cell inj 1
TRANSCRIPT
Any disease process will have:
1. Etiology 2. Pathogenesis3. Morphologic changes4. Signs & symptoms (clinical features)5. Diagnosis, prognosis, treatment & prevention
Physiologic stimulus / Pathologic stimulus
Cellular adaptation
Cell Injury
Normal cell Reversible Irreversible injury
Cell Death
Factors influencing cellular response to an
injurious stimulus:
1. Type of injurious agent
2. Duration of stimulus
3. Type of target cell
4. Status (nutritional & metabolic) of target cell
Response of a cell to injury can be in the form of:
1. Cellular adaptations2. Acute cell injury – reversible & irreversible3. Intra cellular accumulations (metabolic derangements)4. Pathologic calcification5. Aging
Defined as increase in cell size with concomitant increase in size of tissue or organs
Increased synthesis of structural proteins & organelles
Hypertrophy is usually associated with hyperplasia in stable cells
Pure hypertrophy occurs in heart & skeletal muscles (non-dividing permanent cells)
Physiologic hypertrophy occur in:
◦ Skeletal muscles (weight lifters) - Mechanical
◦ Uterine muscles (pregnancy) – Hormonal
◦ Mammary glands (pregnancy) – Hormonal
Pathologic hypertrophy occur in:
◦Heart (hypertension, post-MI) – Mechanical◦ Smooth muscle (achalasia in esophagus,
pyloric stenosis) – Mechanical◦ Kidney (following nephrectomy) –
Compensatory◦ Liver – Compensatory or drug-induced
Defined as an increase in number of cells with proportionate increase in size of tissue or organ
Occur in labile cells & stable cells
Usually associated with hypertrophy
Predisposition to cancer
Physiologic hyperplasia:1. Hormonal e.g.i. Gravid uterusii. Female breast (pregnancy & puberty)2. Compensatory – Parenchymal e.g.i. Liver (influence of GF)3. Compensatory – Mesenchymal e.g.i. Fibroblasts & blood vessels (wound healing)
Pathologic Hyperplasia:
1. Endometrial hyperplasia (hormonal)2. Skin wart (HPV – GF)
3. Prostate hyperplasia (hormonal)
PROSTATE HYPERPLASIA
Testosterone Dihydrotestosterone (DHT)
↑ age --- ↑ ↑ estrogen --- ↑ expression of DHT receptors on prostatic parenchymal cells --- DHT binds to receptors --- Prostate Hyperplasia
Defined as replacement of one adult cell type (either epithelial or mesenchymal) by another adult cell type.
Reversible initially
Epithelial Metaplasia (columnar to squamous):
1. Cigarette smokers (trachea & bronchi)2. Vitamin A deficiency (respiratory epithelium)
Decrease in size of cells, tissues or organs Both nucleus & cytoplasm reduced in size Causes include:
1. Disuse atrophy2. Denervation atrophy
3. Loss of hormonal stimulation4. Ischemia5. Malnutrition (PEM)6. Aging (senile atrophy) Mechanism – Decreased protein synthesis &
increased protein degradation
Protein degradation occurs through:
i. Ubiquitin - Proteasome pathway --- degrade cytosolic & nuclear proteins
ii. Autophagy
Abnormal accumulation of triglycerides in parenchymal cells
Seen in:1. Liver (mostly)2. Heart3. Skeletal muscles4. Kidney etc.
Reversible injury
Causes:
Toxins (CCl4, chloroform, aflatoxins, poisons) Protein malnutrition Diabetes mellitus Obesity Pregnancy Alcohol abuse Starvation Anemia (hypoxia) Reye syndrome
Morphology:
Liver:
◦Gross --Enlarged, yellow, soft & greasy
◦M/s --- Microvesicular change
Macrovesicular change Fatty cysts
Heart:◦Gross --- In anemia --- “tigered effect” In diphtheria --- uniform effect
◦M/s features --- same as above
Phagocytic cells engulf cholesterol --- foam cells e.g.
1. Atherosclerosis 2. Xanthomas (Hyperlipidemic syndrome)
Causes of protein deposition include:
1. Nephrotic syndrome2. Russell bodies 3. Mallory bodies (alcohol )4. Neurofibrillary tangles in Alzheimer disease