Topics A1-5 - General Necrosis, Infarction, Apoptosis Flashcards Preview

Y Pathology I (Dustin) > Topics A1-5 - General Necrosis, Infarction, Apoptosis > Flashcards

Flashcards in Topics A1-5 - General Necrosis, Infarction, Apoptosis Deck (60)
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First 3 steps of necrosis cell death (3 of 6 steps)

1. Damage to mitochondria: toxins, ROS, etc. attack mitochondria
2. MTC damage -> ATP depletion
3. Na+/K+ pump has low E, functions poorly, so sodium builds in the cell and water follows, causing cellular swelling


Last 3 steps (of 6) of necrosis cell death

4. Anaerobic glycolysis -> lactic acid increase -> pH drops, protein synthesis reduced
5. Ca2+ ATPase impairment -> High intracellular [Ca2+] ("Point of No Return!"). Calcium activates many cell death mechanisms.
6. Membrane integrity is lost, cell lyses


5 ways that increased cytosolic Ca2+ causes cell death (try to name at least 4...)

1. Phospholipases activated -> destroys membrane
2. Proteases activated -> destroys cytoskeleton
3. Endonucleases activated -> karyolysis
4. Caspases activated -> apoptosis
5. ATPase activated -> decreased ATP


Key histo features of necrotic cell

Eosinophilic (eosin binds denatured proteins, loss of DNA/RNA), glassy/homogenous "moth-eaten appearance," nucleus karylosis, pyknotic or karyorrhexic


How does a pyknotic nucleus look?

Nucleus shrinks, more basophilic


How does karyorrhexis look?

The nucleus fragments


How does karyolysis look?

Nucleus fades, due to fading of nuclear chromatin via endonuclease activity


6 morphological types of cell necrosis

1. Fat necrosis
2. Gangrene
3. Liquefactive
4. Coagulative
5. Caseatio/"cheesy"
6. Fibrinoid necrosis

"Fat gangs lick coagulating cheese fibers"


What is the order of the breakdown of the nucleus during necrosis? (histologically)

Pyknosis -> karyorrhexis -> karyolysis

"Pick Rex's lice"


How is the nucleus different in necrosis versus apoptosis?

Necrosis: it's pyknotic, karyorrhexic, or karyolytic.

Apoptosis: It's fragmented into nucleosome-size pieces


How is the cell size different in necrosis versus apoptosis?

Necrosis: cell is enlarged

Apoptosis: cell shrinks


What happens to the cellular components in necrosis vs apoptosis?

Necrosis: cellular components leak out, including enzymes - causes enzymatic digestion/damage

Apoptosis: cellular contents are kept intact in apoptotic bodies


What is characteristic of coagulative necrosis?

Outlines of cells are still there. Dominating morphological event is that the proteins are denatured. The structure is preserved bc autolytic enzymes are inactivated. Cell becomes firm and acidophilic. Macrophages/neutrophils required to clear them.


Which organs are more prone to coagulative necrosis?

All solid organs EXCEPT the brain, which is liquefactive

Coagulative necrosis mainly in kidney, heart, liver, adrenal glands, spleen


What usually causes coagulative necrosis?

Infarction: sudden occlusion of vessel


What are the 2 types of infarctions?

1. Ischemic: pale infarct. Happens in denser tissues (kidney, heart, spleen) that prevents RBCs from damaged vessels from diffusing through necrotic tissue

2. Hemorrhagic: red infarct. Lungs, small bowel, testicle. Caused by dual blood supply, venous occlusion, or reperfusion.


What type of infarcts are gangrena humida and pulmonary abcesses?

Anemic liquefactive


What are the anemic types of cerebral infarct called, based on various appearances (reminder that they're liquefactive)

"Encephalomalacia alba" (white necrosis) = earlier infarct

Becomes "flava" (yellow) after 36 hours due to microglial digestion

If they survive and heal, it becomes "cysta post-encephalomalacia" with cyst + glial tissue


What is the hemorrhagic type of cerebral infarct called?

Encephalomalacia rubra - occurs from reperfusion injury.


Why is reperfusion dangerous?

In what situation is a medical treatment a major risk for reperfusion injury?

Enzymes that neutralize ROS are missing, and so many free radicals are generated.

Reperfusion is associated with fibrinolytic therapy after AMI


What is characteristic of liquefactive necrosis?

Tissue becomes soft and leaky. Transformation is due to autolytic enzymes, either from necrotic cell enzymes or neutrophils.


What cells mediate liquefactive necrosis in a CNS infarction?
What about in abscesses due to bacterial infection?

CNS: microglial cells release hydrolytic enzymes

Abscess: microbes stimulate neutrophils to liquefy dead tissue, produce cavity filled with pus


What is gangrene? What are the 2 types?

Not distinct pattern of cell death, but term still used. Usually refers to necrosis of extremities. Black due to Hb + H2S -> black iron sulphide

Gangrena sicca (dry) - coagulative necrosis. Arterial blockage -> hypoxia.

Gangrena humida (wet) - liquefactive due to bacterial infection, venous blockage.


What is a major symptom that gangrene may occur in the leg due to poor blood supply?

Intermittent claudication (limp and have to stop walking frequently to let blood supply catch up to leg)


How does caseous necrosis appear, both grossly and under a microscope? (keep it simple, not the full description for histo exam)

Gross: "Friable, yellow-white" appearance due to excess lipids from TB

With H-E stain appears as a collection of fragmented/lysed cells with amorphous granular pink appearance. Enclosed with a distinct inflammatory border: granuloma


What are the 2 types of fat necrosis?

1. Enzymatic: i.e. pancreas. Activation of lipases -> fats combine with calcium -> saponification. Makes chalky white areas, dystrophic calcification

2. Traumatic: injury to fatty tissue like breast. Not enzyme mediated


What is fibrinoid necrosis?

Not a real necrosis but called one in patho anyway, only visible under microscope. Immune complexes (Ag + Ab) are deposited in walls of arteries with fibrin. Makes eosinophilic amorphous shape called fibrinoid.


Where does fibrinoid necrosis usually occur?

Glomerular capillaries, small muscular arteries and arterioles, venules, valve leaflets, myocardium, subQ tissue


What may cause fibrinoid necrosis?

Immune vasculitis (e.g. Henoch-Schoenlein purpura), malignant hypertension, rheumatic fever


What are 3 ways that the extrinsic pathway to apoptosis can be activated? (no details, just names)

1. Fas Ligand
2. TNF-alpha
3. Cytotoxic T cell (perforins, granzymes)

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