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Factors causing disease are mainly two types. Environmental (or external) factors and Genetic (or Internal) factors. Diseases which present since birth are called Congenital diseases and all other diseases are known as Acquired diseases. Diseases which occur in families are known as
Familial diseases.
evolution.
- Morphology - Study of structural changes in disease (Gross & microscopic) - Clinical Significance - Study of how clinical features are related to changes.
ageing.
Neoplastic disorders are due to excess cell division forming tumours.
Principles
Human disease occurs because of injury to cells / tissue. Most human disease results from injury to epithelium. Injury to one tissue usually affects the adjacent or
seen
under microscopy
Cell Injury
Damage or alteration of one or more cellular components
1. Many types of injury are tissue-specific because of anatomic relationships and tissue response to chemical and infectious agents.
2. Cell injury disrupt cell physiology; so the cell does not function at full capacity.
injurious stimuli
Consequences of Injury
1. (Reversible): No long term effects- the cell damage is repaired, the effects of the injury are reversible. 2. The cell adapts to the damaging stimulus. 3. (Irreversible): The cell dies, undergoing necrosis.
Adaptation to injury
1. Atrophy: decrease in the size and functional capacity of the cell. after normal growth has been attained. ( O2, blood, nerve supply) 2. Hypertrophy: an increase in the size of the cell secondary to an increase in cell function. Increase in the number of mitochondria and ER, etc.
5.
Hypoplasia:
underdevelopment
or
incomplete
development of an organ / tissue (less severe in degree than aplasia). 6. Aplasia: lack of development of an organ or tissue (may have a rudimentary organ). can also refer to lack of production of cells from an organ or tissue (eg aplastic anemia).
Uterine hypertrophy
Muscular hypertrophy
Metaplasia
Cell Atrophy
Causes
1. Loss of blood supply or innervations 2. Loss of endocrine factors (eg. TSH)
Type of injury
Severity of the injury Duration of the injury
4.
alcohol
intoxication,
chronic
illness,
diabetes
mellitus, etc.
This may be due to: An increase in entry of free fatty acids. An increase in synthesis of free fatty acids. A decrease in fatty acid oxidation.
3. Endoplasmic reticulum
4. Nucleus
4. Immunologic reactions
5. Genetic mutations 6. Nutritional imbalances
Cell Death
Apoptosis Necrosis
Apoptosis
Morphology of Necrosis
Pyknosis
Shrunken nucleus with dark staining Seen in a necrotic (dead) cell
Karyorrhexis
Fragmentation of pyknotic nucleus
Karyolysis
Extensive hydrolysis of pyknotic nucleus with loss of staining
Karyolysis
Types of Necrosis
1- Coagulative Necrosis
Dead cells remain as ghost-like remnants of their former self Classically seen in an MI
2- Liquefactive Necrosis
The dead cell undergoes extensive autolysis, caused by the release of lysosomal hydrolases (proteinases, DNases, RNases, lipases, etc.)
infarction.
Liquefactive Necrosis
3- Caseous Necrosis (caseum cheesy) Resembles cottage cheese Soft, friable, whitish-grey Present within infected tissues Seen in Tuberculosis (Mycobacterium tuberculosis)
Caseous Necrosis
Caseous Necrosis
4- Fat Necrosis
Leakage of lipases from dead cells attack triglycerides in surrounding fat tissue and generate free fatty acids and calcium soaps