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DIT Foundation > Fou 6 - Cellular Suffering and Death > Flashcards

Fou 6 - Cellular Suffering and Death Flashcards

1
Q

How many pathway are there for apoptosis ?

A

Two: Intrinsic and extrinsic.

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2
Q

Which is the final step for apoptosis?

A

Activation of cytosolic caspases that mediate cellular breakdown.

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3
Q

What histological findings characterize Apoptosis?

A

Deeply eosinophilic cytoplasm, cell shrinkage, Nuclear shrinkage (pyknosis) and basophilia, membrane blebbing, Nuclear fragmentation (Karyorrhexis), and formation of apoptotic bodies.

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4
Q

What is Pyknosis?

A

Nuclear shrinkage

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5
Q

What is Karyorrhexis?

A

Nuclear fragmentation.

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6
Q

In the Intrinsic pathway, what happened with the proportion of the Anti- and Pro- apoptotic factors?

A

Changes in proportion more pro- than anti-.

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7
Q

Which are the Pro- and Anti- apoptotic factors?

A

Pro- BAX and BAK proteins.

Anti- Bcl-2

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8
Q

What is the BAX and BAK’ functions?

A

Increased mitochondrial permeability and Cytochrome C release.

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9
Q

What is the function of the Apaf-1?

A

Normally induces the activation of caspases.

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10
Q

Which is the process of the Follicular lymphoma?

A

Occurs when Bcl-2 is overexpressed, then decrease caspase activation and tumorigenesis.

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11
Q

Which is the function of the BCL-2?

A

It is the major anti-apoptotic regulator of the mitochondrial permeability.

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12
Q

What is the primary initiator of the apoptosis?

A

Caspases.

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13
Q

Which is the pathway characterized by death receptors?

A

Extrinsic pathway.

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14
Q

Which are the two death receptors?

A

Fas receptor activated by FasL (Fas ligand). TNF receptor activated by TNF-Alpha

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15
Q

What is the function of Granzyme B?

A

Activate caspases directly.

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16
Q

Which defective interaction of the apoptosis process contribute to autoimmune disorders?

A

Defective Fas-FasL interactions.

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17
Q

What is the protein that is use by Killer T cells to make holes in plasma membrane?

A

Perforin punches holes in membrane.

18
Q

Definition of necrosis:

A

Enzymatic degradation and protein denaturation of cell due to exogenous injury produce intracellular components leak. Inflammatory process (unlike apoptosis).

19
Q

What does apoptosis mean?

A

Programmed cell death or orderly cell death process.

20
Q

How many types of necrosis are there?

A

Coagulative, Liquefactive, Caseous, Fat, Fibrinoid, Gangrenous.

21
Q

What is Coagulative necrosis?

A

Seen in: ischemia/infarcts in most tissues(except brain). Due to: ischemia/infarction; proteins denature, enzymatic degradation.
Histology: Cell outlines preserved; increased cytoplasmic binding of acidophilic dyes.

22
Q

What is Liquefactive necrosis.

A

Seen in: Bacterial abscesses, Brain infarcts (due too increase fat content).
Due to: Neutrophils releasing lysosomal enzymes that digest the tissue.
Histology: Early (cellular debris and macrophages) and Late (cystic spaces and cavitation brain).

23
Q

What is Caseous Necrosis

A

Seen in: TB, systemic fungi (histoplasma capsulatum), Nochardia. Due to: Macrophages wall off the infecting microorganism, that produces granular debris. Histology: Fragmented cells and debris surrounded by lymphocytes and macrophages.

24
Q

What is Fat Necrosis?

A

Seen in: Enzymatic (acute pancreatitis, saponification) and Nonenzymatic (Breast trauma). Due to: Damaged cells release lipase, which breaks down fatty acids in cell membranes. Histology: outlines of dead cells without peripheral nuclei;saponification of fat (with calcium) appears dark blue on H&E stain.

25
Q

What is Fibrinoid?

A

Seen in: immune reaction in vessels.
Due to: immune complexes combine with fibrin produce vessel wall damage.
Histology: Vessel walls are thick and pink.

26
Q

What is Gangrenous necrosis?

A

Seen in: Distal extremity, after chronic ischemia. Due to: Dry (ischemia) and Wet (superinfection). Histology: Dry (coagulative) and Wet (Liquefactive).

27
Q

Which are the two types of cell injury?

A

Reversible with O2 and Irreversible.

28
Q

Reversible(R) and Irreversible (I):
1) ATP depletion. 2)Nuclear chromatin clumping. 3)Lysosomal rupture. 4)Fatty change. 5)Plasma membrane damage. 6)Nuclear pyknosis, Karyorrhexis and karyolisis.

A

1)R. 2)R. 3)I. 4)R. 5)I. 6)I.

29
Q

What does infarction mean?

A

It is a tissue death caused by a lack of O2

30
Q

How many types of infarcts are there?

A

Two type: Red and Pale or white

31
Q

What is a Red infarcts?

A

Red (hemorrhagic) infarcts occur in venous occlusion and tissues with multiple blood supplies, such a liver, lung etc.
Reperfusion injury is due to damage by free radicals.

32
Q

What is a Withe or pale infarcts?

A

This occur in solid organs with a single blood supply, such a heart, kidney and spleen.

33
Q

What cellular by-products might you detect in the serum when the cardiac myocytes are injured?

A

Myoglobin, CPK, CKMB and Troponin I. Cardiac enzymes

34
Q

What cellular by-products might you detect in the serum when the skeletal myocytes are injured?

A

CPK, Aldolase and myoglobin.

35
Q

What cellular by-products might you detect in the serum when the Hepatocytes are injured?

A

AST, ALT, Alkaline phosphatase and GGT.

36
Q

What cellular by-products might you detect in the serum when the Salivary gland cells are injured?

A

Amylase.

37
Q

What cellular by-products might you detect in the serum when the pancreatic exocrine cells are injured?

A

Amylase and Lipase.

38
Q

What cellular by-products might you detect in the serum when the Red blood cells (RBCs) are injured?

A

Heme -> Bilirubin.

39
Q

What histology can feature are seen in apoptotic liver cells?

A

Cellular shrinkage, pyknosis, Karyorrhexis, membrane blebbing and apoptotic bodies.

40
Q

What substances do cytotoxic T cells and NK cells use to induce apoptosis in the cells infected with a virus?

A

Perforin and Granzyme B.

41
Q

What highly damagin events can cause irreversible cell injury?

A

Calcium influx, damage to the plasma membrane, rupture of the lysosome, mitochondrial permeability, pyknosis, Karyorrhexis and karyolisis.

42
Q

What cellular enzymes are responsible for handling oxygen free radicals?

A

1)Catalase degrades H2O2 to O2 and H2O. 2)Superoxide Dismutase converts O2 radicals to H2O2. 3)Glutathione per oxidase catalyzes free radical breakdown.

DIT Foundation (9 decks)

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