MLT GlobeBasic Pathology: Cell injury, adaptation & death – page 5
93 Basic Pathology MCQs on Cell injury, adaptation & death with answers and explanations.
In a normal cell, irreparable DNA damage typically triggers apoptosis through which mechanism?
p53 accumulates after DNA damage and induces BAX/PUMA, triggering the mitochondrial pathway. BCL-2 overexpression blocks apoptosis.
Excess iron deposited as haemosiderin in tissues, without organ damage, is called:
Haemosiderosis is iron accumulation (e.g., after repeated transfusion). Haemochromatosis implies iron overload with organ injury.
Inside cells, iron combined with apoferritin forms:
Stored iron is held as ferritin micelles; when excess, they aggregate into haemosiderin granules.
Deficiency of which vitamin causes squamous metaplasia of respiratory and conjunctival epithelium because it is needed for normal epithelial differentiation?
Vitamin A (retinoic acid) regulates epithelial differentiation; deficiency causes keratinising squamous metaplasia, e.g. xerophthalmia.
Besides keratinocytes, which cells commonly contain phagocytosed melanin in the skin?
Melanin released into the dermis is taken up by dermal macrophages, called melanophages, as seen in post-inflammatory pigmentation.
Shrinkage of the brain with neuronal loss in an otherwise healthy 85-year-old is an example of:
Gradual reduction of cell size and number with ageing is senile atrophy, a physiological adaptation. Aplasia is failure of an organ to develop; hypertrophy and hyperplasia are increases.
A newborn of a mother with poorly controlled diabetes develops hypoglycaemia. The neonatal pancreatic islets are expected to show:
Maternal glucose crosses the placenta and stimulates fetal beta cells, causing islet hyperplasia and hyperinsulinism, hence neonatal hypoglycaemia after birth.
Two years after losing one kidney in an accident, the remaining kidney is markedly enlarged. The predominant adaptation is:
The remaining kidney enlarges mainly by increase in size of tubular cells (compensatory hypertrophy), with a minor hyperplastic component.
Six months after blunt trauma to the thigh, a biopsy shows bone trabeculae forming within skeletal muscle. This change is:
Formation of true bone in muscle after injury is osseous metaplasia (myositis ossificans). Calcification is mineral deposition without organised bone formation.
In hypertrophied heart muscle, contractile proteins switch toward fetal isoforms. Which myosin heavy chain change occurs?
During hypertrophy the adult alpha myosin heavy chain is partly replaced by the fetal beta isoform, which contracts more slowly but uses energy more economically.
In ischemic cell injury, which change is the major cause of plasma membrane damage?
Increased cytosolic Ca2+ activates phospholipases and proteases that break down membrane phospholipids and cytoskeleton. Sodium gain and acidosis are early reversible changes.
Which ultrastructural finding indicates that cell injury has become irreversible?
Amorphous mitochondrial densities and membrane rupture mark irreversible injury. Blebbing, ribosome detachment and microvillus loss are reversible changes.
Extracellular dystrophic calcification begins with calcium phosphate crystal formation in:
Calcium concentrates in phospholipid-rich vesicles released from injured cells; phosphatases generate phosphate, and crystals then propagate.