Inflammation and Repair: Lecture 4 - Acute Inflammation

Comprehensive review flashcards covering the cellular events, vascular changes, mechanisms of increased vascular permeability, and fluid classifications (transudate vs. exudate) from Lecture 4 on Acute Inflammation.

What is the primary function of acute inflammation?

To remove defense mechanisms from the vascular system to tissues in response to an injurious stimulus, and to initiate repair.

What are the two major components of acute inflammation?

Vascular changes (which allow circulating blood cells to slow down and infiltrate adjacent tissues) and cellular events (activation of inflammatory cells and tissue repair).

What are the five mechanisms responsible for increased vascular permeability in acute inflammation?

1. Retraction of endothelial cells (in venules)
2. Direct endothelial injury
3. Leukocyte-dependent endothelial injury
4. Increased transcytosis
5. Leakage from new capillaries

In which vessels does endothelial cell retraction primarily occur, and what chemical mediators induce it?

It occurs mainly in venules and is induced by histamine, nitric oxide ($\text{NO}$), bradykinin, leukotrienes, and other inflammatory mediators.

What are the kinetic characteristics and duration of endothelial cell retraction?

It is a rapid, transitory, and reversible response that typically lasts for $15\text{--}30\,\text{minutes}$.

What causes delayed prolonged vascular leakage, and what is its typical timeframe?

It occurs in mild injuries (such as mild burns or UV irradiation) due to endothelial cell contraction and/or mild endothelial degeneration, beginning after a $2\text{--}12\,\text{hour}$ delay and lasting several hours to days.

Which vessels are affected by direct endothelial injury, and what causes it?

It affects arterioles, capillaries, and venules, and is caused by severe injuries such as severe burns, bacterial toxins, and viruses.

What is the onset, duration, and cellular consequence of direct endothelial injury?

It causes endothelial cell necrosis and detachment as an immediate sustained response, beginning immediately after injury and lasting several hours to days until vessels are repaired or thrombosed.

In which vessels does leukocyte-dependent endothelial injury occur, and what mediators drive it?

It occurs in venules and pulmonary capillaries during the later stages of inflammation, mediated by reactive oxygen species ($\text{ROS}$) and proteolytic enzymes released by adhering neutrophils.

What is increased transcytosis, and what factors induce it?

Active transport of fluid across endothelial cells via interconnected, uncoated (pinocytic) vesicles and vacuoles in venules, induced by vascular endothelial growth factor ($\text{VEGF}$) and histamine.

Why does vascular leakage occur from newly formed capillaries during tissue repair?

Proliferating endothelial cells forming new capillaries during neovascularization are inherently leaky; this process is mediated by $\text{VEGF}$.

How do multiple vascular permeability mechanisms participate concurrently during a thermal burn?

Heat directly injures the endothelium; histamine and cytokines cause endothelial retraction; and activated leukocytes release oxygen metabolites ($O_2$) and lysosomal enzymes causing leukocyte-mediated endothelial injury.

What is the etiology and vascular pathogenesis of Epizootic hemorrhagic disease in white-tailed deer?

It is caused by Epizootic hemorrhagic disease virus (an Orbivirus related to Bluetongue virus) that causes direct endothelial damage to the microvasculature of the mucosa and lung, resulting in edema, hemorrhage, and thrombosis.

What are two characteristic morphologic diagnoses of Epizootic hemorrhagic disease virus infection in deer?

1. Severe hydropericardium
2. Acute, severe, multifocal to coalescing hemorrhagic and necrotizing rumenitis

How do a transudate and an exudate differ regarding definition and underlying etiology?

A transudate is non-inflammatory (caused by increased hydrostatic pressure, decreased colloid oncotic pressure, or lymphatic obstruction), whereas an exudate is inflammatory (caused by increased vascular permeability due to inflammation or infection).

What are the specific gravity and protein content thresholds distinguishing an exudate from a transudate?

An exudate has a specific gravity $> 1.025$ and protein content $> 30\,\text{g/L}$, whereas a transudate has a specific gravity $< 1.017$ and protein content $< 25\,\text{g/L}$.

How do nucleated cell counts, clottability, and the presence of bacteria differ between a transudate and an exudate?

Transudates have occasional cells ($< 1{,}500/\mu\text{L}$), rarely clot, and rarely contain bacteria. Exudates have many cells ($> 5{,}000\text{--}7{,}000\,\text{cells}/\mu\text{L}$), often clot, and often contain bacteria.

What are the diagnostic parameters and etiology of a modified transudate?

Arises from long-standing transudates or mildly increased vascular permeability; characterized by specific gravity of $1.017\text{--}1.025$, protein content of $25\text{--}75\,\text{g/L}$, and $1{,}000\text{--}7{,}000\,\text{cells}/\mu\text{L}$.

What are three major morphological types of inflammatory exudates?

Fibrinous, suppurative, and fibrinosuppurative exudates.

How is the abdominal effusion in Feline Infectious Peritonitis (FIP) categorized, and what are its typical laboratory findings?

It is categorized as a modified transudate (high protein, low-to-moderate cells), typically showing yellow-red, viscid fluid with high protein ($60\,\text{g/L}$), intermediate specific gravity ($1.019$), and low numbers of non-degenerate neutrophils and macrophages ($4{,}876\,\text{cells}/\mu\text{L}$).