Gen Path 1: Exam 1

Etiology

Origin of the disease, or why a disease occurs.

Pathogenesis

Development of a disease, or how a disease occurs.

Cell Injury Mechanisms (5 Total)

ATP Depletion
Generation of Reactive Oxygen Species
Loss of CA+ Homeostasis
Altered Membrane Permeability
DNA and Protein Damage

Hypoxia

Low Oxygen Availability, Cells can produce ATP through Anaerobic Glycolysis (Better than Ischemia)

Ischemia

Low Blood Flow (Oxygen and Glucose) Anerobic Glycolysis eventually fails, worse than hypoxia.

Reactive Oxygen Species are associated with

Inflammation
Oxygen Toxicity
Chemicals/Drugs
Radiation
Aging

Major Sites of DNA Damage

Thymidine and Guanine

How is Reactive Oxygen Species (ROS) Controlled

Enzymes such as Catalase, SOD, and Glutathione Peroxidase
Antioxidants such as Vitamins E, A and C, Glutathione, and Cysteine
Serum Proteins that reduce/bind iron and copper to block ROS formation

Degree of Cell Injury is determined by

Physiologic state of the cell
Intensity of the insult
Duration of the insult
# of exposures to the insult

Reversible Cell Injury

Often Acute, short duration and low intensity.

Coagulative Necrosis

Liquefactive Necrosis

Caseous Necrosis

Fat Necrosis

Intrinsic Mechanism for Apoptosis

Mitochondrial Pathway

Extrinsic Mechanism for Apoptosis

Death Receptor PathwayC

Common Node of Apoptosis

Initiator Caspases