Inflammation in Pathology Quiz: Questions and Answers

Questions and Answers

Pyrogens

IL-1 and TNF

PGE2

By vasoconstriction, which reduces heat loss, and activating heat generation in brown fat and skeletal muscle Signup and view all the answers

Most plasma proteins Signup and view all the answers

C-reactive protein Signup and view all the answers

They upregulate the synthesis of prostaglandins Signup and view all the answers

Resetting it to a higher level Signup and view all the answers

Vasoconstriction and effects on brown fat and skeletal muscle Signup and view all the answers

Endogenous and exogenous Signup and view all the answers

Study Notes

Fever is a protective host response, characterized by an elevation of body temperature, often associated with infection.
Pyrogens, such as bacterial products (exogenous pyrogens) and cytokines (endogenous pyrogens), induce fever.
IL-1 and TNF act by stimulating the release of endogenous pyrogens, which upregulate cyclooxygenases to synthesize prostaglandins.
Prostaglandins, primarily PGE2, synthesized by vascular and perivascular cells of the hypothalamus, stimulate the production of neurotransmitters to reset the body's steady-state temperature.

Elevated levels of acute-phase proteins, such as C-reactive protein (CRP), fibrinogen, and serum amyloid A (SAA) protein, are synthesized in the liver.

Inflammation is a protective response to tissue injury or infection, characterized by the 5 'R's: redness, swelling, heat, pain, and loss of function.
Causes of inflammation include physical, chemical, biological, and immune-mediated injuries.

Vasodilation and increased blood flow lead to increased vascular permeability and stasis.
Recruitment of leukocytes to sites of inflammation involves margination, rolling, adhesion, migration, and chemotaxis.
Removal of offending agents via phagocytosis involves recognition and attachment, engulfment, and intracellular destruction.
Endothelial and neuronal NOS are constitutively expressed at low levels, while iNOS is involved in microbial killing and induced when macrophages +/- neutrophils are activated.

Leukocyte-mediated tissue injury occurs via the release of lysosomal enzymes, such as MPO, bactericidal proteins, acid hydrolases, and neutral proteases.
Macrophages also contain acid hydrolases, collagenase, and elastase, which degrade bacteria, debris, extracellular matrix components, and complement proteins.

General morphologic features include vascular dilation and congestion, edema, and inflammatory cellular infiltrate within the extravascular tissue.
Specific morphologic patterns include serous inflammation, fibrinous inflammation, suppurative (purulent) inflammation, and ulcers.

Three possible outcomes of acute inflammation: complete resolution, scarring/fibrosis, and chronic inflammation.
Complete resolution is the ideal outcome, where injury is limited, and removal of cellular debris and microbes by macrophages occurs, allowing for regeneration of damaged cells.