Pathology

The study of dieseae

Etiology

Cause ( enviromental, injury habit?)

Pathogenesis

Mechanisms of its development

( how did it develop?) Acute / Chronic

Morphology

Structural alterations induced in cells and tissue

( on surface or deep?)

Fuctional Consequences

Morphologic changes as observed clinically

( is there a function change?)

4 Aspects of Pathology

1. etiology
2. morphology
3. Pathogenesis
4. funtional consequences

Reversible cell Injury

Can go back to normal

Irreversible Cell Injury

and cell death ( necrosis)

Cellular Adaptation

Atrophy

Wasting away or diminution

Ex. Muscle atrophy is wasting away of the muscle

( a decrease in mucle mass )

Hypertrophy

the enlargment or overgrowth of an organ or part due to an increase in size of its constiuient cells, rather than the number of cells.

( the number of cells stay the same )

Hyperplasia

A condition in which there is a increase in the number of cells in a tissue or organ.

( increase in number of cells )

Metaplasia

A reversible change from one cell type to another

Ex. Squammous --->  Columnar

Dysplasia

Premalignant change characterized by alteration in size, shape, and organization of the cellular components of tissue.

( change, but cannot reverse)

Neoplasia

Abnormal new growth of cells

( reversible ??)

Cells react to adverse influences by:

1. Adapting
2. Sustaining
3. Suffering irriversible injury and dying

( cells either Heal, adapt, or dye)

Name two patterns of cell death :

1. Necrosis - Swelling, breakdown, rupture, inflammation (more common); (unplanned)
2. Apoptosis - Chromation condensation or fragmentation in single or small clusters - lack of inflammation; programmed cell distruction in embryogenesis ( planned )

1. Types of Necrosis:

1. Coagulation Necrosis - Most common type ( ishemia or hyoxia).
2. Liquefaction Necrosis - soft fluid filled (localized infection - oral abcess or like a pimple )
3. Caseous Necrosis - tuberculosis ( cheesy walled off "encased")
4. Fat Necrosis - Lipases

Seven Causes of Cellular Injury :

1. Hypoxia
2. Physical Agents
3. Chemical Agents
4. Infectious Agents
5. Immunological Reactions
6. Genetic Derangements
7. Nutritional Imbalances 

( His Pesky Cat In Indiana Got Nutered )

Cardinal Signs

1. Heat ( Calor )
2. Redness ( Rubor )
3. Edema ( tumor )
4. Pain (palor)
5. Loss of Function (functio laseo)

Exudation

the escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities.

Exudate

An inflammatory extravascular fluid that has a high protein concentration, much cellular debris, and a specific gravity above 1.020

Transudate

A fluid with low protein content and a specific gravity less than 1.012. 

It is essentially an ultrafiltrate of blood plasma and results from hydrostatic imbalance across the vascular epithilium.  ( thinner than exudate )

Edema

Denotes an excess of fluid in the interstitial tissue or serous cavities. 

( it can be either an exudate or a tranudate)

Pus

A purulent ( contains many neutrophils ) inflammatory exudate rich in leukocytes and perenchymal cell debris

(shows infection is present )

Name the five Leukocytes

1. Basophils
2. eosinophils
3. monocytes
4. lymphocytes
5. neutrophils

Three responses to Acute Inflammation:

1. Vascular Resoponse
2. Cellular Response
3. Chemical Response

Phagocytosis

Starlings Law

normal fluid balance is modulated by two opposing forces:

Hydrostatic Pressure - causing fluid to move out of circulation and plasma

Colloid Osmotic Pressure - causing fluid to move into cappilaries