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Pathophysiology:
Terminology:
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Diagnosis: ID of a disease
Etiology: causative factors of disease
o Congenital, genetic, immune/metabolic, environmental,
o Congenital: occurs during development
o Genetic: problem with genetic makeup
o Immune/metabolic: something wrong within the system
o Environmental: caused from something in the environment
Idiopathic disease: unknown cause
Iatrogenic disease: caused by treatment
o Most common is Urinary Tract Infection (UTI)
Manifestations of disease: symptoms or evidence that a disease is present
o Systemic: affect the whole body
o Localized: affect a certain area of the body

Process to pathophysiology:
1
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Cells may be injured
3
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The injurious agent could cause cell death and skip the process
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Call Adaptation: Cells adapt to agent or situation
a
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Cells are not normal but they are not injured either
c
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Ex: during pregnancy, increased breast size and uterine tissue with pregnancy
Atrophy: decrease in cell size
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Effects: on skeletal muscle and brain
A bed ridden or paralyzed person has a decrease in size of skeletal muscles in leg
o Aging
o Malnourishment

Hypertrophy: increase in cell size
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Can effect heart and kidney normally
o Heart: not normal or really good
o Kidney: normal and good
 Loss of kidney, the other grows to compensate

Hyperplasia: increase in cell numbers
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Caused by: increased in cell division rate
o Increased rate caused by something else
Liver and kidney are common

Types of hyperplasia:
Compensatory: kidney and breast
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Adjustment to something happening in body

Hormonal: uterine
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Normal during pregnancy to increase contractions

Pathologic: endometrial
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Good indicator for cancer
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Dysplasia: deranged cell growth varying in shape and size
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Atypical hyperplasia
Epithelial tissue
Strong predictor of breast and cervical cancer

Metaplasia: replacement of one cell type with another
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Ex: ciliated cells replaced by non-ciliated cells due to smoking
o Cant move mucus

Anaplasia: cells with undifferentiated nuclei
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Normally nuclei are easy to see
o Anaplasia results in not being able to identify individual nuclei
Can lead to tumor formation, used for tumor grading or staging

Neoplasm: new cell growth, tumors
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Benign: less serious
Malignant: serious

Cellular Injury:
Stimuli:
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Chemicals (poisons, metals like lead which interferes with neurotransmitters, CO, alcohol)
Reduced O2 levels, hypoxia

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Infectious agents, bacteria or virus
Genetic/nutritional

Most common cause of cell injury is hypoxia
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Both are caused by limited flow followed by blockage
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Manifestations of cell injury: (don’t worry about for test)
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Fatigue, malaise, fever, increased heart rate, pain, presence of enzymes in ECF

Cell Death: autolysis, cells kill themselves
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Necrosis or apoptosis: programmed cell death
o *Coagulative necrosis: (a)-proteins denature
 *Caused by hypoxia and chemicals
 *Heart (MI) and kidneys
o *Liquefactive necrosis: (b)- *hydrolases digest cells;* and during ischemia
 common with bacterial infection or *brain tissue death (stroke)
o Caseous necrosis: occurs in tuberculosis or syphilis infection
 Combines (a) and (b)
o Fat necrosis: Lipases breakdown fatty acids
 Occurs in breast and pancreatic tissue
o *Gangrenous necrosis: *caused by hypoxia

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 Dry (a), wet (b)
 Internal gangrene can occur
Gas necrosis: caused by bacteria
 In muscles
 Gas bubble forms
 Dangerous when it gets into blood vessels

Inflammation Response: after injury, non-lethal cell injury
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Acute inflammation: first step in inflammation response
o Response is immediate
o Arterioles dilate: allows blood flow to the site
o Edema and swelling
o Blood becomes thicker: due to other things coming to the site
o Leukocytes migrate to the area
o Accumulate cells and proteins at site
o Site gets cleaned: macrophages, prep for resolution
Plasma Systems:
o First: complement system
 A series of proteins activated by endotoxins from bacteria
o Second: clotting system
 Formation of meshwork, prevent spread of injury, localizes problem
o Third: Kinin-bradykinin system:
 Bradykinin dilates blood vessels, induces pain, and increase permeability
o Specific protein that controls the systems: C1 esterase inhibitor, dilation
 Hereditary condition: angioneurotic edema
 No C1 esterase inhibitor
o Systems continue to function
Inflammatory cells: leukocytes
o Granulocytes and agranulocytes*
o Granulocytes: contain material in granules that is released to attract other cells to site
o Agranulocytes: do not release anything
 Neutrophils: most common
 Monocytes*: leave blood and invade tissue, can become macrophage
 Lymphocytes*: B and T cells (antibody)
 Eosinophils: parasitic defense
 Throw up on parasite to digest it
 Basophils: mediator release (histamine)
 Mast cells: immune system cells that release mediators

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Chronic Inflammation: second step in inflammatory response
o Neutrophil degranulation
o Activation of lymphocytes
o Fibroblast
Granuloma: third step in inflammatory response
o Walls off area

Resolution and Repair: occur in two overlapping phases
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Resolution: regenerating original tissue, will not work if injury is still there
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o Internal contractures can occur
 Liver: area can be changed causing a problem



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