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MTAP 2 MIDTERMS > Histopathology > Flashcards

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
Q

Hyperplasia:

Happens in response to the need increase in uterus, breast during pregnancy.

Increase in breast size during puberty (glandular stimulation)

A

Physiologic Hyperplasia

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26
Q

Type of hyperplasia:

Erythroid bone marrow hyperplasia in people in high altitude

A

Physiologic hyperplasia

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27
Q

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

A

Pathologic

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28
Q

Occur frequently together with hypertrophy and can be triggered by the same mechanism

A

Compensatory

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29
Q

Involves transformation of adult cell type into another adult type (reversible process)

A

Metaplasia

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30
Q

Mesenchymal metaplasia involves:

A

Connective tissues

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31
Q

Original tissue:

Ciliated columnar epithelium of bronchi

Stimulus: Cigarette smoking

Metaplastic tissue:

A

Squamous epithelium

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32
Q

Original tissue:
Transitional epithelium of bladder

Stimulus:
Trauma of bladder

A

Squamous epithelium

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33
Q

Original tissue: Columnar glandular epithelium

Stimulus: Vitamin A deficiency

Metaplastic tissue:

A

Squamous epithelial cells

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34
Q

Original tissue: Esophageal squamous

Stimulus: Gastric acidity (too much drinking coffee)

Metaplastic tissue:

A

Columnar epithelium

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35
Q

Dysplasia is also known as

A

atypical metaplasia

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36
Q

Pre-neoplastic lesion
Change in cell size, shape, and orientation (reversible).
May lead to cancer but not necessarily

A

Dysplasia (atypical metaplasia)

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37
Q

dedifferentiation (irreversible) transformation of adult cells into embryonic/fetal cells

A

anaplasia

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38
Q

Causes of cell injury

A

Anoxia - lack of oxygen supply
Infectious agents
Mechanical agents/Trauma
Chemical Agents - carcinogens (chloroform, benzene)

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39
Q

No.1 cause of cell injury

A

Oxygen deprivation

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40
Q

Hypoxic cell injury for neuron is irreversible after (minutes)

A

3-5 minutes

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41
Q

Hypoxic cell injury in myocardial cells and hepatocytes is irreversible after (time)

A

1-2 hours

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42
Q

Skeletal muscle hypoxic injury is irreversible after (time)

A

many hours

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43
Q

Appearance of affected organs in gross change

A

Organ pallor (pale), Increased weight

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44
Q

Earliest change of tissue is seen

A

Microscopically

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45
Q

First manifestation of cellular change

A

cellular swelling

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46
Q

Irreversible changes

A

Enzymatic digestion of cells
Protein denaturation
Cytoplasmic changes
Nuclear changes

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47
Q

Cytoplasmic changes includes

A

Increased eosinophilia (pink/orange)
Large cells “cloudy swelling”

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48
Q

Irreversible nuclear changes

A

Pyknosis
Karyolysis
Karyorrhexis

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49
Q

condensation of nucleus

A

pyknosis

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50
Q

fragmentation/segmentation of nucleus

A

Karyorrhexis

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51
Q

Physiologic cell death

Programmed cell death

Death of single cell in a cluster of cells

A

Apoptosis

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52
Q

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

A

Apoptosis

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53
Q

Pathologic cell death

Accidental cell death
Cell swelling
Leakage of cellular components = Inflammation
Change in organ can be seen in gross

A

Necrosis

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54
Q

Type of Necrosis:

due to to sudden cut off of blood supply

A

Coagulative

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55
Q

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

A

Coagulative

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56
Q

Type of Necrosis:

On gross, affected organ appears liquefied, creamy yellow (increased pus)

A

Liquefactive

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57
Q

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

A

Liquefactive

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58
Q

Type of Necrosis:

On gross, tissue organ appears greasy resembling “cheese”

A

Caseous

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59
Q

Type of Necrosis:

Combination of coagulative and liquefactive

Usually seen in TB
Microscopically it appears as amorphous granular debri surrounded by granulomatous inflammation

A

Caseous (cheeselike)

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60
Q

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

A

Fibrinoid

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61
Q

Type of Necrosis:

Destruction of fat cells due to release of pancreatic lipases

A

Fat

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62
Q

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

A

Fat

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63
Q

Type of Necrosis:
necrosis secondary to a ischemia

Not a specific pattern of necrosis

A

Gangrenous

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64
Q

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

A

Gangrenous

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65
Q

due to venous occlusion, example of this is SUPPURATIVE BACTERIAL INFECTION

A

wet gangrene

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66
Q

due to arterial occlusion and example of this is FOOT EMBOLISM

A

Dry gangrene

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67
Q

Tissue reaction to injury

A

Inflammation

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68
Q

Goal of Inflammation:

A

1)To remove the initial cause of the injury

2)To remove the consequences of injury

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69
Q

Cardinal signs of inflammation

A

Dolor
Rubor
Calor
Tumor
Functio laesa

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70
Q

Cardinal sign of inflammation: pain

A

dolor

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71
Q

Cardinal sign of inflammation: redness due to increase blood flow

A

Rubor

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72
Q

Cardinal signs of inflammation: heat

A

Calor

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73
Q

Cardinal signs of inflammation: swelling

A

Tumor

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74
Q

Cardinal Signs of Inflammation: destruction of functioning units of the cell

A

Functio laesa

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75
Q

Type of inflammation:

rapid response to an injurious agent

A

acute inflammation

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76
Q

Hallmark sign of acute inflammation

A

Exudation: escape of fluid proteins, blood cells from the vascular system)

Edema: excess to fluid in interstitial tissues and cavities

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77
Q

escape of fluid proteins, blood cells from the vascular system)

A

Exudation

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78
Q

excess to fluid in interstitial tissues and cavities

A

Edema

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79
Q

Cellular infiltrate of acute inflammation

A

neutrophils

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80
Q

Prolonged duration of inflammation

A

Chronic inflammation

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81
Q

Cellular infiltrate of Chronic inflammation

A

Mononuclear cells (monocytes, macrophage, lymphocytes, plasma cells)

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82
Q

Resolution of inflammation

A

Healing

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83
Q

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

A

Simple resolution

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84
Q

Healing stages:

A

Resolution
Regeneration
Replacement by connective tissue scar

85
Q

Replacement of loss or necrotic or tissues with a new tissue that is similar to those that were destroyed

A

Regeneration

86
Q

Death of the entire body

A

Somatic Death

87
Q

Changes that can be observed immediately after somatic death

A

Primary changes

88
Q

Primary changes in somatic death

A

1)CNS/Nervous failure
2)Respiratory failure
3)Cardiac failure

89
Q

Changes that can be noted/observed few hours after death

A

Secondary changes

90
Q

cooling of the body after death

A

Algor mortis

91
Q

Algor mortis happens at a rate of

A

7 degF/hour

92
Q

Helps establish time of death

Faster in cooling in: cold weather, lean malnourished

Delayed cooling in infectious disease followed by increase in temperature

A

Algor mortis

93
Q

stiffening of the body

A

Rigor mortis

94
Q

Rigor mortis starts ___ following death

95
Q

Rigor mortis completes in ___

96
Q

Rigor mortis remains _____ hours and persists for ____ days

A

12-36 hours
3-4 days

97
Q

Rigor mortis hasten stiffness in:

A

warm environment and in infants

98
Q

Delay of rigor mortis:

A

cold temperature and obese individuals

99
Q

Postmortem hemolysis

A

Livor motis

100
Q

Purplish discoloration of skin

Sinking of fluid blood into capillaries of the dependent body parts

A

Livor mortis

101
Q

Importance of livor mortis

A

determine if body position has changed at the scene of death

102
Q

Occurs slowly or immediately after death

A

Post mortem clotting

103
Q

due to the release of hydrolytic enzymes

104
Q

Rotting and decomposition by bacterial action

A

Putrefaction

105
Q

Refers to the drying and wrinkling of cornea and anterior chamber

A

Dessication

106
Q

Involves examination of a dead body

A

Autopsy/Necropsy

107
Q

Main purpose of autopsy

A

determine cause of death

108
Q

Important requirement to do autopsy

A

consent from the nearest kin

109
Q

Types of autopsy as to purpose

A

1)Routine Hospital Autopsy

2)Medico Legal Autopsy - carried by govt. Agencies

110
Q

Type of autopsy as to completeness of procedure:

A

1)Complete autopsy - from head to foot

2)Partial autopsy - examines the region of the body

111
Q

Types as to manner of incision:

A

Y-shaped incision
Straight incision

112
Q

Type of incision:

cadaver is opened from shoulders down from xiphoid area and incised down to pubis

A

Y-shaped incision

113
Q

Incision done in adult cadaver

A

Y-shaped incision

114
Q

Type of incision:

opened from the midline of the body from the suprasternal notch down to the pubis (for babies)

A

Straight cut

115
Q

Autopsy technique:

organs are removed one by one

A

Rudolf Virchow

116
Q

Autopsy technique:

Involves in-situ dissection (original place)

A

Carl Rokitansky

117
Q

Autopsy Technique:

Involves en-bloc (by system) removal of organs

A

Anthon Ghon

118
Q

Type of autopsy:

Organs are removed “en masses” - all at the same time

A

M. Letulle

119
Q

Advantage: Quick and Suitable for beginners

Disadvantage: Causes loss of continuity

A

Virchow’s method

120
Q

Advantages:

In infected bodies (HIV, Hepa B)

Considered good in children

Disadvantages:

Difficult to perform

A

Rokitansky

121
Q

Cervico-thoracic, abdominal, pelvic organs are removed in three blocks

Neuronal system is removed as another block

A

Ghon’s method

122
Q

Advantage: Excellent preservation

Handling organs easier

Disadvantage:
inter-relationships is difficult to study, if disease is extending to all blocks

A

Ghon’s method

123
Q

Advantage: inter-relationships are preserved body can be handed over quickly

Disadvantage: Organs difficult to handle

A

Lettulle’s method

124
Q

Process of tumor formation

Abnormal proliferation of cells

New cells are produced which are functionless compared to a normal cell

125
Q

Removal of tumor cells

126
Q

Types of tumor

A

Benign
Malignant

127
Q

Type of tumor

Slowly growing mass

Regular surface, capsulated, not attached to deep structures

A

Benign tumor

128
Q

Type of tumor

Rapidly growing mass

Irregular surfaces, Non-capsulated attached to deep structures

A

Malignant tumor

129
Q

Type of tumor

Noninvasive to another organ or tissue

No spread or metastasis

A

Benign tumor

130
Q

Type of tumor

Invasive to other organs

Spread and metastasis

A

Malignant tumor

131
Q

Type of tumor

Well differentiated

No recurrence after surgery

A

Benign tumor

132
Q

Type of tumor

Poorly differentiated, moderately, or well differentiated

Recurrence after surgery

A

Malignant tumor

133
Q

Type of tumor

No bleeding in cut surfaces

Named adding suffix -oma

Slight pressure effect on the neighboring organ

A

Benign tumor

134
Q

Type of tumor

Bleeding from cut

Named by adding suffix sarcoma or carcinoma

Remarkable pressure effect on neighboring tissue

A

Malignant tumor

135
Q

Gradings of tumor:

Different cells

A

normal cells

136
Q

Gradings of tumor

abnormal cells

A

undifferentiated cells

137
Q

Value of grading

A

Guide for treatment
Prognostic guide

138
Q

Broder’s classification

Grade I

A

Differentiated cells: 100-75%

Undifferentiated cells: 0-25%

139
Q

Broder’s Classification

Grade II

A

Differentiated cells: 75-50%

Undifferentiated cells: 25%-50%

140
Q

Broder’s classification

Grade III

A

Differentiated cells: 50-25%

Undifferentiated cells: 50-75%

141
Q

Broder’s classification

Grade IV

A

Differentiated cells: 25-0%

Undifferentiated cells: 75-100%

142
Q

Tumors that are amenable to surgery (good prognosis)

A

Lower grade tumor

143
Q

Tumors that requires radical treatment (chemotherapy, radiation) (poor prognosis)

A

High grade tumor

144
Q

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

A

Staging of tumor

145
Q

TMN Classification

T
N
M

A

T- size of tumor
N - No. of lymph nodes involved
M- Presence or absence of metastasis

146
Q

Tumor:

Unable to assess primary tumor

147
Q

Tumor:

There is no evidence of primary lesions

148
Q

Tumor:

There is no evidence of primary lesions

149
Q

Tumor:

Carcinoma in situ

150
Q

Tumor:

Tuor penetrates submucosa and mucosa

151
Q

Tumor:

The tumor invades but fails to penetrate the muscle layer

152
Q

Tumor:

The tumor penetrates the subserosa

153
Q

Tumor:

Tumors penetrates deep into the peritoneum or other organs

154
Q

N: Lymph node

Unable to assess lymph node involvement

155
Q

N Lymph node

No lymph node involvement

156
Q

N lymph node

There is metastasis in perirectal nodes around one to three

157
Q

N lymph nodes

There is metastasis of four or more perirectal nodes

158
Q

Metastasis

Unable to assess distant metastasis

159
Q

Metastasis

There is no distant metastasis

160
Q

Metastasis

There is distant metastasis

161
Q

Stage IA

Tumor - Node - Metastasis - Grade

A

T1a, T1b
N0
M0
G1,2

162
Q

Stage IB

Tumor - Node - Metastasis - Grade

A

T2a, N0, M0, G1,2

163
Q

Stage IIA

Tumor - Node - Metastasis - Grade

A

T2b, N0, M0, G1, 2

164
Q

Stage IIB

Tumor - Node - Metastasis - Grade

A

T1a, N0, M0, G3,4

165
Q

Stage IIC

Tumor - Node - Metastasis - Grade

A

T2a, N0, M0, G3, 4

166
Q

Stage III

Tumor - Node - Metastasis - Grade

A

T2b, N0, M0, G3,4

167
Q

Stage IV

Tumor - Node - Metastasis - Grade

A

Any T, N1 (any N), M0 (M1), Any G

168
Q

Tumor size

T-1

A

0-2 centimeters

169
Q

Tumor Size

T2

A

2-5 centimeters

170
Q

Tumor size

T3

A

> 5 centimeters

171
Q

Tumor size:

T4

A

Tumor has broken through skin or attached to cell wall

172
Q

Lymph node status

N-0

A

Surgeon can’t feel any nodes

173
Q

Lymph nodes

N-1

A

Surgeon can feel swollen nodes

174
Q

Lymph nodes

N-2

A

Nodes feel swollen and lumpy

175
Q

Lymph node status

N3

A

Swollen nodes located near collarbone

176
Q

Metastasis:

M-0

A

Tested nodes are cancer free

177
Q

Metastasis

M1

A

Tested nodes show cancer cells or micrometastasis

178
Q

Identification of tissue or cellular antigens or phenotypic markers (found in tissues)

A

Immunohistochemistry

179
Q

Make use of antigen antibody reactions by directly labelling of the antibody or by means of secondary labelling method

A

Immunohistochemistry

180
Q

Most commonly used antibody used in IHC

181
Q

Antibodies produced by different cells

Can react with various epitopes (reacts with antibodies)

A

Polyclonal

182
Q

Polyclonal antibody source

A

goats, pigs, sheep

laboratory animals

183
Q

More specific antibodies produced from individual clones of plasma cells

A

Monoclonal

184
Q

Produces one type of antibody can react only with one specific type of epitope

A

Monoclonal

185
Q

Animal source of monoclonal antibodies

186
Q

To detect antigens, antibodies must be

187
Q

Most common enzyme for antigen retrieval

A

Horse Radish Peroxidase

188
Q

Color developer for labeling antibodies

189
Q

Most common method for antigen retrieval

190
Q

Diamino benzedene (DAB) color

191
Q

AEC - 3-amino-9ethylcarbazole color

192
Q

Traditional counterstain for enzyme

A

hematoxylin

193
Q

Alternative phosphatase for horse radish peroxidase

A

alkaline phosphatase

194
Q

Optimum incubation time to link antibody with enzyme peroxidase

A

60 mins at Room temperature

195
Q

Fluorochrome label dye used for fluorescence microscope

A

FITC - Fluorescein isothiocyanate

196
Q

Plant or animal proteins which can bind to tissue carbohydrate

Can also be used to detect antigens, can also be labelled like antibodies

197
Q

Cryostat frozen sections and fixed in a few seconds using

A

absolute methanol or acetone

198
Q

Purpose of cryostat frozen sections

A

To prevent destruction of labile antigenic sites

To preserve position of antigens

199
Q

Processed specimens (antigen retrieval) specimens

A

Formalin fixed
Paraffin embedded

200
Q

Methods of antigen retrieval from processed tissues

A

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
Q

Commonly used enzyme in proteolytic enzyme retrieval

A

trypsin and protease

202
Q

Microwave antigen retrieval/ Heat Induced Epitope retrieval duration

A

20 minutes

203
Q

Waterbath heating temperature

A

90 deg C or 95-98 deg C

204
Q

control:

tissue section with antigen being detected

205
Q

Control:

omit primary antibody from the staining schedule

206
Q

Internal tissue control a.k.a

A

built in control

207
Q

Internal tissue control contains

A

target antigen

208
Q

dissolution of nucleus

A

karyolysis

MTAP 2 MIDTERMS (4 decks)

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