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Worksheetsacute & chronic inflammation
Total questions: 8
Worksheet time: 80secs
A patient steps on a rusty nail and presents with a red, warm, swollen, and painful toe. The initial redness (rubor) at the site is primarily a direct result of:
Increased vascular permeability
Vasodilation of arterioles
Stimulation of nociceptors
Fibrosis and tissue remodeling
The local warmth (calor) experienced in a case of acute inflammation, such as an infected toe, is best explained by:
The production of pus from dead neutrophils
Increased blood flow carrying heat from the body's core to the periphery
The release of endorphins from damaged cells
The activation of plasma cells and lymphocytes
In acute inflammation, swelling (tumor) is caused by the accumulation of fluid and cells in the interstitial space. This process is formally known as:
Vasoconstriction
Necrosis
Oedema
Granulation
The pain (dolor) associated with acute inflammation results from two main mechanisms. These are:
Vasodilation and fever
Chemical mediation by substances like bradykinin and physical pressure from swelling
The presence of lymphocytes and the formation of granulomas
Fibrosis and the loss of function
The fifth cardinal sign of inflammation, "loss of function" (functio laesa), can occur due to:
Pain and physical limitation from swelling
The resolution and complete healing of the tissue
The proliferation of macrophages
All of the above
Which of the following is a key histological difference between acute and chronic inflammation?
Acute inflammation is of longer duration.
Chronic inflammation is primarily mediated by neutrophils.
Acute inflammation is characterized by the presence of macrophages and lymphocytes.
Chronic inflammation is characterized by the presence of macrophages and lymphocytes.
A patient has a persistent, low-grade inflammation in their joints for several months, leading to stiffness and fatigue. This is most consistent with:
Acute inflammation
Chronic inflammation
The resolution phase
Initial vasodilation
The formation of pus, which is rich in dead neutrophils and debris, is a classic feature of a potential outcome in acute inflammation known as:
Fibrosis
Autoimmune disease
Granulation tissue
Abscess formation
