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Pathology I > Session 2 - Tissue Response + Adaptations > Flashcards

Session 2 - Tissue Response + Adaptations Flashcards

1
Q

What is the weakness of labile cells?

A

Highly susceptible to toxic agents (Chemotherapy) _+ Radiation

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2
Q

What are some examples of labile cells given in lecture?

A

Epithelia of the mouth + skin + gut/bladder + bone marrow

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3
Q

What are the three types of cells, based on regenerative capabilities?

A

Labile + Stable + Permanent

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4
Q

What are the characteristics of stable cells?

A

Divide infrequently but if stimulated will divide (aka when cells are lost)

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5
Q

What are some examples given in lecture for stable cells?

A

Liver + Renal tubular + Fibroblasts + Endothelial cells + SM cells + Chondrocytes + Osteocytes of CT

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6
Q

What are the characteristics of permanent cells?

A

Divide only in embryonic and fetal life, then proceed to leave the cell cycle

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7
Q

What is the down side to cells being permanant?

A

Cannot be replaced when lost, there for most (if not all) injured tissue will be replaced with scarring

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8
Q

What are examples of permanent cells given in lecture?

A

Cardiac muscle + Photoreceptors in retinas + Neurons

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9
Q

What are two “options” cells have to “grow”?

A

Hypertrophy + Hyperplasia

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10
Q

What is hypertrophy?

A

Increased functional mass or size of a cell-tissue-organ

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11
Q

What is hyperplasia?

A

Increased number of cells

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12
Q

What is hyperplasia dependent on?

A

Regenerative capacity of cell

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13
Q

Are hypertrophy/hyperplasia irreversible or reversible?

A

Reversible

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14
Q

What are three major causes of pathological hypertrophy or hyperplasia?

A

Abnormal increase in functional demand of the tissue
Excessive hormonal stimulation
Reactive (inflammation or chronic trauma)

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15
Q

What is atrophy?

A

Reduction in functional mass or size of cell-tissue-organ

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16
Q

What are three ways atrophy can be carried out reversibly?

A

Reduction in size, number, or both

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17
Q

How does atrophy become irreversible?

A

Lost cells are then replaced with fatty or fibrous tissue

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18
Q

What is important to remember due to the fact fat or fibrous tissue can replace lost cells?

A

With atrophy organ size doesn’t always decrease

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19
Q

What are three physiological examples of atrophy from lecture?

A

Thymic involution in growing animals
Uterine involution after pregnancy
Testicular atrophy with age

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20
Q

What is the main mechanism for atrophy?

A

Cell loss via apoptosis

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21
Q

What is important to look at when assessing the degree of epithelial damage?

A

Basement membrane and whether it is intact or not

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22
Q

What happens when the basement membrane is destroy in injury to the epithelial tissue?

A

Potential severe acute or chronic hemorrhage

Resolution through scarring

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23
Q

What is erosion?

A

Damage to the epithelial layer without damage to the basement membrane

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24
Q

What is ulceration?

A

Damage to the epithelial tissue with damage to the basement membrane

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25
Q

What makes up an ulcer bed in epithelial tissue?

A

Fibrin + Inflammatory cells

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26
Q

What disease mention in lecture can cause ulcerations in tissue? What is the major characteristic of its lesions?

A

Diphtheria

Membrane over exudation of fibrin and inflammatory cells

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27
Q

What two things occur in hepatic cords in response to injury?

A

Hyperplasia + Pathologic atrophy

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28
Q

Where does pathologic atrophy occur in the hepatic cords as a result of injury?

A

Where scar tissue is forming

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29
Q

Where does hyperplasia occur in the liver when injury occurs?

A

Where there is regeneration taking place

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30
Q

What is the structural result to architectural damage to hepatocytes?

A

Bridging necrosis

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31
Q

What happens after bridging necrosis occurs in hepatocytes?

A

Fibrous scar tissue + Nodular regeneration

Bridging fibrosis

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32
Q

What is the disease process called when there is bridging fibrosis within the liver?

A

Cirrhosis

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33
Q

What is the basic result of cell death within cardiac myocytes?

A

Scaring aka Fibrosis, they are permanent cells and there for regeneration is not an option

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34
Q

Which muscle type is more dynamic, skeletal or cardiac?

A

Skeletal

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35
Q

Why is skeletal cell more dynamic than cardiac?

A

Can regenerate through satellite cell activation, just not well

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36
Q

How can heart and skeletal muscle respond to stress in a reversible manner?

A

Atrophy + Hypertrophy

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37
Q

What are two things that occur after pulmonary hypertension?

A

Arterial hypertrophy + Smooth Muscle hyperplasia

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38
Q

What occurs with hypertrophic cardiomyopathy?

A

Marked myocardial hypertrophy

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39
Q

In what patten does hypertrophy of the heart develop?

A

concentric fashion, from outside in

40
Q

What does eccentric hypertrophy mean?

A

Enlargement of heart in which chamber dilation is superimposed on mural hypertrophy

41
Q

What role does trabecular bone play in regards to bone injury?

A

Alter its alignment with metaphysis creating “growth arrest lines”

42
Q

What are the key responses to injury that occur in bone?

A

Can alter its shape or mass

Bone can replace with woven rather than lamellar structure

43
Q

What part of the bone is responsible for new bone after an injury?

A

Periosteium

44
Q

What are the basic steps in fracture repair?

A 
Disruption of bone trabeculae/haemorrhage 
Granulation tissue aka primary callus 
Osteoclastic bone removal 
Secondary callus formation 
Remodeled
45
Q

What are the three key forms of neurologic injury?

A

Compression
Necrosis
Degeneration

46
Q

What is the general way that the brain heals?

A

NOT fibrosis, rather there is liquefactive necrosis that leads to cavitation

47
Q

What are the two sources of pigments seen in tissues?

A

Exogenous + Endogenous

48
Q

Describe an exogenous pigment.

A

Pigment taken on from an external source

49
Q

Describe an endogenous pigment?

A

Pigment that is produced by the cell

50
Q

What color is anthracosis?

A

Black

51
Q

What is antracosis from?

A

Carbon

52
Q

What is the pathology of antracosis?

A

Found in lung, associated with air pollutants, found in macrophages near airways

53
Q

What color is melanin?

A

Black and brown

54
Q

What is melanin?

A

L-tyrosine bound to sulphur containing proteins

55
Q

What are the two causes of excess melonin?

A

Melanosis + Melanoma

56
Q

What color is lipofuscin?

A

Yellow-brown

57
Q

What is lipofuscin?

A

End product of autophagocytosis that accumulates w/i cells over time
Paritally metabolized protein and lipid

58
Q

What is another name lipofuscin?

A

Wear and tear

59
Q

What is lipofuscin associated with?

A

Aging

60
Q

What color is ceroid?

A

Yellow-green

61
Q

What is ceroid?

A

Also product of oxidized lipids and protein

Can accumulate as specific pathologic condition

62
Q

What are the heme-associated pigments?

A

Hemoglobin + Hemosiderin + Bilirubin + Porphyrins

63
Q

What colors are heme associated pigments?

A

Red + Green + Yellow

64
Q

What is another name for jaundice?

A

Icterus

65
Q

What color is icterus?

A

Yellow

66
Q

What is icterus?

A

Pigmentation due to presence of bilirubin

67
Q

What can cause jaundice?

A

Pre hepatic
Hepatic
Post hepatic

68
Q

What can cause pre-hepatic?

A

Increased rate of hemolysis

69
Q

What can cause hepatic jaundice?

A

Liver disease

70
Q

What can cause post-hepatic jaundice?

A

Biliary obstruction

71
Q

What color is hematin?

A

Brown

72
Q

What is hematin?

A

Artifact of formic acid and heme

Can also be used to describe liver flukes and some other parasites

73
Q

What are the two forms of gout?

A

Articular + Visceral

74
Q

What enzyme is involved in gout?

A

Uricase

75
Q

What is uricase responsible for?

A

Blood uric acid –> Allantoin

76
Q

What animals is gout seen in?

A

Primates + Birds + Reptiles

77
Q

What are aggregates of gout crystals called?

A

Trophi

78
Q

What do trophi cause?

A

Physically irritating to tissues cause chronic inflammatory response

79
Q

What does gout look like histologically?

A

Amorphous to crystaline

Pale grey to eosinophilic

80
Q

What is amyloid made of?

A

Pathologic, misfolded protein

Protein contains mainly beta-sheets and non-branching fibrils

81
Q

What do amyloids look like with H&E stain?

A

Amorphous + Eosinophilic

82
Q

What happens with accumulation of amyloid?

A

Compression + Atrophy of surrounding tissues

83
Q

What is a special stain used for amyloid plaques?

A

Congo red

84
Q

What are the two types of amyloidosis?

A

Primary + Reactive

85
Q

What is the most common form of amyloidosis seen in non-human species?

A

Reactive

86
Q

What is the cause of primary amyloidosis

A

Immunocyte dyscrasia

87
Q

What is reactive amyloidosis?

A

Secondary to inflammation

88
Q

What are the characteristics of primary amyloidosis?

A

Deposits made of light chains from neoplastic plasma cells

89
Q

What are the characteristics of reactive amyloidosis?

A

Amyloid A deposits accumulate as acute phase proteins are produced during inflammation

90
Q

Where are reactive amyloids commonly found?

A

Kidney + Liver + Spleen + Lymph nodes

91
Q

What does calcification look like grossly?

A

Fine, white, gritty appearance and texture

92
Q

What is dystrophic calcification?

A

Found in areas of necrosis

Calcium blood levels are normal

93
Q

What is metastatic calcification?

A

Calcification as a result of hypercalcemia

94
Q

What are things that can cause hypercalcemia, examples given in lecture?

A

Renal failure + Hyperparathyroidism + Lymphoma + Vit D intoxication

95
Q

What are the common causes of intracellular inclusions?

A

Viral

96
Q

Where can inclusions occur in the cell?

A

Cytoplasm + Nucleus + Or both

97
Q

What are the characteristics of liable cells?

A

Proliferate continuously throughout life and have a very high regenerative capacity
Stem cell pool is prsent

Pathology I (19 decks)

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