Chapter 2: Cell Injury, Cell Death Flashcards
It is an adaptive response which is characterized by changes in phenotype of cells
a. Hyperplasia
b. Metaplasia
c. Hypertrophy
d. Atrophy
B
Hyperplasia - increase in number
Hypertrophy - increase in size
Atrophy - decrease in size
It is the structural alterations in cells or tissues that are characteristic of a disease, hence diagnostic of an etiologic process
a. Clinical manifestations
b. Etiology
c. Pathogenesis
d. Morphologic changes
D
Four aspects of disease process
Clinical manifestations - end results of genetic, biochemical, and structural changes in cells and tissues
Etiology - initiating cause
Pathogenesis - sequence that lead to the devt of disease
The progression of cell injury and death
a. loss of cell function -> ultrastructural changes -> biochemical alteration -> light microscopic changes -> gross morphologic changes
b. loss of cell function -> biochemical alteration -> light microscopic changes -> ultrastructural changes -> gross morphologic changes
c. loss of cell function -> biochemical alteration -> ultrastructural changes -> light microscopic changes -> gross morphologic changes
d. loss of cell function -> ultrastructural changes -> biochemical alteration -> light microscopic changes -> gross morphologic changes
c. loss of cell function -> biochemical alteration -> ultrastructural changes -> light microscopic changes -> gross morphologic changes
The following are characteristics of generalized swelling of a cell, except:
a. swelling of organelles
b. blebbing of plasma membrane
c. fragmentation of nucleus
d. clumping of nuclear chromatin
C
It is caused by severe mitochondrial damage with ATP depletion and rupture of lysosomal and plasma membranes
a. Necrosis
b. Apoptosis
c. Necroptosis
d. Ischemic injury
A
Increase serum levels of the following proteins indicate necrosis, except:
a. cardiac-specific variant of troponin
b. specific isoform of alkaline phosphatase
c. transaminases
d. prostaglandins
D
cardiac muscle cells: cardiac-specific variant of troponin
bile duct epithelium: specific isoform of alkaline phosphatase
hepatocytes: transaminases
***necrotic cell: glassy homogenous appearance
It is a pattern of necrosis wherein the affected tissue has a firm texture which usually happens in solid organs
a. Liquefactive necrosis
b. Coagulative necrosis
c. Caseous necrosis
d. Fat necrosis
e. Fibrinoid necrosis
f. Gangrenous necrosis
B: common cause - ischemia or hypoxia
Liquefactive necrosis: digestion of the dead cells, usually in the brain, seen in focal bacterial or fungal infections, necrotic material: creamy yellow -> pus
Caseous necrosis: cheese like, foci of tuberculous infection, usually seen in necrosis dur to TB, friable white appearance of the necrosis -> granuloma
Fat necrosis: focal areas of fat destruction, results from release of activated pancreatic lipases, occurs in acute pancreatitis, fat saponification (chalk-white areas) -> fatty acid + calcium
Fibrinoid necrosis: vascular damage in immune reactions involving blood vessels -> fibrinoid: bright pink and amorphous appearance in H&E stains
Gangrenous necrosis: generally applied to limb (lower leg) that lost its blood supply and undergone necrosis, usually seen in extremities
It is also referred to as the “regulated” cell death which activate intrinsic enzyme that degrade DNA and nuclear/cytoplasmic proteins.
a. Necrosis
b. Apoptosis
c. Necroptosis
d. Ischemic injury
B
It is the hybrid of both apoptosis and necrosis which morphologically and biochemically resembles necrosis and is triggered by signal transduction pathways. It also referred to as programmed necrosis.
a. Autophagy
b. Ferroptosis
c. Necroptosis
d. Pyroptosis
C
Pyroptosis - release of fever-inducing cytokine IL-1, trigger inflammation
Ferroptosis - triggered when excessive intracellular levels of iron or reactive oxygen species overwhelm the glutathione-dependent antioxidant defenses
These are chemical species that have a single unpaired electron in an outer orbit
a. Reactive oxygen species
b. Free radicals
c. Caspases
d. Cytochrome C
B
Reactive oxygen species: type of oxygen-derived free radicals with well-established roles in cell injury
Caspases: marker of cells undergoing apoptosis
Cytochrome C: sustains cell viability, initiates suicide program when released into cytoplasm
It is a condition where there is increased production or decreases scavenging of ROS, which lead to excess of free radicals
a. Mitochondrial membrane damage
b. Plasma membrane damage
c. Oxidative stress
d. Injury to lysosomal membranes
C
Mitochondrial damage occurs by the following mechanisms except:
a. Increased cytosolic calcium ion
b. ROS
c. Oxygen deprivation
d. ATP depletion
D
ATP depletion is a consequence of mitochondrial damage
The following are effects of ATP depletion, except:
a. Activity of plasma membrane energy-dependent sodium pimp is reduced
b. cellular energy metabolism is altered
c. reduction in protein synthesis
d. Apoptosis
D
It should be Necrosis
These act as free radical-scavenging systems and breakdown hydrogen and superoxide anion
a. Enzymes
b. Catalase
c. Superoxide dismutase
d. Glutathione peroxidase
A.
Catalase: present in peroxisomes, decomposes H2O2
Superoxide dismutase: found in many cell types and convert superoxide anion to H2O2
Glutathione peroxidase: catalyzes free radical breakdown
Removal of free radicals
- free radicals are inherently removed unstable and decay spontaneously
- superoxide anion
- different cellular mechanism to remove free radicals: antioxidants (ascorbic acid and glutathione), free iron and copper, enzymes
The pathologic effects of free radicals include the following, except:
a. Lipid peroxidation in membranes
b. Oxidative modification of proteins
c. Lesions in DNA
d. Enzymatic metabolism of exogenous chemicals or drugs
D
Generation of free radicals:
- reduction-oxidation reactions that occur during normal metabolic processes
- absorption of radiant energy
- inflammation
- enzymatic metabolism of exogenous chemicals or drugs
- transition metals: iron and copper
- nitric oxide
These ions normally serve as second messengers in several signaling pathways that when released in excessive amounts can be a source of cell injury
a. Ca2+
b. K+
c. Na+
d. Cl-
A
Increased cytosolic Ca2+ activates enzymes with deleterious effects of cells, which of the following is matched correctly to its effects?
a. Phospholipases: break down membrane & cytoskeletal proteins
b. Proteases: DNA & chromatin fragmentation
c. Endonucleases: cause membrane damage
d. ATPases: hasten ATP depletion
D
Phospholipases: cause membrane damage
Proteases: break down membrane & cytoskeletal proteins
Endonucleases: DNA & chromatin fragmentation
ATPases: hasten ATP depletion
Intracellular accumulation of misfolded proteins are caused by the following, except:
a. Stressors
b. Viral infections
c. Aging
d. Benign mutations
D. deleterious mutations dapat
These antibodies have the propensity to deposit ischemic tissues
a. IgM
b. IgG
c. IgE
d. IgA
A
It is the mechanism wherein chemical combine with critical molecular components to induce cell injury
a. Activation of the complement system
b. Direct toxicity
c. Conversion to toxic metabolites
d. Unfolded protein response
B
Chemicals induce injury through:
- Direct toxicity
- Conversion to toxic metabolites
The following are considered to be pathologic hypertrophy except:
a. enlargement of individual skeletal muscle fibers in response to increased demand
b. hypertrophy of skeletal and cardiac muscles fur to increased workload
c. increase in the number of myofilaments per cell
d. enlargement of the heart in response to pressure overload
A
Physiologic hypertrophy:
- massive growth of the uterus during pregnancy
- enlargement of individual skeletal muscle fibers in response to increased demand - weightlifters
It is the most important in physiologic, exercise-induced hypertrophy
a. G-protein coupled receptor-initiated pathway
b. cardiac hypertrophy
c. degradation and loss of myofibrillar contractile elements
d. Phosphoinositide 3-kinase pathway
D
G-protein coupled receptor-initiated pathway: important in pathologic pathway
It occurs when there is a need to increase functional capacity of hormone sensitive organs or compensatory increase after damage or resection
a. physiologic hyperplasia
b. pathologic hyperplasia
c. physiologic atrophy
d. pathologic atrophy
A
pathologic hyperplasia - excessive or inappropriate actions of hormones or growth factors
physiologic atrophy: common during normal devt (notochord and thyroglossal duct)
pathologic atrophy causes: disuse atrophy (decreased workload), denervation atrophy (loss of innervation), diminished blood supply (ischemia), inadequate nutrition, loss of endocrine stimulation, pressure atrophy
It is a mechanism of atrophy that is marked by appearance of increase number of autophagic vacuoles
a. increased autophagy (self-eating)
b. brown atrophy
c. decreased protein synthesis
d. increased protein degradation
A
