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 replacement of columnar
the 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 Intracellular enzymes 42. This type of necrosis most Gangrenous necrosis
free radicals Exogenous and endogenous often affects the lower
antioxidants extremities or bowel and is
Spontaneous decay secondary to vascular occlusion.

30. is the sum of the degradative Necrosis 43. It is often referred to as Apoptosis
and inflammatory reactions programmed cell death.
occurring after tissue death
caused by injury 44. type of necrosis that has a Caseous necrosis
cheese-like consistency
31. refers to degradative Autolysis
reactions in cells caused by 45. When complicated by Wet gangrene
intracellular enzymes indigenous infective heterolysis and
to the cell consequent liquefactive
necrosis, gangrenous necrosis is
32. occurs after the death of the Post mortem Autolysis called
entire organism and is not
necrosis 46. When characterized Dry gangrene
primarily by coagulative necrosis
33. refers to cellular degradation Heterolysis without liquefaction,
by enzymes derived from gangrenous necrosis is called
sources extrinsic to the cell
47. type of necrosis that is often Fibrinoid necrosis
34. results most often from a Coagulative necrosis associated with immune-
sudden cutoff of blood supply to mediated vascular damage
an organ (ischemia), particularly
the heart and kidney. 48. Two forms of fat necrosis Traumatic fat necrosis
Enzymatic fat necrosis
35. the morphologic hallmark of Nuclear changes
irreversible cell injury and 49. type of necrosis, which is a Enzymatic fat necrosis
necrosis, are characteristic of complication of acute
coagulative necrosis hemorrhagic pancreatitis, a
severe inflammatory disorder of
36. Ischemic injury to the central Liquefactive necrosis the pancreas
nervous system (CNS)
characteristically results in 50. which occurs after a severe Traumatic fat necrosis
injury to tissue with high fat
37. type of necrosis occurs as Caseous necrosis content, such as the breast
part of granulomatous
inflammation 51. type of necrosis characterize Fibrinoid necrosis
by deposition of fibrin-like
38. nuclear changes: proteinaceous material in the
arterial walls appears smudgy
- refers to chromatin Pyknosis and acidophilic
clumping and shrinking
with increased basophilia 52. type of necrosis, on histologic Caseous necrosis
- fragmentation of Karyorrhexis examination has an amorphous
chromatin eosinophilic appearance
- fading of chromatin Karyolysis
material 53. DNA fragmentation is Necrosis
haphazard rather than regular,
39. Suppurative infections Liquefactive necrosis resulting in an electrophoretic
characterized by the formation smudge pattern
of pus (liquefied tissue debris
and neutrophils) by heterolytic 54. DNA fragmentation is regular Apoptosis
mechanisms involve at nucleosomal boundaries,
resulting in an electrophoretic
40. is the leading cause of Tuberculosis “laddered” pattern
caseous necrosis
55. gene product inhibits Bcl-2
41. Caseous necrosis combines Coagulative necrosis and apoptosis
features of both Liquefactive necrosis
56. gene product that facilitates Bax
apoptosis
57. gene product decreases
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
p53 71. Hereditary hemochromatosis Micronodular cirrhosis
results in triad of Diabetes Mellitus
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.

61. It is caused most often by Hyaline change 76. combination of lipofuscin Brown atrophy
nonspecific accumulations of accumulation and atrophy of
proteinaceous material. organs is referred to as

62. plumbism leads to Lead poisoning 77. lipofuscin is often found Hepatocytes
within
63. which may cause a Argyria (silver poisoning)
permanent gray discoloration of 78. lipofuscin is sometimes Wear and tear pigment
the skin and conjunctivae referred to as

64. melanin is a pigment formed Tyrosine 79. cause of metastatic Hypercalcemia

from calcification

65. This pigment is a catabolic Bilirubin 80. is defined as calcification in Dystrophic calcification
product of the heme moiety of previously damaged tissue
hemoglobin and, to a minor
extent, myoglobin.

66. Type of jaundice

- associated with destruction of Hemolytic jaundice
rbc
- associated with parenchymal Hepatocellular jaundice
liver damage
- associated with intra- or Obstructive jaundice
extrahepatic obstruction of
the biliary tract

67. iron-containing pigment Hemosiderin

consists of aggregates of ferritin

68. is defined by accumulation of Hemosiderosis

hemosiderin, primarily within
tissue macrophages, without
associated tissue or organ
damage

69. is more extensive Hemochromatosis

accumulation of hemosiderin,
often within parenchymal cells,
with accompanying tissue
damage, scarring, and organ
dysfunction

70 . It appears in tissues as Hemosiderin

golden brown amorphous
aggregates