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
What makes up an ulcer bed in epithelial tissue?
Fibrin + Inflammatory cells
26
What disease mention in lecture can cause ulcerations in tissue? What is the major characteristic of its lesions?
Diphtheria | Membrane over exudation of fibrin and inflammatory cells
27
What two things occur in hepatic cords in response to injury?
Hyperplasia + Pathologic atrophy
28
Where does pathologic atrophy occur in the hepatic cords as a result of injury?
Where scar tissue is forming
29
Where does hyperplasia occur in the liver when injury occurs?
Where there is regeneration taking place
30
What is the structural result to architectural damage to hepatocytes?
Bridging necrosis
31
What happens after bridging necrosis occurs in hepatocytes?
Fibrous scar tissue + Nodular regeneration | Bridging fibrosis
32
What is the disease process called when there is bridging fibrosis within the liver?
Cirrhosis
33
What is the basic result of cell death within cardiac myocytes?
Scaring aka Fibrosis, they are permanent cells and there for regeneration is not an option
34
Which muscle type is more dynamic, skeletal or cardiac?
Skeletal
35
Why is skeletal cell more dynamic than cardiac?
Can regenerate through satellite cell activation, just not well
36
How can heart and skeletal muscle respond to stress in a reversible manner?
Atrophy + Hypertrophy
37
What are two things that occur after pulmonary hypertension?
Arterial hypertrophy + Smooth Muscle hyperplasia
38
What occurs with hypertrophic cardiomyopathy?
Marked myocardial hypertrophy
39
In what patten does hypertrophy of the heart develop?
concentric fashion, from outside in
40
What does eccentric hypertrophy mean?
Enlargement of heart in which chamber dilation is superimposed on mural hypertrophy
41
What role does trabecular bone play in regards to bone injury?
Alter its alignment with metaphysis creating "growth arrest lines"
42
What are the key responses to injury that occur in bone?
Can alter its shape or mass | Bone can replace with woven rather than lamellar structure
43
What part of the bone is responsible for new bone after an injury?
Periosteium
44
What are the basic steps in fracture repair?
``` Disruption of bone trabeculae/haemorrhage Granulation tissue aka primary callus Osteoclastic bone removal Secondary callus formation Remodeled ```
45
What are the three key forms of neurologic injury?
Compression Necrosis Degeneration
46
What is the general way that the brain heals?
NOT fibrosis, rather there is liquefactive necrosis that leads to cavitation
47
What are the two sources of pigments seen in tissues?
Exogenous + Endogenous
48
Describe an exogenous pigment.
Pigment taken on from an external source
49
Describe an endogenous pigment?
Pigment that is produced by the cell
50
What color is anthracosis?
Black
51
What is antracosis from?
Carbon
52
What is the pathology of antracosis?
Found in lung, associated with air pollutants, found in macrophages near airways
53
What color is melanin?
Black and brown
54
What is melanin?
L-tyrosine bound to sulphur containing proteins
55
What are the two causes of excess melonin?
Melanosis + Melanoma
56
What color is lipofuscin?
Yellow-brown
57
What is lipofuscin?
End product of autophagocytosis that accumulates w/i cells over time Paritally metabolized protein and lipid
58
What is another name lipofuscin?
Wear and tear
59
What is lipofuscin associated with?
Aging
60
What color is ceroid?
Yellow-green
61
What is ceroid?
Also product of oxidized lipids and protein | Can accumulate as specific pathologic condition
62
What are the heme-associated pigments?
Hemoglobin + Hemosiderin + Bilirubin + Porphyrins
63
What colors are heme associated pigments?
Red + Green + Yellow
64
What is another name for jaundice?
Icterus
65
What color is icterus?
Yellow
66
What is icterus?
Pigmentation due to presence of bilirubin
67
What can cause jaundice?
Pre hepatic Hepatic Post hepatic
68
What can cause pre-hepatic?
Increased rate of hemolysis
69
What can cause hepatic jaundice?
Liver disease
70
What can cause post-hepatic jaundice?
Biliary obstruction
71
What color is hematin?
Brown
72
What is hematin?
Artifact of formic acid and heme | Can also be used to describe liver flukes and some other parasites
73
What are the two forms of gout?
Articular + Visceral
74
What enzyme is involved in gout?
Uricase
75
What is uricase responsible for?
Blood uric acid --> Allantoin
76
What animals is gout seen in?
Primates + Birds + Reptiles
77
What are aggregates of gout crystals called?
Trophi
78
What do trophi cause?
Physically irritating to tissues cause chronic inflammatory response
79
What does gout look like histologically?
Amorphous to crystaline | Pale grey to eosinophilic
80
What is amyloid made of?
Pathologic, misfolded protein | Protein contains mainly beta-sheets and non-branching fibrils
81
What do amyloids look like with H&E stain?
Amorphous + Eosinophilic
82
What happens with accumulation of amyloid?
Compression + Atrophy of surrounding tissues
83
What is a special stain used for amyloid plaques?
Congo red
84
What are the two types of amyloidosis?
Primary + Reactive
85
What is the most common form of amyloidosis seen in non-human species?
Reactive
86
What is the cause of primary amyloidosis
Immunocyte dyscrasia
87
What is reactive amyloidosis?
Secondary to inflammation
88
What are the characteristics of primary amyloidosis?
Deposits made of light chains from neoplastic plasma cells
89
What are the characteristics of reactive amyloidosis?
Amyloid A deposits accumulate as acute phase proteins are produced during inflammation
90
Where are reactive amyloids commonly found?
Kidney + Liver + Spleen + Lymph nodes
91
What does calcification look like grossly?
Fine, white, gritty appearance and texture
92
What is dystrophic calcification?
Found in areas of necrosis | Calcium blood levels are normal
93
What is metastatic calcification?
Calcification as a result of hypercalcemia
94
What are things that can cause hypercalcemia, examples given in lecture?
Renal failure + Hyperparathyroidism + Lymphoma + Vit D intoxication
95
What are the common causes of intracellular inclusions?
Viral
96
Where can inclusions occur in the cell?
Cytoplasm + Nucleus + Or both
97
What are the characteristics of liable cells?
Proliferate continuously throughout life and have a very high regenerative capacity Stem cell pool is prsent