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26 Cards in this Set

  • Front
  • Back
Differentiate between reversible and irreversible cell injury.
Cell injury occurs with exposure to persistent sublethal environmental stress; if the stress is removed in time, or if the cell is able to withstand the assault, structural and functional integrity is restored and the injury is tus reversed. Sufficiently severe stress beyond point of no return results in irreversible injury and death of the cell.
Four ultrastructural changes of intracellular organelles which may occur in the hydropic swelling of reversible cell injury.
1. Endoplasmic reticulum become distended by fluid.

2. Mitochondria swell.

3. Plasma membrane form cytoplasmic blebs.

4. Nucleolus fibrillar and granular components may segregate.
Six major cellular adaptive responses to chronic stress;
1. Atrophy - Decrease in size and function of a cell or organ.

2. Hypertrophy - An increase in the size of a cell/organ accompanied by augmented functional capacity.

3. Hyperplasia - An increase in the number of cells in an organ or tissue.

4. Metaplasia - Conversion of one differential cell type to another.

5. Intracellular storage
Three common intracellular nutritional constituents which can accumulate abnormally during dysfunction of intracellular storage.
1. Fat

2. Glycogen

3. Iron
Three of the most common causes of cellular death
Viruses, ischemia, physical agents (radiation, extreme temps, toxic chemicals)
Morphological stages which occur during coagulative necrosis
The cell nucleus shows clumping of chromatic with redistribution along the nuclear membrane.

The nucleus becomes smaller (pyknosis) and may fragment throughout the cytoplasm (karyorrhexis), or the pyknotic nucleus may be extruded from the cell. The nucleus may show progressive loss of chromatic staining (karyolysis)
Conditions under which liquefactive necrosis may occur.
Polymorhonuclear leukocytes (PMNs) are acute inflammation cells which congregate generally in response to a bacterial infection; they contain hydrolases (enzymes) which are capable of completely digesting dead cells, often forming an abscess. This dissolution of tissue is called liquefactive necrosis.
Etiology of Fat necrosis
Fat necrosis specifically affects adipose tissue and most commonly results from pancreatitis or trauma. Digestive enzymes found in the pancreatic duct and small intestine are relesed from injured pancreatic cells and ducts into the exracellular space; they digest the pancreas and surrounding tissue including adipose cells.
Differentiate caseous necrosis from coagulative and liquefactive necrosis.
Caseous - Typical lesion of TB in which dead cells persist indefinitely as amorphous, coarsely granular, eosinophilic debris.

Coagulative - changes in cell cytoplasm and the nucleus common to al forms of cellular death.

Liquefactive - When a localized collection of acute inflammatory cells produce rapid death and dissolution of a tissue, often resulting in an abscess.

*Difference is - in caseous necrosis, the necrotic cells do not retain their cellular outlines; however, the cells fail to disappear by lysis as in liquefactive necrosis.
An important cause of coagulative and liquefactive necrosis.
Ischemia is the most important cause of coagulative necrosis; complication of atherosclerosis are a common cause of ischemic cell injury in the brain, heart, small intestines, kidney, and lower extremities.
Differentiate between direct and indirect cytopathic viruses.
The infection of a cell by a directly cytopathic virus causes lethal injury without the involvement of the host immune system, while indirect cytopathic viruses require the participation of the immune system.
Describe two types of pathologic calcification
Dystrophic calcification refers to deposition of calcium salts in the extracellular fluid of injured tissue; it is often visible with the naked eye. Metastatic calcification reflects deranged calcium metabolism and is associated with increased serum calcium concentration.
3 Steps in inflammation
INITIATION - of the mechanisms responsible for the localization and clearance of foreign substances and injured tissues.

AMPLIFICATION - of the inflammatory response in which mediators and cellular inflammatory systems are activated

TERMINATION - of the inflammatory response after generation of inflammatory agents and elimination of the foreign agent.
Three Vascular wall changes produced by inflammatory mediators at the site of injury.
LOSS of endothelial cell integrity

LEAKAGE of fluid and plasma components from the intravascular compartment.

EMIGRATION of erythrocytes and leukocytes from the intraluminal space into the extravascular tissue.
Four possible outcomes of acute inflammatory response.
1. Resolution
2. Abscess
3. Scar
4. Persistent (chronic) inflammation.
Inflammatory vs. noninflammatory edema.
When the movement of fluid into the extravascular space exceeds its clearance by the lymphatics, noninflammatory edema fluid accumulates;

inflammatory edema occurs in response to tissue injury and consequent changes in vasculature.
How the microvasculature is altered by vasoactive mediators in early response to tissue injury causing edema.
1. TRANSIENT vasoconstriction of the arterioles at the site of injury.

2. Vasodilation of precapillary arterioles increases blood flow to the injured tissue.

3. Increase in the permeability of the endothelial cell barrier resulting in leakage of fluid from intravascular into extravascular space.
8 types of extravascular accumulation in response to cellulary Injury.
1. Effusion - excess fluid
2. Transudate - edema, low protein.
3. Exudate - edema with high protein count.
4. Serous - effusion/exudate with absence of cellular response components.
5. Serosanguinous - effusion/exudate with erythrocytes.
6. Fibrinous - Exudate with large amounts of fibrin from activation of teh coagulation system.
7. Purulent - Effusion/exudate with prominent cellular components.
8. Suppurative - purulent exudate (excess fluid + high protein and cellular components) accompanied by significant liquefactive necrosis.
Six cell types with are potent sources of vasoactive mediators
1. Platelets
2. Tissue mast cells
3. Basophils
4. Polymorph leuocytes (polys, PMNs)
5. Endothelial cells
6. Monocyte / Macrophage
Describe the ed result of complement pathway activation (whether classical or alternative)
A) Formation of a membrane attack complex capable of inducing cell lysis.

B) Generation of the biologically active anaphylatoxins C3a and C5a
Tell what happens during he second phase (cellular recruitment phase) of the acute inflammatory response.
Cellular recruitment involves the accumulation of leukocytes, especially polymorphonuclear leukocytes, at the site of tissue injury.
Four physiologic response of circulating leukocytes exposed to chemotactic factors.
A: With the slowing of blood flow in response to vasodilation in the injured tissue, leukocytes concentrate adjacent to endothelial cells, called amargination.

B: Adherence of inflammatory cells to the endothelium.

C: Emigration along chemical gradients to the source of chemotactic stimulus; in most types of acute inflammation, neutrophils emigrate first and monocytes later.

D: Chemotaxis or binding of chemotactic agents to specific receptors on the cell membranes of leukocytes which leads to subsequent phagocytosis.
Three events involved inteh process of phagocytosis.
1. RECOGNITION of immunoglobulin molecules by the binding of opsonized (more susceptible to phagocytes) particles to specific receptors on phagocytic cells.

2. INTERNALIZATION of the opsonized particle

3. DIGESTION of foreign material.
TEll how chronic inflammation might occur, and the purpose that it serves.
Chronic inflammation may occur as a sequel to acute inflammation (nonimmunologic), or in an immune response to a foreign antigen. It serves primarily to contain and remove a pathologic agent or process within a tissue. Acute and chronic inflammation represent a continuum in which teh features may overlap.
List the cellular components of the chronic response.
1. Macrophage

2. Plasma cell

3. Lymphocyte

4. Eosinophil
Describe the systemic manifestations of inflammation


Decrease appetitite

Altered sleep pattern

Changes in plasma levels on acute phase proteins.