PRELIM LEC: INTRO CONTINUATION (CELL DEATH) Flashcards
1
Q
Occurs after irreversible injury
A
CELL DEATH
2
Q
2 TYPES OF CELL DEATH
A
APOPTOSIS
NECROSIS
3
Q
Reduced
Cell Size
A
Apoptosis
4
Q
Fragmentation into nucleosome-size fragments
Nucleus
A
Apoptosis
5
Q
Pyknosis (clumping) Karyorrhexis
(fragmentation) Karyolysis (dissolution)
Nucleus
A
Necrosis
6
Q
Intact
Plasma Membrane
A
Apoptosis
7
Q
Disrupted
Plasma Membrane
A
Necrosis
8
Q
Intact
Cellular contents
A
Apoptosis
9
Q
Enzymatic digestion; may leak out of cell
Cellular contents
A
Necrosis
10
Q
No (because phagocytes rapidly devour the cells)
Adjacent Inflammation
A
Apoptosis
11
Q
Frequent (due to leakage of cellular contents)
Adjacent Inflammation
A
Necrosis
12
Q
- Physiologic
- Death by destiny
Physiologic or Pathologic?
A
Apoptosis
13
Q
- Pathologic
- Death by disease
Physiologic or Pathologic?
A
Necrosis
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
15
Q
Presence of cleaved, active caspases (cysteine proteases that cleave aspartic acid residue) is a marker for cells undergoing apoptosis
A
APOPTOSIS
16
Q
Cells break up into apoptotic bodies, which are tasty targets for phagocytes
A
APOPTOSIS
17
Q
Reasons for Apoptosis in Following Conditions: Physiologic
A
Eliminates cells that are no longer needed, or those that have served their purposes
18
Q
Reasons for Apoptosis in Following Conditions: Pathologic
A
Eliminates cells that are injured beyond repair without eliciting host reaction
19
Q
consequence of severe injury
A
NECROSIS
20
Q
Pathologic cell death
A
NECROSIS
21
Q
NECROSIS 2 TYPES ACCORDING TO LOCATION OF EXTENT
A
FOCAL
MASSIVE
22
Q
tissue or organs with large numbers of dead cells
A
Necrotic
23
Q
Types of Necrosis According to Morphology
A
- Coagulative
- Liquefactive
- Gangrenous
- Caseous
- Fat
- Fibrinoid
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
25
* Tissue becomes liquid viscous mass due to digestion of dead cells
* Occurs during microbial infection
* Creamy yellow because of pus
* Affects CNS
Liquefactive
26
* Due to ischemia and superimposed bacterial infection
* Combination of coagulation and liquefaction necrosis
Gangrenous
27
* Means ‘cheese-like’
* Friable white appearance of necrotic area
* Seen in tuberculosis, granuloma
Caseous
28
Seen in immune reactions when antigen- antibody complexes are deposited in walls of arteries
Fibrinoid
29
* Fat destruction due to pancreatic lipase
* Seen in acute pancreatitis
Fat
30
2 TYPES OF Gangrenous
1. Dry Gangrene
2. Wet Gangrene
31
Immune complex + fibrin =
fibrinoid (bright pink and amorphous appearance in H&E staining)
32
* Sterile necrosis
* Arterial occlusion, sharp demarcation line, less foul odor
Dry Gangrene
33
* Nonsterile necrosis (due to bacterial infection)
* Vein occlusion, no sharp demarcation line, foul odor
Wet Gangrene
34
ARTERIAL
| OCCLUSION
Dry Gangrene
35
LESS FOUL
| ODOR
Dry Gangrene
36
SHARP
| DEMARCATION
Dry Gangrene
37
VENOUS
| OCCLUSION
Wet Gangrene
38
MORE FOUL
| ODOR
Wet Gangrene
39
NONE
| DEMARCATION
Wet Gangrene
40
TISSUE TO DISCOLARTION DUE TO
BLOOD PIGMENTS
41
WHAT IS THE CAUSE OF FOUL SMELL IN WET GANGRENOUS NECROSIS?
STAGNATION OF VENOUS BLOOD
42
Fatty Acids + Calcium =
Chalky-white areas (fat saponification)
43
LIPASE SPILLS FAT INTO FATTY ACIDS (FA) AND GLYCEROL. T OR F?
| FAT NECROSIS
TRUE
44
fountain damage and isolate injury
INFLAMMATION
45
* contain damage & isolate injury
* destroy cause of injury (microorganism/toxins)
* destroy resulting necrotic cells and tissues
* prepare tissue for healing & repair
INFLAMMATION
46
Harmful effects of inflammaion:
1. Digestion of normal tissues
2. Swelling
3. Inappropriate inflammatory response
47
Cardinal Signs:
1. Rubor – redness
2. Calor – heat
3. Tumor – swelling
4. Dolor – pain
5. Functio laesa – loss of function
48
COMPONENTS OF INFLAMMATION
VASCULAR REACTION
CELLULAR REACTION
49
VASCULAR REACTION 3 TYPES:
Vasoconstriction
Vasodilation
Endothelial Activation
50
Occurs first and lasts only for seconds
Vasoconstriction
51
Increased diameter of blood vessels
Increased blood flow to area Erythema (heat and redness on site of infection)
Vasodilation
52
Increased vascular permeability Edema (extravasation of liquid portion of blood)
Endothelial Activation
53
Cellular Response:
Neutrophil Activation
54
WBCs enter site of injury
Kill organism, mop debris
Release chemokines (substances that attract other immune substances to site of inflammation)
Neutrophil Activation
55
Classes of Inflammation:
1. According to Duration
2. According to Character of Exudate
3. According to Location
56
3 TYPES According to Duration
| Classes of Inflammation
Acute
Chronic
Sub-acute/chronic
57
5 TYPES According to Character of Exudate
| Classes of Inflammation
1. Serous
2. Fibrinous
3. Catarrhal
4. Hemorrhagic
5. Suppurative / Purulent
58
2 TYPES According to Location
| Classes of Inflammation
1. Localized
2. Generalized / Systemic
59
Sudden onset; usually mild and self-limiting; Polymorphonuclear (PMNs) cells
| According to Duration
Acute
60
Involves persistence of injurious agent; often severe and progressive; Mononuclear cells
| According to Duration
Chronic
61
* watery, protein-poor
* Out-pouring of relatively protein-poor fluid; common in cavities
| According to Character of Exudate
Serous
62
* 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
Fibrinous
63
* mucus and debris
* Increased blood flow to mucosal vessels, enlargement of secretory vessels discharge of mucus and epithelial debris
| According to Character of Exudate
Catarrhal
64
* RBC leakage
* Disruption of blood vessel wall leakage of large number of RBCs
| According to Character of Exudate
Hemorrhagic
65
* Mainly due to bacterial infection or secondary condition
* Collection of large amount of Pus
| According to Character of Exudate
Suppurative / Purulent
66
Collection of large amount of Pus Composed of :
Neutrophil
Necrotic cells
Edema fluid
67
composed of dead neutrophils, necrotic cells and edema fluid
pus
68
collection of pus
Abscess
69
One site; not widespread
| According to Location
Localized
70
Whole organ; area of tissue; region
of tissue
| According to Location
Generalized / Systemic
71
Sequential Steps of a Typical Inflammatory Reaction
1. recognition of stimulus
2. recruitment of WBCs and proteins to site
3. removal of stimulus
4. regulation of response
5. repair
72
If inflammatory reaction is not controlled, adverse tissue effects may occur, such as:
abscess formation and chronic inflammation
73
ABNORMALITIES IN CELL GROWTH
* Retrogressive Changes
* Progressive Changes
* Degenerative Changes
74
organs are smaller than the normal
Retrogressive Changes
75
4 Developmental Defects
1. Aplasia
2. Hypoplasia
3. Agenesia
4. Atresia
76
incomplete development of the organ
Aplasia
77
failure of an organ to develop fully
Hypoplasia
78
complete non-appearance of an organ
Agenesia
79
failure of an organ to form an opening
Atresia
80
acquired decrease of the size of a normally developed organ
Atrophy
81
organs become larger than normal
Progressive Changes
82
increase of cell size
Hypertrophy
83
due to increase work load or endocrine stimulation
True
84
Hypertrophy 3 TYPES
1. True
2. Compensatory
3. False
85
Progressive Changes 2 TYPES
Hypertrophy
Hyperplasia
86
true for paired organs, where one is excised and the other incresases in size to “take responsibility’ for its pair
Compensatory
87
due to ECF buildup and CT proliferation
False
88
increase in cell population
Hyperplasia
89
HYPERPLASIA 2 TYPES
Physiologic
Pathologic
90
as in pregnancy
Physiologic
91
as in typhoid fever affecting lymphoid follicles
Pathologic
92
changes in the adult form of cell
Degenerative Changes
93
Degenerative Changes 4 TYPES
1. Metaplasia
2. Dysplasia
3. Anaplasia
4. Neoplasia
94
replacement of one cell type of cells to another type in the same site (reversible)
Metaplasia
95
means “disordered growth”; development of
abnormal cell types within a tissue (reversible)
Dysplasia
96
lack of differentiation of cells (irreversible)
Anaplasia
97
means “new growth”; uncontrolled proliferation of cells with no purpose; due to carcinogens, or DNA alteration (irreversible)
Neoplasia
98
mass of neoplastic cells
Tumor/Neoplasms
99
General Characteristics of Tumors
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
actively dividing cells
Parenchyma
100
Parts of Tumor
Parenchyma
Stroma
101
connective tissue framework and lymphatic and vascular channels
Stroma
102
monstrous tumors
TERATOMA
103
well differentiated cell
good prognosis
104
Classification of Tumor
Benign
Malignant
105
Usually does not
cause death except
for infants and brain
tumors
| Death
Benign
106
Usually causes death
| Death
Malignant
107
Well-differentiated
| Differentiation
Benign
108
Some lack of
differentiation
| Differentiation
Malignant
109
# ```
Usually progressive
and slow; may come
to a standstill or
regress
| Rate of Growth
Benign
110
Erratic; may be slow
to rapid
| Rate of Growth
Malignant
111
Absent
| Metastasis
Benign
112
Frequent
| Metastasis
Malignant
113
- 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
Grading of Tumors
114
tumor cells resemble normal cells
Well-differentiated
115
tumor cells do not resemble normal cells
Undifferentiated
116
Limitation of Grading:
1. It is subjective
2. Higher grades of tumor have more tendency to metastasize
3. Most sarcomas cannot be graded
