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What are the two processes via which an organ can increase in size?
Hyperplasia (increase in number of cells) and hypertrophy (increase in size of cells)
Hyperplasia
Increased number of cells
Hypertrophy
Increase in cell size
What are three processes/events that occur in hypertrophy?
Gene activation, protein synthesis, production of organelles
Where do the new cells in hyperplasia come from?
Stem cells
What tissues cannot undergo hyperplasia, only hypertrophy?
Permanent tissue, i.e. skeletal muscle, cardiac muscle, nerve tissue
What is the only type of muscle that can undergo hyperplasia?
Smooth muscle (i.e. uterus)
How do cardiac myocytes respond to hypertension?
Hypertrophy, not hyperplasia
Hyperplasia that occurs due to underlying pathologic process
Pathologic hyperplasia
Pathologic hyperplasia pathway
Hyperplasia --> dysplasia --> cancer
exception is BPH
What is one exception to the rule that pathologic hyperplasia can lead to cancer?
Benign prostatic hyperplasia does not increase the risk for cancer
What leads to atrophy?
Decrease in stress
What are the two processes that cause atrophy?
A decrease in the size of cells (via ubiquitin-proteosome degradation of the cytoskeleton and autophagy) and a decrease in the number of cells (via apoptosis)
Where are the three places stem cells are found?
Bone marrow, skin, base of intestinal crypts
Ubiquitin
Protein put on intermediate filaments of the cytoskeleton to mark them for degradation in ubiquitin-proteosome degradiation (decrease cell size)
Proteosome
Destroys ubiquitin-tagged proteins, often intermediate filaments
What destroys ubiquitin tagged proteins?
Proteosomes
Autophagy
Cell consumes its own components in vacuoles, which fuse with lysozomes, whose hydrolytic enzymes break the cellular components in the vacuoles down
What are the two processes in atrophy that can decrease cell size
Ubiquitin-proteosome degradation (to decrease cytoskeleton) and autophagy (to decrease organelles)
What promotes metaplasia?
A change in stress on a cell
Epithelium
Cells that line body surfaces
What type of cells are most commonly involved in metaplasia?
Change of one type of surface epithelium to another (i.e. squamous, columnar, urethelial/transitional)
Barrett's Esophagus
Non-keratinized squamous epithelium of the esophagus becomes non-ciliated, mucin producing columnar cells (normal cell in stomach)
Is metaplasia reversible?
Yes
How does metaplasia occur?
Via reprogramming of stem cells
What type of metaplasia does not produce an increase in cancer risk?
Apocrine metaplasia of the breast, which is seen in fibrocystic change of the breast
Metaplasia to cancer pathway
Metaplasia --> dysplasia --> cancer
What vitamin deficiency can result in metaplasia?
Vitamin A deficiency
Vitamin that differentiates specialized epithelial surfaces (i.e. conjunctiva of the eye)
Vitamin A
What happens to the conjunctiva of the eye during Vitamin A deficiency?
Undergoes metaplasia from goblet cell/columnar epithelium to keratinizing squamous epithelium
Xerophthalmia
Dry eyes (caused by vitamin A deficiency and metaplasia); can lead to keratomalacia
Keratomalacia
Corneal destruction due to vitamin A deficiency; can eventually result in blindness; example of metaplasia, columnar epithelium becomes squamous, and can lead to xerophthalmia (dry eye)
Myositis ossificans
Connective tissue within muscle changes to bone during healing after a trauma; example of mesenchymal metaplasia
Example of mesenchymal (connective) tissue metaplasia
Myositis ossificans
Sign of vitamin A deficiency
Loss of night vision
Types of mesenchymal/connective tissue
Bone, blood vessels, fat, cartilage
Dysplasia
Disordered cell growth, most often referring to proliferation of precancerous cells
CIN
Cervical intraepithelial neoplasia is an example of dysplasia and is a precursor to cervical cancer
What two processes commonly lead to dysplasia?
Pathologic hyperplasia and metaplasia
Is dysplasia reversible?
Yes, if the inciting stress is relieved
Is carcinoma reversible?
No
Aplasia (and give an example)
Failure of cell production during embryogenesis; unilateral renal agenesis
Hypoplasia
Decrease in cell production during embryogenesis, resulting in a small organ
Example of hypoplasia
Streak ovary in Turner's (45 X)
When does cellular injury occur?
When stress exceeds a cells ability to adapt
What does cellular adaptation versus cellular injury depend on?
Type of stress 2.Severity of stress 3. Type of cell
Neurons versus skeletal muscle in ischemic injury
Neurons are highly susceptible (3-5 minutes) whereas skeletal muscle more resistant
Slowly developing ischemia versus acute ischemia
Slowly developing ischemia will lead to adaptation (i.e. renal artery atherosclerosis will result in renal atrophy) whereas acute ischemia (i.e. renal artery embolus) will result in injury
Hypoxia
Low oxygen delivery to tissues
Why does hypoxia cause problems?
Oxygen is the final electron acceptor in oxidative phosphorylation electron transport chain. Without oxygen to complete oxidative phosphorylation, low ATP results in cell injury
Name three general causes of hypoxia
Ischemia, hypoxemia, decreased oxygen carrying capacity of the blood
Ischemia
Decreased blood flow through an organ
What are three causes of ischemia?
Decreased arterial blood flow, backed up venous blood (Budd-Chiari Syndrome), shock (hypotension/low cardiac output resulting in decreased perfusion to tissues)
What is the most common cause of Budd Chiari Syndrome, and what is a second cause?
Polycythemia Vera (too many red blood cells, causing blood to be viscous and unable to flow well through hepatic vein). Second cause is lupus, due to lupus anticoagulant
Budd Chiari Syndrome
Thrombosis of hepatic vein, preventing fresh blood flowing through the liver
Hypoxemia
Low partial pressure of oxygen in the blood (PaO2 < 60 mmHg, resulting in SaO2 < 90%)
Path of oxygen from atmosphere to hemoglobin
FiO2 --> PAO2 --> PaO2 --> SaO2
Shock definition and the different types
Decreased perfusion of vital organs (cardiogenic, hypovolemic, anaphylactic, septic)
Disease where air is trapped in the lung
COPD
Example of diffusion defect
Interstitial Pulmonary Fibrosis
PaO2 and SaO2 in anemia
Normal
Anemia
Decreased RBC mass
PaO2 and SaO2 in CO poisoning
PaO2 normal; SaO2 decreased
Treatment for CO poisoning
100% O2
Cherry Red Appearance of Skin
CO poisoning
First sign of CO poisoning
Headache
PaO2 and SaO2 in Methemoglobinemia
PaO2 normal; SaO2 decreased
Drug causes of methemoglobinemia
Sulfa and nitrate drugs
Methemoglobinemia
Fe2+ oxidized to Fe3+
Two signs of methemoglobinemia
Cyanosis and chocolate colored blood
Treatment for methemoglobinemia
Methylene blue (ascorbic acid as ancillary treatment)
Population susceptible to methemoglobinemia
Newborns
Three functions low ATP (as a result of hypoxia) disrupts
Na-K pump
Ca pump
Aerobic glycolysis (pyruvate and produces 34 ATP)
Hallmark of reversible cell injury
Cellular swelling (including loss of microvilli, membrane blebbing, and decreased protein synthesis due to ribosomes popping off ER)
Goal for Ca in cytosol, and why?
Goal is to keep Ca low in the cytosol, because Ca can activate enzymes. When the Ca pump is dysfunctioning due to a lack of ATP, Ca concentration increases in the cytosol of the cell
Hallmark of irreversible cellular injury
Membrane damage (phospholipid, mitochondrial, and lysosome membrane)
Two results of phospholipid membrane damage due to low ATP
Enzymes leak into the blood (i.e. what you are measuring when you get troponins and LFTs) Increased Ca in the cytosol
Where is the electron transport chain?
Inner mitochondrial membrane
Two results of mitochondrial membrane damage due to low ATP
No electron transport chain, 2. Cytochrome c leaks into the cytosol, activating apoptosis
One result of lysosome membrane damage due to low ATP
Hydrolytic enzymes leak into the cell, are activated by Ca
Morphologic hallmark of cell death
Loss of the nucleus
Steps in losing the nucleus in cell death
Pyknosis (condensation), karyorrhexis (fragmentation), karyolysis (dissolution)
Two mechanisms of cell death
Apoptosis and necrosis
Necrosis definition
Death of a large group of cells followed by acute inflammation
What follows necrosis?
Acute inflammation and neutrophils
Necrotic tissue that remains firm, with cell shape and organ structure preserved by coagulation of proteins, but the nucleus disappears
Coagulative necrosis
What type of necrosis follows ischemic infarction in all organs except the brain?
Coagulative necrosis (liquefactive in the brain)
What is the shape and color of infarcted tissue due to ischemia/coagulative necrosis?
Wedge shaped with pale color
Two causes of acute inflammation
Infection
When can a red infarction (as opposed to pale) arise?
Blood reenters a loosely organized tissue (lungs, testicle, bowel)
What is the pathogenesis of ischemia in a testicular infarction?
The testicle twists on the spermatic cord, causing the vein to be compressed but the artery is not compressed, so blood gets backed up and fresh blood can't flow into the tissue
Necrotic tissue becomes liquefied due to enzymatic lysis of cells and proteins, causing liquefaction
Liquefactive necrosis
Three processes that present with liquefactive necrosis
Brain infarction
What causes liquefactive necrosis in the brain?
Microglial cells (equivalents of monocytes) release proteolytic enzymes, which liquefy the brain
Abscess
Walled off area of dead tissue (neutrophils inside walled off area)
Why does an abscess present with liquefactive necrosis?
Proteolytic enzymes of neutrophils liquefy the tissue
Why does pancreatitis present with liquefactive necrosis?
Proteolytic enzymes from the pancreas liquefy the parenchyma
Gangrenous necrosis
Coagulative necrosis that resembles mummified tissue
What artery is commonly occluded in diabetics, leading to gangrenous necrosis of the foot?
Popliteal artery
Wet gangrene
Superimposed infection on top of dry gangrene, resulting in liquefactive necrosis
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