Path INFLammation Dr Johnson Part 2

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.

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.

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.

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

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.

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.

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.

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.

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.

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

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

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.

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.

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)

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

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.