I - Cell Injury, Cell Death and Adaptations Flashcards
1
Q
Hypertrophy(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 34
A
Increase in SIZE of cells resulting in increased size of organ.
2
Q
Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.35
A
Increase in NUMBER of cells
3
Q
Both. Estrogen stimulates SM hyperthrophy and hyperplasia (TOPNOTCH)Robbins Basic Pathology, 9th ed. p.34
A
Hypertrophy of hyperplasia?Uterus during pregnancy
4
Q
Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.4
A
Hypertrophy or hyperplasia?Wound healing
5
Q
Both. (TOPNOTCH) Robbins Basic Pathology 9th ed., p 36
A
Hypertrophy or hyperplasia?
Female breast at puberty
6
Q
Hypertrophy (TOPNOTCH)
A
Cellular adaptation of non-dividing cells (i.e., myocardial fibers)
7
Q
Hypertrophy (TOPNOTCH)
A
50 y/o male with untreated hypertension for several years. What cellular adaptation will be most likely seen in the myocardium?
8
Q
Hyperplasia(TOPNOTCH)
A
40 y/o male underwent partial hepatectomy. What cellular adaptation will the liver most likely undergo?
9
Q
Increased workload (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.34
A
The most common stimulus for hypertrophy of muscle
10
Q
Hyperplasia(Case of BPH) (TOPNOTCH)
A
Hypertrophy or hyperplasia? Benign prostate enlargement that can cause lower urinary tract symptoms (weak stream, straining, hesitancy) *SEE SLIDE 1.1
11
Q
Hormonal stimulation by androgens. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 36
A
Stimulus for hyperplasia in BPH
12
Q
Hyperplasia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 36
A
Cellular adaptation in papilloma virus infection
13
Q
Atrophy(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 35
A
Reduction in the size of an organ or tissue due to decrease in cell size and number
14
Q
Atrophy(in menopause)(TOPNOTCH)
A
60 y/o female has been experiencing hot flushes and irritability. Her uterine epithelium will most likely reveal what type of cellular adaptation?
15
Q
Tumor necrosis factor (TNF)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 35
A
Chronic production of this cytokine is thought to be responsible for appetite suppression and lipid depletion, culminating in muscle atrophy and marked muscle wasting (cachexia)
16
Q
Metaplasia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 37
A
A reversible change in which one differentiated cell type is replaced by another cell type.
17
Q
Metaplasia. This is a case of Barret’s esophagus (squamous to glandular epithelium) (TOPNOTCH)
A
A 49 y/o female had a chronic history of heartburn. Biopsy done showed glandular changes in the distal epithelium of the esophagus. What cellular adaptation is present? *SEE SLIDE 1.2
18
Q
Columnar to squamous(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 37
A
Most common epithelial metaplasia
19
Q
Columnar to squamous(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 37
A
Type of metaplasia in trachea and bronchi in habitual cigarette smoking
20
Q
Cellular swelling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.8 *SEE SLIDE 1.3
A
This is the first manifestation of almost all forms of injury to cells.
21
Q
Apoptosis(TOPNOTCHRobbins Basic Pathology, 8th ed. p.7
A
Type of cell death characterized by nuclear dissolution, WITHOUT complete loss of membrane integrity.
22
Q
Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.7
A
Type of cell death which is energy-dependent, tightly regulated, and associated with normal cellular functions. Often physiologic. Undergoes shrinkage and fragmentation.
23
Q
Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.9
A
Type of cell death which results from a pathologic cell injury. Undergoes cellular swelling and eventual pyknosis, karyorrhexis, and karyolysis.
24
Q
Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
A
Type of cell death associated with inflammation.
25
Pyknosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.42
It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. There is nuclear shrinkage with increased basophilia.
26
Karyorrhexis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
It is the destructive fragmentation of the nucleus of a dying cell.
27
Karyolysis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
It is the complete dissolution of the chromatin of a dying cell.
28
Cellular swelling, hydropic change or vacuolar degeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23 *SEE SLIDE 1.3
Small clear vacuoles within the cytoplasm, representing pinched-off segments of the endoplasmic reticulum.
29
Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23 *SEE SLIDE 1.4
Appearance of lipid vacuoles in the cytoplasm. Often seen in cells participating in fat metabolism (liver, heart)
30
Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
REVERSIBLE or IRREVERSIBLE INJURY: Surface blebs, increased eosinophilia of the cytoplasm, cellular swelling.
31
Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 9th ed., p.41
REVERSIBLE or IRREVERSIBLE INJURY: loss of microvilli, blunting, appearance of smal amorphous densities, ER dilation and disaggregation of granular and fibrillar elements.
32
Irreversible/ Necrotic cellular injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
REVERSIBLE or IRREVERSIBLE INJURY: loss of nuclei, cellular fragmentation and leakage of cellular contents.
33
Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology , 9th ed. p.43
Characterized by digestion of dead cells, resulting in transformation of the tissue into a liquid viscous mass. Often seen in INFECTIONS (pus) and in hypoxic death of cells within the CNS. *SEE SLIDE 1.5
34
Coagulative necrosis (i.e., HSK - Heart, Kidney, Spleen) (TOPNOTCH)Robbins Basic Pathology, 9th ed. p.43 *SEE SLIDE 1.6
A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved. The affected tissues take on a firm texture. Often seen in INFARCTS of all solid organs except the brain.
35
Fat necrosis (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 44
Refers to focal areas of fat destruction, typically seen in acute pancreatitis. There is release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. The foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits (SAPONIFICATION), surrounded by an inflammatory reaction.
36
Fibrinoid necrosis (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 44
A special form of necrosis usually seen in immune reactions involving blood vessels. Deposits of IMMUNE COMPLEXES, together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called "fibrinoid" (fibrin-like) by pathologists. *SEE SLIDE 1.7
37
Liquefactive necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
Seen in focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes digest the tissue. *SEE SLIDE 1.5
38
Gangrenous necrosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.43
This term is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulative necrosis with superimposed liquefactive necrosis involving multiple tissue layers.
39
Caseous necrosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.43
Friable, white appearance of necrosis. It appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border (GRANULOMA). Cheese-like. *SEE SLIDE 1.8
40
Liquefactive necrosis (TOPNOTCH)
Obstruction of the blood supply would lead to which type of NECROSIS in the brain parenchyma?
41
Caseation necrosis (TOPNOTCH) *SEE SLIDE 1.8
A 32 y/o male complains of chronic cough and weight loss. CXR showed an ill-defined mass along the apex of the right lobe. Sputum AFB was positive. Biopsy of the lung will most likely reveal what kind of necrosis?
42
Free radicals(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
These are chemical species with a single unpaired electron in the outer orbital.
43
Antioxidants(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 48
They block free radical formation or inactivate free radicals. Examples of these are the lipid-soluble vitamins E, A, and C, and glutathione in the cytosol.
44
Ischemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
Most common cause of cell injury in clinical medicine.
45
Apoptotic Bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.19
Composed of membrane-bound vesicles of cytosol and organelles seen in programmed-cell death.
46
ApoptosisTOPNOTCH) Robbins Basic Pathology, 9th ed., p. 53
Characterized by cell shrinkage, chromatic condensation, formation of cytoplasmic blebs and apoptotic bodies, and phagocytosis by macrophages.
47
ApoptosisTOPNOTCH) Robbins Basic Pathology, 9th ed., p. 52
Type of cell death in embryogenesis
48
ApoptosisTOPNOTCH) Robbins Basic Pathology, 9th ed., p. 52
Type of cell death in menopause
49
Ischemia-Reperfusion Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
Restoration of blood flow to ischemic but otherwise viable tissue paradoxically results in exacerbated and accelerated injury.
50
Mitochondrial / Intrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22
Pathway of apoptosis triggered by loss of survival signals, DNA damage and accumulation of misfolded proteins. Inhibited by Anti-apoptotic members of the Bcl family.
51
Death Receptor / Extrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22
Pathway of apoptosis responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes. Initiated by TNF receptors.
52
Autophagy(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 61
It involves sequestration of cellular organelles into cytoplasmic autophagic vacuoles that fuse with lysosomes and digest enclosed material.
53
Fatty change/Steatosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62 *SEE SLIDE 1.4
Refers to any abnormal accumulation of triglycerides within parenchymal cells. Most often seen in the liver but can also occur in the heart and kidneys.
54
Foam cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24
Other name for macrophages in contact with lipid debris of necrotic cells or abnormal forms of lipoproteins. Filled with minute, membrane-bound vacuoles of lipid, imparting a foamy appearance to their cytoplasm.
55
Xanthomas(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24
Presence of cholesterol-filled macrophages in subepithelial connective tissue of skin or tendons.
56
Hypertrophy due to increased workload(TOPNOTCH)
Hypertrophy or hyperplasia?Cardiomegaly due to hypertension
57
Carbon(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Most common exogenous pigment?
58
Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
"Wear and Tear pigment"? *SEE SLIDE 1.9
59
Melanin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Pigment produced by tyrosinase-catalyzed oxidation of tyrosine to dihydroxyphenylalanine.
60
Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Hemoglobin-derived granular pigment that is golden-yellow to brown in color. Accumulates in excess of iron.
61
Prussian blue test(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26 *SEE SLIDE 1.10
Histochemical reaction used to identify hemosiderin.
62
Dystrophic calcification.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Abnormal calcium deposition occuring in the absence of calcium metabolic derangements.
63
Metastatic calcification (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
Calcium deposition in normal tissues occuring in the presence of hypercalcemia.
64
Calcium salts(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.27
Grossly seen as fine white granules or clumps, often felt as gritty deposits. Histologically, intra/extracellular basophilic deposits.
65
Cellular aging(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.29
A result of a progressive decline in the proliferative capacity and lifespan of cells.
66
Apoptotic cell(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20
Appears as round or oval masses with intensely eosinophilic cytoplasm, nuclei with various stages of chromatin condensation and aggregation, karyorrhexis.
67
Apoptotic bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20
Membrane bound vesicles of cytosol and organelles quickly extruded and phagocytosed without eliciting inflammatory response.
68
Fatty change of the heart(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24
Focal, intracellular fat deposits creating alternating bands of yellowed myocardium with alternating bands of darker red-brown uninvolved heart or "tigered effect".
69
Russel bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25
Rounded, eosinophilic accumulation of newly synthesized immunoglobulins in the rough ER of plasma cells.
70
Mallory body / "alcoholic hyalin"(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25
Eosinophilic cytoplasmic inclusion in liver cells composed of aggregated intermediate filaments which resist degradation. Seen in patients woth alcoholic liver disease. *SEE SLIDE 1.11
71
Neurofibrillary tangles in Alzheimer's disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26 *SEE SLIDE 1.12
Aggregated protein inclusions that contain microtubule-associated proteins and neurofilaments, reflecting disrupted neuronal cytoskeleton.
72
Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
An insoluble brownish-yellow granular intracellular material that accumulates as a function of age and atrophy. Appears as perinuclear electron-dense granules on electron microscopy. *SEE SLIDE 1.9
73
Triglyceride (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62
What substance accumulates in the cytoplasm of liver cells in steatosis?
74
Defective transport (TOPNOTCH)
Mechanism of triglyceride accumulation in malnutrition
75
Alzheimer's Disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 21
DISEASE PATHOGENESIS: Abnormal folding of AB peptides causing aggregation within neurons and apoptosis.
76
Creutzfeldt-Jacob disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 58
DISEASE PATHOGENESIS: abnormal folding of PrPSC causing neuronal death (affected prion protein)
77
Alpha-1-antitrypsin deficiency (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 58
Pathogenesis: absence of enzymatic activity in lungs causing destruction of elastic tissue
78
Reduction in ATP levels(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 45
Fundamental cause of necrotic cell death
79
Alcohol abuse and non-alcoholic fatty liver disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62
Most common causes of significant fatty change in the liver
80
Hyaline change(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 61
Alteration within the cells or in the extracellular space that gives a homogeneous, glassy, pink appearnce in H&E histologic section
81
Diabetes mellitus(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 64
In this disease, glycogen can be seen in renal tubular epithelial cells, liver cells, B cells of islets of Langerhans, and heart muscle cells.
82
Hemosiderosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 65
A condition when there is systemic overload of iron, hemosiderin may be deposited in many organs and tissues.
83
Hemochromatosis. (TOPNOTCH)
An inherited disease characterized by extreme accumulation of iron, associated with liver, heart, and pancreatic damage, and resulting in liver fibrosis, heart failure, and diabetes mellitus. *SEE SLIDE 1.10
84
Alkaptonuria(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 64
A rare metabolic disease causing black pigment deposition in the skin, connective tissue, and cartilage. *SEE SLIDE 1.13
85
Psammoma bodies (TOPNOTCH)
Foci of dystrophic calcification which appears as lamellated configurations because of their resemblance to grains of sand. Seen in some types of papillary cancer. *SEE SLIDE 1.14
86
Bilirubin (TOPNOTCH)
Jaundice is due to accumulation of what pigment?
87
Coagulative necrosis (TOPNOTCH)
What type of necrosis is most characteristic of ischemia involving the heart or kidney?
88
Coagulative necrosis (TOPNOTCH)
What type of necrosis is most often caused by sudden ischemia from vascular occlusion?
89
Metastatic calcification (TOPNOTCH)
Dystrophic or metastatic calcification? Renal nephrocalcinosis
90
Dystrophic calcification(TOPNOTCH)
Dystrophic or metastatic calcification? Calcific aortic stenosis
91
Dystrophic calcification(TOPNOTCH)
Dystrophic or metastatic calcification?Left anterior descending coronary artery with atheromatous plaques
92
Metastatic calcification (TOPNOTCH)
Dystrophic or metastatic calcification? Sarcoidosis
93
Metastatic calcification (TOPNOTCH)
Dystrophic or metastatic calcification? Paget disease
94
Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
30 year old thalassemic male receiving multiple blood transfusions. What is the expected intracellular accumulation in the cells of his liver, heart, and endocrine organs? *SEE SLIDE 1.10
95
DYSTROPHIC calcification (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp26-27.
Accumulation of calcium despite absence of calcium derangements.
96
Alcohol abuse and diabetes (TOPNOTCH) Robbins Basic Pathology, 8th ed. P 23.
Two most common causes of fatty change in the liver in industrialized nations.
97
Endometrial cells show shrinkage and nuclear accumulation (Apoptosis) (TOPNOTCH) Robbins Basic Pathology 8th ed., pp 19-20
A 22 yo female is on the first day of her menses. How would you characterize the events in her endometrial cells?
98
Reversible Injury (TOPNOTCH)Robbins Basic Pathology, 9th ed., p.9
REVERSIBLE or IRREVERSIBLE INJURY: mitochondrial changes such as swelling and appearacne of phospholipid-rich amorphous densities
99
Seen in both, but irreversible injury is marked by karyolysis, pyknosis, and karyorrhexis. (TOPNOTCH)Robbins Basic Pathology, 9th ed., p.9
REVERSIBLE or IRREVERSIBLE INJURY: nuclear alterations
100
Myelin figures (TOPNOTCH)Robbins Basic Pathology, 9th ed., p.9
Phospholipid masses seen in the cytoplasm, derived from damaged cellular membranes.
101
Tay-Sachs Disease (TOPNOTCH)Robbins Basic Pathology, 9th ed., p.22
DISEASE PATHOGENESIS: Lack of hexosaminidase enzyme, which leads to accumulation of GM2 gangliosides in neurons
102
Cystic fibrosis (TOPNOTCH)Robbins Basic Pathology, 9th ed., p.22
DISEASE PATHOGENESIS: Loss of CFTR leading to defects in chloride transport
