1
Q
Prior to starting the Post mortem exam
one should:
1. Bathe the body
2. Assess the risks
3. Remove clothes & accessories
4. Check signed consent form
A
Answer: B (2 and 4 only)
2
Q
- Causes of Cell Injury:
- Oxygen deprivation
- Bacterial infection
- Glucose
- Maramus
A
Answer: E (all of the above)
3
Q
- Nuclear change/s in Necrosis:
- Karyolysis
- Pyknosis
- Karyorrhexis
- Basophilia
A
Answer: C (1, 2 & 3 only)
4
Q
- Stain/s glycogen best:
- PAS
- Congo Red
- Best carmine
- H & E stain
A
Answer: A (1 & 3 only)
5
Q
- Appears as yellow-brown, finely granular,
cytoplasmic, often perinuclear pigments: - Melanin
- Lipochrome
- Hemosiderin
- Lipofuscin
A
Answer: B (2 and 4 only)
6
Q
- Most common & medically important cause/s of
Inflammation: - Foreign bodies
- Tissue necrosis
- Immune reactions
- Infections
A
Answer: D (4 only)
7
Q
- Morphologic pattern/s of cause inflammation:
- Vasodilation
- Leukocyte Infiltration
- Exudation
- Edema
A
Answer: C (1, 2 & 3 only)
8
Q
- Reversible cell injury in characteristics by:
- Cellular swelling
- Blebbing of plasma membrane
- Detachment of ribosomes
- Clumping of nuclear chromatin
A
Answer: E (all of the above)
9
Q
- Cause/s of the morphological changes associated
with cell injury: - Decreased generation of ATP
- Loss of cell membrane integrity
- Defects of protein injury
- Inflammation
A
Answer: C (1, 2 & 3 only)
10
Q
- Morphology seen in Apoptosis:
- Cell shrinkage
- Formation of apoptotic bodies
- Formation of cytoplasmic blebs
- Chromatin condensation
A
Answer: E (all of the above)
11
Q
- Pathway/s pf abnormal intracellular accumulations:
- Deposition and accumulation of abnormal
exogenous substance - Accumulation of an abnormal endogenous
substance - Failure to degrade a metabolite
- Abnormal metabolism
A
Answer: E (all of the above)
12
Q
- Exogenous pigment/s:
- Coal worker’s pneumoconiosis
- Lipochrome
- Anthracosis
- Hemosidirosis
A
Answer: A (1 and 3 only)
13
Q
- Dystrophic calcification:
- Normal tissues
- Hypercalcemia
- Hyperparathroidism
- Necrotic tissues
A
Answer: D (4 only)
14
Q
- Major component/s of Acute inflammation:
- Dilatation of blood vessels
- Increased permeability of the microvasculature
- Emigration of leukocytes
- Activation of mediators
A
Answer: C (1, 2 & 3 only)
15
Q
- Feature/s of reversible cell injury seen under the
light microscope: - Cellular swelling
- Plasma membrane blebbing
- Fatty change
- Nuclear clumping
A
Answer: A (1 & 3 only)
16
Q
- Most characteristic/s feature/s of Apoptosis:
- Cell shrinkage
- Formation of apoptotic bodies
- Formation pf cytoplasmic blebs
- Chromatin condensation
A
Answer: D (4 only)
17
Q
- Function/s of Autophagy:
- Survival mechanism
- Removal of unwanted cells to maintain cell
population - Recycling of cells and it’s metabolites
- Normal cellular process
A
Answer: A (1 & 3 only)
18
Q
- Etiology/ies of protein deposition:
- Nephrotic syndrome
- Multiple myeloma
- Emphysema
- Amyloidosis
A
Answer: E (all of the above)
19
Q
- Endogenous pigment/s:
- Coal worker’s pneumoconiosis
- Lipochrome
- Anthracosis
- Hemosidirosis
A
Answer: B (2 and 4 only)
20
Q
- Main characteristic/s of Acute Inflammation:
- Rapid response
- Edema
- Short in duration
- Emigration of leukocytes
A
Answer: B (2 & 4 only)
21
Q
- Source/s of Histamine:
- Basophils
- Platelets
- Mast cells
- Eosinophils
A
Answer: C (1,2,3 only)
22
Q
- Cell/s in chronic inflammation:
- Lymphocytes
- Neutrophils
- Macrophages
- Eosinophils
A
Answer: E (all of the above)
23
Q
- Cell/s that are involved in Fat metabolism:
- Hepatocytes
- Skeletal muscle cells
- Myocardial cells
- Neurons
A
Answer: A (1 & 3 only)
24
Q
- Process/ess of Apoptosis:
- Initiation
- Mitochondrial
- Execution
- Death receptor
A
Answer: A (1 and 3 only)
25
25. Morphologic alteration/s in necrosis:
1. Increased eosinophilia
2. Formation of myelin figures
3. Vacuolated cytoplasm
4. Moth-eaten appearance of the cytoplasm
Answer: E (all of the above)
26
26. Abnormal accumulations of triglycerides within
parenchymal cells:
1. Atherosclerosis
2. Fatty change
3. Saponification
4. Steatosis
Answer: B (2 and 4 only)
27
27. Known as the wear and tear pigments:
1. Melanin
2. Lipochrome
3. Hemosiderin
4. Lipofuscin
Answer: B (2 and 4 only)
28
28. Cell type/s that produce prostaglandins:
1. Mast cells
2. Macrophages
3. Endothelial cells
4. Basophils
Answer: C (1, 2 and 3 only)
29
29. Pyrogen/s
1. IL-1
2. Prostaglandins
3. TNF
4. Lipopolysaccharides
Answer: E (all of the above)
30
30. Process/es of the Autophagy:
1. Formation of phagophore
2. Elongation
3. Degradation
4. Maturation of the autophagosome
Answer: E (all of the above)
31
31. Pathway/s of Apoptosis:
1. Initiation
2. Mitochondrial
3. Execution
4. Death receptor
Answer: B (2 & 4 only)
32
32. Types of Autophagy:
1. Chaperone-mediated autophagy
2. Macroautophagy
3. Microautophagy
4. Chaperone-independent autophagy
Answer: C (1, 2 and 3 only)
33
33. Metastatic calcifications:
1. Normal tissues
2. Hypercalcemia
3. Hyperparathyroidism
4. Necrotic tissue
Answer: C (1, 2 and 3 only)
34
34. Stimuli/s for Histamine release:
1. Trauma
2. Allergic reactions
3. Anaphylatoxins
4. Neuropeptides
Answer: E (all of the above)
35
35. Outcome/s of Acute inflammation:
1. Complete restitution
2. Scarring
3. Connective tissue and replacement
4. Chronic inflammation
Answer: E (all of the above)
36
36. Major participant/s in the inflammatory response:
1. Complement proteins
2. Leukocytes
3. Arachidonic acid metabolites
4. Blood vessels
Answer: B (2 and 4 only)
37
37. Major mechanism/s of apoptosis in all mammalian
cells:
1. Intrinsic
2. Extrinsic
3. Mitochondrial
4. Death receptor
Answer: A (1 and 3 only)
38
38. Considered as the main domain of Pathology:
a. Etiology
b. Morphologic changes
c. Clinical manifestations
d. Pathogenesis
Answer: D Pathogenesis
39
39. AA, 65 years old. Female, diabetic, currently
maintained on Metformin 500 mg/tab daily with poor
compliance come in to the clinic because of a
nonhealing wound on her left leg. On examination you
noted, that all of the toes on her leg has green to black
discoloration with yellowish to green foul smelling
discharge. What type of necrosis is expected in the
foot?
a. Gangrenous necrosis
b. Wet gangrene
c. Liquifactive necrosis
d. Coagulative necrosis
Answer: B Wet grangrene
40
40. A special form of necrosis usually seen in immune
reactions involving blood vessels:
a. Fibrinoid necrosis
b. Liquifactive necrosis
c. Coagulative necrosis
d. Fat necrosis
Answer: A Fibrinoid necrosis
41
41. Caspase-independent programmed cell death:
a. Apoptosis
b. Necrosis
c. Cell injury
d. Necroptosis
Answer: D Necroptosis
42
42. Sequential steps of a typical inflammatory reactions:
Answer: A. Recognition, Recruitment, Activation,
Elimination, Regulation, Repair
43
43. Earliest manifestation of acute inflammation:
a. Vasodilation
b. Increased blood agar
c. Increased permeability of postcapillary venules
d. Redness
Answer: A Vasodilation
44
44. Steps in leukocyte recruitment:
Answer: A. Margination, Rolling, Adhesion, Diapedesis,
Chemotaxis
45
45. Formation of new blood vessels:
a. Angiogenesis
b. Chemotaxis
c. Fibrosis
d. Scarring
Answer: A Angiogenesis
46
46. Based on the correct answer in number 45, what is
the stimulus?
a. VEGF
b. Histamine
c. Leukotrienes
d. Endothelial injury
Answer: VEGF
47
47. Adaptations are reversible:
true
48
48. KS, 30 years old, female, took a pregnancy test at
home due to her late menses and it was positive. What
is the principle of the cellular adaptation that will
occur?
a. Atrophy
b. Hypertrophy
c. Hyperplasia
d. Metaplasia
Answer: B Hypertrophy
49
49. Based on the question in number 48, what is the
mechanism that governs this cellular adaptation?
a. Increased in the production of cellular proteins
b. Increase in the number of cells
c. Decrease in cell size
d. Increase in cell size
Answer: A Increased in the production of cellular
proteins.
50
50. Based on your answer in number 48, what cells are
capable of undergoing this cellular adaptation?
a. Labile cells
b. Quiescent cells
c. Terminally differentiated cells
d. None of the above
Answer: A Labile cells
51
51. This is considered the first manifestation of almost
all forms of cell injury:
a. Cellular swelling
b. Plasma cell membrane blebbing
c. Clumping of the nuclear chromatin
d. Presence of vacuoles
Answer: A Cellular swelling
52
52. Based on your answer number 50, what is the
pathogenesis of the correct answer?
a. Failure to maintain ionic and fluid homeostasis
b. Failure of energy-dependent ion pumps in the
plasma membrane
c. All of the above
d. None of the above
e. A only
Answer: C all of the above
53
53. CD, 60 years old, known diabetic and hypertensive
with poor compliance to medications had sudden loss
of consciousness. On the walking, she presented with
slurring of speech and right sided weakness. She was
diagnosed with ischemic stroke. What is likely
consequence of resolution from the following cellular
events?
a. Coagulative necrosis
b. Apoptosis
c. Inflammation
d. Liquefactive necrosis
Answer: D Liquefactive Necrosis
54
54. It is used as a descriptive term rather than a
specific marker for cell injury:
a. Fibrinoid necrosis
b. Hyaline change
c. Basophilia
d. Vacuoles in the cytoplasm
Answer: B Hyaline change
55
55. Inhibit neutrophil chemotaxis and endothelial
adhesion:
a. Prostaglandins
b. Lipoxins
c. Leukotrienes
d. Vasocactive amines
Answer: B Lipoxins
56
56. Supress inflammation by inhibiting the recruitment
of leukocytes:
a. Prostaglandins
b. Lipoxins
c. Leukotrienes
d. Vasocactive amines
Answer: B Lipoxins
57
57. Considered the most important factor for declining
post mortem examination:
a. Religious and cultural practices
b. Additional anxiety and grief of the family
c. High cost of the procedure
d. Risk of malpractice
Answer: A Religious and cultural practice
58
58. AC, 55 years old, male, chronic alcoholic complained
of a slow growing mass on his abdomen, on further
examination, there was a 5x5 cm mass noted on the left
lobe of his liver, his doctor suggested a frozen section
biopsy. What is the cellular adaptation that could occur
after removal of the mass?
a. Hypertrophy
b. Hyperplasia
c. Metaplasia
d. Atrophy
Answer: B Hyperplasia
59
59. Based on your answer number 58, what is the
stimulus for the response?
a. Hormonal
b. Compensatory
c. Stress
d. Increased workload
Answer: B Compensatory
60
60. Intracellular accumulation are:
a. Reversible
b. Irreversible
c. Inflammatory
d. None of the above
Answer: A Reversible
61
61. Hallmark of acute inflammation:
a. Vasodilation
b. Increased blood flow
c. Increased permeability of postcapillary venules
d. Redness
Answer: C increased permeability of postcapillary
venules
62
62. Based on correct answer 61, what is the mechanism
of the response?
a. Due to the actions of histamine
b. Contraction of endothelial cells
c. Vasodilation of arterioles
d. Increase blood flow
Answer: B contraction of endothelial cells
63
63. Al, 56 years old, female, noted profuse vaginal
bleeding for 7 days consuming 3 fully soaked pads per
day associated with hypogastric pain and dizziness. She
consulted her doctor for her condition. What cellular
adaptation is likely occurring?
a. Hyperplasia
b. Metaplasia
c. Atrophy
d. Hypertrophy
Answer: A Hyperplasia
64
64. Based on answer num 63, what is the stimulus for
response?
Hormonal
65
65. Based on number 63, the condition is:
a. Pathologic
b. Compensatory
c. Normal
d. Hormonal
Answer: A pathologic
66
66. Based on answer number 63, what is the etiology of
the condition?
Answer: A Excessive actions of hormones or growth
factors
67
67. Hallmark of repair:
a. Granulation tissue formation
b. Scab formation
c. Angiogenesis
d. Fibrin deposition
Answer: A Granulation tissue formation
68
68. Inadequate formation of granulation tissue or scar:
a. Dehiscence
b. Keloid
c. Hypotrophic scar
d. Hypertrophic scar
Answer: A Dehiscence
69
69. Cell injury is reversible:
true
70
70. RR, 23 years old, male, complains of one-month.
Non-productive cough, associated with rapid weight
loss, and night sweats. Based on the case what is the
pattern of tissue necrosis expected?
Answer: D. Caseous necrosis
71
71. Based on 70, a chest x-ray was requested and they
were multiple opacities seen on the film. If the nodules
were sent to the laboratory for a biopsy, what
morphology will you see under the microscope?
Answer: A. Granuloma formation
72
72. Based number 70, grossly, the nodule will appear:
Answer: A. Cheese-like, friable, with white appearance
73
73. Involved in leukocyte recruitment:
a. Prostaglandins
b. Lipoxins
c. Leukotrienes
d. Vasoactive amines
Answer: C Leukotrienes
74
74. Extremely time consuming if unexperienced and
requires a larger incision:
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
Answer: A. Letulle
75
75. Removal of individual organs one by one:
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
Answer: B. Virchow
76
76. Excessive amounts of granulation tissue:
a. Ulceration
b. Keloid
c. Proud flesh
d. Contractures
Answer: C. Proud flesh
77
77. Method used commonly in perinatal autopsies:
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
Answer: A. Letulle
78
78. CC, 4 years old, male was diagnosed with
thyroglossal duct cyst and was advised to have it
removed, What cellular adaptation is dysfunctional?
a. Hyperplasia
b. Atrophy
c. Hypertrophy
d. Metaplasia
79
79. What is the mechanism of the corrected answer in
number 78?
Answer: A. Decreased protein synthesis increased
protein degradation
80
80. The results from inadequate vascularization during
healing:
a. Ulceration
b. Dehiscence
c. Keloid
d. Hypertrophic scar
Answer: A. Ulceration
81
81. Excessive formation of components of repair?
a. Ulceration
b. Keloid
c. Proud flesh
d. Contractures
Answer: B. Keloid
82
82. Quick but preserves inter-organ relationships:
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
Answer: D. Ghon
83
83. This technique is rarely performed:
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
Answer: C. Rokitansky
84
84. AL, 80 years old, male, chronic smoker, he noticed
that he was prone to upper respiratory tract infections.
What cellular adaptation is likely occurring?
a. Metaplasia
b. Atrophy
c. Hyperplasia
d. Hypertrophy
Answer: A. Metaplasia
85
85. Is the cellular adaptation in number 84?
a. Reversible
b. Irreversible
c. None of the above
Answer: A. Reversible
86
86. What is the mechanism of the correct answer in
number 84?
Answer: A. Reprogramming of the stem cells
87
87. What is the stimulus of the correct answer in
number 84?
Answer: B. Stress
88
88. Based on the case num 84, what is the predisposing
factor of the patient for the cellular adaptation?
Answer: Chronic smoker
89
89. Exudation of cell-poor fluid into spaces due to cell
injury or into body cavities:
a. Serous inflammation
b. Purulent inflammation
c. Effusion
d. Edema
Answer: A. Serous inflammation
90
90. This inflammation is characteristically seen in the
lining of the body cavities?
Answer: C. Fibrinous inflammation
91
91. Method used for those with communicable disease:
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
Answer: C. Rokitansky
92
92. Embryogenesis
a. Physiologic apoptosis
b. Pathologic Apoptosis
c. none of the above
A
93
93. Genetic mutations
a. Physiologic apoptosis
b. Pathologic Apoptosis
c. none of the above
A
94
94. Viral infections
a. Physiologic apoptosis
b. Pathologic Apoptosis
c. none of the above
b
95
95. Acute Inflammatory Response
a. Physiologic apoptosis
b. Pathologic Apoptosis
c. none of the above
A
96
96. Menopause
a. Physiologic apoptosis
b. Pathologic Apoptosis
c. none of the above
A
97
97. Hypoxia
a. Physiologic apoptosis
b. Pathologic Apoptosis
c. none of the above
B
98
98. This process is known as the increase transport of
fluid and proteins through the endothelial cells:
a. Transcytosis
b. Exudation
c. Vascular leakage
d. Transmigration
Answer: A. Transcytosis
99
99. Based on number 98, what is the stimulus for this
response?
a. Histamine
b. VEGF
c. Bradykinin
d. Complement
B. VEGF
100
100. Based on number 90, what is deposited on the site of inflammation?
a. Cell-poor fluid
b. Pyogenic bacteria and leukocytes
c. Fibrin
d. Inflamed necrotic tissue
c. Fibrin
101
101. Based on number 90, how does this inflammatory
reaction develop?
Answer: B.Vascular leaks are large or precoagulant
states
102
102. These generally develop after thermal or traumatic
injuries that involve the deeper layers of the dermis:
a. Dehiscence
b. Keloid
c. Hypotrophic scar
d. Hypertrophic scar
Answer: D. Hypertrophic scar
103
103. AM, 46 years old, complained of severe abdominal
pain. She was brought to ER and laboratories were
taken showing elevated amylase and lipase. What is the likely pattern of necrosis manifested?
Answer: C. Fat necrosis
Diagnosis to patient: Acute pancreatitis
104
104. Based number 103, what is diagnosis:
Answer: B. Acute pancreatitis
105
105. Based on number 103, what will be the gross
appearance of the organ affected?
Answer: A. Grossly visible chalky white areas
106
106. Based on number 103, what is the mechanism for
the gross appearance of the affected organ?
Answer: A. Fat saponification
107
107. These are usually seen in burn patients:
a. Ulceration
b. Keloid
c. Proud flesh
d. Contractures
Answer: D. Contractures
108
108. Extremely quick techniques
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
Answer: B. Virchow
109
109. Accumulation of excessive amounts of collagen
giving rise to a raised scar:
a. Keloid
b. Hypertrophic scar
c. Dehiscence
d. Ulceration
Answer: B. Hypertrophic scar
110
110. SD, 65 years old, hypertensive, chronic smoker,
currently maintained on Losartan. 50 mg/tab daily
complained sudden, crushing left sided chest pain and
shortness of breath. He was brought on ER, and lab
were taken and showed elevated levels of Troponin I
and CK-MB. What type of necrosis could be manifested
by the cardiac muscles?
a. Coagulative necrosis
b. Liquefactive necrosis
c. Fibrinoid necrosis
d. Gangrenous necrosis
Answer: A. Coagulative necrosis
111
111. Based on 110, what is the microscopic morphology
seen in the cardiac cells?
Answer: C. Preservation of architecture of cells
112
112. The scar tissue grows beyond its borders and doors
not regress:
a. Keloid
b. Hypertrophic scar
c. Dehiscence
d. Ulceration
a. keloid
113
113. Removing all organs at one time:
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
a. letulle
114
114. unregulated cell death
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
a
115
115. inflammation
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
a
116
116. regulated cell death
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
b
117
117. pathologic cell death
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
a
118
118. damage of cell membranes
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
a
119
119. leaking of cellular contents
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
a
120
120. loss of ion hemostasis
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
a
121
121. nuclear dissolution
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
b
122
122. fragmentation of cell
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
b
123
123. no inflammatory reactions
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
b
124
124. always a pathologic process
a. necrosis
b. apoptosis
c. all of the above
d. none of the above
a
125
125. initial responses
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
a
126
126. angiogenesis
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
b
127
127. edema
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
a
128
128. scarring
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
b
129
129. emigration of leukocytes
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
a
130
130. leukocytes
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
a
131
131. monocytes
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
b
132
132. lymphocytes
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
b
133
133. adaptive immunity
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
b
134
134. days to weeks
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
b
135
135. innate immunity
a. acute inflammation
b. chronic inflammation
c. all of the above
d. none of the above
a
136
The following statements are true regarding cell injury and cell death except:
a. Cell injury is reversible up to a certain point
b. The functional and structural alterations in mild forms of injury are reversible even if the stimulus is not removed
c. Necrosis and apoptosis are the two types of principle cell death
d. Necrosis is always pathologic
b. The functional and structural alterations in mild forms of injury are reversible even if the stimulus is not removed
137
The earliest manifestation of cell injury
a. Cellular swelling
138
The following statements are true regarding the morphological patterns of tissue necrosis except
a. b. All organs undergo coagulative necrosis except the brain
An infarct is a localized area of coagulative necrosis
c. The cellular outline is maintained in liquefactive necrosis
d. Fibrinoid necrosis is found in vasculitis syndromes
c. The cellular outline is maintained in liquefactive necrosis
139
Prescence of these enzymes is a marker of cells undergoing apoptosis
a. Caspases
b. Active caspases
c. Cytochrome c
d. BCL-2
b. active caspases
140
The following statements are true regarding apoptosis except
a. Apoptosis does not elicit an inflammatory reaction
b. Chromatin condensation is the most characteristics feature of apoptosis
c. Mitochondrial pathway is responsible for apoptosis in mammalian cells
d. Apoptosis is always pathologic
d. Apoptosis is always pathologic
141
Initiates the C-side program of apoptosis
a. BCL-2
b. Cytochrome C
c. Caspases
d. Active caspases
b. Cytochrome C
142
The following statements are true regarding hypertrophy
a. Hypertrophy can be physiologic or pathologic
b. The mechanism if hypertrophy is increased in the size of the cell
c. Physiologic hypertrophy can be caused by increased functional demand
d. Cardiac hypertrophy is pathologic
b. The mechanism if hypertrophy is increased in the size of the cell
143
The following states are true regarding hyperplasia, except:
a. Hyperplasia and hypertrophy can be triggered by the same stimulus
b. Hyperplasia can occur in cells that are capable of dividing
c. Hyperplasia has an increased risk for cancer
d. DPH is an example of physiologic hyperplasia
d. DPH is an example of physiologic hyperplasia
144
Considered the main domain of pathology
pathogenesis
145
The following statements are true regarding inflammation, except
a. Blood vessels respond to an inflammatory stimuli by vasodilation and decreased their permeability
b. Different mediators of inflammation can initiate an amplified inflammatory response
c. Chronic inflammation may follow acute inflammation or arise de novo
d. Acute inflammation is characterized by edema and immigration of leukocytes
a. Blood vessels respond to an inflammatory stimuli by vasodilation and decreased their permeability
146
147
The following statements are true regarding acute inflammation, except:
a. Lymph flow is increased in inflammation and helps drain edema fluid
b. Contraction of endothelial cells is elicited by histamine and bradykinin
c. Exudation is the process by there is an escape of fluid, protein and blood cells from the vascular system into the interstitial tissue or cavities
d. As stasis develop leukocyte accumulate along the central axial column
d. As stasis develop leukocyte accumulate along the central axial column
148
The following statements are true regarding the morphological patterns of acute inflammation
except
a. Purulent inflammation is characterized by the production of pus
b. The fluid in serous inflammation contains large number of microbes or large number of leukocytes
c. Fibrinous inflammation can be relapse if there is a procoagulant stimulus
d. Abscesses are produced when there is seeding of pyogenic bacteria in the tissues
b. The fluid in serous inflammation contains large number of microbes or large number of leukocytes
149
The following statements are true regarding acute inflammation except
a. Acute inflammation can undergo complete healing scarring or progression to chronic inflammation
b. The hallmark of acute inflammation is the increased permeability of arterioles and capillaries
c. The most important leukocytes are neutrophils and macrophages
d. Histamines and serotonins are the major vasoactive amines
b. The hallmark of acute inflammation is the increased permeability of arterioles and capillaries
150
The following statements are true regarding tissue repair except
a. Infection is one of the most important causes of delayed healing
b. Excessive amounts of collagen will give rise to a hypertrophic scar
c. If the injured tissue is capable of regeneration repair occurs by scar formation
d. Androgenesis is critical in healing at sites of injury
c. If the injured tissue is capable of regeneration repair occurs by scar formation
151
The following statements are true of chronic inflammation, except:
a. Chronic inflammation is a response of prolonged duration in which inflammation, tissue injury in attempts repair coexists
b. Hypersensitivity reactions are examples of chronic inflammation
c. Infiltration of polymorphonuclear cells is one of the morphological features of chronic inflammation
d. Neutrophils are also found in chronic inflammation
c. Infiltration of polymorphonuclear cells is one of the morphological features of chronic inflammation
152
The following statements are true regarding pathologic calcification except:
a. Pathologic calcification is the abnormal deposition of calcium salts only
b. Metastatic calcification is encountered when there is hypercalcemia
c. Dystrophic calcification will occur in necrotic tissue
d. Renal failure can cause metastatic calcification
a. Pathologic calcification is the abnormal deposition of calcium salts only
153
A form of apoptosis that releases inflammatory mediators
a. Necroptosis
b. Autophagy
c. Ferroptosis
d. Pyroptosis
d. Pyroptosis
154
The following statements are true regarding intracellular accumulation except
a. The most common endogenous pigment is carbon
b. An example of localized hemosiderosis is a bruise
c. Russel bodies are example of intracellular hyaline accumulations
d. Amyloidosis is an example of aggregation of an abnormal protein
a. The most common endogenous pigment is carbon
155
The following statements are true regarding intracellular accumulations except
a. This accumulation can be located in the cytoplasm within the organelles or in the nucleus
b. The overload can be controlled or stopped, the accumulation is reversible
c. Emphysema is the result of failure of the degeneration of metabolite
d. All major classes of lipids can accumulate in the cells
c. Emphysema is the result of failure of the degeneration of metabolite
156
Also termed as programmed necrosis
a. Necroptosis
b. Apoptosis
c. Necrosis
d. Ferroptosis
a. necroptosis
157
An example of physiologic compensatory hyperplasia
a. Breasts during puberty
b. Uterus during pregnancy
c. Breasts after weaning
d. Liver after resection
d. Liver after resection
158
The following statements are true regarding tissue repair except:
a. Stable tissues are continuously being loss and replaced
b. An example of labile tissues are hematopoietic stem cells
c. When permanent tissues are injured healing in first scar formation
d. An example of permanent tissues are cardiac muscles
a. Stable tissues are continuously being loss and replaced
159
23. The following statements are true regarding post-mortem examination except:
a. Evisceration is the opening of body during autopsy and removal of organs
b. One of the disadvantage of an En-masse section is that it is time-consuming
c. Virchow method is considered the best method in observing the pathological and anatomical relationship between structures
d. Enbloc removal is a combination between Virchow and Letulle
c. Virchow method is considered the best method in observing the pathological and anatomical relationship between structures
160
24. The following statements are true regarding post-mortem examination except:
a. Rokitansky method is rarely performed
b. Enbloc removal was developed by Ghon
c. En-masse technique is usually used for adult autopsy
d. Prior to starting a post-mortem examination, one should check the consent forms
c. En-masse technique is usually used for adult autopsy
161
25. Critical initiator caspase of the mitochondrial pathway:
a. Caspase-3
b. Caspase-9
c. Caspase-8
d. Caspase-10
b. Caspase-9
162
IP, 55 years old female, complains that she hasn’t had her menstruation for a year.
26. What is the mechanism of the cellular adaptation?
a. decreased protein synthesis and increased protein degradation
b. reduction in the size of the organ due to a decrease in cell size or number
c. loss of endocrine stimulation
d. decreased blood supply
a. decreased protein synthesis and increased protein degradation
163
IP, 55 years old female, complains that she hasn’t had her menstruation for a year.
27. What is the cause of the cellular adaptation?
a. decreased protein synthesis and increased protein degradation
b. reduction in the size of the organ due to a decrease in cell size or number
c. loss of endocrine stimulation
d. decreased blood supply
c. loss of endocrine stimulation
164
IP, 55 years old female, complains that she hasn’t had her menstruation for a year.
28. The cellular adaptation is:
a. physiologic
b. pathologic
a. physiologic
165
HG, 42 years old female, complains of prolonged heavy menstrual bleeding.
29. What is the stimulus for the cellular adaptation?
a. Hormonal
b. Compensatory
c. None of the above
a. hormonal
166
HG, 42 years old female, complains of prolonged heavy menstrual bleeding.
30. The cellular adaptation is:
a. physiologic
b. pathologic
b. pathologic
167
JJ, 23 years old male, complains of on and off productive cough for 3 months associated with weight loss and night sweats.
31. What is the inflammation that is being presented?
a. chronic inflammation
b. granulomatous inflammation
c. acute inflammation
d. A and B
e. none of the above
a. chronic inflammation
168
JJ, 23 years old male, complains of on and off productive cough for 3 months associated with weight loss and night sweats.
32. What could be the gross appearance of the lesions in the lungs?
a. friable white appearance of the area
b. chalky white deposits
c. wedge-shaped discoloration on the area
d. liquid viscous mass
a. friable white appearance of the area
169
JJ, 23 years old male, complains of on and off productive cough for 3 months associated with weight loss and night sweats.
33. On microscopy of the lesion, there is:
a. necrotic areas with distinct inflammatory borders
b. preservation of the outlines of the cells
c. shadowy outlines of necrotic fat cells with calcium deposits
d. bright pink amorphous appearance
a. necrotic areas with distinct inflammatory borders
170
34. Cell injury is reversible.
True
171
35. Metaplasia is irreversible.
False
172
36. Necrosis always produces an inflammatory response.
True
173
37. Vasodilation is the earliest manifestation of chronic inflammation.
False
174
38. In hypertrophy, there is production of new cells.
False
175
39. Nephrotic syndrome can cause production of excessive amounts of normally secreted proteins.
False
176
40. Hyaline change is a specific marker for cell injury.
False
177
41. Melanin is the only endogenous pigment.
False
178
42. Method used for those with communicable diseases:
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
c. rokitansky
179
43. Formation of excessive amounts of granulation tissue:
a. Contraction
b. Proud flesh
c. Keloid
d. Hypertrophic scar
b. proud flesh
180
44. The most characteristic feature of apoptosis:
a. Cellular swelling
b. Apoptosis
c. Chromatin condensation
d. Cellular shrinkage
c. Chromatin condensation
181
45. Mechanism of metaplasia
a. Stress
b. Reprogramming of cells
c. Increased protein synthesis
d. Change of phenotype of the cell
b. Reprogramming of cells
182
46. It is the process by which leukocytes would move in the tissues toward the site of inflammation along a chemical gradient:
a. Transcytosis
b. Diapedesis
c. Transmigration
d. Chemotaxis
d. chemotaxis
183
47. Hallmark of repair:
a. Granulation tissue
b. Scab formation
c. Angiogenesis
d. Fibrin deposition
a. Granulation tissue
184
48. Caspase-independent programmed cell death:
a. Necrosis
b. Apoptosis
c. Necroptosis
d. Autophagy
c. Necroptosis
185
49. This causes vascular congestion during inflammation
a. Increased permeability of the vasculature
b. Stasis
c. Vasodilation
d. Migration of leukocytes
b. stasis
186
50. Described the 5th cardinal sign of inflammation:
a. Rudolp Virchow
b. Celsus
c. Ellie Metchnikoff
d. John Hunter
a. Rudolp Virchow
187
51. The scar tissue that grows beyond its borders and does not regress:
a. Keloid
b. Hypertrophic scar
c. Dehiscence
d. Ulceration
a. keloid
188
52. Extremely quick technique:
a. Letulle
b. Virchow
c. Rokitansky
d. Ghon
b. virchow
189
53. This metabolite suppresses inflammation by inhibiting the recruitment of leukocytes
a. Leukotrienes
b. Lipoxin
c. Chemokines
d. Arachidonic acid
b. lipoxin
190
54. This causes vasocontriction
a. Histamine
b. Serotonin
c. Prostaglandin
d. Arachidonic acid
b. serotonin
191
55. Steps in leukocyte recruitment:
a. Margination -> rolling -> adhesion -> diapedesis -> chemotaxis
b. Margination -> rolling -> diapedesis -> adhesion -> chemotaxis
c. Margination -> adhesion -> rolling -> diapedesis -> chemotaxis
d. Margination -> adhesion -> diapedesis -> rolling -> chemotaxis
a. Margination -> rolling -> adhesion -> diapedesis -> chemotaxis
192
neutrophils
a. acute
b. chronic
c. all of the above
c
193
edema
a. acute
b. chronic
c. all of the above
a
194
innate immunity
a. acute
b. chronic
c. all of the above
a
195
mast cells
a. acute
b. chronic
c. all of the above
b
196
increased vascular permeability
a. acute
b. chronic
c. all of the above
a
197
vasodilation
a. acute
b. chronic
c. all of the above
a
198
angiogenesis
a. acute
b. chronic
c. all of the above
b
199
appendicitis
a. acute
b. chronic
c. all of the above
a
200
proliferation of lymphatics
a. acute
b. chronic
c. all of the above
a
201
plasma cells
a. acute
b. chronic
c. all of the above
b
202
fibrosis
a. acute
b. chronic
c. all of the above
b
203
asthma
a. acute
b. chronic
c. all of the above
b
204
effusion
a. acute
b. chronic
c. all of the above
a
205
necrosis
a. reversible
b. irreversible
b
206
ischemia
a. reversible
b. irreversible
b
207
anemia
a. reversible
b. irreversible
a
208
hydropic change
a. reversible
b. irreversible
a
209
wet gangrene
a. reversible
b. irreversible
b
210
tuberculosis
a. reversible
b. irreversible
b
211
anorexia
a. reversible
b. irreversible
a
212
apoptosis
a. reversible
b. irreversible
b
213
necroptosis
a. reversible
b. irreversible
b
214
atrophy
a. reversible
b. irreversible
a
215
pancreatitis
a. reversible
b. irreversible
b
216
pyknosis
a. reversible
b. irreversible
b
217
Morphology of Necrosis
1. Increased basophilia
2. Vacuolated cytoplasm
3. Cytoplasmic Blebbing
4. Karyorrhexis
2 & 4
218
Organs that undergo steatosis
1. Liver
2. Muscle
3. Heart
4. Kidney
all
219
Proapoptotic proteins
1. BCL 1
2. BAX
3. Cytochrome C
4. BAK
2&4
220
Pathologic Apoptosis
1. Embryogenesis
2. Duct obstruction
3. Neutrophils in acute inflammation
4. Anticancer drugs
2&4
221
Causes fever
1. IL 1
2. Prostaglandins
3. TNR
4. Lipopolysaccharides
all
222
Abnormal accumulation of proteins
1. Nephritic syndrome (nephrotic)
2. Multiple Myeloma
3. Parkinson’s disease (alzheimer's disease)
4. Amyloidosis
2&4
223
Causes of Inflammation
1. Fungal infections
2. Hypersensitivity
3. Autoimmune Disease
4. Sutures
all
224
Major components of acute inflammation
1. Dilatation of blood vessels
2. Edema
3. Immigration of leukocytes
4. Release of histamine
1,2,3
225
Acute inflammation
1. Initial rapid response
2. Edema
3. Innate immunity
4. Proliferation of blood vessels
1,2,3
226
Functions of autophagy
1. Survival mechanism
2. Removal of unwanted cells to maintain cell population
3. Recycling of cells and its metabolites
4. Normal cellular process
1&3
227
Cells in chronic inflammation
1. Lymphocytes
2. Neutrophils
3. Macrophage
4. Eosinophils
all
228
Endogenous pigments
1. Coal worker’s pneumoconiosis
2. Lipochrome
3. Anthracosis
4. Hemosiderosis
2&4
229
Atrophy
1. Marasmus
2. Menopause
3. Loss of nerve supply
4. Cachexia
all
230
Pathways of abnormal intracellular accumulation - E
1. Deposition and accumulation of abnormal exogenous substance
2. Accumulation of an abnormal endogenous substance
3. Failure to degrade a metabolite
4. Abnormal Metabolism
all
231
Reversible Cell Injury
1. Clumping of nuclear chromatin
2. Cellular swelling
3. Detachment of ribosomes from the ER
4. Fatty change
all
232
Extrinsic death receptor pathway -B
1. Caspase 3
2. Caspase 10
3. Caspase 6
4. Caspase 8
2&4
233
Executioner caspases
1. Caspase 3
2. Caspase 10
3. Caspase 6
4. Caspase 8
1&3
234
Produces prostaglandins
1. Mast cells
2. Endothelial cells
3. Macrophages
4. Platelets
1,2,3
235
Appears as yellow brown finely granular cytoplasmic often perinuclear pigment
1. Melanin
2. Lipochrome
3. Hemosiderin
4. Lipofuscin
2&4
active recalls
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