactions.

Basophils release mediators that help orchestrate inflammation.

Monocytes are macrophages in the blood which are responsible for phagocytosis.

C5a is responsible of chemotaxis of PMNs.

C3a & C5a are anaphylatoxins and are major mediators of increased vascular permeability and edema seen in inflammation and anaphylaxis. Please see slide 51 (Fig 2-13) for further details.

The presence of eosinophilic muscle fibers with only a few karyorrhectic and pyknotic nuclei remaining suggests that the myocardial infarct is in the subacute phase. This phase typically occurs around 2 days after the initial injury, as indicated by the presence of many polys at the margin of the area. Therefore, the most likely age of this myocardial infarct is 2 days.

Lipopolysaccharide (LPS) is a component of the outer membrane of gram-negative bacteria. It is a potent activator of the immune system and can induce the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1). In this case, the 72-year-old man developed gram-negative bacterial peritonitis, and the fever, macrophage activation, and B-cell mitogenicity are all mediated by the induction of host cytokines, including TNF and IL-1, which are activated by the presence of LPS.

Neutrophils release degradative enzymes that completely digest tissue and cause liquefactive necrosis as seen in the center of this abscess.

Lymphokines are molecules released by immune cells, specifically lymphocytes, in response to an immune reaction. In the case of chronic inflammation in a delayed hypersensitivity reaction, lymphokines play a crucial role in mediating the inflammatory response. They attract immune cells to the site of inflammation, promote the activation and migration of immune cells, and regulate the immune response. This leads to the sustained inflammation observed in delayed hypersensitivity reactions. Histamine, bradykinin, and complement are also involved in inflammation but are not specifically responsible for the chronic inflammation seen in delayed hypersensitivity reactions.

Hagman factor activation initiates the complement, coagulation, kinin, and fibrinolytic system.

Plasmin is produced and degrades thrombin and the fibrin in an insoluble clot.

Thrombin cleaves fibrinogen and produces fibrin which causes an insoluble clot to form. Thrombin also enhances WBC adhesion to endothelium by generating fibrinopeptides (during fibrinogen cleavage). Thrombin causes increased vascular permeability and chemotaxis of WBCs.

High molecular weight kininogen cofactor is important in the activation of Hageman factor (XII). When the kinin system is activated the formation of bradykinin occurs. Bradykinin is responsible for pain and increased vascular permeability which causes edema.

A shift to the left means that immature band forms are seen in the peripheral blood.

Thrombocytopenia is a decrease in PLT numbers.

Anemia is a decrease in hemoglobin and hematocrit.

Increase in mature PMNs is a neutrophilic leukocytosis.

Immature lymphocytes or lymphoblasts may be seen in cases of severe chronic inflammation in which there is a lymphocytic hyperplasia in the bone marrow and an increase loss of lymphocytes from the blood supply.

Mast cells can liberate histamine. See Slide 43 (Fig 2-11)

Lymphangitis-- is an inflammation of the lymphatic channels that occurs as a result of infection at a site distal to the channel. The most common cause of lymphangitis in humans is Streptococcus pyogenes (Group A strep). Lymphangitis is also sometimes called "blood poisoning".

Signs and symptoms include a deep reddening of the skin, warmth, lymphadenitis, and a raised border around the affected area. The person may also have chills and a high fever along with moderate pain and swelling. A person with lymphangitis should be hospitalized and closely monitored by medical professionals.
Thin red lines may be observed running along the course of the lymphatic vessels in the affected area, accompanied by painful enlargement of the nearby lymph nodes

The presence of a granuloma in the lung indicates an accumulation of white blood cells (WBCs) that are actively fighting persistent bacterial infections. This is the best explanation to provide to the patient regarding the pathology report.

Microscopic examination of the contents of a chronic abscess would most likely show an acute inflammatory infiltrate of polymorphonuclear leukocytes (PMNs). This is because PMNs, also known as neutrophils, are the first immune cells to arrive at the site of infection or inflammation. They play a crucial role in the body's defense mechanism by engulfing and destroying bacteria and other foreign substances. In the case of a chronic abscess, the presence of PMNs indicates an ongoing inflammatory response to the persistent infection.

The ESR is governed by the balance between pro-sedimentation factors, mainly fibrinogen, and those factors resisting sedimentation, namely the negative charge of the erythrocytes (zeta potential). When an inflammatory process is present, the high proportion of fibrinogen in the blood causes red blood cells to stick to each other. The red cells form stacks called 'rouleaux,' which settle faster. Rouleaux formation can also occur in association with some lymphoproliferative disorders in which one or more immunoglobulin are secreted in high amounts

The ESR is increased by any cause or focus of inflammation. The ESR is increased in pregnancy or rheumatoid arthritis, and decreased in polycythemia, sickle cell anemia, hereditary spherocytosis, and congestive heart failure. The basal ESR is slightly higher in females

Caseous necrosis is a form of cell death in which the tissue maintains a cheese-like appearance. The dead tissue appears as a soft and white proteinaceous dead cell mass.

Frequently, caseous necrosis is encountered in the foci of tuberculous infections. It can also be caused by syphilis and certain fungi.
A similar appearance can be associated with histoplasmosis, cryptococcosis, and coccidioidomycosis

Venules, followed by capillaries and rarely arterioles are the most likely sites where WBC emigration or diapedesis occurs.

Complement (C5a) is an important chemotactic agent, particularly for PMNs.

Hageman factor (XII), kinins, serotonin and histamine are all chemical mediators of inflammation but do not cause chemotaxis.

Histamine causes arteriolar dilation and results in venular endothelial contraction & interendothelial gaps and ultimately increased vascular permeability

Hageman factor (XII) activation initiates 4 systems involved in plasma derived mediators that regulate many of the effects inflammation. These 4 systems inlcude:
1) Kinin system (activation leads to formation of Bradykinin which causes pain & increased vascular permeability
2) Clotting system (activation results in thrombin which is responsible for the conversion of soluble circulating fibrinogen
to become an insoluble fibrin clot (cement between the PLTs (bricks or blocks)
3) Fibrinolytic system (activation results in formation of plasmin which cleaves fibrin to solubilize the clot (secondary
hemostatic clot)
4) Complement system (activation leads to opsonization (C3b), chemotaxis of WBCs, and cell lysis (C5-9)

Serotonin (5-hydroxytryptamine) is a preformed vasoactive mediator with similar effects to histamine. It is found primarily within platelet dense body granules and released during platelet aggregation.

Hageman factor is a protein synthesized by liver which circulates in an inactive form and activates when it encounters collagen, basement membrane, or activated platelets (at site of endothelial injury)

The multinucleated giant cells seen in this granuloma are a result of fusion or nuclear division of macrophages (IL-4 & Inteferon gamma).

Macrophages release TNF& IL-1 which both act on the thermoregulatory centers of the hypothalamus via prostaglandin E (PGE) to induce fever.

Basophils release mediators of inflammation, mainly histamine

Lymphocytes release lymphokines that activate macrophages

Eosinophils release major basic protein to kill parasites

Neutrophils release degradative enzymes to kill bacteria