PATHOLOGY I- CELLULAR

REACTION TO INJURY

1. increase in the size of an organ hypertrophy 17. is exemplified by the squamous metaplasia
or tissue due to an increase in the replacement of columnar
size of cells epithelium at the
squamocolumnar junction of the
2. is an increase in the size of an hyperplasia cervix by squamous epithelium
organ or tissue caused by an
increase in the number of cells. 18. Hypoxic cell injury results ischemia
from various mechanisms which anemia
3. is a failure of cell production aplasia includes (5) carbon monoxide poisoning
decreased perfusion of tissues by
4. is a decrease in cell production hypoplasia oxygen-carrying blood
that is less extreme than in poor oxygenation of blood
aplasia

5. during fetal development, agenesis 19. first part of cell affected by mitochondria
aplasia results in hypoxic cell injury

6. AGENESIS means absence of organ due to failure 20. Reversible morphologic signs myelin figures
of production of damage in hypoxic cellular cell blebs
injury include the formation of:
7. It is seen in the partial lack of hypoplasia
growth and maturation of 21. Enzymes that have been lactate dehydrogenase ldh
gonadal structures in Turner useful in the diagnosis of creatine kinase (ck)
syndrome and Klinefelter myocardial infarction aspartate aminotransferase (ast)
syndrome

8. It is exemplified by glandular hyperplasia 21. whorl-like structures, myelin figures

proliferation in the breast during probably originating from
pregnancy. damaged membranes

9. is a decrease in the size of an atrophy 22. a cell surface deformity, most cell bleb
organ or tissue and results from likely caused by disorderly
a decrease in the mass of function of the
preexisting cells cellular cytoskeleton

10. is the replacement of one metaplasia 23. Hypoxic injury become

differentiated tissue by another irreversible after how many
minutes/ hrs in the:
10. characteristic features of autophagic granules - neurons 3-5 minutes
ATROPHY often include the - myocardial cells 1-2hrs
presence of - hepatocytes 1-2hrs

11. atrophy is thought to be ubiquintin-proteasome 24. are more susceptible to purkinje cells of the cerebellum
mediated in part by the ______ hypoxic injury than are other neurons of the hippocampus
pathway of protein degradation. neurons.

13. refers to intracytoplasmic autophagic granules 25. these molecules have a free radicals
vacuoles containing debris from single unpaired electron in the
degraded organelles. outer orbital

14. is proliferation of myeloid metaplasia 26. is an ocular disorder of retrolental fibroplasia

hematopoietic tissue at sites premature infants that leads to
other than the bone marrow, blindness
such as the liver and spleen
27. are classic ultrastructural proliferation and hypertrophy of
15. is the formation of new bone osseous metaplasis markers of barbiturate the ser of the hepatocyte
at sites of tissue injury intoxication

16. most common cause of ischemia 28. mechanisms the generate normal metabolism, oxygen
hypoxic cell injury free radicals toxicity, ionizing radiation, uv
light, drugs and chemicals,
reperfusion after ischemic injury
29. mechanisms that degrade
free radicals
30. is the sum of the degradative
and inflammatory reactions
occurring after tissue death
caused by injury
31. refers to degradative
reactions in cells caused by
intracellular enzymes indigenous
to the cell
32. occurs after the death of the
entire organism and is not
necrosis
33. refers to cellular degradation
by enzymes derived from
sources extrinsic to the cell
34. results most often from a
sudden cutoff of blood supply to
an organ (ischemia), particularly
the heart and kidney.
35. the morphologic hallmark of
irreversible cell injury and
necrosis, are characteristic of
coagulative necrosis
36. Ischemic injury to the central
nervous system (CNS)
characteristically results in
37. type of necrosis occurs as
part of granulomatous
inflammation
38. nuclear changes:
- refers to chromatin
clumping and shrinking
with increased basophilia
- fragmentation of
chromatin
- fading of chromatin
material
39. Suppurative infections
characterized by the formation
of pus (liquefied tissue debris
and neutrophils) by heterolytic
mechanisms involve
40. is the leading cause of
caseous necrosis
41. Caseous necrosis combines
features of both
Intracellular enzymes 42. This type of necrosis most
Exogenous and endogenous often affects the lower
antioxidants extremities or bowel and is
Spontaneous decay secondary to vascular occlusion.
Apoptosis
Necrosis 43. It is often referred to as
programmed cell death.
Caseous necrosis
44. type of necrosis that has a
cheese-like consistency
Autolysis Wet gangrene
45. When complicated by
infective heterolysis and
consequent liquefactive necrosis,
gangrenous necrosis is called
Post mortem Autolysis
46. When characterized Dry gangrene
primarily by coagulative necrosis
without liquefaction, gangrenous
Heterolysis necrosis is called
47. type of necrosis that is often Fibrinoid necrosis
associated with immune-
Coagulative necrosis mediated vascular damage
48. Two forms of fat necrosis Traumatic fat necrosis
Enzymatic fat necrosis
Nuclear changes 49. type of necrosis, which is a Enzymatic fat necrosis
complication of acute
hemorrhagic pancreatitis, a
severe inflammatory disorder of
the pancreas
Liquefactive necrosis
50. which occurs after a severe Traumatic fat necrosis
injury to tissue with high fat
content, such as the breast
Caseous necrosis
51. type of necrosis characterize Fibrinoid necrosis
by deposition of fibrin-like
proteinaceous material in the
arterial walls appears smudgy
and acidophilic
Pyknosis
52. type of necrosis, on histologic Caseous necrosis
examination has an amorphous
Karyorrhexis eosinophilic appearance
Karyolysis 53. DNA fragmentation is Necrosis
haphazard rather than regular,
resulting in an electrophoretic
Liquefactive necrosis smudge pattern
54. DNA fragmentation is regular Apoptosis
at nucleosomal boundaries,
resulting in an electrophoretic
“laddered” pattern
Tuberculosis
55. gene product inhibits Bcl-2
apoptosis
Coagulative necrosis and
Liquefactive necrosis 56. gene product that facilitates Bax
apoptosis
57. gene product decreases
Gangrenous necrosis transcription of bcl-2 and
increases transcription of bax,
thus facilitating apoptosis
58. is characterized by the
accumulation of intracellular
parenchymal triglycerides
59. This term denotes a
characteristic (homogeneous,
glassy, and eosinophilic)
appearance in hematoxylin and
eosin sections.
60. fatty change is observed
most frequently in the
61. It is caused most often by
nonspecific accumulations of
proteinaceous material.
62. plumbism leads to
63. which may cause a
permanent gray discoloration of
the skin and conjunctivae
64. melanin is a pigment formed
from
65. This pigment is a catabolic
product of the heme moiety of
hemoglobin and, to a minor
extent, myoglobin.
66. Type of jaundice
- associated with destruction of
rbc
- associated with parenchymal
liver damage
- associated with intra- or
extrahepatic obstruction of
the biliary tract
67. iron-containing pigment
consists of aggregates of ferritin
68. is defined by accumulation of
hemosiderin, primarily within
tissue macrophages, without
associated tissue or organ
damage
69. is more extensive
accumulation of hemosiderin,
often within parenchymal cells,
with accompanying tissue
damage, scarring, and organ
dysfunction
70 . It appears in tissues as
golden brown amorphous
aggregates
p53
Skin Pigmentation
72. the triad of hereditary Bronze diabetes
fatty change hemochromatosis is referred as
73. secondary hemochromatosis Multiple blood transfusion
is often caused by
hyaline change
74. Hereditary hemochromatosis Hfe gene on chromosome 6
is most often caused by a
mutation in
75. This yellowish, fat-soluble Lipofuscin
Liver, heart, kidney pigment is an end product of
membrane lipid peroxidation.
Hyaline change 76. combination of lipofuscin Brown atrophy
accumulation and atrophy of
organs is referred to as
Lead poisoning 77. lipofuscin is often found Hepatocytes
within
Argyria (silver poisoning)
78. lipofuscin is sometimes Wear and tear pigment
referred to as
Tyrosine 79. cause of metastatic Hypercalcemia
calcification
Bilirubin 80. is defined as calcification in Dystrophic calcification
previously damaged tissue
81. toxic metabolites of Smooth ER
acetaminophen are generated
by which organelle?
Hemolytic jaundice
82. proteins most likely played a p53
Hepatocellular jaundice key role in triggering radiation-
induced cell death
Obstructive jaundice
83. adaptation to chronic injury Hyperplasia
in patient with psoriasis?
Hemosiderin 84. ingests carbon tetrachloride Mixed function oxygenase
(CCl4) and develop acute liver (P450)
failure, which cellular proteins
Hemosiderosis was directly involved in the
development of hepatotoxicity in
this patient?
85. Individual cells display Dysplasia
hyperchromatic nuclei, a larger
Hemochromatosis nucleus-to-cytoplasm ratio, and
disorderly tissue arrangement.
86. cellular adaptations in the Hyperplasia
bone marrow best explains the
increased hematocrit
Hemosiderin 87. Actinic Keratosis, response of Dysplasia
the skin to chronic sunlight
exposure?
71. Hereditary hemochromatosis Micronodular cirrhosis 88. patient with progeria, it is
results in triad of Diabetes Mellitus caused by mutation in
 102. Myocardial Infarction, Coagulative necrosis
89. type of necrosis in malignant Fibrinoid necrosis demonstrate which of the
hypertension following morphologic changes?

90. karyorrhexis and karyolysis Decrease in intracellular pH 103. necrotic cells contain higher Calcium
evident renal tubular epithelial intracellular concentrations of
cells. Which biochemical events
preceded these pathologic 104. the necrosis of virally Humoral and cellular immunity
changes? infected neurons was mediated
primarily by which mechanism
91. proteins plays the most Cytochrome c
important role in mediating 105. A chest X-ray reveals Caseous necrosis
programmed cell death in findings “consistent with a Ghon
squamous cell carcinoma of skin complex.”, this patient would
most likely demonstrate which of
92. bone trabeculae have formed Myositis ossificans the following pathologic
within the striated skeletal Metaplasia (osseous) changes?
muscle at the site of tissue injury,
This pathologic condition which 106. central nervous system Plasma membrane sodium
is known as ____, is an example neurons display hydropic transport
of which of the following degeneration. This manifestation
morphologic adaptations to of sublethal neuronal injury was
injury? most likely mediated by
impairment of which cellular
93. morphologic adaptations to Atrophy process?
partial ischemia
107. Barret esophagus, Glandular metaplasia
94. acidophilic (Councilman) Apoptosis morphologic adaptation
body, which cellular processes
best accounts for the presence of 108. Acute pancreatitis, Fat necrosis
scattered acidophilic bodies? morphologic changes

95. Which biochemical changes Fragmentation of DNA

characterizes the formation of
acidophilic bodies?

96. wound has enlarged to Liquefactive necrosis

become a 1-cm sore that drains
thick, purulent material. This skin
wound illustrates which of the
following morphologic types of
necrosis?

97. Which substance was most Reactive oxygen species

likely cause of reperfusion injury
in transplanted liver

98. chronic cystitis, morphologic Metaplasia

response

99. is the major intracellular iron Hemosiderin

storage protein in hepatocytes

100. golden cytoplasmic granules Lipofuscin

that do not stain with Prussian
blue

101. yellow brown granules in Hemosiderin

cytoplasm which turn blue with
Prussian blue

Lamin