• Atrophy, Hypertrophy, Hyperplasia, Metaplasia, Dysplasia: pathophysiology, what makes them different, examples of each type of cellular adaptation
• Most common cause(s) of cellular injury
• What changes occur dur
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• Atrophy, Hypertrophy, Hyperplasia, Metaplasia, Dysplasia: pathophysiology, what makes them different, examples of each type of cellular adaptation
• Most common cause(s) of cellular injury
• What changes occur during cellular injury to the cell, when lack of ATP leads to ischemia and hypoxia (from class, what electrolytes move out of cell, into cell, etc.)
• Types of Necrosis: Liquefactive vs. Coagulative vs. Gangrene vs. Fatty
o Gangrene-large are of necrosis, Severe hypoxic injury, severe lack of oxygen, commonly occurring due to arteriosclerosis (blockage) of major arteries ESPECIALLY in the lower leg—larger area than liquefactive
• Apoptosis
o cell death resulting from activation of intracellular signaling cascades that course cell death.
• Complications of impaired wound healing
o Dysfunction during inflammatory response
o Wound disruption
Dehiscence
o Impaired epithelialization
Antiinflammatory steroids, hypoxemia, and nutritional
Innate Immunity: Inflammation (Ch. 7):
• Vascular response associated with inflammation & local manifestations
• Main functions of the three protein systems (complement, coagulation, & kinin), not every little detail, stick to the basic and most important features
• Role of “General” Mast cell in the inflammatory response
• Chemotaxis and chemotactic factors: role in inflammatory response
o Chemotaxis – directional movement of cells along a chemical gradient;
• Role of Phagocytes & Phagocytosis (neutrophils, macrophages, eosinophils only)
o Macrophages – mature monocytes #2
Monocytes produced in bone marrow, enter circulation,
o Eosinophils – parasitic #3
• Chemical mediators that induce pain during an inflammatory response
• Local vs. Systemic signs (clinical manifestations) of inflammation
• Exudative Fluids: types and description of each
o Serous exudate
• Age related changes associated with immunity and wound healing
o Neonates - infants
• Primary characteristics that differentiate the adaptive response from the innate inflammatory response • Origins of B & T cells
o B cells -from bone marrow • Clonal Diversity vs. Clonal Selection
o Clonal diversity:
• Passive vs. Active immunity and examples of each
• Humoral vs. Cell-Mediated Immunity: major differences and roles of each
o Humoral immunity
• Antigens: Role and definition of antigen and immunogens, the most important determinant of an antigen being able to initiate an immune response, antigen binding
• Antibody Production and protective mechanisms
o produced by plasma cells.
o Job is to Protect against infection.
• Antibody classes: IgM, IgG, IgE (difference between these only, major points)
• Age related changes in immune function
o Decreased T-cell activity (leads to viral infections or cancer.)
Alterations in Immunity & Inflammation (Ch. 9) & Infection (Ch. 10):
• Hypersensitivity and Hypersensitivity Reactions: Type I to Type IV, major pathophysiological differences, class of antibody associated with each, and examples of each
• Alloimmunity vs. Autoimmunity: definition, patho, examples of each
• Transplant Rejection
• Transplant rejection: Classified according to time.
• HIV & AIDS: pathophysiology, diagnosis criteria, clinical manifestations
o HIV:
• Host lines of defense
• Types of Organisms that cause infection (bacteria, viruses, fungi, parasites): characteristics of each
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