Pathology Module 2: Cell injury and adaptation

What is hypertrophy?

Increase in protein synthesis —> Increase in size of cells —> Increase in organ/tissue size

What is hyperplasia?

Excessive hormone production/ growth factors —> Increased number of cells

What is hypoplasia?

Incomplete or underdevelopment of tissues or an organ

What is atrophy?

Decrease in mass of pre-existing cells —> smaller tissue/organ

Common causes of atrophy

lack of use

poor nutrition

lack of oxygen

lack of endocrine stimulation

aging

injury of the nerves

What is metaplasia?

Replacement of one tissue by another tissue

What is hypoxic cell injury?

Complete lack of oxygen/ decreased oxygen

What is anoxia?

Worst and complete lack of oxygen to the brain

What is hypoxia?

Reduced supply of oxygen to the brain

During hypoxic cell injury, how long till there is irreversible damage in neurons?

3-5 minutes

During hypoxic cell injury, how long till there is irreversible damage in myocardial cells and hepatocytes?

1-2 hours

During hypoxic cell injury, how long till there is irreversible damage in skeletal muscles?

Many hours

What causes cell death?

severe or prolonged injury

What causes cell death?

Irreversible damage to the cell membrane

Calcium influx

Mitochondria calcifies

What is a free radical?

Chemical species that contain single unpaired electron in an outer orbit

Why are free radicals dangerous?

They bind to macromolecules

through oxidation that cause cell damage

What are the intracellular enzymes?

glutathione peroxidase

catalase

superoxide dismutase

What are important for cell antioxidant defense?

Glutathione peroxidase (GPX)

superoxide dismutase (SOD)

catalase

Describe apoptosis?

Controlled cell death

No inflammation

Induced by physiological stimuli

Energy (ATP) dependent

Describe necrosis?

Affects groups of cells

Evoked by non-physiological stimuli

Inflammation

Swelling of cytoplasm

No energy requirement

Ca overload

What is necrosis?

The sum of all the reactions in an injured tissue

What is autolysis?

Cells enzymes auto digest cell

What is heterolysis?

Extrinsic enzymes of lysins digest cells

What is coagulative necrosis?

Cell outline usually remains intact after cell death

Due to interruption of blood -ischemia

Ex: poor collateral circulation

What is the most common type of necrosis?

Coagulative

What is karyolysis?

Nuclear fading

What is pyknosis?

Nuclear shrinkage

What is Karyorrhexis?

pyknotic nuclei membrane ruptures and nucleus

What is liquefactive necrosis?

Lysosomal and hydrolytic enzymes release by necrotic cells or neutrophils liquefy the tissue —> pseudo cyst

What is caseous necrosis?

Coagulative + Liquefactive

Part of granulomatous

What is gangrenous necrosis?

Interruption of the blood supply to the lower extremities or bowels

What are the two types of gangrenous necrosis?

Wet: Complicated by liquefactive necrosis

Dry: complicated by coagulative necrosis

What is fibrinoid necrosis?

Immune mediated vascular damage

Protein like material in the blood vessels

What is fat necrosis?

Benign condition when fat is injured due to trauma, radiation, or surgery

Can self-resolve

What inhibits apoptosis?

BCL-2

What facilitates apoptosis?

BAX

BAK

P53

Which is a tumor suppressor gene?

P53

What is BAX and BAK activated by?

heat

changes in pH

chemicals

What appearance does hyaline change have?

Glassy

Where can hyaline change occur?

Intracellular and extracellular

Where is pathologic calcifications?

Previously damaged tissues

What is hypercalcemia - “metastatic calcification”?

Deposition of calcium salts in normal tissue because of elevated calcium