MLT GlobeBasic Pathology: Cell injury, adaptation & death – page 3
93 Basic Pathology MCQs on Cell injury, adaptation & death with answers and explanations.
When hydropic swelling affects many cells of an organ, the organ grossly appears:
Widespread cellular swelling compresses capillaries, making the organ pale and heavy. Yellow greasy change indicates fatty change.
When removing the damaging stimulus no longer restores a cell's structure and function, the injury is described as:
Irreversible injury is the point of no return, marked by mitochondrial dysfunction and membrane damage, leading to cell death.
A yellow-brown, perinuclear granular pigment accumulating in ageing heart muscle and neurons is:
Lipofuscin is 'wear-and-tear' pigment of lipid peroxidation, marking free-radical injury. Haemosiderin is iron-derived and Prussian-blue positive.
Abnormal deposition of calcium salts, with small amounts of iron, magnesium and other minerals, in tissues is termed:
Pathological calcification includes dystrophic and metastatic types. Amyloidosis is deposition of misfolded protein.
A golden-yellow to brown granular pigment in macrophages stains blue with Perls' Prussian blue. It is:
Haemosiderin is iron-containing pigment derived from haemoglobin; its ferric iron gives a positive Prussian blue reaction.
Melanocytes, which synthesise the brown-black pigment melanin, are normally found in which skin layer?
Melanocytes lie among basal keratinocytes of the epidermis and transfer melanin to them. Melanin seen in the dermis is usually within macrophages (melanophages).
Enlargement of the breast glandular epithelium at puberty and during pregnancy is an example of:
Hormone-driven increase in glandular cell number at puberty and pregnancy is normal physiological hyperplasia. Pathological hyperplasia results from excessive or inappropriate stimulation.
After partial hepatectomy in a living donor, the remaining liver cells re-enter the cell cycle and restore liver mass. This adaptation is termed:
Loss of tissue stimulates the remaining cells to divide, restoring mass: compensatory hyperplasia. Hormonal hyperplasia is driven by hormones such as oestrogen.
Gradually worsening narrowing of one renal artery reduces, but does not abolish, blood flow to that kidney. Over months, the kidney will most likely show:
Chronic partial ischaemia lowers the supply of oxygen and nutrients, so cells shrink and the organ becomes smaller (atrophy). Hypertrophy and hyperplasia follow increased demand, not reduced supply.
A bladder biopsy from a man with long-standing cystitis shows islands of glandular (columnar) epithelium replacing the normal urothelium, with chronic inflammation but no atypia. This change is termed:
Replacement of one differentiated epithelial type by another in response to chronic irritation is metaplasia (here, glandular metaplasia). Dysplasia would require cytological atypia, which is absent.
At autopsy of a patient with acute pancreatitis, the peripancreatic fat shows opaque, chalky-white foci. What is this?
Released lipases split fat into fatty acids that bind calcium (saponification), producing chalky-white areas. Caseous necrosis is cheesy and friable.
Calcium deposits in a damaged heart valve of a patient with normal serum calcium are best explained by:
Dystrophic calcification occurs in dead or damaged tissue despite normal serum calcium. Metastatic calcification affects normal tissue in hypercalcaemia.
Chronic smoking converts bronchial ciliated columnar epithelium into squamous epithelium. This change is:
Metaplasia is a reversible replacement of one adult cell type by another better suited to chronic irritation, e.g. smoke.
Which finding in an injured cell is still reversible?
Cell swelling, ER dilation and blebbing are reversible. Nuclear fragmentation (karyorrhexis) or dissolution (karyolysis) and lysosomal rupture mark irreversible injury.
Which adaptive change provides a fertile background from which cancer may later develop?
Pathological hyperplasia (e.g., endometrial hyperplasia under excess estrogen) is itself not cancer but raises the risk of malignant transformation. Physiological adaptations carry no such risk.
Muscle wasting (atrophy) involves increased protein breakdown. Which hormone opposes rather than promotes this catabolism?
Glucocorticoids, thyroid hormone and TNF stimulate ubiquitin-proteasome protein degradation. Insulin is anabolic and suppresses protein breakdown.
Most conditions below involve excessive apoptosis. Which one is instead driven mainly by too little apoptosis?
Tumor cells often escape apoptosis (e.g., BCL2 overexpression, p53 loss), which favours their survival. The other conditions show increased apoptotic cell death.
During pregnancy the uterus enlarges greatly. Besides smooth muscle hypertrophy, which other process contributes?
Estrogen drives both enlargement of individual smooth muscle cells (hypertrophy) and an increase in their number (hyperplasia).
Raised cytosolic calcium in injured cells activates several enzymes. Which one is directly responsible for fragmenting nuclear DNA?
Calcium activates endonucleases that cleave DNA and chromatin. Phospholipases damage membranes, proteases break down cytoskeleton, and ATPases deplete ATP.
Which change marks the point of no return in cell injury?
Inability to restore mitochondrial function (ATP generation) and severe membrane damage define irreversible injury. Swelling, fatty change and ribosome detachment are reversible.