Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

PRELIM LEC: INTRO CONTINUATION (CELL DEATH) Flashcards

1
Q

Occurs after irreversible injury

A

CELL DEATH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

2 TYPES OF CELL DEATH

A

APOPTOSIS
NECROSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Reduced

Cell Size

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Fragmentation into nucleosome-size fragments

Nucleus

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

Nucleus

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Intact

Plasma Membrane

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Disrupted

Plasma Membrane

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Intact

Cellular contents

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Enzymatic digestion; may leak out of cell

Cellular contents

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

No (because phagocytes rapidly devour the cells)

Adjacent Inflammation

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Frequent (due to leakage of cellular contents)

Adjacent Inflammation

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  • Physiologic
  • Death by destiny

Physiologic or Pathologic?

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  • Pathologic
  • Death by disease

Physiologic or Pathologic?

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

APOPTOSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

APOPTOSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Reasons for Apoptosis in Following Conditions: Physiologic

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Reasons for Apoptosis in Following Conditions: Pathologic

A

Eliminates cells that are injured beyond repair without eliciting host reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

consequence of severe injury

A

NECROSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Pathologic cell death

A

NECROSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

NECROSIS 2 TYPES ACCORDING TO LOCATION OF EXTENT

A

FOCAL
MASSIVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

tissue or organs with large numbers of dead cells

A

Necrotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Types of Necrosis According to Morphology

A
  1. Coagulative
  2. Liquefactive
  3. Gangrenous
  4. Caseous
  5. Fat
  6. Fibrinoid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
  • Due to ischemia and superimposed bacterial infection
  • Combination of coagulation and liquefaction necrosis
A

Gangrenous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q
  • Means ‘cheese-like’
  • Friable white appearance of necrotic area
  • Seen in tuberculosis, granuloma
A

Caseous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

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

A

Fibrinoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q
  • Fat destruction due to pancreatic lipase
  • Seen in acute pancreatitis
A

Fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

2 TYPES OF Gangrenous

A
  1. Dry Gangrene
  2. Wet Gangrene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Immune complex + fibrin =

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q
  • Sterile necrosis
  • Arterial occlusion, sharp demarcation line, less foul odor
A

Dry Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q
  • Nonsterile necrosis (due to bacterial infection)
  • Vein occlusion, no sharp demarcation line, foul odor
A

Wet Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

ARTERIAL

OCCLUSION

A

Dry Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

LESS FOUL

ODOR

A

Dry Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

SHARP

DEMARCATION

A

Dry Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

VENOUS

OCCLUSION

A

Wet Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

MORE FOUL

ODOR

A

Wet Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

NONE

DEMARCATION

A

Wet Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

TISSUE TO DISCOLARTION DUE TO

A

BLOOD PIGMENTS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A

STAGNATION OF VENOUS BLOOD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Fatty Acids + Calcium =

A

Chalky-white areas (fat saponification)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

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

FAT NECROSIS

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

fountain damage and isolate injury

A

INFLAMMATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Harmful effects of inflammaion:

A
  1. Digestion of normal tissues
  2. Swelling
  3. Inappropriate inflammatory response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

60
Q

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

According to Duration

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

According to Character of Exudate

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

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

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

68
Q

collection of pus

69
Q

One site; not widespread

According to Location

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

77
Q

failure of an organ to develop fully

A

Hypoplasia

78
Q

complete non-appearance of an organ

79
Q

failure of an organ to form an opening

80
Q

acquired decrease of the size of a normally developed organ

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

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

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)

96
Q

lack of differentiation of cells (irreversible)

97
Q

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

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

102
Q

monstrous tumors

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

106
Q

Usually causes death

Death

107
Q

Well-differentiated

Differentiation

108
Q

Some lack of
differentiation

Differentiation

109
Q

```

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

Rate of Growth

110
Q

Erratic; may be slow
to rapid

Rate of Growth

111
Q

Absent

Metastasis

112
Q

Frequent

Metastasis

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 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions