TEST BANK For Robbins & Kumar Basic Pathology, 11th
Edition by Vinay Kumar, Abul K. Abba
Hypertrophy - ANSWER:Increased cell and organ size, often in response to increased
workload: induced by mechanical stress, and by growth factors; occurs in tissue
incapable of cell division.
Hyperplasia - ANSWER:Increased cell numbers in response to hormones and other
growth factors; occurs in tissues whose cells are able to divide.
Atrophy - ANSWER:Decreased cell and organ size, as a result of decreased nutrient
supply or disuse: associated with decreased synthesis and increased proteolytic
breakdown of cellular organelles.
Metaplasia - ANSWER:Change in phenotype of differentiated cells, often a response
to chronic irritation that makes cells better able to withstand the stress.
Hypoxia - ANSWER:Oxygen deficiency which interferes with aerobic oxidative
respirations and is an extremely important and common cause of cell injury and
death.
Ischemic - ANSWER:Loss of blood supply in a tissue due to impeded arterial flow or
reduced venous drainage.
Coagulative necrosis - ANSWER:A form of tissue necrosis in which the component
cells are dead, but the basic tissue architecture is preserved for at least several days.
Liquefactive necrosis - ANSWER:A form of necrosis seen in focal bacterial or
occasionally fungal infections, because microbes stimulate the accumulation of
inflammatory cells and the enzymes of leukocytes digest the tissue.
Caseous necrosis - ANSWER:A form of necrosis encountered most often in foci of
tuberculosis infections.
Fat necrosis - ANSWER:Term referring to focal areas of fat destruction, typically
resulting from release of activated, pancreatic lipases into the peritoneal cavity.
Fibrinous necrosis - ANSWER:A special form of necrosis usually seen in Immune
reactions involving blood vessels.
Autophagy - ANSWER:Lysosomal digestion of the cells own components.
Apoptosis - ANSWER:A pathway of cell death that is induced by a tightly regulated
suicide program in which the cells destined to die activate enzymes capable of
degrading the cells own nuclear DNA.
,Steatosis (fatty change) - ANSWER:Refers to any abnormal accumulation of
triglycerides within parenchymal cells. It is most often seen in the liver.
Dystrophic calcification - ANSWER:Depositions of calcium at sites of cell injury, and
necrosis
Metastatic calcification - ANSWER:Deposition of calcium in normal tissues, caused by
Hypercalcemia (usually a consequence of parathyroid hormone excess).
Inflammation - ANSWER:A protective response intended to eliminate the initial
cause of cell injury as well as the necrotic cells and tissues resulting from the original
insult.
Acute Inflammation - ANSWER:A rapid response to injury or microbes and other
foreign substance that is designed to deliver leukocytes and plasma proteins to sites
of injury.
Serous inflammation - ANSWER:An outpouring of a watery, relatively protein-poor
fluid that, depending on the site of injury, derives either from the serum or from the
secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities.
Effusion - ANSWER:Fluid in a serous cavity.
Fibrinous inflammation - ANSWER:Inflammation occurring as a consequence of more
severe injuries, resulting in greater vascular permeability that allows large molecules
(such as fibrinogen) to pass the endothelial barrier
Abscess - ANSWER:Focal collections of pus that may be caused by seeding of
pyogenic organisms into a tissue or by secondary infections of necrotic foci.
Ulcer - ANSWER:A local defect or excavation of the surface of an organ or tissue that
is produced by necrosis of cells and sloughing of inflammatory necrotic tissue
Cytokines - ANSWER:Polypeptide products of many cell types that function as
mediators of inflammation and immune responses.
chronic inflammation - ANSWER:Prolonged inflammation in which active
inflammation, tissue injury, and healing proceed simultaneously
Granulomatous inflammation - ANSWER:A distinctive pattern of chronic
inflammation characterized by aggregates of activated macrophages that assume an
epithelioid appearance.
Repair - ANSWER:The restoration of tissue architecture and function after an injury.
, Regeneration - ANSWER:The process of replacing damaged tissue components and
essentially returning to a normal state.
Fibrosis - ANSWER:The extensive deposition of collagen that occurs in the lungs,
liver, kidney and other organs as a consequence of chronic inflammation.
Angiogenesis - ANSWER:A critical process in healing at sites of ischemia where a
preexisting vessel sends out capillary sprouts to produce new vessels.
Keloid - ANSWER:A prominent raised scar caused by the accumulation of exuberant
amounts of collagen.
Edema - ANSWER:Significant increased fluid in the interstitial tissue spaces.
Anasarca - ANSWER:Severe and generalized edema with profound subcutaneous
tissue swelling.
Hyperemia - ANSWER:A local increase in blood volume that is an active process from
augmented blood flow due to arteriolar dilation
Congestion - ANSWER:A local increase in blood volume that is a passive process
resulting from impaired venous return out of a tissue.
Hemorrhage - ANSWER:The extravasation of blood from vessels into the
extravascular space.
Hematoma - ANSWER:The accumulation of blood confined within a tissue after a
hemorrhage
Normal hemostasis - ANSWER:A tightly regulated process that maintains blood in a
fluid, clot-free state in normal vessels while inducing the rapid formation of a
localized hemostatic plug at the site of vascular injury.
Thrombosis - ANSWER:Blood clot (thrombus) formation in uninjured vessels or
thrombotic occlusion of a vessel after relatively minor injury.
Lines of Zahn - ANSWER:The grossly and microscopically apparent lamination in a
thrombi representing pale platelet and fibrin layers alternating with darker
erythrocyte-rich layers
Embolism - ANSWER:A detached intravascular solid, liquid, or gaseous mass that is
carried by the blood to a site distant from its point of origin.
Infarct - ANSWER:An area of ischemic necrosis caused by occlusion of either the
arterial supply or the venous drainage in a particular tissue.
Edition by Vinay Kumar, Abul K. Abba
Hypertrophy - ANSWER:Increased cell and organ size, often in response to increased
workload: induced by mechanical stress, and by growth factors; occurs in tissue
incapable of cell division.
Hyperplasia - ANSWER:Increased cell numbers in response to hormones and other
growth factors; occurs in tissues whose cells are able to divide.
Atrophy - ANSWER:Decreased cell and organ size, as a result of decreased nutrient
supply or disuse: associated with decreased synthesis and increased proteolytic
breakdown of cellular organelles.
Metaplasia - ANSWER:Change in phenotype of differentiated cells, often a response
to chronic irritation that makes cells better able to withstand the stress.
Hypoxia - ANSWER:Oxygen deficiency which interferes with aerobic oxidative
respirations and is an extremely important and common cause of cell injury and
death.
Ischemic - ANSWER:Loss of blood supply in a tissue due to impeded arterial flow or
reduced venous drainage.
Coagulative necrosis - ANSWER:A form of tissue necrosis in which the component
cells are dead, but the basic tissue architecture is preserved for at least several days.
Liquefactive necrosis - ANSWER:A form of necrosis seen in focal bacterial or
occasionally fungal infections, because microbes stimulate the accumulation of
inflammatory cells and the enzymes of leukocytes digest the tissue.
Caseous necrosis - ANSWER:A form of necrosis encountered most often in foci of
tuberculosis infections.
Fat necrosis - ANSWER:Term referring to focal areas of fat destruction, typically
resulting from release of activated, pancreatic lipases into the peritoneal cavity.
Fibrinous necrosis - ANSWER:A special form of necrosis usually seen in Immune
reactions involving blood vessels.
Autophagy - ANSWER:Lysosomal digestion of the cells own components.
Apoptosis - ANSWER:A pathway of cell death that is induced by a tightly regulated
suicide program in which the cells destined to die activate enzymes capable of
degrading the cells own nuclear DNA.
,Steatosis (fatty change) - ANSWER:Refers to any abnormal accumulation of
triglycerides within parenchymal cells. It is most often seen in the liver.
Dystrophic calcification - ANSWER:Depositions of calcium at sites of cell injury, and
necrosis
Metastatic calcification - ANSWER:Deposition of calcium in normal tissues, caused by
Hypercalcemia (usually a consequence of parathyroid hormone excess).
Inflammation - ANSWER:A protective response intended to eliminate the initial
cause of cell injury as well as the necrotic cells and tissues resulting from the original
insult.
Acute Inflammation - ANSWER:A rapid response to injury or microbes and other
foreign substance that is designed to deliver leukocytes and plasma proteins to sites
of injury.
Serous inflammation - ANSWER:An outpouring of a watery, relatively protein-poor
fluid that, depending on the site of injury, derives either from the serum or from the
secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities.
Effusion - ANSWER:Fluid in a serous cavity.
Fibrinous inflammation - ANSWER:Inflammation occurring as a consequence of more
severe injuries, resulting in greater vascular permeability that allows large molecules
(such as fibrinogen) to pass the endothelial barrier
Abscess - ANSWER:Focal collections of pus that may be caused by seeding of
pyogenic organisms into a tissue or by secondary infections of necrotic foci.
Ulcer - ANSWER:A local defect or excavation of the surface of an organ or tissue that
is produced by necrosis of cells and sloughing of inflammatory necrotic tissue
Cytokines - ANSWER:Polypeptide products of many cell types that function as
mediators of inflammation and immune responses.
chronic inflammation - ANSWER:Prolonged inflammation in which active
inflammation, tissue injury, and healing proceed simultaneously
Granulomatous inflammation - ANSWER:A distinctive pattern of chronic
inflammation characterized by aggregates of activated macrophages that assume an
epithelioid appearance.
Repair - ANSWER:The restoration of tissue architecture and function after an injury.
, Regeneration - ANSWER:The process of replacing damaged tissue components and
essentially returning to a normal state.
Fibrosis - ANSWER:The extensive deposition of collagen that occurs in the lungs,
liver, kidney and other organs as a consequence of chronic inflammation.
Angiogenesis - ANSWER:A critical process in healing at sites of ischemia where a
preexisting vessel sends out capillary sprouts to produce new vessels.
Keloid - ANSWER:A prominent raised scar caused by the accumulation of exuberant
amounts of collagen.
Edema - ANSWER:Significant increased fluid in the interstitial tissue spaces.
Anasarca - ANSWER:Severe and generalized edema with profound subcutaneous
tissue swelling.
Hyperemia - ANSWER:A local increase in blood volume that is an active process from
augmented blood flow due to arteriolar dilation
Congestion - ANSWER:A local increase in blood volume that is a passive process
resulting from impaired venous return out of a tissue.
Hemorrhage - ANSWER:The extravasation of blood from vessels into the
extravascular space.
Hematoma - ANSWER:The accumulation of blood confined within a tissue after a
hemorrhage
Normal hemostasis - ANSWER:A tightly regulated process that maintains blood in a
fluid, clot-free state in normal vessels while inducing the rapid formation of a
localized hemostatic plug at the site of vascular injury.
Thrombosis - ANSWER:Blood clot (thrombus) formation in uninjured vessels or
thrombotic occlusion of a vessel after relatively minor injury.
Lines of Zahn - ANSWER:The grossly and microscopically apparent lamination in a
thrombi representing pale platelet and fibrin layers alternating with darker
erythrocyte-rich layers
Embolism - ANSWER:A detached intravascular solid, liquid, or gaseous mass that is
carried by the blood to a site distant from its point of origin.
Infarct - ANSWER:An area of ischemic necrosis caused by occlusion of either the
arterial supply or the venous drainage in a particular tissue.
