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Pathology I > Lecture 2: Tissue Responses to Injury and Adaptations > Flashcards

Lecture 2: Tissue Responses to Injury and Adaptations Flashcards

1
Q

What are labile cells

A

Continuously cycling cells that proliferate at high rate, high regenerative capacity

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2
Q

What are some examples of labile cells

A

Epithelia of the mouth, skin , gut, bladder, and bone marrow cells

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3
Q

What are quiescent tissue

A

Stable cells, divide infrequently but can be stimulated to divide when the cells are lost. In Go until stimulated to G1

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4
Q

What are some examples of quiescent tissues

A

Liver, renal tubular cells, fibroblasts, endothelial cells, smooth muscle cells, chondrocytes, osteocytes

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5
Q

What are permanent cells

A

Non-dividing tissue that divide in embryonic and fetal life then leave cell cycle. Cells can’t be replaced when lost and have limited capacity to divide

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6
Q

What are some examples of permanent cells

A

Neurons, cardiac, photoreceptors

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7
Q

Is the following: normal, atrophy, hypertrophy, or hyperplasia

A

normal

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8
Q

Is the following: normal, atrophy, hypertrophy, or hyperplasia

A

Hyperplasia

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9
Q

Is the following: normal, atrophy, hypertrophy, or hyperplasia

A

hypertrophy

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10
Q

Is the following: normal, atrophy, hypertrophy, or hyperplasia

A

Atrophy

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11
Q

The left picture is normal, what tissue change is noted in right image (note: image at same magnification

A

Atrophy

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12
Q

What is the mechanism of cell loss in the following atrophies: thymus involution, uterine involution after pregnancy, mammary glands following lactation, testicular atrophy in old age

A

Apoptosis- programmed cell death not pathological

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13
Q

What is the pathogensis of hydronephrosis

A
  1. Blockage in urinary bladder (ex: transitional cell carcinoma)
  2. Block ureter outflow
  3. Increase pressure on renal pelvis
  4. Renal and cortical medically atrophy
  5. Hydronephrosis
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14
Q

What are some reasons for pathological hyperplasia and hypertrophy

A
  1. Abnormal increase in functional demand
  2. Excessive hormonal stimulation
  3. Reactive-response to inflammation or chronic trauma
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15
Q

Which image is normal and which abnormal, what is wrong with abnormal image

A

Left: normal epidermis
Right: epidermal hyperplasia

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16
Q

What tissue is this? Which is normal vs abnormal? What is abnormality

A

Cardiomyocytes
Left: hypertrophic cardiomyopathy
Right: normal

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17
Q

Is the following erosion and ulceration and how do you know

A

erosion because basement membrane is intact

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18
Q

In terms of regeneration, what is the capacity of epithelium to response to injury

A

High regeneration capacity due to epithelial cells being labial cells that are continuously going through cell cycle

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19
Q

Is this ulceration or erosion and how do you know

A

ulceration- damage the basement membrane

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20
Q

Ulceration can lead to severe/acute or chronic ___ and perforated ___

A

Hemorrhage, perforated ulcer

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21
Q

Does regeneration occur in ulceration injuries?

A

No, damage basement membrane with stem cells, resolution through scaring/fibrosis

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22
Q

Identify which image shows erosion vs ulceration

A

Left: erosion
Right: ulceration

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23
Q

What is the most common cause of stricture in the esophagus

A

Circumferential erosion or ulceration by pressure necrosis

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24
Q

What is the worst outcome of ulceration in the stomach

A

Perforation leading to peritonitis

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25
Q

This image shows an esophagus, what is wrong

A

ulcerated

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26
Q

This image shows a stomach what is wrong

A

ulcerated

27
Q

Can the liver regenerate after an acute injury

A

Yes, quiescent cells can regenerate

28
Q

Can liver regenerate after repeated injury

A

No fibrosis will occur—> leading to modular regeneration/cirrhosis of the liver

29
Q

Identify the pathologies of the liver

A

top left: normal
Bottom left: cirrhosis
Top right: lipidosis

30
Q

What do both of these stains of the liver show

A

Cirrhosis—> increase in fibrosis connective tissue

31
Q

What stain stains the fibrous CT blue to identify cirrhosis of the liver

A

Trichrome stain

32
Q

How does the heart and skeletal muscle respond to reversible injury

A

Atrophy and hypertrophy

33
Q

How does the heart respond to irreversible injury? What is its regenerative capacity

A

Cardiomyocytes are permanent cells and therefore can’t regenerate—> outcome is fibrosis/scaring

34
Q

What is concentric hypertrophy

A

Thickening of the outside of the heart towards the lumen, add sarcomeres on top

35
Q

What is eccentric hypertrophy

A

Caused by addition of sacromeres to the side of the heart allowing for enlargement and dilation

36
Q

Identify the tissue type? Identify normal vs abnormal? What is causing abnormality?

A

Cardiomyocytes
Left: normal
Right: abnormal- myocardial fibrosis

37
Q

What are the key forms of neurological injury

A
  1. Compression
  2. Necrosis
  3. Degeneration
38
Q

How does the brain respond to injury and heal

A

Minimal regeneration of nerve fibers or neurons, but does not heal via fibrosis but damage leaves cavitation

39
Q

Does the brain heal by fibrosis

A

No, damage results in cavitation

40
Q

What is anthracosis

A

Exogenous black pigment found in lungs as a result of air pollutants

41
Q

What does the following image of the lung show

A

anthracosis

42
Q

How is melanin formed

A

Oxidation of tyrosine

43
Q

What is the endogenous pigment lipofuscin

A

“Wear and tear” pigment, age indicator

44
Q

What does the endogenous pigment ceroid show

A

Pathogenic indicator, associated with vitamin E deficiency

45
Q

Both images show melanin pigmentation, which is benign and which is malignant

A

left: benign- look more like discoloration marks rather than masses
Right: more like black masses

46
Q

What do both these histologies show? What is the difference between them and how do you know

A

both show melanin
Left: malignant melanoma- can tell due to high cellular atypica
Right: pigment are incontinence- benign reaction to inflammation

47
Q

Describe the mechanism in which cooper deficiency causes a fading in coat color of sheep and cattle

A

Melanin is formed by oxidation of tyrosine which requires a copper containing enzyme tyrosinase, therefore copper deficiency—> decreased melanin

48
Q

What causes jaundice coloration

A

Presence of bilirubin

49
Q

What causes hematin (brown) coloration

A
  1. Artifact of Formica acid and heme
  2. Liver flukes
50
Q

How would you describe this pigmentation

A

jaundice- excess bilirubin as a result of liver tumor

51
Q

How would you describe this pigmentation

A

Hematin

52
Q

What is the mechanism that normally makes us avoid gout

A

Blood uric acid uses enzyme Uricase to form Allantoin which is then excreted in urine

53
Q

How does gout occur

A

Increase in blood uric acid due to lack of uricase enzyme so not converted to allantoin

54
Q

What does the following image show

A

gout crystals

55
Q

What is the most common form of amyloid/amyloidosis in animals

A

Reactive secondary to inflammation- amyloid A deposits accumulate as acute phase proteins produced during inflammation

56
Q

Where are amyloid deposits commonly found

A

Kidney, liver, spleen, and lymph nodes

57
Q

Which image is normal? What is abnormality?

A

left: normal
Right: abnormal: amyloidosis

58
Q

What is wrong here and what stain was used

A

amyloidosis identified with Congo red stain

59
Q

What is wrong here and what stain was used

A

amyloidosis identified with congo red stain that turned apple green under polarized light

60
Q

What is the difference between dystrophic calcification and metastatic calcification

A
  1. Dystrophic calcification: localized increase in calcium, blood calcium levels are normal
  2. Metastatic calcification: blood Ca2+ levels are increased-> hypercalcemia
61
Q

In general what is indicated by the arrows in both pictures

A

viral inclusions

62
Q

What staining technique do you want to use to identify viral inclusion bodies in lead poisoning and what tissue are they found in.

A

Acid fast
Tissue: renal tubules

63
Q

what is shown here? Blood ca2+ is normal

A

Dystrophic calcification

64
Q

What is shown here? Patient was hyperglycemic

A

metastatic calcification

Pathology I (11 decks)

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