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