SM53_CellInjury

Question 1

Major causes of cell injury and death

Answer 1

oxygen deprivation (hypoxia/anoxia)
physical agents (radiation induced trauma)
chemical agents (poisons, pharmaceuticals)
infectious agents (virus, bacteria)
immune system (autoimmune)
genetic disease 
nutritional abnormalities (malabsorption, starvation)

Question 2

Molecular and biological changes following cell injury include:

Answer 2

• Decreased ATP synthesis due to absence of oxygen or chemical toxic injury
• Mitochondrial damage leads to mitochondrial transitional pore –> loss of mito function
• Calcium influx –> opens mito transition pore and activates other enzymes
• ROS accumulation –> DNA damage/mutations, membrane damage, protein modifications and misfolding
• Membrane permeability: damage to cell, lysosomal, or mito membrane
• DNA damage

Question 3

Necrosis during reoxygenation of ischemic (low blood supply) organs is called ______ _____ and is in most part due to a sudden burst of _____

Answer 3

reperfusion injury, ROS

Question 4

Reversible changes in cell morphology following injury are called _______ or ______

Answer 4

hydropic change, vacuolar degeneration

Question 5

List the changes seen in cell morphology under a light microscope in reversible cell injury

Answer 5

Swelling of cells/organelles; small cytoplasmic vacuoles, increased eosinophilic staining

Question 6

List the changes seen in cell morphology under an electron microscope in reversible cell injury

Answer 6

Blebbing (protrusions) of plasma membrane, mitochondrial swelling, detachment of ribosomes from ER, clumping of chromatin, accumulation of phospholipid masses derived from cell membrane (aka myelin figures)

Question 7

List the changes seen in cell morphology under an electron microscope in IRreversible cell injury

Answer 7

markedly swollen mitochondria with electron dense deposits, swelling/fragmentation of organelles (especially lysosomes), disrupted plasma membranes, abnormal intracellular depositions and calcifications

Question 8

List the changes seen in cell morphology under a light microscope in IRreversible cell injury

Answer 8

Nuclear shrinkages, fragmentation, or dissolution, breakdown of membranes and leakage of cell, increased eosinophilic staining

Question 9

Terms for

1) nuclear dissolution
2) nuclear fragmentation
3) nuclear shrinkage

Answer 9

1. Karyolysis
2. Karyorrhexis
3. Pyknosis

Question 10

Newly found/additional cell death pathways with features of both necrosis and apoptosis

Answer 10

Necroptosis, pryoptosis

Question 11

Define necrosis

Answer 11

Local death of a group of cells || always pathologic in nature || defined mainly by inflammation, and cells show morphology of irreversible cell death

Question 12

Morphology of coagulative, liquefactive, and caseous necrosis

Answer 12

Coagulative: nuclei may be absent but cell outlines and cytoplasm still discernible.

Liquefactive: necrotic area rapidly liquefied due to extensive lysis

Caseous: characteristics of both above + granuloma formation (necrotic cells surrounded by macrophages and multi-nucleated giant cells) + whitish/gray and sharply demarcated from surrounding healthy tissue

Question 13

Morphology of fat necrosis, fibrinoid necrosis, and gangrenous necrosis

Answer 13

fat: found in adipose tissue contiguous to pancreas; foci of necrosis are yellowish white and soft
fibrinoid: bright pink, amorphous appearance of vesssel
gangrenous: clinical variant of coagulation in soft tissues of lower limbs, where bacteria/leukocytes enter site of necrosis –> extensive liquefaction

Question 14

Causes of coagulative, liquefactive, and caseous necrosis

Answer 14

coagulative: when enzymes are denatured and can’t breakdown dead cells; following ischemia or due to exposure to toxic agents
liquefactive: most frequently seen in brain after ischemic injury, resulting in extensive lysis (arterial occlusion, severe cerebral trauma, bacterial infection of brain)
caseous: tuberculous infection in tissues

Question 15

Causes of fat, fibrinoid, and gangrenous necrosis

Answer 15

fat: leakage of lipase and other hydrolytic enzymes from acutely injured acinar cells of the pancreas
fibrinoid: immune reactions (immune complex deposition) in blood vessels
gangrenous: Soft tissue of lower limb compromised by protracted hypoxia/ischemia –> devitalized overlying skin –> bacteria/leukocytes entering area of necrosis

Question 16

True of False: apoptosis is only physiological, while necrosis is only pathological

Answer 16

False; apoptosis can occur due to either pathologic or physiologic purposes

Question 17

Key components (2) of apoptosis

Answer 17

1. Enzymatic degradation of proteins and DNA (triggered by caspases)
2. Immediate recognition and removal of dead cells (by phagocytes)

Question 18

Differentiate the intrinsic and extrinsic pathways of apoptosis

Answer 18

Intrinsic: DNA damage, ER stress, loss of survival signals –> leakage of pro-apoptotic proteins from mitochondria into cytoplasm

Extrinsic: ligand binds to death receptors on cell surface (TNF receptor family!)