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Questions and Answers
Which cell types are the principal sources of TNF-α in acute inflammation?
Which cell types are the principal sources of TNF-α in acute inflammation?
- Macrophages, other cells
- Macrophages, endothelial cells, epithelial cells
- Macrophages, mast cells, T lymphocytes (correct)
- Endothelial cells, T lymphocytes, mast cells
Which of the following best describes the outcome when acute inflammation leads to little tissue damage?
Which of the following best describes the outcome when acute inflammation leads to little tissue damage?
- Formation of an ulcer
- Presence of multiple bacterial abscesses
- Healing by connective tissue replacement (correct)
- Progression to chronic inflammation
What is the characteristic of a morphological pattern that is fibrinous in nature during acute inflammation?
What is the characteristic of a morphological pattern that is fibrinous in nature during acute inflammation?
- Scar formation and limitation of function
- Presence of fibrinous exudate (correct)
- Pus filled fluid consisting of neutrophils and dead cells
- Copious effusion of nonviscous serous fluid
In acute inflammation, what kind of cells are typically found in the abscesses that form?
In acute inflammation, what kind of cells are typically found in the abscesses that form?
What is the typical cause of a purulent morphological pattern seen in acute inflammation?
What is the typical cause of a purulent morphological pattern seen in acute inflammation?
Which of the following is NOT a common cause that can trigger acute inflammation?
Which of the following is NOT a common cause that can trigger acute inflammation?
Which cellular component acts as phagocytes or releases enzymatic granules?
Which cellular component acts as phagocytes or releases enzymatic granules?
What is the process called when leukocytes emigrate toward the site of injury driven by chemoattractants?
What is the process called when leukocytes emigrate toward the site of injury driven by chemoattractants?
What is the receptor type that recognizes Toll-like receptors (TLRs), G protein-coupled receptors for short bacterial peptides, and receptors for opsonins?
What is the receptor type that recognizes Toll-like receptors (TLRs), G protein-coupled receptors for short bacterial peptides, and receptors for opsonins?
What are the 4 cardinal clinical signs of acute inflammation described by Celsus?
What are the 4 cardinal clinical signs of acute inflammation described by Celsus?
What is the function of Nitric Oxide (NO) in acute inflammation?
What is the function of Nitric Oxide (NO) in acute inflammation?
Which action contributes to vessel dilation in acute inflammation?
Which action contributes to vessel dilation in acute inflammation?
What is the main cause of oedema in acute inflammation?
What is the main cause of oedema in acute inflammation?
What is the major function of leukocytes in acute inflammation?
What is the major function of leukocytes in acute inflammation?
How long does acute inflammation typically last?
How long does acute inflammation typically last?
Which term describes the movement of leukocytes from vessel lumen to interstitial tissue in acute inflammation?
Which term describes the movement of leukocytes from vessel lumen to interstitial tissue in acute inflammation?
What is the role of bradykinin in vascular reactions during acute inflammation?
What is the role of bradykinin in vascular reactions during acute inflammation?
What is the source of histamine in acute inflammation?
What is the source of histamine in acute inflammation?
Which of the following is NOT one of the major components of acute inflammation?
Which of the following is NOT one of the major components of acute inflammation?
What was Virchow's contribution to Celsus' description of acute inflammation?
What was Virchow's contribution to Celsus' description of acute inflammation?
Neutrophils are the principal source of TNF-α in acute inflammation.
Neutrophils are the principal source of TNF-α in acute inflammation.
Serous effusion in acute inflammation is typically thick and viscous in nature.
Serous effusion in acute inflammation is typically thick and viscous in nature.
Phagocytes only release enzymatic granules but do not act as phagocytes themselves in acute inflammation.
Phagocytes only release enzymatic granules but do not act as phagocytes themselves in acute inflammation.
VCAM-1 is an example of an exogenous chemoattractant in leukocyte chemotaxis.
VCAM-1 is an example of an exogenous chemoattractant in leukocyte chemotaxis.
Leukocytes release cytokines that help in resolving the inflammatory response.
Leukocytes release cytokines that help in resolving the inflammatory response.
Leukocytes recognize Toll-like receptors (TLRs) through opsonins.
Leukocytes recognize Toll-like receptors (TLRs) through opsonins.
Phagocytosis involves the fusion of engulfed particles with lysosomes to form phagolysosomes.
Phagocytosis involves the fusion of engulfed particles with lysosomes to form phagolysosomes.
Ulcerative loss of tissue from the surface leading to the formation of an abscess is a typical example of acute inflammation.
Ulcerative loss of tissue from the surface leading to the formation of an abscess is a typical example of acute inflammation.
Complete resolution is an outcome of acute inflammation where fibroblasts grow into the area of damage.
Complete resolution is an outcome of acute inflammation where fibroblasts grow into the area of damage.
Acute inflammation can progress to chronic inflammation if there is substantial tissue damage and fibroblasts grow into the damaged area.
Acute inflammation can progress to chronic inflammation if there is substantial tissue damage and fibroblasts grow into the damaged area.
Leukocytes migrate from the interstitial tissue to the vessel lumen in acute inflammation.
Leukocytes migrate from the interstitial tissue to the vessel lumen in acute inflammation.
Vascular dilation in acute inflammation results in decreased blood flow.
Vascular dilation in acute inflammation results in decreased blood flow.
Endothelial cell contraction is not involved in the mechanism of allowing plasma fluid and protein to escape into extracellular tissue.
Endothelial cell contraction is not involved in the mechanism of allowing plasma fluid and protein to escape into extracellular tissue.
The main function of histamine during acute inflammation is vasoconstriction.
The main function of histamine during acute inflammation is vasoconstriction.
Nitric Oxide (NO) is mainly produced by macrophages during acute inflammation.
Nitric Oxide (NO) is mainly produced by macrophages during acute inflammation.
The 5th cardinal clinical sign of acute inflammation described by Celsus is Functio Laesa (Loss of function).
The 5th cardinal clinical sign of acute inflammation described by Celsus is Functio Laesa (Loss of function).
Chronic Inflammation lasts for a shorter duration compared to Acute Inflammation.
Chronic Inflammation lasts for a shorter duration compared to Acute Inflammation.
Allergic reactions can trigger Acute Inflammation.
Allergic reactions can trigger Acute Inflammation.
Virchow's contribution to Celsus' description of acute inflammation was adding the sign Dolor (Pain).
Virchow's contribution to Celsus' description of acute inflammation was adding the sign Dolor (Pain).
Increased vascular permeability is mainly caused by Nitric Oxide during acute inflammation.
Increased vascular permeability is mainly caused by Nitric Oxide during acute inflammation.
Acute inflammation is a fundamentally harmful process that leads to tissue injury.
Acute inflammation is a fundamentally harmful process that leads to tissue injury.
Leukocyte recruitment involves leukocytes moving from the interstitial tissue to the vessel lumen.
Leukocyte recruitment involves leukocytes moving from the interstitial tissue to the vessel lumen.
Study Notes
- Acute inflammation: host's protective response to noxious stimuli like infections, trauma, burns, and allergic reactions
- First described by Celsus with the four cardinal signs: rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function)
- Consists of vascular and cellular reactions to deliver leukocytes and plasma proteins to injury sites
- Vascular reaction: vessel dilation and increased blood flow caused by histamine, bradykinin, and nitric oxide
- Allows plasma fluid and proteins to escape from circulation into extracellular tissue, causing oedema
- Cellular components: leukocytes, primarily neutrophils and monocytes, emigrate from the microvasculature and release inflammatory mediators
- Chemotaxis: leukocytes are attracted to the site of injury by chemotactic agents, such as bacterial products and complement components
- Phagocytosis: removal of offending agents through recognition, attachment, engulfment, and killing
- Acute inflammatory cytokines: TNF-α, IL-1, and IL-6, produced by macrophages, mast cells, and T lymphocytes, among others, to maintain the inflammatory response
- Morphological patterns: fibrinous (scar formation), purulent (pus-filled), and serous (copious effusion)
- Outcomes: complete resolution with limited tissue damage or fibrosis, or substantial tissue damage leading to chronic inflammation
- Acute inflammation responds to infection, trauma, burns, and allergies.
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Description
Test your knowledge on the processes, mechanisms, morphology, and outcomes of acute inflammation. Learn about the principal sources of inflammatory cytokines, lysosomal enzymes, and the morphological patterns associated with acute inflammation.
