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1. Growth Adaptations, Cellular Injury, Cell Death

Growth Adaptations Hyperplasia, hypertrophy, atrophy, metaplasia, dysplasia, aplasia, and hypoplasia - Caused by a change in physiologic stress away from homestasis
Hyperplasia & Hypertrophy (cause) Increase in physiologic stress
Hypertrophy Increase in cell size. Involves gene activation, protein synthesis, and organelle production.
Hyperplasia Increase in cell number developed by stem cells. Does not occur in permanent tissues.
Permanent Tissues Cardiac muscle, skeletal muscle, and nerves. Only undergo hypertrophy, not hyperplasia.
Pathologic Hyperplasia Can progress to dysplasia and cancer. EXCEPTION: Benign Prostatic Hyperplasia (BPH)
Atrophy (cause) Decrease in physiologic stress
Atrophy Decrease in cell size via Ubiquitin-Proteosome degradation of cytoskeleton and autophagy of cellular components. Decrease in cell number via apoptosis.
Metaplasia Change in type of physiologic stress on organ leads to a change in cell type via reprogrammed stem cells. Most commonly in epithelium. REVERSIBLE, but can progress to dysplagia and cancer. EXCEPTION: Apocrine Metaplasia of breast.
Barrett Esophagus Under acidic stress, non-keratinizing squamous epithelium of the esophagus changes into non-ciliated, mucin-produing columnar.
Keratomalacia Vitamin A deficiency leads to night blindness and metaplasia of the conjuctiva into stratified keratinizing squamous epithelium.
Myositis Ossificans A type of mesenchymal tissue metaplasia. After trauma, muscle tissue changes to bone during healing.
Dysplasia Disordered cellular growth. Most often referring to precancerous cells. Arises from longstanding pathologic hyperplasia or metaplasia. REVERSIBLE. If stress persists, then progresses to carcinoma.
Cervical Intraepithelial Neoplasia (CIN) Cervical dysplasia - precursor to cervical cancer.
Aplasia Failure of cell production during embryogenesis.
Hypoplasia Decrease in cell production during embryogenesis, resulting in a relatively small organ.
Hypoxia Low oxygen delivery to tissue - low oxygen leads to low ATP via oxidative phosphorylation. Three causes: ischemia, hypoxemia, and decreased O2-carrying capacity of blood.
Ischemia Decreased blood flow through an organ. Via: decreased arterial perfusion, decreased venous drainage, or shock (generalized hypotension)
Hypoxemia Low partial pressure of oxygen in the blood (PaO2 < 60mm Hg, SaO2 < 90%)
Causes of hypoxemia Think atmosphere (FiO2) to alveoli (PAO2) to arteries (PaO2) to RBC (SaO2). High altitude (low FiO2), hypoventilation (low PAO2 from high PACO2), diffusion defect (thick alveolar barrier causes low PaO2), or V/Q mismatch.
Causes of decreased O2 carrying capacity of blood Hemoglobin loss or dysfunction. Examples: Anemia (PaO2 normal, SaO2 normal), CO poisoning, and Methemoglobinemia.
Carbon Monoxide (CO) Poisoning CO has higher affinity for Hb (PaO2 normal, low SaO2). Classic finding: cherry-red appearance of skin and lips. Early sign is headache. Can progress to coma and death.
Methemoglobinemia Think Fe2 binds O2. Under oxidant stress, Fe2 is changed to Fe3 which cannot bind O2 (PaO2 normal, low SaO2). Seen with sulfa and nitrate drugs or in newborns. Classic finding: cyanosis with chocolate-colored blood. Treatment: IV methylene blue
Describe the key cellular functions that low ATP disrupts Na-K pump (Na and water builds up in cell - swelling), Ca pump (Ca builds up in cell - enzyme activator), Aerobic glycolysis (changes to anaerobic - lactic acid builds up, lowers pH which denatures proteins and precipitates DNA).
Hallmarks of reversible cellular injury Cellular swelling (from disrupted Na-K pump) - causes loss of microvilli, membrane blebbing, and RER swelling (which results in dissociation of ribosomes and decreased protein synthesis).
Hallmarks of irreversible cellular injury Membrane damage - Plasma membrane (leaking out cytosolic enzymes and additional Ca enters cell), Mitochondrial membrane (loss of electron transport chain and cytochrome c into cytosol [apoptosis]), and lysosome membrane (leaks hydrolytic enzymes)
Hallmarks of cell death Loss of nucleus. Occurs via pyknosis, karyorrhexis, and karyolysis. Two types: Necrosis and Apoptosis.
Pyknosis Nuclear condensation.
Karyorrhexis Nuclear fragmentation.
Karyolysis Nuclear dissolution.
Necrosis Death of large groups of cells followed by acute inflammation. Never physiologic. 6 Types: Coagulative, Liquefactive, Gangrenous, Caseous, Fat, and Fibrinoid.
Coagulative Necrosis Tissue remains firm. Cell shape and organ structure preserved, but nucleus disappears. Characteristic of ischemic infarction of any organ (except brain). Wedge-shaped and pale. Red (hemorrhagic) infarction arises if blood re-enters tissue (lungs/testes).
Liquefactive Necrosis Necrotic tissue becomes liquified due to enzymatic lysis of cells and proteins. Characteristic of: Brain infarct (enzymes from microglial cells), Abscess (enzymes from neutrophils), and Pancreatitis (enzymes from pancreas).
Gangrenous Necrosis Coagulative necrosis that resembles mummified tissue (dry gangrene). Characteristic of ischemia of lower limb and GI. If followed by infection of dead tissue, then wet gangrene (liquefactive necrosis).
Caseous Necrosis "Cottage cheese-like" soft and friable necrotic tissue. Characteristic of granulomatous inflammation (TB or fungal infection).
Fat Necrosis Chalky-white appearance of necrotic adipose tissue due to calcium deposition. Characteristic of fat trauma (breast) and pancreatitis-mediated damage to peripancreatic fat. Fatty acids released by trauma or lipase bind with calcium via saponification.
Saponification Fatty acids bind with calcium in damaged adipose tissue. An example of Dystrophic Calcification. Necrotic tissue acts as a nidus for calcification in the setting of normal serum calcium and phosphate.
Metastatic Calcification High serum calcium or phasphate levels lead to calcium deposition in normal tissues.
Fibrinoid Necrosis Necrotic damage to blood vessel wall. Proteins (including Fibrin) leak into vessel wall resulting in bright pink staining of vessel wall. Characteristic of malignant hypertension, pre-eclampsia, and vasculitis.
Apoptosis Energy dependent, genetically programmed cell death involving small groups of cells. Dying cells shrinks (more eosinophilic), then pyknosis and karyorrhexis. Then apoptotic bodies are removed by macrophages (no inflammation). Mediated by Caspases.
Caspase Mediator of Apoptosis. Activates proteases to breakdown cytoskeleton and endonucleases to breakdown DNA. Activated in 3 pathways: Intrinsic Mitochondrial Pathway, Extrinsic Receptor-Ligand Pathway, and Cytotoxic CD8+ T Cell-Mediated Pathway.
Intrinsic Mitochondrial Pathway Cellular injury, DNA damage, or loss of hormonal stimulation leads to inactivation of Bcl2 (an inner mitochondrial membrane stabilizer). Lack of Bcl2 allows Cytochrome C to leak into cytoplasm activating Caspases.
Extrinsic Receptor-Ligand Pathway FAS ligand binds FAS death receptor (CD95) on target cell, activating caspases (negative selection of thymocytes in thymus). Or, Tumor Necrosis Factor (TNF) binds TNF receptor on target cell, activating Caspases.
Cytotoxic CD8+ T Cell-Mediated Pathway Perforins (secreted by CD8+ T cells) create pores in target cell. Granzyme (from CD8+ T cells) enters pores and activates caspases. Allows CD8+ T cells to kill virally infected cells.
Free Radical Chemical species with an unpaired electron in outer orbit. Cause injury via peroxidation of lipids and oxidation of DNA/proteins. DNA damage is associated with aging and oncogenesis.
Physiologic generation of Free Radicals Via Oxidative Phosphorylation. Cytochrome c oxidase (complex IV) transfers electrons to oxygen. Partial reduction of O2 yields Superoxide (O2*-), Hydrogen Peroxide (H2O2), and Hydroxyl Radicals (OH*). Hydroxyl radicals most damaging of all free radicals.
Pathologic generation of Free Radicals Arises with Ionizing Radiation (water hydrolyzed to hydroxyl free radicals), Inflammation (NADPH oxidase generates Superoxide via neutrophils), Metals (copper, iron - Fe2+ generates hydroxyl free radicals via Fenton reaction), and Drugs/Chemicals (P450)
Mechanisms of Free Radical elimination Anti-oxidants (glutathione, Vit A, C, E), Metal Carrier Proteins (Transferrin), and Enzymes (Superoxide Dismutase [mitochondria: O2*- to H2O2], Catalase [peroxisomes: H2O2 to O2 & H2O], and Glutathione Peroxidase [mitochondria: GSH + OH* to GSSG & H2O])
Carbon Tetrachloride (CCl4) Organic solvent in dry cleaning. In liver, P450 converts to CCl3* free radical. Results in RER swelling, detachment of ribosomes, and impairment of protein production. Less apolipoproteins leads to fatty change in liver.
Reperfusion Injury Return of blood post ischemic injury also returns oxygen and inflammation factors which results in production of O2-derived free radicals. Leads to continued rise in organ enzymes post reperfusion (ex. troponin after myocardial infarct).
Amyloid Misfolded protein that deposits in extracellular space. Characteristics: Beta-pleated sheet configuration and Congo Red staining (with apple-green birefringence under polarized light). Systemic or localized.
Primary Systemic Amyloidosis Systemic deposition of AL amyloid (derived from immunoglobulin light chain). Associated with plasma cell dyscrasias (plasma cells produce Ig light chain in balance with heavy chains). Example of plasma cell dyscrasias: multiple myeloma.
Secondary Systemic Amyloidosis Systemic deposition of AA amyloid derived from Serum Amyloid-Associated protein (SAA). SAA is an acute phase reactant increased in chronic inflammatory states, malignancy, and Familial Mediterranean Fever.
Familial Mediterranean Fever Autosomal Recessive dysfunction of neutrophils in people with Mediterranean origin. Episodes of fever and acute serosal inflammation (can mimic appendicitis, arthritis, or MI). High SAA during attacks deposits as AA amyloid in tissues.
Clinical Findings of Systemic Amyloidosis Nephrotic Syndrome (kidney is most common organ involved), Restrictive Cardiomyopathy or Arrhythmias, Tongue enlargement, malabsorption, and hepatosplenomegaly.
How to diagnose Systemic Amyloidosis Tissue Biopsy. Typically abdominal fat pad or rectum.
Treatment of Systemic Amyloidosis Damaged organs must be transplanted. Amyloid cannot be removed.
6 types of Localized Amyloidosis Senile Cardiac Amyloidosis, Familial Amyloid Cardiomyopathy, Non-Insulin-Dependent Diabetes Mellitus (type II), Alzheimer disease, Dialysis-associated Amyloidosis, and Medullary Carcinoma of the Thyroid.
Senile Cardiac Amyloidosis Non-mutated serum Transthyretin (2nd most common protein in blood) deposits in heart. Usually assymptomatic; present in 25% of people over 80.
Familial Amyloid Cardiomyopathy Mutated serum Transthyretin deposits in heart leading to restrictive cardiomyopathy. 5% of African Americans carry the mutated gene.
Non-Insulin-Dependent Diabetes Mellitus (type II) Amylin (derived from insulin) deposits in islets of pancreas.
Alzheimer disease Alpha-Beta Amyloid (derived from Beta-amyloid Precursor Protein [Beta-APP]) deposits in brain forming amyloid plaques. Gene for Beta-APP is located on chromosome 21 (most Down Syndrome [Trisomy 21) patients develop early onset [<40 y.o.] Alzheimers.
Dialysis-Associated Amyloidosis Beta2-microglobulin (associated with MHC-1) deposits in joints.
Medullary Carcinoma of the Thyroid Cancer of thyroid C-cells which produce excess Calcitonin. Calcitonin deposits within the tumor. Sometimes seen in setting of "Tumor cells in an amyloid background" in a thyroid biopsy.
Created by: zackao1



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