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

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

1
Q

First 3 steps of necrosis cell death (3 of 6 steps)

A
  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
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2
Q

Last 3 steps (of 6) of necrosis cell death

A
  1. Anaerobic glycolysis -> lactic acid increase -> pH drops, protein synthesis reduced
  2. Ca2+ ATPase impairment -> High intracellular [Ca2+] (“Point of No Return!”). Calcium activates many cell death mechanisms.
  3. Membrane integrity is lost, cell lyses
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3
Q

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

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

Key histo features of necrotic cell

A

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

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5
Q

How does a pyknotic nucleus look?

A

Nucleus shrinks, more basophilic

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6
Q

How does karyorrhexis look?

A

The nucleus fragments

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7
Q

How does karyolysis look?

A

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

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8
Q

6 morphological types of cell necrosis

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

“Fat gangs lick coagulating cheese fibers”

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9
Q

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

A

Pyknosis -> karyorrhexis -> karyolysis

“Pick Rex’s lice”

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10
Q

How is the nucleus different in necrosis versus apoptosis?

A

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

Apoptosis: It’s fragmented into nucleosome-size pieces

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11
Q

How is the cell size different in necrosis versus apoptosis?

A

Necrosis: cell is enlarged

Apoptosis: cell shrinks

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12
Q

What happens to the cellular components in necrosis vs apoptosis?

A

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

Apoptosis: cellular contents are kept intact in apoptotic bodies

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13
Q

What is characteristic of coagulative necrosis?

A

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.

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14
Q

Which organs are more prone to coagulative necrosis?

A

All solid organs EXCEPT the brain, which is liquefactive

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

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15
Q

What usually causes coagulative necrosis?

A

Infarction: sudden occlusion of vessel

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16
Q

What are the 2 types of infarctions?

A
  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.
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17
Q

What type of infarcts are gangrena humida and pulmonary abcesses?

A

Anemic liquefactive

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18
Q

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

A

“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

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19
Q

What is the hemorrhagic type of cerebral infarct called?

A

Encephalomalacia rubra - occurs from reperfusion injury.

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20
Q

Why is reperfusion dangerous?

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

A

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

Reperfusion is associated with fibrinolytic therapy after AMI

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21
Q

What is characteristic of liquefactive necrosis?

A

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

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22
Q

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

A

CNS: microglial cells release hydrolytic enzymes

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

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23
Q

What is gangrene? What are the 2 types?

A

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.

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24
Q

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

A

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

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25
Q

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

A

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

26
Q

What are the 2 types of fat necrosis?

A
  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
27
Q

What is fibrinoid necrosis?

A

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.

28
Q

Where does fibrinoid necrosis usually occur?

A

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

29
Q

What may cause fibrinoid necrosis?

A

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

30
Q

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

A
  1. Fas Ligand
  2. TNF-alpha
  3. Cytotoxic T cell (perforins, granzymes)
31
Q

In general, what is the mechanism that the different initiators use in the extrinsic pathway of apoptosis? (again, very general.. need to know more than this)

A
  1. Mediator binds to death receptor, activates initiator caspases
  2. Initiator caspases turn to executioner caspases (proteases and nucleases)
  3. Proteases destroy cytoskeleton, endonucleases destroy nucleus
32
Q

What is general layout of the intrinsic pathway to apoptosis?

A
  1. Cell injury, DNA damage, misfolded proteins -> BCL-2 sensor genes activated
  2. Activation of BAX and BAK genes produce mitochondrial channels that cause leakage of cytochrome C into cytosol
  3. Cytochrome C complexes lead to activation of Caspase 9, which activates other caspases (proteases, endonucleases)
33
Q

Deficiency in apoptosis can cause what diseases?

Excessive apoptosis can cause what diseases?

A

Deficiency -> cancer, autoimmune diseases, atresia

Excessive -> sepsis, AMI, ischemia, neurodegenerative diseases, diabetes mellitus

34
Q

What are 4 examples of anemic coagulative necrosis?

A

Kidney infarct, splenic infarct, non-reperfusion AMI, and gangrena sicca

35
Q

What are 3 examples of hemorrhagic coagulative necrosis?

A

Reperfusion AMI, pulmonary infarct, intestinal infarct

36
Q

What normally causes renal and splenic infarcts?

A

Thrombosis or emboli, mostly coming from the heart (more commonly from A-fib, but also maybe embolism arising from endocarditis or AMI)

37
Q

What, morphologically do you see in both renal and splenic infarcts? (prototypical coagulative infarcts)

A

Beginning has wedge-shaped anemic pale yellowish tissue, after a day surrounded by red hyperemic ring, then necrotic tissue digested -> fibroblasts come -> scar tissue that contracts to make “flower-bed” depressed tissue.

The functional parenchyma does not recover

38
Q

What does p53 do in relation to apoptosis? How can it be activated?

A

p53 is a tumor suppressor gene that can activate apoptosis. Activated by:

  1. DNA damage
  2. hypoxia
  3. aberrant oncogene expression
39
Q

What does p53 promote? (3 things)

A
  1. cell-cycle checkpoints
  2. DNA repair
  3. cellular sensecence and apoptosis
40
Q

How does gangrena sicca usually progress?

Which blood supply blockage is it associated with?

A

Distal-to-proximal

Associated with arterial blockage

41
Q

How does gangrena humida result from venous blockage?

A

Affected limb is saturated with stagnant blood, allowing for proliferation of bacteria

42
Q

What allows a pulmonary infarct to have reperfusion injury?

A

Although the pulmonary artery is obstructed, the bronchial arteries allow oxygenation and bleeding into the area

43
Q

What are 4 major sources of embolism? (will be in later topics too, but ties in here and it’s essential)

A
  1. Deep veins
  2. Periprostatic veins
  3. Perimetrial veins
  4. Auricles of heart (left auricle from A-fib, right auricle embolism origin more common in IV drug users)
44
Q

How does a hemorrhagic infarct in the lungs appear as it progresses?

A

Usually affects lower lobes. Wedge-shaped, apex pointing towards hilus. First appears as red-blue area.

After 48 hours, infarct becomes pale, then red-brown as hemosiderin accumulates

45
Q

Why do hemorrhagic infarcts occur in the intestines?

A

Mesenteric arteries have anastomoses, and so the double circulation means there can be hemorrhage and reperfusion injury

46
Q

Cerebral infarcts are often prevented, but can still be hemorrhagic because of what mechanism?

A

The circle of Willis anastomoses system allows oxygenation, often life-saving but can allow reperfusion injury too

47
Q

What type of blood supply is involved in encephalomalacia rubra?

A

Venous thrombosis or “borderline” between 2 areas of arterial blood supply

48
Q

What are emollition cysts?

A

“Pseudocysts” that occur in the brain after liquefactive necrosis. Don’t have epithelial lining, so they’re not real cysts but just necrotic material

49
Q

What type of necrosis is a pulmonary abscess? What occurs?

A

Liquefactive anemic necrosis.

Bacterial infection causes immune cells to kill large amount of parenchyma and form an abscess

50
Q

What is the Wave-Front Theory?

A

Myocardial infarctions start at the subendocardial area, then progress to the transmural area step-by-step as a “wave-front.” Fast treatment limits extent of necrosis.

51
Q

What are the 3 reasons behind the Wave-Front Theory?

A
  1. Coronaries run in the subepicardium, and the endocardium only gets the distal branches
  2. Myocardial fibers twist like a spiral, and subendocardium works harder (more sensitive to O2 deprivation)
  3. Ventricle has higher pressure, which compresses the subendocardium more than subepicardium
52
Q

What enzyme reaction can be used to detect an early myocardial infarction?

A

Diaphorase: bc dehydrogenases are the first enzymes disrupted during an infarct

53
Q

What is the first morphological sign you see of myocardial infarction? When do you see it?

A

Dilated cells under a microscope. Seen 30 minutes to 4 hours after infarction (before that it’s not clearly different)

54
Q

When do you start seeing evidence of full-blown myocardial infarction? What are the major morphological changes?

A

12-24 hours after infarct. See pale, firm tissue

55
Q

What do you see at 1-2 days after a myocardial infarction has occurred?

A

Degeneration: Reddish hyperemic ring around pale area. Enzymatic leakage makes the tissue necrotic tissue soft.

56
Q

What occurs 3-12 days after a myocardial infarction?

A

Capillarization of tissue: endothelial cells grow into tissue, change into fibroblasts, produce collagen. May also see myocardial rupture during this period..

57
Q

From 12 to 20 days, what occurs morphologically after a myocardial infarction?

A

The whole necrotic tissue is replaced by scar tissue, which is white/ “egg shell” colored

58
Q

When is the ideal time for reperfusion therapy in myocardial infarction? Why?
(4 specific effects are listed)

A

3-6 hours after infarction. Effects:

  1. Free radicals are produced after reperfusion, damaging myocytes
  2. Myocyte hypercontracture: ischemia caused high intracellular calcium levels, impaired calcium cycling and sarcolemma damage. Reperfusion causes uncontrolled contraction because they lack ATP to undergo relaxation. Can also kill myocytes
  3. Leukocytes aggregate + platelets and complement are activated, injuring tissue and the microvasculature
  4. Vascular injury/leakiness can cause bleeding into necrotic area (major risk)
59
Q

What are 5 consequences of myocardial infarction?

A
  1. Pump failure / heart failure: can cause hypotension, pulmonary edema, cardiogenic shock
  2. Arrythmias: conducting system impaired
  3. Myocardial rupture: usually 5-6 days after due to inflammatory cells digesting tissue. May cause hemiparcardium, cardiac tamponade
  4. Aneurysm: soft infarct tissue bulges from pressure
  5. Chronic ischemic heart disease: heart failure in long run, hypertrophy
60
Q

Note that MIs are covered again (and more thoroughly) in topic B2

A

OK

Y Pathology I (Dustin) (20 decks)

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