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HISTOPATHOLOGY > PRELIM LEC: INTRO CONTINUATION (CELL DEATH) > Flashcards

PRELIM LEC: INTRO CONTINUATION (CELL DEATH) Flashcards

1
Q

Occurs after irreversible injury

A

CELL DEATH

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2
Q

2 TYPES OF CELL DEATH

A

APOPTOSIS
NECROSIS

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3
Q

Reduced

Cell Size

A

Apoptosis

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4
Q

Fragmentation into nucleosome-size fragments

Nucleus

A

Apoptosis

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5
Q

Pyknosis (clumping)  Karyorrhexis
(fragmentation)  Karyolysis (dissolution)

Nucleus

A

Necrosis

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6
Q

Intact

Plasma Membrane

A

Apoptosis

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7
Q

Disrupted

Plasma Membrane

A

Necrosis

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8
Q

Intact

Cellular contents

A

Apoptosis

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9
Q

Enzymatic digestion; may leak out of cell

Cellular contents

A

Necrosis

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10
Q

No (because phagocytes rapidly devour the cells)

Adjacent Inflammation

A

Apoptosis

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11
Q

Frequent (due to leakage of cellular contents)

Adjacent Inflammation

A

Necrosis

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12
Q
  • Physiologic
  • Death by destiny

Physiologic or Pathologic?

A

Apoptosis

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13
Q
  • Pathologic
  • Death by disease

Physiologic or Pathologic?

A

Necrosis

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14
Q

Induced by a tightly regulated suicide program in which cells destined to die activate enzymes that degrade the cells’ own proteins and nuclear DNA

A

APOPTOSIS

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15
Q

Presence of cleaved, active caspases (cysteine proteases that cleave aspartic acid residue) is a marker for cells undergoing apoptosis

A

APOPTOSIS

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16
Q

Cells break up into apoptotic bodies, which are tasty targets for phagocytes

A

APOPTOSIS

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17
Q

Reasons for Apoptosis in Following Conditions: Physiologic

A

Eliminates cells that are no longer needed, or those that have served their purposes

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18
Q

Reasons for Apoptosis in Following Conditions: Pathologic

A

Eliminates cells that are injured beyond repair without eliciting host reaction

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19
Q

consequence of severe injury

A

NECROSIS

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20
Q

Pathologic cell death

A

NECROSIS

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21
Q

NECROSIS 2 TYPES ACCORDING TO LOCATION OF EXTENT

A

FOCAL
MASSIVE

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22
Q

tissue or organs with large numbers of dead cells

A

Necrotic

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23
Q

Types of Necrosis According to Morphology

A
  1. Coagulative
  2. Liquefactive
  3. Gangrenous
  4. Caseous
  5. Fat
  6. Fibrinoid
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24
Q
  • Tissue is firm because architecture of dead tissue is preserved
  • Eosinophilic due to denaturation of proteins AND enzymes
  • Occurs on affected tissue when vessel is obstructed, except brain
A

Coagulative

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25
Q
  • Tissue becomes liquid viscous mass due to digestion of dead cells
  • Occurs during microbial infection
  • Creamy yellow because of pus
  • Affects CNS
A

Liquefactive

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26
Q
  • Due to ischemia and superimposed bacterial infection
  • Combination of coagulation and liquefaction necrosis
A

Gangrenous

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27
Q
  • Means ‘cheese-like’
  • Friable white appearance of necrotic area
  • Seen in tuberculosis, granuloma
A

Caseous

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28
Q

Seen in immune reactions when antigen- antibody complexes are deposited in walls of arteries

A

Fibrinoid

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29
Q
  • Fat destruction due to pancreatic lipase
  • Seen in acute pancreatitis
A

Fat

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30
Q

2 TYPES OF Gangrenous

A
  1. Dry Gangrene
  2. Wet Gangrene
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31
Q

Immune complex + fibrin =

A

fibrinoid (bright pink and amorphous appearance in H&E staining)

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32
Q
  • Sterile necrosis
  • Arterial occlusion, sharp demarcation line, less foul odor
A

Dry Gangrene

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33
Q
  • Nonsterile necrosis (due to bacterial infection)
  • Vein occlusion, no sharp demarcation line, foul odor
A

Wet Gangrene

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34
Q

ARTERIAL

OCCLUSION

A

Dry Gangrene

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35
Q

LESS FOUL

ODOR

A

Dry Gangrene

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36
Q

SHARP

DEMARCATION

A

Dry Gangrene

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37
Q

VENOUS

OCCLUSION

A

Wet Gangrene

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38
Q

MORE FOUL

ODOR

A

Wet Gangrene

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39
Q

NONE

DEMARCATION

A

Wet Gangrene

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40
Q

TISSUE TO DISCOLARTION DUE TO

A

BLOOD PIGMENTS

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41
Q

WHAT IS THE CAUSE OF FOUL SMELL IN WET GANGRENOUS NECROSIS?

A

STAGNATION OF VENOUS BLOOD

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42
Q

Fatty Acids + Calcium =

A

Chalky-white areas (fat saponification)

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43
Q

LIPASE SPILLS FAT INTO FATTY ACIDS (FA) AND GLYCEROL. T OR F?

FAT NECROSIS

A

TRUE

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44
Q

fountain damage and isolate injury

A

INFLAMMATION

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45
Q
  • contain damage & isolate injury
  • destroy cause of injury (microorganism/toxins)
  • destroy resulting necrotic cells and tissues
  • prepare tissue for healing & repair
A

INFLAMMATION

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46
Q

Harmful effects of inflammaion:

A
  1. Digestion of normal tissues
  2. Swelling
  3. Inappropriate inflammatory response
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47
Q

Cardinal Signs:

A
  1. Rubor – redness
  2. Calor – heat
  3. Tumor – swelling
  4. Dolor – pain
  5. Functio laesa – loss of function
48
Q

COMPONENTS OF INFLAMMATION

A

VASCULAR REACTION
CELLULAR REACTION

49
Q

VASCULAR REACTION 3 TYPES:

A

Vasoconstriction
Vasodilation
Endothelial Activation

50
Q

Occurs first and lasts only for seconds

A

Vasoconstriction

51
Q

Increased diameter of blood vessels 
Increased blood flow to area  Erythema (heat and redness on site of infection)

A

Vasodilation

52
Q

Increased vascular permeability  Edema (extravasation of liquid portion of blood)

A

Endothelial Activation

53
Q

Cellular Response:

A

Neutrophil Activation

54
Q

WBCs enter site of injury
 Kill organism, mop debris
 Release chemokines (substances that attract other immune substances to site of inflammation)

A

Neutrophil Activation

55
Q

Classes of Inflammation:

A
  1. According to Duration
  2. According to Character of Exudate
  3. According to Location
56
Q

3 TYPES According to Duration

Classes of Inflammation

A

Acute
Chronic
Sub-acute/chronic

57
Q

5 TYPES According to Character of Exudate

Classes of Inflammation

A
  1. Serous
  2. Fibrinous
  3. Catarrhal
  4. Hemorrhagic
  5. Suppurative / Purulent
58
Q

2 TYPES According to Location

Classes of Inflammation

A
  1. Localized
  2. Generalized / Systemic
59
Q

Sudden onset; usually mild and self-limiting; Polymorphonuclear (PMNs) cells

According to Duration

A

Acute

60
Q

Involves persistence of injurious agent; often severe and progressive; Mononuclear cells

According to Duration

A

Chronic

61
Q
  • watery, protein-poor
  • Out-pouring of relatively protein-poor fluid; common in cavities

According to Character of Exudate

A

Serous

62
Q
  • protein-rich (such as fibrinogen)
  • More severe injury  more vascular permeability  more protein leaking (such as
    fibrinogen which is the precursor of fibrin)

According to Character of Exudate

A

Fibrinous

63
Q
  • mucus and debris
  • Increased blood flow to mucosal vessels, enlargement of secretory vessels  discharge of mucus and epithelial debris

According to Character of Exudate

A

Catarrhal

64
Q
  • RBC leakage
  • Disruption of blood vessel wall  leakage of large number of RBCs

According to Character of Exudate

A

Hemorrhagic

65
Q
  • Mainly due to bacterial infection or secondary condition
  • Collection of large amount of Pus

According to Character of Exudate

A

Suppurative / Purulent

66
Q

Collection of large amount of Pus Composed of :

A

Neutrophil
Necrotic cells
Edema fluid

67
Q

composed of dead neutrophils, necrotic cells and edema fluid

A

pus

68
Q

collection of pus

A

Abscess

69
Q

One site; not widespread

According to Location

A

Localized

70
Q

Whole organ; area of tissue; region
of tissue

According to Location

A

Generalized / Systemic

71
Q

Sequential Steps of a Typical Inflammatory Reaction

A
  1. recognition of stimulus
  2. recruitment of WBCs and proteins to site
  3. removal of stimulus
  4. regulation of response
  5. repair
72
Q

If inflammatory reaction is not controlled, adverse tissue effects may occur, such as:

A

abscess formation and chronic inflammation

73
Q

ABNORMALITIES IN CELL GROWTH

A
  • Retrogressive Changes
  • Progressive Changes
  • Degenerative Changes
74
Q

organs are smaller than the normal

A

Retrogressive Changes

75
Q

4 Developmental Defects

A
  1. Aplasia
  2. Hypoplasia
  3. Agenesia
  4. Atresia
76
Q

incomplete development of the organ

A

Aplasia

77
Q

failure of an organ to develop fully

A

Hypoplasia

78
Q

complete non-appearance of an organ

A

Agenesia

79
Q

failure of an organ to form an opening

A

Atresia

80
Q

acquired decrease of the size of a normally developed organ

A

Atrophy

81
Q

organs become larger than normal

A

Progressive Changes

82
Q

increase of cell size

A

Hypertrophy

83
Q

due to increase work load or endocrine stimulation

A

True

84
Q

Hypertrophy 3 TYPES

A
  1. True
  2. Compensatory
  3. False
85
Q

Progressive Changes 2 TYPES

A

Hypertrophy
Hyperplasia

86
Q

true for paired organs, where one is excised and the other incresases in size to “take responsibility’ for its pair

A

Compensatory

87
Q

due to ECF buildup and CT proliferation

A

False

88
Q

increase in cell population

A

Hyperplasia

89
Q

HYPERPLASIA 2 TYPES

A

Physiologic
Pathologic

90
Q

as in pregnancy

A

Physiologic

91
Q

as in typhoid fever affecting lymphoid follicles

A

Pathologic

92
Q

changes in the adult form of cell

A

Degenerative Changes

93
Q

Degenerative Changes 4 TYPES

A
  1. Metaplasia
  2. Dysplasia
  3. Anaplasia
  4. Neoplasia
94
Q

replacement of one cell type of cells to another type in the same site (reversible)

A

Metaplasia

95
Q

means “disordered growth”; development of
abnormal cell types within a tissue (reversible)

A

Dysplasia

96
Q

lack of differentiation of cells (irreversible)

A

Anaplasia

97
Q

means “new growth”; uncontrolled proliferation of cells with no purpose; due to carcinogens, or DNA alteration (irreversible)

A

Neoplasia

98
Q

mass of neoplastic cells

A

Tumor/Neoplasms

99
Q

General Characteristics of Tumors

A
  1. May resemble and function like a normal cell
  2. Autonomous; non-responsive to normal growth factors
  3. Parasitic nature; competes with cells for metabolic needs
100
Q

actively dividing cells

A

Parenchyma

100
Q

Parts of Tumor

A

Parenchyma
Stroma

101
Q

connective tissue framework and lymphatic and vascular channels

A

Stroma

102
Q

monstrous tumors

A

TERATOMA

103
Q

well differentiated cell

A

good prognosis

104
Q

Classification of Tumor

A

Benign
Malignant

105
Q

Usually does not
cause death except
for infants and brain
tumors

Death

A

Benign

106
Q

Usually causes death

Death

A

Malignant

107
Q

Well-differentiated

Differentiation

A

Benign

108
Q

Some lack of
differentiation

Differentiation

A

Malignant

109
Q

```

Usually progressive
and slow; may come
to a standstill or
regress

Rate of Growth

A

Benign

110
Q

Erratic; may be slow
to rapid

Rate of Growth

A

Malignant

111
Q

Absent

Metastasis

A

Benign

112
Q

Frequent

Metastasis

A

Malignant

113
Q
  • Attempts to establish an estimate of the level of malignancy of a tumor
  • Based on cytologic differentiation of tumor cells and number of mitoses
  • Different from Staging, as staging accounts for size, extent of spread to lymph nodes, and presence of metastasis
A

Grading of Tumors

114
Q

tumor cells resemble normal cells

A

Well-differentiated

115
Q

tumor cells do not resemble normal cells

A

Undifferentiated

116
Q

Limitation of Grading:

A
  1. It is subjective
  2. Higher grades of tumor have more tendency to metastasize
  3. Most sarcomas cannot be graded

HISTOPATHOLOGY (8 decks)

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