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Flashcards in Pathoma Ch1 Deck (15):

Why don't permanent tissues do hyperplasia? What are the permanent tissues?

cardiac myocytes, skeletal muscle, and nerve
only do hyperplasia b/c they don't have the stem cells to do hyperplasia


How does atrophy occur?

and decr. in cell size. Mechanism is ubiquitin-proteosome degradation of the cytoskeleton AND autophagy of cellular components


How does metaplasia occur?

reprogramming of stem cells that is REVERSIBLE with the removal of the driving stressor


What is an exception to the rule that metaplasia can progress to cancer?

apocrine metaplasia of the breast.


How does vitamin A deficiency lead to metaplasia? Vitamin A review?

vitamin A can cause night blindness.
can also cause immune deficiency- needed for maturation of the immune system. Can be used in some therapeutis for promyelocytic anemia.
also needed to maintain specialized epithelia, like the conjunctiva of the eye. patient might get keratomalacia: vitamin A metaplasia


What are examples of mesenchymal tissues undergoing metaplasia?

myositis ossificans: skeletal muscle undergoes trauma and the musclke gets inflamed. the muscle is metaplastic to bone. Don't confuse with osteosarcoma! other bone will look separate and normal


What is the key difference btw dysplasia and carcinoma?

dysplasia is reversible, but cancer is not


What are some common causes of cell injury?

inflammation, hypoxia, nutritional excess or deficiency, trauma, genetic mutations


Causes of hypoxia: 3 causes and mechanisms for each

1. ischemia: decr. blood flow through an organ. may be arterial block, venous backup (Budd Chiari syndrome: blockage of hepatic veins that leads to liver infarction, most commonly caused by polycythemia vera or lupus anti-coagulant). Shock can also cause ischemia.
2. Hypoxemia: low O2 in the blood. problems with fraction of inhaled oxygen, alveolar pressure, areterial pressure, saturation)
3. Decr. O2-carrying capacity within the blood d/t hemoglobin loss or dysfunction: (ex. anemia, CO poisoning)


What is the early sign of CO exposure?



What is methemoglobinemia?

heme in hemoglobin has iron.
Fe2+ binds O2. Fe3+ can't bind O2. If Fe2+ becomes FE3+. the hemoglobin can't bind oxygen. PaO2 is normal, SaO2 is decreased. Seen with oxidant stress, like sulfa drugs and nitrate drugs, or in newborns


What is the classic finding in methemoglobinemia? treatment?

cyanosis with chocolate colored blood
treatment is IV methylene blue that helps reduce Fe3+ to Fe2+


What is the consequence of hypoxia?

low ability to generate ATP d/t impaired oxidative phosphorylation.
ATP is needed for Na/K pump to push Na out of the cell. Too much Na causes swelling of the cell.
ATP also needed for calcium pump. Ca in cytosol is supposed to be low. This can activate enzymes that are dangerous.
And, switch to anaerobic glycolysis, which can cause lactic acidosis.


What are the findings in reversible hyoxia?

cellular swelling, which causes loss of microvilli, membrane blebbing, and swelling of RER (rough ER). RER fills with water, and the ribosomes are attached with loose association- ribosomes will pop off- so you can have a decr. of protein synthesis.


What is the hallmark of irreversible cellular damage?

membrane damage.
Plasma membrane damage: enzymes leak out, calcium comes in.
mitochondrial damage: inner mitochondrial membrane crucial for metabolism, so this makes the damage irreversible. also, mitochondrial membrane damage causes cytochrome C to leak out- this activates apoptosis.
lysosome membrane is damage: lytic enzymes leak out, and they are very active enzymes b/c of all of the calcium in the cytosol from plasma membrane damage.

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