Basic Pathology: Tissue repair & healing – page 2
59 Basic Pathology MCQs on Tissue repair & healing with answers and explanations.
Which is the most important systemic factor impairing wound healing?
Diabetes impairs healing through microangiopathy and poor neutrophil function. Infection, foreign bodies and mechanical stress are local factors.
During tissue repair, which cell is the principal source of growth factors that stimulate fibroblasts and new blood vessel formation?
Activated macrophages secrete PDGF, TGF-beta, FGF and VEGF, driving fibroblast proliferation, collagen deposition and angiogenesis. Neutrophils mainly clear debris early and contribute little to repair signalling.
When tissue loss is too extensive for regeneration, the defect is filled by scar produced mainly by:
Fibroblasts proliferate and deposit collagen to form scar when parenchymal cells cannot regenerate. Monocytes/macrophages signal and clean up, but do not lay down the collagen.
Extensive collagen deposition in the lung, liver or kidney as a consequence of chronic inflammation, or in the myocardium after ischaemic necrosis, is called:
Fibrosis is excess collagen deposition in organs due to persistent injury. A keloid is an exuberant skin scar, and a desmoid is a fibromatosis (neoplasm).
If the supporting framework of a tissue is severely damaged so that complete restitution is impossible, healing proceeds by:
Regeneration requires intact stroma and proliferative cells. Severe damage to the framework or non-dividing cells leads to repair by connective tissue (scar).
Which feature is NOT expected in healing by first intention (primary union)?
Primary union occurs in clean, sutured incisions with little tissue loss, so only minimal granulation tissue forms. Abundant granulation tissue and contraction mark secondary union.
Proper hydroxylation of proline and lysine residues, needed for stable collagen in a healing scar, requires which vitamin?
Ascorbic acid is a cofactor for prolyl and lysyl hydroxylases; deficiency (scurvy) causes weak collagen and poor wound healing.
A sutured eyebrow laceration is examined 1–2 days later. Macrophages have entered the wound. Their main task at this stage is:
Early in healing, macrophages ingest dead cells, fibrin and bacteria and release growth factors. Collagen is made by fibroblasts, antibodies by plasma cells, and contraction by myofibroblasts.
A clean puncture wound is dressed with sterile gauze. What is the very first event in the healing sequence?
Haemostasis comes first: the clot plugs the defect and provides a scaffold for incoming cells. Neutrophils, macrophages and collagen deposition follow in that order.
Whether a skin laceration heals by first intention or by second intention depends mostly on:
Healing by primary union requires closely apposed edges with little tissue loss; gaping wounds fill with granulation tissue (secondary union). Nutrition and blood supply affect speed, not the mode.
Two months after a sutured arm laceration, the scar has become raised, irregular and nodular, extending beyond the original wound. This is best described as:
A keloid is excessive collagen deposition that grows past the wound margins. Dehiscence is wound reopening; resolution means restoration without scarring.
Neurones and cardiac muscle cells cannot divide after maturity. In terms of regenerative capacity they are:
Permanent cells have left the cell cycle, so injury heals by scarring. Labile cells (epithelia, marrow) divide continuously; stable cells (hepatocytes) divide when stimulated.
A mature scar mainly contains fibrillar collagens. Which set of collagen types is involved?
Fibrillar collagens in scars and connective tissue are types I, III and V. Type IV is non-fibrillar basement membrane collagen and type II is cartilage collagen.
A large open wound heals by secondary intention. Which feature most distinguishes it from a sutured incision healing by primary intention?
Both types of healing show inflammation, angiogenesis and fibroblast activity. Secondary healing forms more granulation tissue and undergoes wound contraction by myofibroblasts.
A patient on long-term high-dose corticosteroids has a surgical wound that heals poorly. The main reason is:
Glucocorticoids suppress inflammation and TGF-beta production, reducing fibroblast activity and collagen deposition, so wound strength is poor.
Which of the following is a systemic (host-wide) factor that delays wound healing?
Malnutrition, especially protein and vitamin C deficiency, impairs collagen synthesis throughout the body. Infection, foreign bodies and mechanical stress are local factors.
About how long after a clean sutured skin incision is the site mostly acellular connective tissue without inflammation, under intact epidermis?
By the end of the first month the scar is largely acellular collagen with little inflammation. At one week granulation tissue and collagen are still being laid down.
Wound contraction, prominent in healing by second intention, is mainly brought about by:
Myofibroblasts have smooth-muscle-like contractile features and pull wound edges together, reducing the defect size.
In healing by first intention, granulation tissue fills the incision and neovascularisation peaks at about:
By day 5 new vessels peak and granulation tissue fills the incisional space. At 72 hours granulation tissue is only beginning to form.
A raised scar made of excess collagen that remains within the original wound margins and often regresses is a:
Hypertrophic scars stay within wound boundaries and may regress. Keloids extend beyond the margins and seldom regress.