1. Catalase: H20 2. Glutathione peroxidase: Hydroxide + Hydroxy-radical 3. Fenton reaction with iron or copper: Hydroxide + Hydroxy-radical

Cell Injury, Death, and Adaptations Flashcards by Brittany Byerley

Molecular Cause of Hypereosinophilia

Degradation of cellular protein and cytoplasmic RNA

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What is aplasia?

failure in cell production during fetal development or later by loss of precursor cells in proliferative tissue

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Cell types unable to undergo hyperplasia

Cells that are incapable of mitotic division:

Skeletal muscle
Cardiac muscle
Neurons
Glomeruli
Retinal epithelium

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Cause (and tissue type) of thicking of uterus during normal cycle

Hyperplasia of the endometrial glands and stroma

(+) Estrogen

(-) Progesterone

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Cause (and tissue type) of thicking of uterus during pregnancy

Hyperplasia of smooth muscle

(+) Estrogen

(-) Progesterone

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Cause (and tissue type) of breast growth during puberty/pregnancy

hyperplasia of glandular epithelium

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In cardiac m hypertrophy, what are the vasoactive compounds and growth factors that initiates gene activation?

Vasoactive compounds:

Angiotensin II
Endothelin

Growth factors:

TGF-ß
Insulin-like GF

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What are the structural/molecular changes that accompany cardiac hypertrophy?

change from a to fetal ß-myosin
- decreases ATPase

slower, energy-efficient contraction

Change to fetal ANF
- increases Na excretion, with water, to decrease blood volume and pressure

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What is Cachexia? What causes it? MOA?

Muscle wasting

Causes: Marasmus, chronic inflammation

Overproduction of TNF suppresses appetite and induces muscle atrophy

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Mechanisms of protein degradation associated with atrophy

Lysosomal enzymes
Ubiquitin-proteasome pathway

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What is shown in the picture? What does it signal?

Lipochrome pigment: autophagic granules signify atrophy

Also: lipofuscin pigments

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What type of cellular process is shown? What is this condition called? What type of transformation? Cause?

Metaplasia

Barrett’s esophagus

In the esophagus: squamous to columnar (secreting) epithelium

Result of acid reflux disease

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What type of cellular process is shown? What is this condition called? What type of transformation? Cause?

Metaplasia

Laryngeal metaplasia

Respiratory epithelium (columnar) to squamous

Smoking

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What type of cellular process is shown? Characteristics?

Dysplasia of squamous epithelium of cervix

Hyperchromatic nuclei and mitotic spindles: Mitosis occurs at all tissue levels

Loss of cell polarity

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Damage to cell following ischemia

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Damage to mitochondria following increased Ca lvls, ROS damage, or lipid peroxidation

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Cell damage following loss of Ca homeostasis

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ROIs formed from radiation

Hydrolyzes water to hydroxyl and hydrogen free radicals

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Metabolism of Superoxide

SOD and forms H2O2

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Metabolism of H2O2

Catalase: H20
Glutathione peroxidase: Hydroxide + Hydroxy-radical
Fenton reaction with iron or copper: Hydroxide + Hydroxy-radical

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Significance of Malondialdehyde in blood or urine

oxidative damage (due to lipid peroxide radical formation)

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Characteristics of necrotic cells

cytoplasmic eosinophilia (degradation of cytoplasmic RNA and denaturation of proteins)
Karyolysis, Pyknosis, and Karyorrhexis

**causes inflammation from leakage of cytoplasmic contents

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Characteristics of Coagulative necrosis

Results from hypoxic death (of all tissues except the brain)
Denaturation of proteins (from low ATP -> anaerobic -> increased lactic acid) which results in preservation of outline of dead cells
firm texture
wedge-shape

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Characteristics and causes of liquifactive necrosis

Causes:

brain hypoxia (microglia)
Abcess (neutrophils)
Pancreatitis (proteases)
Bacterial/fungal infection

Characteristics:

viscous liquid mass (enzymatic digestion)
focal accumulation of inflammatory cells

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Dry gangrene

Coagulative necrosis from anoxic injury (frostbite)

Wet gangrene

Liquefactive necrosis associated with secondary bacterial infection

Causes and Characteristics of Caseous Necrosis

Causes: 1. TB 2. Fungal infection Characteristics: (form of coagulative necrosis) 1. cheesy appearance 2. Granular center with inflammatory border 3. Tissue architecture is obliterated

Causes and Characteristics of Fat necrosis

Causes: 1. Trauma to breast 2. Acute pancreatitis Characteristics: 1. fat destruction 2. fat saponification: FAs combine with Ca

What is pictured? Cause?

Fibrinoid Necrosis Deposition of immune complexes in the blood vessels causing vasculitis (fibrin leaks out)

Type of necrosis?

Caseous necrosis

Type of necrosis?

Coagulative

Type of necrosis?

Coagulative

Type of necrosis?

Coagulative

Type of necrosis?

Fat necrosis

Type of necrosis?

Fat necrosis with saponification

Type of necrosis?

Liquifactive

Type of necrosis?

Liquifactive

What is shown? With what cellular process is it associated?

Myelin figures (swirls of phospholipids from membrane damage) Associated with apoptosis

Effect of mercuric chloride

binds sulfhydryl groups increase membrane permeability

Effect of cyanide

Inhibit oxidative phosphorylation (bind cytochrome C)

Characteristics of apoptotic cells

1. shrunken cell (results in eosinophilia) 2. condensed chromatin (may form crescents) 3 Nucleus may break up into fragments

Role of p53

cell cycle arrest if DNA damage is present If irreparable, induces apoptosis.

Extrinsic pathway apoptosis receptors

FAS ligand and TNF

Causes of Intrinsic pathway apoptosis and MOA

1. Withdrawal of GFs/Hormones 2. Protein misfolding 3. Cellular Injury Mechanism: pro- vs anti-apoptotic molecule concentrations determine fate

Proteins from Tc cells to induce apoptosis

1. Perforin (punctures membrane to allow Granzyme in) 2. Granzyme

What is shown? With what disease is it associated?

Mallory bodies (or alcoholic hyaline) composed of IFs Alcoholic liver disease

Accumulation of Triglycerides 1. Disease 2. Causes 3. Changes

Steatosis Causes: 1. Alcohol ((+) triglyceride synthesis) 2. Protein malnutrition ((-) apolipoprotien) 3. Malnutrition (increased FAs) Changes: 1. Liver enlargens and turns yellow 2. liposomes in cells --\> fatty cysts when cells lyse

Atherosclerosis 1. What is the accumulation? 2. What are cell characteristics?

1. Cholesterol 2. Atheromas: foam cells and crystalized cholesterol clefts Affects foam cells (macrophages) and smooth mm cells

Xanthomas ## Footnote 1. What is the accumulation? 2. What are cell characteristics? 3. Causes?

1. Cholesterol 2. Foamy macrophages (collect in connective tissue of skin, forming mass) 3. Hyperlipidemia, neoplasms, xanthelasma (no underlying disorder

1. What is shown? 2. What is the accumulation? 3. What are cell characteristics?

1. Cholesterolosis 2. Cholesterol in the gall bladder 3. Foamy macrophages

Neimann-Pick type C ## Footnote 1. Disease type? 2. What is the accumulation?

1. Lysosomal storage disease 2. Cholesterol

Alpha-anti-trypsin deficiency 1. What is the accumulation? 2. What is an associated disease?

1. Protein (anti-trypsin) due to misfolding 2. Emphysema

Chloride Channel protein of lung deficiency 1. What is the accumulation? 2. With what disease is it associated?

1. Protein (misfolded Cloride Channel) 2. Cystic fibrosis

1. What type of accumulation is pictured? 2. What diseases are associated with this type of accumulation?

1. Glycogen 2. Diabetes and Pompe's disease (glycogen storage disease)

1. What type of accumulation is pictured? 2. What is the disease? Characteristics?

1. Carbon or coal dust 2. Anthracosis: Transport via macrophage to regional lymph nodes, turning them black

1. What type of accumulation is pictured? 2. What does it signal? 3. Where does it come from?

1. Lipofuscin 2. Oxidative stress of cell 3. End product of lipid peroxidation

Hemosiderosis ## Footnote 1. What is the accumulation? 2. Causes?

1. Hemosiderin 2. Hb degradation or Fe overload - Hemorrage and lysis of RBCs (bruising) - Hemolytic anemia - Blood transfusion - Increased dietary iron or defective metabolism

Jaundice ## Footnote 1. What is the accumulation? 2. What is the origin of the accumulation?

1. Bilirubin 2. derived from Hb but no iron

Dystrophic vs Metastatic calcification

Dystrophic: occurs in dying tissue; calcium lvl normal Metastatic: occurs in normal tissue; elevated calcium lvls

Initiation of intracellular vs extracellular dystrophic calcification

Intracellular: Mitochondria (accumulates Ca) Extracellular: phospholipids in membrane vesicles from dead cells

Causes of Hypercalcemia

1. Hyperparathyroidism (bone resorption) 2. Bone destruction 3. Increased Vit D (increases absorption of Ca from intestine and kidney) 4. Renal failure (reuptake of PO4, secondary hyperparatyroidism)