Histopathology Flashcards

1
Q

Cell that frequently divide to replace lost cells

A

Labile cells

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2
Q

not typically dividing to replace injured cells

Do not frequently go cell division

Only undergo replication to replace injured cells

A

Stable cells

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3
Q

Stable cells examples

A

Parenchymal cells of liver and kidneys

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4
Q

Cell class that do not undergo replication following maturation

A

Permanent Cell

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5
Q

Permanent cell example

A

neurons (nerve cell)

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6
Q

incomplete or defective development of tissue/organ. Shows no resemblance to the normal mature structure. Usually happens in paired organs (kidneys, gonads)

A

Aplasia

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7
Q

complete non-appearance of organ.

A

Agenesia

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8
Q

failure of tissue/organ to reach normal mature adult size

A

Hypoplasia

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9
Q

Failure of organ to form an opening

Example:
Imperforate anus (without opening)

Microtia - absence of ear canal

A

Atresia

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10
Q

Cellular adaptation mechanisms

A

Atrohpy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
Anaplasia

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11
Q

acquired decrease in tissue or organ size

A

Atrophy

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12
Q

Atrophy that occurs as consequence of maturation

example:

Atrophy of thymus at puberty

Decrease in uterus size after childbirth

A

Physiologic

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13
Q

Pathologic atrophy:

occurs if blood supply becomes reduced or below the critical level (may develop as a result of pressure atrophy)

A

Vascular atrophy

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14
Q

Pathologic atrophy:

persistent pressure on the organ or tissue may directly injure the cell or may secondarily promote diminution of blood supply

A

Pressure atrophy

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15
Q

Pathology atrophy:

due to lack of hormones needed to maintain normal size and structure

A

Endocrine atrophy

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16
Q

Pathologic atrophy:

due to lack of nutritional supply to sustain normal growth

A

Hunger/Starvation atrophy

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17
Q

Pathologic atrophy:

too much workload can cause general wasting of tissues

A

Exhaustion atrophy

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18
Q

Pathologic atrophy:

Inactivity/diminished activity/functions

A

Atrophy of disuse

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19
Q

Increase in tissue/organ size due to an increase in size of cells making up the organ

A

Hypertrophy

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20
Q

hypertrophy of skeletal muscles due to frequent exercise

A

Physiologic hypertrophy

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21
Q

Hypertrophy of the myocardium (hypertension)

Aortic valve disease

A

Pathologic hypertrophy

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22
Q

Type of hypertrophy that may develop as response to a deficiency (usually in paired organs– when one is removed)

A

Compensatory

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23
Q

Example of compensatory hyperthrophy

A

Renal hypertrophy

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24
Q

Increase in tissue or organ size due to an increase in the number of the cells making up the organ (new cells are formed)

A

Hyperplasia

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25
Hyperplasia: Happens in response to the need increase in uterus, breast during pregnancy. Increase in breast size during puberty (glandular stimulation)
Physiologic Hyperplasia
26
Type of hyperplasia: Erythroid bone marrow hyperplasia in people in high altitude
Physiologic hyperplasia
27
Type of hyperplasia: Grave’s disease - diffuse crowding of epithelial cells Hyperplasia of endometrium due to excessive estrogen TB of cervical lymph nodes - there is increase in the number of lymph nodules
Pathologic
28
Occur frequently together with hypertrophy and can be triggered by the same mechanism
Compensatory
29
Involves transformation of adult cell type into another adult type (reversible process)
Metaplasia
30
Mesenchymal metaplasia involves:
Connective tissues
31
Original tissue: Ciliated columnar epithelium of bronchi Stimulus: Cigarette smoking Metaplastic tissue:
Squamous epithelium
32
Original tissue: Transitional epithelium of bladder Stimulus: Trauma of bladder
Squamous epithelium
33
Original tissue: Columnar glandular epithelium Stimulus: Vitamin A deficiency Metaplastic tissue:
Squamous epithelial cells
34
Original tissue: Esophageal squamous Stimulus: Gastric acidity (too much drinking coffee) Metaplastic tissue:
Columnar epithelium
35
Dysplasia is also known as
atypical metaplasia
36
Pre-neoplastic lesion Change in cell size, shape, and orientation (reversible). May lead to cancer but not necessarily
Dysplasia (atypical metaplasia)
37
dedifferentiation (irreversible) transformation of adult cells into embryonic/fetal cells
anaplasia
38
Causes of cell injury
Anoxia - lack of oxygen supply Infectious agents Mechanical agents/Trauma Chemical Agents - carcinogens (chloroform, benzene)
39
No.1 cause of cell injury
Oxygen deprivation
40
Hypoxic cell injury for neuron is irreversible after (minutes)
3-5 minutes
41
Hypoxic cell injury in myocardial cells and hepatocytes is irreversible after (time)
1-2 hours
42
Skeletal muscle hypoxic injury is irreversible after (time)
many hours
43
Appearance of affected organs in gross change
Organ pallor (pale), Increased weight
44
Earliest change of tissue is seen
Microscopically
45
First manifestation of cellular change
cellular swelling
46
Irreversible changes
Enzymatic digestion of cells Protein denaturation Cytoplasmic changes Nuclear changes
47
Cytoplasmic changes includes
Increased eosinophilia (pink/orange) Large cells "cloudy swelling"
48
Irreversible nuclear changes
Pyknosis Karyolysis Karyorrhexis
49
condensation of nucleus
pyknosis
50
fragmentation/segmentation of nucleus
Karyorrhexis
51
Physiologic cell death Programmed cell death Death of single cell in a cluster of cells
Apoptosis
52
Cell shrinkage - integrity of membrane remains intact Cellular components do not leak out = no inflammation Chief morphologic features: Chromatin condensation Chromatin fragmentation Cell shrinkage Cytoplasmic bleb formation Phagocytosis of apoptotic cells
Apoptosis
53
Pathologic cell death Accidental cell death Cell swelling Leakage of cellular components = Inflammation Change in organ can be seen in gross
Necrosis
54
Type of Necrosis: due to to sudden cut off of blood supply
Coagulative
55
Type of Necrosis: Due to ischemia Appears ghostly (cell outline is maintained) Usually happens in solid organs (liver, kidneys, heart) Microscopically cell outlines are preserved On gross, affected organs somewhat firm, appearing like a boiled material Actions of hydrolytic enzyme is blocked (normal cell death releases lysozyme - hydrolytic enzyme for cell self destruction) I.e. Myocardial Infarct
Coagulative
56
Type of Necrosis: On gross, affected organ appears liquefied, creamy yellow (increased pus)
Liquefactive
57
Type of Necrosis: Softening of organs is due to actions of hydrolytic enzymes Complete digestion of cells i.e. brain infarct and supporative bacterial infections
Liquefactive
58
Type of Necrosis: On gross, tissue organ appears greasy resembling “cheese”
Caseous
59
Type of Necrosis: Combination of coagulative and liquefactive Usually seen in TB Microscopically it appears as amorphous granular debri surrounded by granulomatous inflammation
Caseous (cheeselike)
60
Type of Necrosis: Seen in immune reactions of the blood vessel Deposition of fibrin in vessel wall Cannot be seen in gross examination Can only be microscopically
Fibrinoid
61
Type of Necrosis: Destruction of fat cells due to release of pancreatic lipases
Fat
62
Type of Necrosis: Death of fat tissues due to loss of blood supply On gross, appears chalky white Microscope, infiltrates of foamy macrophage adjacent to adipose tissues Seen in pancreatitis Affected organ is usually breasts
Fat
63
Type of Necrosis: necrosis secondary to a ischemia Not a specific pattern of necrosis
Gangrenous
64
Type of Necrosis: Refers to a limb that loss its blood supply in the lower extremities Skin - dry, black, and is observed in various stages of decomposition
Gangrenous
65
due to venous occlusion, example of this is SUPPURATIVE BACTERIAL INFECTION
wet gangrene
66
due to arterial occlusion and example of this is FOOT EMBOLISM
Dry gangrene
67
Tissue reaction to injury
Inflammation
68
Goal of Inflammation:
1)To remove the initial cause of the injury 2)To remove the consequences of injury
69
Cardinal signs of inflammation
Dolor Rubor Calor Tumor Functio laesa
70
Cardinal sign of inflammation: pain
dolor
71
Cardinal sign of inflammation: redness due to increase blood flow
Rubor
72
Cardinal signs of inflammation: heat
Calor
73
Cardinal signs of inflammation: swelling
Tumor
74
Cardinal Signs of Inflammation: destruction of functioning units of the cell
Functio laesa
75
Type of inflammation: rapid response to an injurious agent
acute inflammation
76
Hallmark sign of acute inflammation
**Exudation**: escape of fluid proteins, blood cells from the vascular system) **Edema**: excess to fluid in interstitial tissues and cavities
77
escape of fluid proteins, blood cells from the vascular system)
Exudation
78
excess to fluid in interstitial tissues and cavities
Edema
79
Cellular infiltrate of acute inflammation
neutrophils
80
Prolonged duration of inflammation
Chronic inflammation
81
Cellular infiltrate of Chronic inflammation
Mononuclear cells (monocytes, macrophage, lymphocytes, plasma cells)
82
Resolution of inflammation
Healing
83
Healing stage: No destruction of normal tissues Offending agent is neutralized Vessels return to their normal permeability state Excess fluids is reabsorbed Clearance of mediators and inflammatory cells
Simple resolution
84
Healing stages:
Resolution Regeneration Replacement by connective tissue scar
85
Replacement of loss or necrotic or tissues with a new tissue that is similar to those that were destroyed
Regeneration
86
Death of the entire body
Somatic Death
87
Changes that can be observed immediately after somatic death
Primary changes
88
Primary changes in somatic death
1)CNS/Nervous failure 2)Respiratory failure 3)Cardiac failure
89
Changes that can be noted/observed few hours after death
Secondary changes
90
cooling of the body after death
Algor mortis
91
Algor mortis happens at a rate of
7 degF/hour
92
Helps establish time of death Faster in cooling in: cold weather, lean malnourished Delayed cooling in infectious disease followed by increase in temperature
Algor mortis
93
stiffening of the body
Rigor mortis
94
Rigor mortis starts ___ following death
2-3 hours
95
Rigor mortis completes in ___
6-8 hours
96
Rigor mortis remains _____ hours and persists for ____ days
12-36 hours 3-4 days
97
Rigor mortis hasten stiffness in:
warm environment and in infants
98
Delay of rigor mortis:
cold temperature and obese individuals
99
Postmortem hemolysis
Livor motis
100
Purplish discoloration of skin Sinking of fluid blood into capillaries of the dependent body parts
Livor mortis
101
Importance of livor mortis
determine if body position has changed at the scene of death
102
Occurs slowly or immediately after death
Post mortem clotting
103
due to the release of hydrolytic enzymes
autolysis
104
Rotting and decomposition by bacterial action
Putrefaction
105
Refers to the drying and wrinkling of cornea and anterior chamber
Dessication
106
Involves examination of a dead body
Autopsy/Necropsy
107
Main purpose of autopsy
determine cause of death
108
Important requirement to do autopsy
consent from the nearest kin
109
Types of autopsy as to purpose
1)Routine Hospital Autopsy 2)Medico Legal Autopsy - carried by govt. Agencies
110
Type of autopsy as to completeness of procedure:
1)Complete autopsy - from head to foot 2)Partial autopsy - examines the region of the body
111
Types as to manner of incision:
Y-shaped incision Straight incision
112
Type of incision: cadaver is opened from shoulders down from xiphoid area and incised down to pubis
Y-shaped incision
113
Incision done in adult cadaver
Y-shaped incision
114
Type of incision: opened from the midline of the body from the suprasternal notch down to the pubis (for babies)
Straight cut
115
Autopsy technique: organs are removed one by one
Rudolf Virchow
116
Autopsy technique: Involves in-situ dissection (original place)
Carl Rokitansky
117
Autopsy Technique: Involves en-bloc (by system) removal of organs
Anthon Ghon
118
Type of autopsy: Organs are removed “en masses” - all at the same time
M. Letulle
119
Advantage: Quick and Suitable for beginners Disadvantage: Causes loss of continuity
Virchow's method
120
Advantages: In infected bodies (HIV, Hepa B) Considered good in children Disadvantages: Difficult to perform
Rokitansky
121
Cervico-thoracic, abdominal, pelvic organs are removed in three blocks Neuronal system is removed as another block
Ghon's method
122
Advantage: Excellent preservation Handling organs easier Disadvantage: inter-relationships is difficult to study, if disease is extending to all blocks
Ghon's method
123
Advantage: inter-relationships are preserved body can be handed over quickly Disadvantage: Organs difficult to handle
Lettulle's method
124
Process of tumor formation Abnormal proliferation of cells New cells are produced which are functionless compared to a normal cell
Neoplasia
125
Removal of tumor cells
Biopsy
126
Types of tumor
Benign Malignant
127
Type of tumor Slowly growing mass Regular surface, capsulated, not attached to deep structures
Benign tumor
128
Type of tumor Rapidly growing mass Irregular surfaces, Non-capsulated attached to deep structures
Malignant tumor
129
Type of tumor Noninvasive to another organ or tissue No spread or metastasis
Benign tumor
130
Type of tumor Invasive to other organs Spread and metastasis
Malignant tumor
131
Type of tumor Well differentiated No recurrence after surgery
Benign tumor
132
Type of tumor Poorly differentiated, moderately, or well differentiated Recurrence after surgery
Malignant tumor
133
Type of tumor No bleeding in cut surfaces Named adding suffix -oma Slight pressure effect on the neighboring organ
Benign tumor
134
Type of tumor Bleeding from cut Named by adding suffix sarcoma or carcinoma Remarkable pressure effect on neighboring tissue
Malignant tumor
135
Gradings of tumor: Different cells
normal cells
136
Gradings of tumor abnormal cells
undifferentiated cells
137
Value of grading
Guide for treatment Prognostic guide
138
Broder's classification Grade I
Differentiated cells: 100-75% Undifferentiated cells: 0-25%
139
Broder's Classification Grade II
Differentiated cells: 75-50% Undifferentiated cells: 25%-50%
140
Broder's classification Grade III
Differentiated cells: 50-25% Undifferentiated cells: 50-75%
141
Broder's classification Grade IV
Differentiated cells: 25-0% Undifferentiated cells: 75-100%
142
Tumors that are amenable to surgery (good prognosis)
Lower grade tumor
143
Tumors that requires radical treatment (chemotherapy, radiation) (poor prognosis)
High grade tumor
144
Used to determine the spread of cancer in a patient Based on the size of primary lesions, extent of spread to regional lymph nodes and presence or absence of metastases
Staging of tumor
145
TMN Classification T N M
T- size of tumor N - No. of lymph nodes involved M- Presence or absence of metastasis
146
Tumor: Unable to assess primary tumor
Tx
147
Tumor: There is no evidence of primary lesions
T0
148
Tumor: There is no evidence of primary lesions
T0
149
Tumor: Carcinoma in situ
Tis
150
Tumor: Tuor penetrates submucosa and mucosa
T1
151
Tumor: The tumor invades but fails to penetrate the muscle layer
T2
152
Tumor: The tumor penetrates the subserosa
T3
153
Tumor: Tumors penetrates deep into the peritoneum or other organs
T4
154
N: Lymph node Unable to assess lymph node involvement
Nx
155
N Lymph node No lymph node involvement
N0
156
N lymph node There is metastasis in perirectal nodes around one to three
N1
157
N lymph nodes There is metastasis of four or more perirectal nodes
N2
158
Metastasis Unable to assess distant metastasis
Mx
159
Metastasis There is no distant metastasis
M0
160
Metastasis There is distant metastasis
M1
161
Stage IA Tumor - Node - Metastasis - Grade
T1a, T1b N0 M0 G1,2
162
Stage IB Tumor - Node - Metastasis - Grade
T2a, N0, M0, G1,2
163
Stage IIA Tumor - Node - Metastasis - Grade
T2b, N0, M0, G1, 2
164
Stage IIB Tumor - Node - Metastasis - Grade
T1a, N0, M0, G3,4
165
Stage IIC Tumor - Node - Metastasis - Grade
T2a, N0, M0, G3, 4
166
Stage III Tumor - Node - Metastasis - Grade
T2b, N0, M0, G3,4
167
Stage IV Tumor - Node - Metastasis - Grade
Any T, N1 (any N), M0 (M1), Any G
168
Tumor size T-1
0-2 centimeters
169
Tumor Size T2
2-5 centimeters
170
Tumor size T3
>5 centimeters
171
Tumor size: T4
Tumor has broken through skin or attached to cell wall
172
Lymph node status N-0
Surgeon can't feel any nodes
173
Lymph nodes N-1
Surgeon can feel swollen nodes
174
Lymph nodes N-2
Nodes feel swollen and lumpy
175
Lymph node status N3
Swollen nodes located near collarbone
176
Metastasis: M-0
Tested nodes are cancer free
177
Metastasis M1
Tested nodes show cancer cells or micrometastasis
178
Identification of tissue or cellular antigens or phenotypic markers (found in tissues)
Immunohistochemistry
179
Make use of antigen antibody reactions by directly labelling of the antibody or by means of secondary labelling method
Immunohistochemistry
180
Most commonly used antibody used in IHC
IgG
181
Antibodies produced by different cells Can react with various epitopes (reacts with antibodies)
Polyclonal
182
Polyclonal antibody source
goats, pigs, sheep laboratory animals
183
More specific antibodies produced from individual clones of plasma cells
Monoclonal
184
Produces one type of antibody can react only with one specific type of epitope
Monoclonal
185
Animal source of monoclonal antibodies
mice
186
To detect antigens, antibodies must be
labeled
187
Most common enzyme for antigen retrieval
Horse Radish Peroxidase
188
Color developer for labeling antibodies
chromogen
189
Most common method for antigen retrieval
Enzyme
190
Diamino benzedene (DAB) color
brown
191
AEC - 3-amino-9ethylcarbazole color
brick red
192
Traditional counterstain for enzyme
hematoxylin
193
Alternative phosphatase for horse radish peroxidase
alkaline phosphatase
194
Optimum incubation time to link antibody with enzyme peroxidase
60 mins at Room temperature
195
Fluorochrome label dye used for fluorescence microscope
FITC - Fluorescein isothiocyanate
196
Plant or animal proteins which can bind to tissue carbohydrate Can also be used to detect antigens, can also be labelled like antibodies
Lectins
197
Cryostat frozen sections and fixed in a few seconds using
absolute methanol or acetone
198
Purpose of cryostat frozen sections
To prevent destruction of labile antigenic sites To preserve position of antigens
199
Processed specimens (antigen retrieval) specimens
Formalin fixed Paraffin embedded
200
Methods of antigen retrieval from processed tissues
1)Proteolytic enzyme retrieval (PIER) 2)Microwave antigen retrieval/ Heat Induced Epitope retrieval 3)Pressure cooking antigen retrieval 4)Autoclave heating 5)Waterbath heating 6)Steamer heating 7)Decloaker heating 8)Combination of microwave and enzyme digestion
201
Commonly used enzyme in proteolytic enzyme retrieval
trypsin and protease
202
Microwave antigen retrieval/ Heat Induced Epitope retrieval duration
20 minutes
203
Waterbath heating temperature
90 deg C or 95-98 deg C
204
control: tissue section with antigen being detected
positive
205
Control: omit primary antibody from the staining schedule
negative
206
Internal tissue control a.k.a
built in control
207
Internal tissue control contains
target antigen
208
dissolution of nucleus
karyolysis