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HISTOPATH 1 Flashcards

1
Q

study of all changes in cells, tissues, and organs that underlie a disease

A

Pathology

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2
Q

starting point in every disease process

A

Cells

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3
Q

3 CLASSES
OF CELLS

A

Labile
Stable
Permanent

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4
Q

Cells frequently dividing to replace lost body cells

A

LABILE CELL

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5
Q

Replaces majority of body cells due to their limited lifespan

A

LABILE CELL

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6
Q

example of LABILE cell

A

Epithelial cells of skin

Exception: cancer cells
(immortalized cells)

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7
Q

Cells not frequently dividing; only divides to replace injured cells

A

STABLE CELL

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8
Q

example of STABLE cell

A

Parenchymal cells of liver and kidneys

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9
Q

Cells that do not undergo replication upon maturation

A

PERMANENT CELL

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10
Q

example of PERMANENT cell

A

neurons (nerve cells)

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11
Q

4 ABNORMALITIES IN CELL GROWTH

A

Aplasia
Agenesia
Hypoplasia
Atresia

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12
Q

T/F

Young cells typically undergo maturation with interval in between. There could be abnormalities along the way before it reaches maturation

A

TRUE

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13
Q

Incomplete/defective development of tissue/organ

A

Aplasia

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14
Q

abnormalities in cell growth wherein the affected organ shows no resemblance to the normal mature structure

A

Aplasia

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15
Q

abnormalities in cell growth that usually occur in PAIRED ORGANS (KIDNEYS, GONADS)

A

Aplasia

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16
Q

Complete non-appearance of organ

A

Agenesia

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17
Q

Failure of tissue/organ to reach normal mature adult size

A

Hypoplasia

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18
Q

Failure of organ to form an opening

A

Atresia

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19
Q

Imperforate anus and microtia (absence of ear canal) are both abnormalities in cell growth called as

A

Atresia

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20
Q

T/F

Body cells may be exposed to stressful stimuli. Under normal condition, cells will able to adapt (through several adaptation mechanisms). If exposure to stressful stimuli is prolonged and the degree of stress is severe, cells will fail to adapt which can cause injury (reversible or irreversible).

A

TRUE

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21
Q

6 CELLULAR ADAPTATION MECHANISMS

A

Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
Anaplasia

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22
Q

Acquired decrease in tissue/organ size

A

Atrophy

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23
Q

Normal decrease in tissue/organ size as a consequence of maturation

A

Physiologic atrophy

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24
Q

Decrease
in tissue/organ size is associated
with a disease

A

Pathologic atrophy

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25
Q

State the cellular adaptation mechanism:

Thymus at puberty

A

PHYSIOLOGIC atrophy

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26
Q

State the cellular adaptation mechanism:

Decrease in uterus size after birth

A

PHYSIOLOGIC atrophy

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27
Q

TYPES OF PATHOLOGIC ATROPHY

A

“HE VAPE”

Hunger/starvation atrophy
Exhaustion atrophy
Vascular atrophy
Atrophy of disuse
Pressure atrophy
Endocrine atrophy

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28
Q

Decreased tissue/organ size if blood supply to an organ becomes reduced/below critical level

A

Vascular atrophy

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29
Q

Decreased tissue/organ size due to persistent pressure on the organ or tissue that may directly injure the cell or may secondarily promote diminution of blood supply (vascular atrophy)

A

Pressure atrophy

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30
Q

A correlated types of PATHOLOGIC ATROPHY

A

Pressure atrophy
Vascular atrophy

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31
Q

Decreased tissue/organ size due to lack of hormones needed to maintain normal size and structure

A

Endocrine atrophy

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32
Q

Decreased tissue/organ size due to lack of nutritional supply to sustain normal growth

A

Hunger/starvation atrophy

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33
Q

Too much workload, causing general wasting of tissues – leading to decreased tissue/organ size

A

Exhaustion atrophy

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34
Q

Inactivity/diminished activity or function causing decreased tissue/organ size

A

Atrophy of disuse

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35
Q

Increase in tissue/organ size due to increase in cell size making up the organ

A

Hypertrophy

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36
Q

Increase in tissue/organ size but NO NEW CELLS PRODUCED

A

Hypertrophy

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37
Q

Increase in tissue/organ size due to increase in cell number making up the organ

A

Hyperplasia

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38
Q

Increase in tissue/organ size; NEW CELLS PRODUCED

A

Hyperplasia

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39
Q

Reversible type of hypertrophy

A

Physiologic Hypertrophy

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40
Q

Normal increase in tissue/organ size due to increased cell size
Reversible

A

Physiologic
Hypertrophy

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41
Q

Increased tissue/organ size due to increased cell size caused by a disease

A

Pathologic
Hypertrophy

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42
Q

Increased cell size as a response to a deficiency

A

Compensatory
hypertrophy

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43
Q

Increase in tissue/organ size when one of the paired organs is removed

A

Compensatory
hypertrophy

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44
Q

State the cellular adaptation mechanism:

Bulging of skeletal muscles due to frequent exercise

A

Physiologic
Hypertrophy

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45
Q

State the cellular adaptation mechanism; also state the reason for its occurrence:

Increased size of myocardium (heart muscle)

A

Pathologic
Hypertrophy

due to HTN or aortic valve disease

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46
Q

cellular adaptation mechanism that may occur if a patient is experiencing hypertension or aortic valve dse

A

Pathologic
Hypertrophy

(inc. size of myocardium)

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47
Q

cellular adaptation mechanism that may occur if an individual is consistently exercising

A

Physiologic
Hypertrophy

(bulging of skeletal muscles)

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48
Q

State the cellular adaptation mechanism:

Enlargement of one kidney (renal)

A

Compensatory hypertrophy
(occur when one of the kidney is removed)

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49
Q

Normal increase in cell no.

Happens in response to a need

A

Physiologic
hyperplasia

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50
Q

Abnormal increase in cell no.

A

Pathologic
hyperplasia

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51
Q

T/F

If there is a compensatory hypertrophy, there is also compensatory hyperplasia.

A

TRUE!!

Hypertrophy and hyperplasia are two different processes but usually occur together. Triggered by the same stimulus.

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52
Q

State the cellular adaptation mechanism:

↑ breast & uterus size during pregnancy

A

Physiologic
hyperplasia

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53
Q

State the cellular adaptation mechanism:

↑ breast size during puberty due to glandular stimulation

A

Physiologic
hyperplasia

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54
Q

State the cellular adaptation mechanism:

Erythroid bone marrow hyperplasia (red cell precursor/immature RBCs in the bone marrow may undergo an ↑ in size, usually in individuals living in high altitude)

A

Physiologic
hyperplasia

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55
Q

what cellular adaptation mechanism that usually occur in individuals living in high altitude

A

Physiologic hyperplasia

(reversible if they transfer to low altitude)

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56
Q

State the cellular adaptation mechanism:

Graves disease

A

Pathologic
hyperplasia

*Graves disease is also described as diffuse crowding of epithelial cells

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57
Q

State the cellular adaptation mechanism:

Endometriosis due to inc. estrogen

A

Pathologic
hyperplasia

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58
Q

State the cellular adaptation mechanism:

TB of cervical lymph nodes (↑ no. of lymph nodules)

A

Pathologic
hyperplasia

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59
Q

Involves transformation of adult cell type into another adult cell type

REVERSIBLE

A

Metaplasia

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60
Q

2 types of metaplasia

A

Epithelial Metaplasia
Mesenchymal Metaplasia

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61
Q

Cells involved in transformation from adult cell type to another adult cell type are epithelial cells

A

Epithelial Metaplasia

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62
Q

Cells involved in transformation from adult cell type to another adult cell type are connective tissue cells

A

Mesenchymal Metaplasia

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63
Q

Original tissue: Ciliated columnar epithelium of bronchi

Stimulus: ?
Metaplastic tissue: ?

A

Stimulus: Cigarette smoking
Metaplastic tissue: Squamous epithelium

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64
Q

Original tissue: Transitional epithelium of bladder

Stimulus: ?
Metaplastic tissue: ?

A

Stimulus: Bladder trauma
Metaplastic tissue: Squamous epithelium

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65
Q

Original tissue: Columnar glandular epithelium

Stimulus: ?
Metaplastic tissue: ?

A

Stimulus: Vit K deficiency
Metaplastic tissue: Squamous epithelium

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66
Q

Original tissue: Esophageal squamous epithelium

Stimulus: ?
Metaplastic tissue: ?

A

Stimulus: Gastric acidity (triggered by excessive coffee
Metaplastic tissue: Columnar epithelium

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67
Q

What is the affected tissue when a person is a persistent cigarette smoker? What will be the resulting metaplastic tissue?

A

Ciliated columnar epithelium of bronchi –> Squamous epithelium

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68
Q

What is the affected tissue when a person experienced a bladder trauma? What will be the resulting metaplastic tissue?

A

Transitional epithelium of bladder –> Squamous epithelium

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69
Q

What is the affected tissue when a person has Vit K deficiency? What will be the resulting metaplastic tissue?

A

Columnar glandular epithelium –> Squamous epithelium

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70
Q

What is the affected tissue when a person consumes excessive coffee causing gastric acidity? What will be the resulting metaplastic tissue?

A

Esophageal squamous epithelium –> Columnar epithelium

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71
Q

aka Dysplasia

A

Atypical metaplasia/
Pre-neoplastic lesion

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72
Q

aka Anaplasia

A

Dedifferentiation

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73
Q

No transformation; only change in cell size, shape, & orientation (cell arrangement)

May lead to cancer, but not necessarily

A

Dysplasia

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74
Q

Dysplasia: reversible or irreversible?

A

Reversible

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75
Q

Anaplasia: reversible or irreversible?

A

Irreversible

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76
Q

With transformation of adult cells into embryonic or fetal cells (young)

A

Anaplasia

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77
Q

T/F

Neoplasia is also considered as a cellular adaptation mechanism

A

FALSE

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78
Q

Causes of cell injury

A

Anoxia
Infectious agents
Mechanical agents
Chemical agents

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79
Q

No. 1 cause of cell injury

A

Anoxia (O2 deprivation) - can also lead to cell death

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80
Q

Type of injury wherein the affected cell may recover

A

Reversible Injury

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81
Q

Type of injury wherein the affected cell will never recover (further undergo cell death); considered as a point of no return

A

Irreversible injury

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82
Q

Duration for a hypoxic injury to be IRREVERSIBLE in neurons

A

3-5 minutes

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83
Q

Duration for a hypoxic injury to be IRREVERSIBLE in myocardial cells and hepatocytes

A

1-2 hours

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84
Q

Duration for a hypoxic injury to be IRREVERSIBLE in skeletal muscles

A

many hours

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85
Q

Gross changes that can be observed to assume that the cell injury is still REVERSIBLE

A
  1. Organ pallor/pale
  2. Increased organ weight
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86
Q

Earliest microscopic changes to assume that the cell injury is still REVERSIBLE

A
  1. Cellular swelling (reason for inc. wt) – 1st to occur
  2. Fatty degeneration
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87
Q

IRREVERSIBLE INJURY changes are due to

A

Enzymatic digestion of cells
Protein denaturation

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88
Q

To determine that the cell injury is IRREVERSIBLE, these cell parts are observed

A

Cytoplasm
Nucleus

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89
Q

Cytoplasmic changes in irreversible injury

A
  1. Larger cells “cloudy swelling”
  2. ↑ eosinophilia (orange or bright pink cytoplasm)
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90
Q

Nuclear changes in
irreversible injury

A
  1. Pyknosis – nuclear condensation (small nucleus)
  2. Karyorrhexis – nuclear fragmentation/segmentation
  3. Karyolysis – dissolution of nucleus
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91
Q

ending of irreversible injury

A

CELL DEATH

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92
Q

PATTERNS OF CELL DEATH

A

Apoptosis
Necrosis

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93
Q

Physiologic (programmed) cell death

A

Apoptosis

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94
Q

Normal cell death for all cells except for permanent cells (neuron)

A

Apoptosis

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95
Q

Death of single cell in a cluster of cells

A

Apoptosis

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96
Q

Course of events in APOPTOSIS

A

Cell shrinkage →
Intact membrane integrity →
No leakage of cellular components →
NO INFLAMMATION

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97
Q

Course of events in NECROSIS

A

Cell swelling →
Non-intact membrane →
Leakage of cellular components →
INFLAMMATION

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98
Q

Pathologic (accidental) cell death

A

Necrosis

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99
Q

5 Chief morphologic features in apoptosis

A
  1. Chromatid condensation
  2. Chromatid fragmentation
  3. Cell shrinkage
  4. Cytoplasmic bleb formation
  5. Phagocytosis of apoptotic cells – removed by neighboring cells
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100
Q

TYPES OF NECROSIS

A

Coagulative
Liquefactive
Caseous
Fibrinoid
Fat
Gangrenous

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101
Q

Necrosis due to sudden cut off of blood supply (O2)/ischemia

A

Coagulative
necrosis

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102
Q

Hydrolytic enzymes’ action is blocked (lysozyme released upon cell death) in this type of necrosis

A

Coagulative
necrosis

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103
Q

MICROSCOPIC APPEARANCE of coagulative necrosis

A

Preserved cell
outline, empty
(ghostly)

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104
Q

GROSS APPEARANCE of coagulative necrosis

A

Somewhat firm,
boiled-like
material

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105
Q

Coagulative necrosis is usually common in these organs

A

Solid organs (liver, kidneys, myocardial infarct)

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106
Q

Softening of organs due to action of hydrolytic enzymes

A

Liquefactive
necrosis

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107
Q

Complete digestion of cells

A

Liquefactive
necrosis

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108
Q

GROSS APPEARANCE of liquefactive necrosis

A

Soft, liquefied, creamy yellow

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109
Q

Liquefactive necrosis usually occur in these conditions

A

Brain infarct

Suppurative bacterial infection

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110
Q

Coagulative + Liquefactive

A

Caseous
necrosis

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111
Q

cheese-like

A

Caseous
necrosis

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112
Q

MICROSCOPIC APPEARANCE of caseous necrosis

A

Amorphous granular debri surrounded by granulomatous inflammation

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113
Q

GROSS APPEARANCE of caseous necrosis

A

Greasy
resembling
“cheese”

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114
Q

Caseous necrosis is usually seen in these condition

A

TB

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115
Q

Fibrin deposition in vessel wall

A

Fibrinoid
Necrosis

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116
Q

MICROSCOPIC APPEARANCE of Fibrinoid Necrosis

A

Thickened blood vessels

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117
Q

GROSS APPEARANCE of Fibrinoid Necrosis

A

NO GROSS changes!!!

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118
Q

Fibrinoid necrosis usually occur in this condition

A

Immune reactions of the blood vessels

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119
Q

Destruction of fat cells due to release of pancreatic lipases

Death of fat tissues (adipose cells) due to blood supply loss

A

Fat Necrosis

120
Q

MICROSCOPIC APPEARANCE of Fat Necrosis

A

Infiltrates of foamy macrophage adjacent to adipose tissues

121
Q

GROSS APPEARANCE of Fat Necrosis

A

Chalky white precipitates

122
Q

Fat necrosis usually occur in these condition

A

pancreatitis

123
Q

Fat necrosis usually affect this organ

124
Q

Necrosis secondary to ischemia

A

Gangrenous
necrosis

125
Q

NOT a specific pattern of necrosis

A

Gangrenous
necrosis

126
Q

usually refer to a limb/lower extremity that has interrupted blood supply

A

Gangrenous

127
Q

GROSS APPEARANCE of gangrenous necrosis

A

Skin is dry, black, and observed in various stages of decomp.

128
Q

gangrene due to venous occlusion

A

Wet gangrene

129
Q

gangrene due to arterial occlusion

A

Dry gangrene

130
Q

type of gangrene:
foot embolism

A

DRY gangrene

131
Q

type of gangrene:
suppurative bacterial infection

A

WET gangrene

132
Q

Immediate tissue reaction to injury

A

INFLAMMATION

133
Q

Ultimate goal of INFLAMMATION

A
  1. To remove the initial cause of injury
  2. To remove consequences of injury
134
Q

5 Cardinal signs

A

rubor (redness)
calor (warmth/heat)
tumor (swelling)
dolor (pain)
functio laesa (loss of function/destruction of functioning units of the cell)

135
Q

cardinal sign: pain

136
Q

cardinal sign: redness

137
Q

cardinal sign: heat

138
Q

cardinal sign: swelling

139
Q

cardinal sign: destruction of functioning units of the cell/loss of function

A

FUNCTIO LAESA

140
Q

Rapid response to an injurious agent
May progress to chronic inflammation if it fails to subside in several weeks

A

Acute
Inflammation

141
Q

Hallmark signs of an acute inflammation

A

Exudation
Edema

142
Q

escape of fluid, proteins, & blood cells from vascular system

143
Q

excess fluid in interstitial tissues and serous cavities

144
Q

Cellular infiltrate in acute inflammation

A

NEUTROPHILS

145
Q

Inflammation of prolonged duration
Occur from nonresolution of acute inflammation

A

Chronic
inflammation

146
Q

Cellular infiltrate in chronic inflammation

A

MONONUCLEAR CELLS (macrophage, lymphocytes, plasma cells)

147
Q

RESOLUTION OF INFLAMMATION

148
Q

TYPES OF HEALING

A

• Simple resolution
• Regeneration
• Replacement by a connective tissue scar

149
Q
  • No destruction of normal tissues
  • Offending agent is neutralized
  • Vessels return to their normal permeability state
  • Excess fluid (edema) is reabsorbed
  • Clearance of mediators and inflammatory cells
A

Simple resolution

150
Q

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

A

Regeneration

151
Q

Replacement of loss/necrotic tissues with a new tissue that is not that
similar to those that were destroyed

A

Replacement by a connective tissue scar

152
Q

Death of the entire body

A

SOMATIC DEATH

153
Q

Changes that can be observed immediately after death

A

Primary changes

154
Q

Primary changes in somatic death

A
  1. CNS failure
  2. Respiratory failure
  3. Cardiac failure
155
Q

Changes that can be observed few hours after death

A

Secondary changes

156
Q

Secondary changes in somatic death

A
  1. Algor mortis
  2. Rigor mortis
  3. Livor mortis
  4. Post mortem clotting
  5. Autolysis
  6. Putrefaction
  7. Desiccation
157
Q

cooling of the body

A

Algor mortis

158
Q

stiffening of the body

A

Rigor mortis

159
Q

post mortem
hemolysis

A

Livor mortis

160
Q

Used to establish time of death

A

Algor mortis
(cooling of the body)

161
Q

Algor mortis (cooling of the body) happens at a rate of _____

A

70ºF/hour

162
Q

Algor mortis (cooling of the body) is FASTER in:

A

cold weather
lean malnourished individuals

163
Q

Algor mortis (cooling of the body) is DELAYED in:

A

infectious diseases followed by ↑ temp.

164
Q

Rigor mortis (stiffening of the body) STARTS ____ after death

165
Q

Rigor mortis (stiffening of the body) COMPLETES at ____ after death

166
Q

Rigor mortis (stiffening of the body) STIFFNESS REMAINS for ____ after death

A

12-36 hours,
persist for 3-4 days

167
Q

Hasten rigor mortis (stiffness):

A

warm environment
in infants

168
Q

Delays rigor mortis (stiffness):

A

cold temperature
obese individuals

169
Q

Purplish discoloration of the skin

A

Livor mortis (post mortem hemolysis)

170
Q

Sinking of fluid blood into capillaries of dependent body part

A

Livor mortis (post mortem hemolysis)

171
Q

Determine if body position has changed at the scene of death

A

Livor mortis (post mortem hemolysis)

172
Q

Occur slowly or immediately after death
Settling and separation of RBCs from the fluid phase

A

Post mortem clotting

173
Q

Cell destruction due to the release of hydrolytic enzymes

174
Q

Rotting and decomposition by bacterial action

A

Putrefaction

175
Q

Drying and wrinkling of cornea and anterior chamber

A

Desiccation

176
Q

examination of a dead body (NOT mandatory)

A

AUTOPSY/NECROPSY

177
Q

aka AUTOPSY

178
Q

Main purpose of autopsy/necropsy

A

To determine cause of death

179
Q

Most important requirement before performing autopsy/necropsy

A

Consent from the nearest kin

180
Q

Autopsy types as to PURPOSE

A

Routine Hospital Autopsy – performed in hospital

Medico Legal Autopsy – performed by government agencies

181
Q

Autopsy types as to COMPLETENESS OF PROCEDURE

A

Complete autopsy – examine the body from head to foot

Partial autopsy – examine only a few regions of the body

182
Q

Autopsy types as to the MANNER OF INCISION

A

Y-shaped incision
Straight cut incision

183
Q

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

A

Y-shaped incision

184
Q

manner of incision usually done in adult cadaver

A

Y-shaped incision

185
Q

manner of incision usually done in children/infant cadaver

A

Straight cut incision

186
Q

cadaver is opened from the midline of the body from the suprasternal notch down to the pubis

A

Straight cut incision

187
Q

4 AUTOPSY TECHNIQUES by:

A

Rudolf Virchow
Carl Rokitansky
Anton Ghon
Maurice Lettulle

188
Q

Father of pathology

A

Rudolf Virchow

189
Q

Organs are removed separately one by one, studied individually

A

technique by Rudolf Virchow

190
Q

Cranial cavity →
thoracic cavity →
cervical region →
abdominal cavity

A

technique by Rudolf Virchow

191
Q

Autopsy technique is quick and suitable for beginners (advantage)

A

technique by Rudolf Virchow

192
Q

Autopsy technique that causes loss of continuity (disadvantage)

A

technique by Rudolf Virchow

193
Q

“In-situ” dissection (no removal, dissection in original place), combined with en bloc removal

A

technique by Carl Rokitansky

194
Q

advantage:

  • Infected bodies
    (HIV, hepa B)
  • Good in children
A

technique by Carl Rokitansky

195
Q

disadvantage:
* Difficult to perform

A

technique by Carl Rokitansky

196
Q

“En-bloc” removal of organs (removal of organs that belong to the same system)

A

technique by Anton Ghon

197
Q

Cervico-thoracic, abdominal, pelvic organs are removed in 3 blocks

Neuronal system is removed as another block

A

technique by Anton Ghon

198
Q

Advantage:
* Excellent preservation
* Handling of organs easier

A

technique by Anton Ghon

199
Q

Disadvantage:
* Interrelationships are difficult to study; if disease is extending to all blocks

A

technique by Anton Ghon

200
Q

“En masses” method
All organs are removed en masse and dissected as organ block

A

technique by Maurice Lettulle

201
Q

Advantage:
* Organs interrelationships are preserved
* Body can be handed over quickly

A

technique by Maurice Lettulle

202
Q

Disadvantage:
* Organs difficult to handle

A

technique by Maurice Lettulle

203
Q

Process of tumor formation (abnormal proliferation of cells)

204
Q

New cells are produced but functionless and immortalized

205
Q

Practical remedy for NEOPLASIA

A

surgical removal of tumor → biopsy (to determine if benign or malignant)

206
Q

PARTS OF TUMOR

A
  1. Parenchyma
  2. Stroma
207
Q

neoplastic cells

A

Parenchyma

208
Q

connective tissue framework; supplies blood supply to tumor → proliferation

209
Q

Types of tumor as to CAPACITY TO CAUSE DEATH

A

BENIGN TUMORS
MALIGNANT TUMORS

210
Q

Slowly growing mass

A

BENIGN TUMORS

211
Q

Rapidly growing mass

A

MALIGNANT TUMORS

212
Q

Regular surface, capsulated, not
attached to deep structures

A

BENIGN TUMORS

213
Q

type of tumor with irregular surface, non-capsulated, attached to deep surfaces

A

MALIGNANT TUMORS

214
Q

Type of tumor noninvasive to another organ/tissues

A

BENIGN TUMORS

215
Q

Invasive to other organs

A

MALIGNANT TUMORS

216
Q

No spread or metastasis

A

BENIGN TUMORS

217
Q

Spread and metastasis

A

MALIGNANT TUMORS

218
Q

Well differentiated tumor

A

BENIGN TUMORS

219
Q

Type of tumor that may be poorly differentiated, moderately or well differentiated

A

MALIGNANT TUMORS

220
Q

tumor with NO recurrence after surgery

A

BENIGN TUMORS

221
Q

Type of tumor with recurrence after surgery

A

MALIGNANT TUMORS

222
Q

Tumor: No bleeding in cut surfaces

A

BENIGN TUMORS

223
Q

Tumor: Bleeding from cut surfaces is common

A

MALIGNANT TUMORS

224
Q

Named by adding suffix “-oma”

A

BENIGN TUMORS

225
Q

Named by adding suffix
“sarcoma” or “carcinoma”

A

MALIGNANT TUMORS

226
Q

Type of tumor with slight pressure effect on the
neighboring organ

A

BENIGN TUMORS

227
Q

Type of tumor with remarkable pressure effect on neighboring tissue

A

MALIGNANT TUMORS

228
Q

PURPOSE of grading tumor

A

To determine the percentage of differentiated and undifferentiated cells

229
Q

Differentiated cells

A

Normal cells

230
Q

Undifferentiated cells

A

Abnormal/neoplastic cells

231
Q

Value of grading

A
  1. Guide for treatment
  2. Prognostic guide
232
Q

Characteristics of cancerous cells:

A
  1. Many cells continue to grow and divide
  2. Variations in cell size and shape
  3. Nucleus is larger and darker than normal
  4. Abnormal no. of chromosomes arranged in a disorganized fashion
  5. Cluster of cells without a boundary
233
Q

Used to grade tumor

A

BRODER’S CLASSIFICATION

234
Q

Differentiated cells: 100-75%

Undifferentiated cells: 0-25%

235
Q

Differentiated cells: 75-50%

Undifferentiated cells: 25-50%

236
Q

Differentiated cells: 50-25%

Undifferentiated cells: 50-75%

237
Q

Differentiated cells: 25-0%

Undifferentiated cells: 75-100%

238
Q

prognosis of tumor with LOWER grades

A

GOOD prognosis
amenable to surgery

239
Q

prognosis of tumor with HIGHER grades

A

POOR prognosis
requires radical tx (chemo, rad)

240
Q

Purpose of staging tumors

A

To determine the spread of cancer

Based on the size of primary lesions, extent of spread to regional lymph nodes and presence or absence of metastases

241
Q

Used to STAGE tumors

A

TNM classification

T = Size of tumor
N = Number of lymph nodes involved
M = Presence/absence of metastasis

243
Q

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

A

Immunohistochemistry

244
Q

Purpose of IHC

A

Identification of tissue or cellular antigens or phenotypic markers

245
Q

In IHC, detected in cells is ____.

246
Q

Used as detector in IHC

A

Antibodies

247
Q

Most common form of antibody used in IHC

248
Q

Antibodies produced by different cells

A

Polyclonal Ab

249
Q

React with various epitopes (part of antigen that reacts with an antibody)

A

Polyclonal Ab

250
Q

May be obtained from laboratory animal sources

A

Polyclonal Ab

251
Q

Main source of Polyclonal Ab

A

Rabbits (immunized to produced Abs)

252
Q

Other sources of Polyclonal Ab

A

Goat
Pig
Sheep

253
Q

Produced from individual clone of plasma cells – MORE SPECIFIC

A

Monoclonal Ab

254
Q

Produces only 1 type of antibody and reacts with 1 specific type of epitope

A

Monoclonal Ab

255
Q

Animal source of Monoclonal Ab

256
Q

Used in labeling antibodies

A

Enzymes
Fluorochrome label
Radioisotopes
Colloidal metal/gold
Lectins

257
Q

most widely used enzyme for labeling Ab

A

Horse Radish Peroxidase (HRP)

258
Q

requires the use of CHROMOGEN (color developer)

259
Q

Chromogen used in HRP

A

DAB (3,3’-Diaminobenzidine)
AEC (3-amino-9-ethylcarbazole)

260
Q

Chromogen with BROWN as resulting color

A

DAB (3,3’-Diaminobenzidine)

261
Q

Chromogen with BRICK-RED as resulting color

A

AEC (3-amino-9-ethylcarbazole)

262
Q

alternative enzyme

A

Alkaline phosphatase

263
Q

traditional counterstain used in labeling antibodies

A

hematoxylin

264
Q

Optimum incubation time to link antibody with enzyme peroxidase

A

30-60 mins at RT

265
Q

used in Fluorochrome label

A

FITC (Fluorescein Isothiocyanate)

266
Q

Plant or animal proteins which can bind to tissue carbohydrate

267
Q

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

268
Q

specimens for IHC

A

Cryostat Frozen sections

Processed specimens (formalin-fixed/paraffin-embedded)

269
Q

Must be fixed in a few seconds using absolute methanol or acetone

A

Cryostat frozen sections

270
Q

used to fix cryostat frozen sections

A

absolute methanol
acetone

271
Q

Purpose of fixation of Cryostat frozen sections

A

a) To prevent destruction of labile antigenic sites
b) To preserve antigen position

272
Q

IHC specimen that requires antigen retrieval

A

Processed specimens

273
Q

Processed specimens

A

Formalin-fixed
Paraffin-embedded

274
Q

Methods of antigen retrieval from processed tissues

A

Proteolytic enzyme retrieval (PIER)
Microwave antigen retrieval/Heat Induced Epitope retrieval
Pressure cooking antigen retrieval
Autoclave heating
Waterbath heating (90ºC or 95-98º)
Steamer heating
Decloaker heating
Combination of microwave & enzyme digestion

275
Q

most common method of antigen retrieval

A

Proteolytic enzyme retrieval (PIER)

276
Q

commonly used in PIER

A

trypsin
protease

277
Q

Duration of Microwave antigen retrieval/Heat Induced Epitope retrieval

A

20 minutes

278
Q

not preferred method of antigen retrieval

A

Pressure cooking antigen retrieval

279
Q

Tissue section with the antigen being detected

A

Positive control

280
Q

To prepare, primary antibody is omitted from staining sched

A

Negative control

281
Q

Contains the target antigen, not only in the tissue but also in adjacent tissue elements

A

Internal tissue control (Built-in control)

282
Q

necrosis due to fungal infections? what are the examples?

A

Caseous necrosis

• Histoplasmosis
• Blastomycosis
• Coccidioidomycosis

283
Q

site involved in DRY gangrene

284
Q

site involved in WET gangrene

A

more common in bowel

285
Q

mechanism of DRY gangrene

A

arterial occlusion

286
Q

mechanism of WET gangrene

A

venous obstruction

287
Q

Macroscopic appearance of DRY gangrene

A

dry
shrunken
black

288
Q

Macroscopic appearance of WET gangrene

A

moist
soft
swollen
rotten
dark

289
Q

Putrefaction in DRY gangrene

A

limited due to less blood supply

290
Q

Putrefaction in WET gangrene

A

MARKED due to congestion of organ with blood

291
Q

Line of demarcation: DRY gangrene

292
Q

Line of demarcation: WET gangrene

A

no clear cut line

293
Q

bacteria in DRY gangrene

A

fail to survive

294
Q

bacteria in WET gangrene

A

numerous bacteria present

295
Q

prognosis in DRY gangrene

A

better (due to septicemia)

296
Q

prognosis in WET gangrene

A

POOR (due to toxemia)

MTAP 2 (23 decks)

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