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Pathology I > Lecture 1: Cell injury > Flashcards

Lecture 1: Cell injury Flashcards

1
Q

Which of the following is considered an unselective injury: necrosis or apoptosis

A

Necrosis

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2
Q

Which of the following is considered a selective injury: necrosis or apoptosis

A

Apoptosis

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3
Q

What are the 4 categories of causes of cell injury

A
  1. Deficiency in critical material
  2. Lack of cellular energy production
  3. Accumulation of abnormal substances
  4. Physical injury
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4
Q

What is ischemia

A

Inadequate blood supply to an organ or part of the body

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5
Q

List some of the events that occur in reversible cell injuries

A
  1. Decrease oxidative phosphorylation
  2. Decrease ATP and increase glycolysis
  3. Disrupt ion pumps: decrease Na/K ATPase—> increase Na+ intracellularly
  4. Influx H20
  5. Decrease protein synthesis
  6. Chromatin dysfunction
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6
Q

List some of the morphological changes in reversible cell injury

A

Cell swelling, ER swelling, loss of Microvilli, blebs, clumped chromatin, lipid accumulation

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7
Q

List some of the events that occur in irreversible cell injury

A
  1. Mitochondrial dysfunction
  2. Produce ROS
  3. Release lysozymes
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8
Q

What are some causes of cell injury due to oxygen deprivation

A

Anemia, vascular obstruction, cardiac failure

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9
Q

Describes the steps of cell injury to irreversible injury from oxygen deprivation

A
  1. Hypoxia
  2. Aerobic metabolism stops
  3. Decrease oxidative phosphorylation
  4. Decrease ATP—> disrupt Na+/K+ pump—> increase Na+ intracellular, influx H20
  5. Anaerobic cell metabolism starts
  6. Intracellular acidosis
  7. Protein synthesis decreases
  8. Ribosomes lost
  9. Cell membrane defects
  10. Lysosome rupture- release RNAases, and DNAases—> digest cell
  11. Rupture and cell death
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10
Q

Do cells have the ability to regenerate with large numbers of deaths

A

No- replace gap with fibrous CT

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11
Q

What is hydropic degeneration

A

Water movement into cells- causing acute swelling

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12
Q

What is the pathogens is of hydropic degeneration

A
  1. Cell injury (hypoxia)
  2. Decrease mitochondrial fx
  3. Cell membrane damage
  4. Interfere with ion channels
  5. Disrupt Na/k+ pump—> increase Na+ intracellularly—> influx h20
  6. Mitochondria and ER swelling
  7. Hydropic degeneration
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13
Q

Is hydropic degeneration reversible or irreversible

A

Reversible

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14
Q

What bovine disease caused by parapoxivrus can result in ballooning degeneration/hydropic degeneration

A

Bovine papular stomatitis

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15
Q

What is the gross change noted in hydropic degeneration

A

Swelling of tissue

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16
Q

What is the microscopic change in hydropic degeneration

A

Single or multiple cytoplasmic vacuoles

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17
Q

Image shows bovine papular stomatitis: what cellular injury can be seen in this image

A

Hydropic degeneration

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18
Q

What is the pathogensis of hepatic lipodosis

A
  1. Excessive FFA from fat stores or diet
  2. Decrease oxidation or use of FA
  3. Impaired apoprotein synthesis
  4. Impaired protein and triglyceride synthesis to form lipoprotein
  5. Accumulation of lipoprotein in hepatocytes
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19
Q

The following is an image of a cat liver: what does this show

A

Hepatic lipidosis

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20
Q

How can ketosis and pregnancy toxemia lead to hepatic lipidosis

A

Excess fat stores and drive for increased mobilization in late pregnancy and early lactation

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21
Q

How can inappetance and anorexia lead to hepatic lipidosis

A

Both will drive fat mobilization

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22
Q

What are some common causes of hepatic lipidosis

A

High fat diets, obesity, hepatotoxins, hypoxia, DM, hypothyroidism

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23
Q

How does the gross color and texture of a liver differ from lipid accumulation vs glycogen accumulation

A

Lipid: pale, yellow friable
Glycogen: pale-tan- white, firm

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24
Q

How does the histology of a liver differ from lipid vs glycogen accumulation

A

Lipid: nuclei pushed to periphery, vacuoles have distinct borders

Glycogen: nuclei stay central, vacuoles have no distinct borders

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25
Is the following image characteristics of lipid of glycogen accumulation in the liver
glycogen
26
What is wrong here
hepatic lipidosis
27
What is the difference between these two liver histologies
Left: hepatic lipidosis, increase number of fat cells, nuclei moved to the side Right: normal
28
Is hepatic lipidosis reversible or irreversible
Reversible
29
Identify the liver with fat accumulation and the liver with glycogen accumulation
Left: fat Right: glycogen
30
Necrosis or apoptosis: hypoxia, ischemia, direct cell membrane injury
Necrosis
31
Necrosis or apoptosis: death following swelling
Necrosis
32
Necrosis or apoptosis: programmed cell death
Apoptosis
33
Necrosis or apoptosis: cell death with shrinkage
Apoptosis
34
Necrosis or apoptosis: no inflammation, organized
Apoptosis
35
Necrosis or apoptosis: adjacent inflammation
Necrosis
36
Necrosis or apoptosis: release cellular content
Necrosis
37
What are the key morphological factors of cellular necrosis
1. Pyknosis 2. Karyorrhexis 3. Karyolysis 4. Absence of nucleus
38
What is pyknosis
Irreversible condensation of chromatin in nucleus
39
What is karyorrhexis
Fragmentation of nucleus
40
What is karyolysis
Nucleus extremely pale and eventually gone
41
What are the two pathways in the mechanism of apoptosis
1. Mitochondrial/intrinsic pathway 2. Death receptor/extrinsic pathway
42
List the steps in the mitochondrial/instrinsic pathway of apoptosis
1. Cell injury 2. Signal to BCL2 family sensors 3. Activate BCL2 effectors-BAX and BAK 4. Mitochondria release cytochrome C and other apoptotic proteins 5. Initiator capsase 9 6. Execution capsases: 3, 6, 7,12 7. Endonucleus activation-nucleus fragmentation and breakdown of cytoskeleton 8. Cytoplasmic blob 9. Apoptotic body 10. Phagocytosis
43
List the steps in the death receptor/intrinsic pathway
1. Ligand FAS binds to receptor TNF 2. Adaptor proteins 3. Initiator capsase 8 4. Executioner capsases: 3, 6, 7, 12 5. Endonucleus activation-nucleus fragmentation and cytoskeleton breakdown 6. Cytoplasmic bleb 7. Apoptotic body 8. Phagocytosis
44
What are some key morphological features of apoptosis
Cell shrinkage, chromatin condensation, cytoplasmic blebs and apoptotic bodies, phagocytosis
45
What does hematoxylin stain and what color
Stains Nucleus, bacteria and calcium purple
46
What does eosin stain and what color
Stains cytoplasm, collagen, fibrin, RBC, proteins in pink
47
What are some key morphological features of necrosis on HE stain
1. Increased eosinophilia (more red) 2. Glassy 3. Cytoplasmic vacuolation 4. Karryorrhexis to karyolysis 5. Ghost cells 6. Lysozyme release
48
What is coagulative necrosis and an example
Desaturation with dense/rigid texture to dead cells Ex: myocardial, hepatic or nephrotic necrosis
49
What is liquefactive necrosis and an example
Process of complete enzymatic digestion of cells Ex: brain abscess
50
What is caseous necrosis and an example
Cheesy, coagulative granulomatous reaction Ex: lung tuberculosis
51
What is fat necrosis and an. Example
Fatty acids mixed with calcium Ex: acute pancreatitis
52
What is gangrene necrosis and an example
Necrosis due to ischemia of distal limb Moist: liquefactive Dry: necrosis secondary to infarct Gas: clostridium perfringes
53
Which image is normal vs necrotic and what kind of necrosis
Left: coagulative necrosis of the heart Right: normal
54
What type of necrosis is this
Renal papillary necrosis- form of coagulative necrosis
55
What is the pathogensis of renal papillary necrosis from NSAIDS
1. NSAIDS block COX-1 and COX-2 2. Block PG synthesis 3. Block vasodilation of kidneys 4. Hypoperfusion and ischemia
56
What is suppurative necrosis
Form of liquefactive necrosis- acute inflammatory cells release proteolytic enzymes that destroy surrounding tissues
57
The following image is from brain tissue- what form of necrosis is this
Liquefactive Many macrophages to the right- remove everything resulting in liquefaction
58
What type of necrosis is this
liquefactive necrosis
59
what type of necrosis is this?
Caseous necrosis of the lung infected with TB
60
What type of necrosis is this
Fat necrosis
61
What is wet gangrene necrosis
Combination of coagulative necrosis from loss of blood supply with a liquefactive component due to superimposed infection

Pathology I (23 decks)

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