Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is ischemia

A

Inadequate blood supply to an organ or part of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List some of the events that occur in irreversible cell injury

A
  1. Mitochondrial dysfunction
  2. Produce ROS
  3. Release lysozymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some causes of cell injury due to oxygen deprivation

A

Anemia, vascular obstruction, cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

No- replace gap with fibrous CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is hydropic degeneration

A

Water movement into cells- causing acute swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Is hydropic degeneration reversible or irreversible

A

Reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Bovine papular stomatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the gross change noted in hydropic degeneration

A

Swelling of tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the microscopic change in hydropic degeneration

A

Single or multiple cytoplasmic vacuoles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Hydropic degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

Hepatic lipidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How can inappetance and anorexia lead to hepatic lipidosis

A

Both will drive fat mobilization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some common causes of hepatic lipidosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Is the following image characteristics of lipid of glycogen accumulation in the liver

A

glycogen

26
Q

What is wrong here

A

hepatic lipidosis

27
Q

What is the difference between these two liver histologies

A

Left: hepatic lipidosis, increase number of fat cells, nuclei moved to the side

Right: normal

28
Q

Is hepatic lipidosis reversible or irreversible

A

Reversible

29
Q

Identify the liver with fat accumulation and the liver with glycogen accumulation

A

Left: fat
Right: glycogen

30
Q

Necrosis or apoptosis: hypoxia, ischemia, direct cell membrane injury

A

Necrosis

31
Q

Necrosis or apoptosis: death following swelling

A

Necrosis

32
Q

Necrosis or apoptosis: programmed cell death

A

Apoptosis

33
Q

Necrosis or apoptosis: cell death with shrinkage

A

Apoptosis

34
Q

Necrosis or apoptosis: no inflammation, organized

A

Apoptosis

35
Q

Necrosis or apoptosis: adjacent inflammation

A

Necrosis

36
Q

Necrosis or apoptosis: release cellular content

A

Necrosis

37
Q

What are the key morphological factors of cellular necrosis

A
  1. Pyknosis
  2. Karyorrhexis
  3. Karyolysis
  4. Absence of nucleus
38
Q

What is pyknosis

A

Irreversible condensation of chromatin in nucleus

39
Q

What is karyorrhexis

A

Fragmentation of nucleus

40
Q

What is karyolysis

A

Nucleus extremely pale and eventually gone

41
Q

What are the two pathways in the mechanism of apoptosis

A
  1. Mitochondrial/intrinsic pathway
  2. Death receptor/extrinsic pathway
42
Q

List the steps in the mitochondrial/instrinsic pathway of apoptosis

A
  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
Q

List the steps in the death receptor/intrinsic pathway

A
  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
Q

What are some key morphological features of apoptosis

A

Cell shrinkage, chromatin condensation, cytoplasmic blebs and apoptotic bodies, phagocytosis

45
Q

What does hematoxylin stain and what color

A

Stains Nucleus, bacteria and calcium purple

46
Q

What does eosin stain and what color

A

Stains cytoplasm, collagen, fibrin, RBC, proteins in pink

47
Q

What are some key morphological features of necrosis on HE stain

A
  1. Increased eosinophilia (more red)
  2. Glassy
  3. Cytoplasmic vacuolation
  4. Karryorrhexis to karyolysis
  5. Ghost cells
  6. Lysozyme release
48
Q

What is coagulative necrosis and an example

A

Desaturation with dense/rigid texture to dead cells
Ex: myocardial, hepatic or nephrotic necrosis

49
Q

What is liquefactive necrosis and an example

A

Process of complete enzymatic digestion of cells

Ex: brain abscess

50
Q

What is caseous necrosis and an example

A

Cheesy, coagulative granulomatous reaction

Ex: lung tuberculosis

51
Q

What is fat necrosis and an. Example

A

Fatty acids mixed with calcium

Ex: acute pancreatitis

52
Q

What is gangrene necrosis and an example

A

Necrosis due to ischemia of distal limb

Moist: liquefactive
Dry: necrosis secondary to infarct
Gas: clostridium perfringes

53
Q

Which image is normal vs necrotic and what kind of necrosis

A

Left: coagulative necrosis of the heart
Right: normal

54
Q

What type of necrosis is this

A

Renal papillary necrosis- form of coagulative necrosis

55
Q

What is the pathogensis of renal papillary necrosis from NSAIDS

A
  1. NSAIDS block COX-1 and COX-2
  2. Block PG synthesis
  3. Block vasodilation of kidneys
  4. Hypoperfusion and ischemia
56
Q

What is suppurative necrosis

A

Form of liquefactive necrosis- acute inflammatory cells release proteolytic enzymes that destroy surrounding tissues

57
Q

The following image is from brain tissue- what form of necrosis is this

A

Liquefactive

Many macrophages to the right- remove everything resulting in liquefaction

58
Q

What type of necrosis is this

A

liquefactive necrosis

59
Q

what type of necrosis is this?

A

Caseous necrosis of the lung infected with TB

60
Q

What type of necrosis is this

A

Fat necrosis

61
Q

What is wet gangrene necrosis

A

Combination of coagulative necrosis from loss of blood supply with a liquefactive component due to superimposed infection

Pathology I (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions