Mechanism of Injury

Cells

________ can either die by necrosis which causes inflammation or apoptosis which is silent.

Extrinsic Pathway

________: death receptor- mediated (ligand binds the receptor)

Hyperplasia

________: increase in the number of cells (dividing cells only)

Dysplasia

________: Change in how cells look.

Microscopic

________: at the cellular level, inclusions (could be iron, fat, lipofuscin (aging)), pigmentation, multinucleation, apoptosis, necrosis.

pigmentation

Macroscopic: at the organ level, hypertrophy, atrophy, dysplasia, ________, calcification (like in severe atherosclerosis), fatty change (liver)

Endoplasmic Reticulum Stress Pathway

________: Mediated by too little or too much Calcium.

Hypertrophy

________: cells increase in size, organs increase in size (dividing and non- dividing cells)

Metaplasia

________: cells change from one cell type to another. INCREASES THE RISK OF CANCER

Pathological Hypertrophy

________: Myocytes in the heart become over-stressed due to prolonged hypertension or valve disease.

Intestinal Metaplasia

________: AKA gastro- esophageal junction or Barretts esophagus, squamous epithelium switches to glandular columnar epithelium due to GERD.

Necrosis

________ is enzymatic digestion and leakage of cellular components; violent tissue death.

Physiological Hypertrophy

________: Uterus during pregnancy (both organ and cells) and muscle growth.

Prostate Hyperplasia

________ → Benign prostatic hyperplasia (BPH) (aka nodular hyperplasia), due to testosterone being converted into DHT which is more potent.

Physiological Atrophy

________: shrinkage of the uterus after pregnancy, occurs due to loss of hormonal stimulation from the placenta and developmental gene regulation.

Pathological Atrophy

________: Muscle atrophy after a fracture, brain with Alzheimers (due to inactivity, lack of innervation, loss of perfusion, lack of nutrition, loss of hormonal stimulation, aging, or pressure)

Macroscopic

at the organ level, hypertrophy, atrophy, dysplasia, pigmentation, calcification (like in severe atherosclerosis), fatty change (liver)

Hypertrophy

increase in size

Atrophy

decrease in size

Dysplasia

Change in how cells look

Microscopic

at the cellular level, inclusions (could be iron, fat, lipofuscin (aging)), pigmentation, multinucleation, apoptosis, necrosis

Hypertrophy

cells increase in size, organs increase in size (dividing and non-dividing cells)

Hyperplasia

increase in the number of cells (dividing cells only)

Atrophy

Shrinkage in cell size (or organ)

Metaplasia

cells change from one cell type to another

Physiological Hypertrophy

Uterus during pregnancy (both organ and cells) and muscle growth

Pathological Hypertrophy

Myocytes in the heart become over-stressed due to prolonged hypertension or valve disease

Physiological Atrophy

shrinkage of the uterus after pregnancy, occurs due to loss of hormonal stimulation from the placenta and developmental gene regulation

Pathological Atrophy

Muscle atrophy after a fracture, brain with Alzheimers (due to inactivity, lack of innervation, loss of perfusion, lack of nutrition, loss of hormonal stimulation, aging, or pressure)

Squamous Metaplasia

Occurs in the upper airways usually in smokers, columnar epithelium switches to squamous epithelium due to stress

Intestinal Metaplasia

AKA gastro-esophageal junction or Barretts esophagus, squamous epithelium switches to glandular columnar epithelium due to GERD

Murder weapon

oxygen deprivation, physical injury (heat/cold/electric), chemical, infectious agent, immune system (friendly fire), genetic defects, or nutritional deficiencies

Extrinsic

death receptor-mediated (ligand binds the receptor)

Intrinsic

Mitochondrial-mediated

Endoplasmic Reticulum Stress Pathway

Mediated by too little or too much Calcium

Myocardial Infarct

ischemic necrosis of the myocardium

Coagulation Necrosis

"dry necrosis" where the basic cell outline is maintained, Nuclei lost, cytoplasm, eosinophils, hypoxic cell death

Liquefactive Necrosis

"liquid/wet necrosis" where tissue dissolves, every structure is lost, NO cells visible (infections like TB or ANYTHING in the brain)

Gangrene (Gangrenous Necrosis)

dry or wet necrosis, often after a loss of blood supply (diabetic foot, peripheral artery disease, frostbite (dry))

Caseous Necrosis

in TB the lung cavity is filled with "cheesy" white-yellow material

Fat Necrosis

Fat destruction of the Mesentery (tissue-fat sheet in the belly), frequently occurs after pancreatitis, Lipase or other digestive enzymes meet lipids and calcium and complex to form chalky "soap" deposits

macroscopic

On the organ level, hypertrophy, atrophy, dysplasia, pigmentation, calcification, fatty changes

Squamous Metaplasia

Upper airways of smokers, Columnar epithelium turns into squamous epithelium due to stress

benign prostatic hyperplasia

aka nodular Hyperplasia, due to an increase in hormonal stimulation of DHT which is 10x more potent than testosterone

Intrinsic Pathway

Mitochondria mediated apoptosis

Endoplasmic Reticulum Stress Pathway

Mediated by too much or too little calcium

Silent

death by apoptosis

Causes inflammation

death by necrosis

coagulation necrosis

"Dry necrosis" where the basic cell outline is maintained, the nuclei are lost, hypoxic cell death (infarcts)

Liquefactive necrosis

"Wet necrosis" where the tissue dissolves, every structure is lost, no cells visible

BRAIN

The _____ shows liquefactive necrosis always.

Gangrene

wet or dry necrosis, often after blood loss (diabetic foot, peripheral arterial disease, frost bite)

Caseous Necrosis

TB infections, the lung cavity is filled with "cheesy" white-yellow material

Fat Necrosis

Fat destruction of the Mesentery (tissue-fat sheet in the belly), frequently occurs after pancreatitis. Digestive enzymes meet with lipids and complex with calcium to form chalky "soap" deposits