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1 Foundations of Disease and Therapy > PATH: Irreversible Cell Injury and Cellular Death > Flashcards

PATH: Irreversible Cell Injury and Cellular Death Flashcards

1
Q

What cellular damage must occur for irreversible damage to be inevitable?

A

Unrecoverable mitochondrial damage occurs with loss of ATP synthetic capacity and cell membrane damage of such severity that regulation of internal milieu is impossible

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2
Q

Describe the feed-forward cycle of irreversible cell injury

A

Membrane dysfunction leads to influx of Ca++ which activates phospholipases, which further contribute to membranal damage and further influx of Ca++

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3
Q

The detection of what hepatocyte enzymes are non-specific indicators of liver inflammation?

A

AST and ALT

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4
Q

What pancreas proteins can be only detected in the serum in cases of pancreatitis?

A

Lipase and amylase

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5
Q

What are the morphological changes of irreversible mitochondrial injury?

A

Marked swelling, dense body formation (calcium phosphate)

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6
Q

What is karyolysis?

A

Marker of irreversible nuclear damage where the nucleus “fades away”

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7
Q

What is pyknosis?

A

Marker of irreversible nuclear damage where the nucleus is hard and dark and becomes “clumped” and actually shrinks

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8
Q

What is karyorrhexis?

A

Marker of irreversible nuclear damage where there is random breakup of nucleus into many fragments

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9
Q

How long can it take for nuclear morphological signs of damage to be clinically observed?

A

6-12 hours

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10
Q

What is reperfusion injury? What is thought to be the underlying mechanism of this damage?

A

Damage that occurs upon resumption of blood supply and reoxygenation of previously ischemic tissue; thought to be due to generation of ROS, including oxygen-derived free radicals

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11
Q

What are three common examples of oxygen-derived free radicals?

A

Superoxide anion, hydrogen peroxide, and hydroxyl radical

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12
Q

What are physiologic generators of ROS?

A

Oxidative phosphorylation, Neutrophilic respiratory burst, xanthine oxidase

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13
Q

What types of damage can be induced by ROS?

A

Lipid peroxidation (form lipid peroxides); Protein-protein cross-linking; single-stranded DNA breaks

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14
Q

What are the antioxidant mechanisms that protect from ROS?

A

Superoxide Dismutase (mitochondria) , Glutathione peroxidase and reductase (mitochondria), and catalase (peroxisomes)

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15
Q

How does carbon tetrachloride cause cellular damage?

A

CCl4 is metabolized by cyP450 to form CCL3-, which is esp. damaging to the rER, inhibiting protein synthesis and export (esp. apoproteins), resulting in lipid accumulation within injured hepatocytes

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16
Q

What vitamins serve as free radical scavengers?

A

Vit. E and A

17
Q

How does the cell regulate molecules that propagate free radical production?

A

Fe is bound by transferrin and/or ferritin; Cu is bound by ceruloplasmin

18
Q

After cell death via necrosis what two concurrent processes may be present in the cell?

A

Protein denaturation and enzymatic digestion of cell constituents

19
Q

What is the difference is autolysis and heterolysis?

A

Autolysis is enzymatic digestion of cellular contents by the cell’s own lysosome; Heterolysis is by inflammatory cells

20
Q

What cytoplasmic change can be observed following cell necrosis? Why does this happen?

A

Increased eosinophilia dueto loss of basophlic ribosomes and increased uptake of eosin dye by denatured proteins

21
Q

What is coagulation necrosis?

A

Cell necrosis in which denaturation (coagulation) of cellular proteins predominates, typically by autolysis

22
Q

What is an infarct? What is the difference between a pale/anemic infarct and hemorrhagic /red infarct?

A

An infarct is a circumscribed area of an organ undergoing coagulation necrosis due to ischemia; Pale infarcts are found in end organs (spleen, heart, kidney) which have no dual blood supply; Red infarcts happen in organs with dual blood supply (lung) or with large amounts of CT (gut)

23
Q

What kind of necrosis is gangrene? What is the cause?

A

A special type of coagulation necrosis caused by gradual ischemia of the distal extremities

24
Q

In which type of necrosis occurs in tissues in which the initial digestion of cells and tissue predominates, with resulting loss of tissue structure? What is the mechanism of this digestion?

A

Liquefactive necrosis; heterolysis

25
Q

In which organ is liquefactive necrosis seen following infarction rather than coagulation necrosis?

A

Brain

26
Q

What are the causes of caseous necrosis and what are the common characteristics they share?

A

Mycobacterial (TB) and some fungal infections; difficult for the body to eliminate, resulting in chronic inflammation

27
Q

What is the appearance of caseous necrotic tissue, grossly?

A

Necrotic tissue is walled off and transformed into focus of granular “cheesy” material, surrounded by granulomatous inflammation and fibrosis

28
Q

In which organ is fat necrosis likely to occur? What is the mechanism?

A

Pancreatic cells undergo necrosis and spill their hydrolytic enzymes, esp. lipases, which act on adjacent adipocytes to release fatty acids, which combine with calcium to undergo saponification

29
Q

Where does fibrinoid necrosis occur? When does it occur?

A

Arterial walls; Occurs in extreme hypertension or immune complex deposition in arterial walls

30
Q

True or False: Both Necrosis and Apoptosis are energy-requiring?

A

False- Apoptosis is energy-requiring but not necrosis

31
Q

What are the morphologic changes associated with apoptosis?

A

Cell shrinks and detaches from neighbors, blebbing, chromatin condensation, fragmentation into apoptotic bodies, little to no inflammatory response

32
Q

What class of proteins are caspases and what are their cellular functions? Which are initiators and which are effectors?

A

Cysteine proteases which cleave cytoskeletal proteins and cleave nuclear scaffolding; initiators are -2,-8, and -9; executioners are capases-3, -6, - and -7

33
Q

What is the function of Bcl-2 and where can it be found?

A

Bcl-2 is an anti-apoptotic protein normally found in the outer mitochondrial membrane, which stabilizes the membrane, prevents pore formation, prevents release of cytochrome c, binds to and sequesters Apaf-1

34
Q

What are the common pro-apoptotic members of the Bcl-2 family?

A

Bax and Bad

35
Q

What proteins form the apoptosome?

A

Apaf-1, cytochrome-c, and proCaspase 9

36
Q

What are the best known triggers of the extrinsic apoptotic pathway? What is the mechanism of activation?

A

Fas and TNFR1 receptors binding to their ligands (Fas-L or TNF-alpha); Interaction with the appropriate ligand results in trimerization, and trimerization of Fas interact with Fas Associated Death Domain which activates proCaspase 8 and triggers the cascade

1 Foundations of Disease and Therapy (30 decks)

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