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MCBD Jenna > Week 3 Pathology > Flashcards

Week 3 Pathology Flashcards

1
Q

What are the 3 major effects of free radical attack on lipids, proteins and DNA?

A

1) Lipid peroxidation
2) DNA fragmentation
3) Protein crosslinking

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2
Q

What does reversible and irreversible injury do to the plasma membrane?

A

Reversible injury: blebbing, loss of microvilli

Irreversible injury: disruption/lysis

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3
Q

What does reversible and irreversible injury do to the mitochondria?

A

Reversible injury: modest swelling

Irreversible injury: massive swelling, leakage

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4
Q

What does reversible and irreversible injury do to the endoplasmic reticulum?

A

Reversible injury: dilation with detachment of polysomes

Irreversible injury: extensive disruption and fragmentation

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5
Q

What is karyolysis?

A

Loss of basophilia of DNA - DNAase activity (nuclei fading). Occurs in Necrosis.

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6
Q

What is pyknosis?

A

Shrinkage of the nucleus, occurs in necrosis AND apoptosis

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7
Q

What is karyorrhexis?

A

Fragmentation of a pyknotic (shrunken) nucleus, occurs in necrosis AND apoptosis

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8
Q

What are the 6 main patterns of necrosis?

A

1) coagulative
2) liquefactive
3) gangrenous
4) caseous
5) fibrinoid
6) fat

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9
Q

What happens in the cytoplasm in apoptosis?

A

1) Cell shrinkage
2) Formation of cytoplasmic blebs/apoptotic bodies
3) Mitochondria remain relatively intact

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10
Q

What happens to the nucleus in apoptosis?

A

1) Chromatin condensation
2) Pyknosis
3) Nuclear remnants packaged into apoptotic bodies

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11
Q

Which cell processes have ONLY pathologic causes?

A

necrosis and atrophy

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12
Q

Extrinsic apoptosis is triggered by the ligands ______ or _________ that when bound to receptors triggers a cascade that eventually activates __________

A

Extrinsic apoptosis is triggered by the ligands Fasl or tumor necrosis factor (TNF) that when bound triggers a cascade that eventually activates caspases.

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13
Q

Caspases function as __________ and __________

A

endonucleases (eat DNA) and proteases (eat protein)

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14
Q

Intrinsic apoptosis from cell stress is caused by the leakage of __________ from the __________ that eventually triggers the caspases.

A

Intrinsic apoptosis is caused by the leakage of cytochrome C from the mitochondria that eventually triggers the caspases.

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15
Q

Normally, _________ keeps cytochrome C inside the mitochondria but in intrinsic apoptosis, it is inhibited by _____, ______, _____, ______ when these are activated by the apoptotic signal _________.

A

Normally, Bcl2 keeps cytochrome C inside the mitochondria but in intrinsic apoptosis, it is inhibited by Bax, Bak, Bid, Bim when these are activated by the apoptotic signal P53.

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16
Q

Ischemia is an example of _________ necrosis

A

coagulative

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17
Q

TB is an example of __________ necrosis

A

caseous

18
Q

Peripheral vascular disease can cause ___________ necrosis

A

dry gangrene/coagulative

19
Q

Which type of necrosis preserves the architecture of the cell?

A

Coagulative - cell outline still there, no nucleus

20
Q

Damage to which organ would most likely cause fat saponification and fat necrosis?

A

Pancreas

21
Q

Bacterial abscesses and fungal infection is likely which type of necrosis?

A

Liquefactive necrosis

22
Q

Which type of necrosis is caused by leakage of proteinaceous material caused by damage to vessels (i.e. vasculitis)?

A

Fibrinoid necrosis

23
Q

Increase in size of the liver is most likely due to what process?

A

Hyperplasia

24
Q

GERD will likely result in which type of cell adaptation?

A

Metaplasia

25
Q

Increase in size of heart is likely due to what process?

A

Hypertrophy

26
Q

What is necrosis?

A

Morphologic changes causing enzymatic degradation of lethally injured cells. Occurs in living tissue and is accompanied by INFLAMMATION!!!

27
Q

What is apoposis?

A

Programmed cell death by a highly regulated cascade of enzymes that neatly package the cell for phagocytosis.
Does NOT incite inflammatory response!

28
Q

Lack of oxygen to a cell is _________ while lack of blood flow is _________?

A

Hypoxia and Ischemia

29
Q

Name some mechanisms of cell injury.

A
  1. Decreased ATP
  2. Mitochondrial damage
  3. Ca2+ entering mitochondria
  4. Increase reactive oxygen species (AKA free radicals)
  5. Membrane damage
  6. Protein misfolding
30
Q

Describe the apoptotic intrinsic pathway

A

P53 arrests the cell cycle and activates Bax, Bak, Bim and Bid (simultaneously inactivating BCL-2 and BCL-X).
Bax, Bak, Bim and Bid borrow themselves into the mitochondria promoting the release of cytochrome-C and pro-apoptotic proteins.
This initiates caspases to be released breaking down the cytoskeleton and chewing up the DNA for packaging into phagocytes.

31
Q

Describe the apoptotic extrinsic pathway

A

Every cell has death receptors. When the death receptors are initiated by a ligand (FAS or TNF) that provokes adapter proteins to initiate caspases to be released breaking down the cytoskeleton and chewing up the DNA for packaging into phagocytes.

32
Q

When would you see coagulative necrosis? What do you see microscopically?

A

See this in infarcts in any tissue (except brain)
Due to loss of blood
Gross: tissue is firm
Micro: Cell outlines are preserved (cells look ghostly), and everything looks red

33
Q

When would you see liquefactive necrosis? What do you see microscopically?

A

See this in infections and, for some unknown reason, in brain infarcts
Due to lots of neutrophils around releasing their toxic contents, “liquefying” the tissue
Gross: tissue is liquidy and creamy yellow (pus)
Micro: lots of neutrophils and cell debris

34
Q

When would you see caseous necrosis? What do you see microscopically?

A

See this in tuberculosis
Due to the body trying to wall off and kill the bug with macrophages
Gross: White, soft, cheesy-looking (“caseous”) material
Micro: fragmented cells and debris surrounded by a collar of lymphocytes and macrophages (granuloma)

35
Q

When would you see fat necrosis? What do you see microscopically?

A

See this in acute pancreatitis
Damaged cells release lipases, which split the triglyceride esters within fat cells
Gross: chalky, white areas from the combination of the newly-formed free fatty acids with calcium (saponification)
Micro: shadowy outlines of dead fat cells; sometimes there is a bluish cast from the calcium deposits, which are basophilic

36
Q

When would you see fibrinoid necrosis? What do you see microscopically?

A

See this in immune reactions in vessels
Immune complexes (antigen-antibody complexes) and fibrin are deposited in vessel walls
Gross: changes too small to see grossly
Micro: vessel walls are thickened and pinkish-red (called “fibrinoid” because the deposits look like fibrin deposits)

37
Q

When would you see gangrenous necrosis? What do you see microscopically?

A

See this when an entire limb loses blood supply and dies (usually the lower leg)
This isn’t really a different kind of necrosis, but people use the term clinically so it’s worth knowing about
Gross: skin looks black and dead; underlying tissue is in varying stages of decomposition
Micro: initially there is coagulative necrosis from the loss of blood supply (this stage is called “dry gangrene”); if bacterial infection is superimposed, there is liquefactive necrosis (this stage is called “wet gangrene”)

38
Q

Describe hypertrophy and what it is caused by.

A

Hypertrophy is an increase in cell SIZE which will lead to increase in tissue SIZE.
Either pathological (hypertrophic cardial myophathy) or physiologic (muscle building).
Caused by increase in 1) proteins, 2) cellular activity, 3) metabolic induction

39
Q

Describe hyperplasia and what it is caused by.

A

Hyperplasia is an increase in the NUMBER of cells which causes increase in tissue size.
Either pathological (BPH) or physiologic (breast enlargement due to hormones).
Caused by increase in 1) proteins, 2) cellular activity, 3) metabolic induction

40
Q

Describe atrophy, what it is caused by, and how it is mediated.

A

Atrophy is a DECREASE in cell SIZE and NUMBER which causes decrease in tissue size.
Only PATHOLOGICAL!
Cause by denervation and age and decreases in: 1) nutrients 2) hormone stimulation
Mediated by autophagy to degrade affected tissue via ubiquitin-proteasome pathway.

41
Q

Describe metaplasia and what it is caused by.

A 
Metaplasia is a CHANGE is cell type due to adverse stimuli. It is REVERSIBLE! 
Either pathological (epithelia change in trachea due to smoking) or physiological (transformation zone of cervix).

MCBD Jenna (8 decks)

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