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Disease and Defense > Unit 2: Tissue Injury, Neoplasia > Flashcards

Unit 2: Tissue Injury, Neoplasia Flashcards

1
Q

Major Mechanisms of Cell Injury (5)

A 
ATP depletion
Mitochondria Damage
Calcium Influx
ROS
Membrane Permeability
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2
Q

How does ischemia/hypoxia cause cell injury?

A
  • Under hypoxic conditions, oxidative phosphorylation fails and mitos release ROS.
  • ROS production increases w/ high oxygen therapy
  • Nuetorphils produce ROS during inflammatory response.
  • xanthine oxidase produced during hypoxia makes ROS when O2 is restored
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3
Q

Cellular Adaptations to Injury (4)

A

Hypertrophy: increase in size
Hyperplasia: increase in number
Atrophy: reduction in size
Metaplasia: change in cell type

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4
Q

Changes in organelles during cell injury (4)

A

Membrane: perforation, loss of pump function, lipid peroxidation.
Mitochondria: accumulation of H2O2, reduced ATP production.
ER: ribosome detachment, reduced protein synthesis.
Nucleus: nucleolus changes, reduced rRNA

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5
Q

Four types of necrosis

A

Coagulative: ishemia/infarction, tissue architecture preserved, pale cells in wedge shape
Liquefactive: immune response damage, damage from digestive enzymes, infection/CNS damage
Caseous: TB, white collection of fragmented cells/granular debris w/ distinctive border.
Fat: fat hydrolysis from pancreatic enzyme release, chalky precipitate w/ calcium
Fibrinoid: vasculitis, deposition of AB-AG w/ fibrin in vessel walls, appears pink.

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6
Q

Reversible Morphology/Biochemical Alterations

A 
Low ATP
Low pump activity (swelling)
high Glycolysis
Low pH
Low protein synthesis
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7
Q

Irreversible Injury Morphology/Biochemical Alterations

A

Lysosomal enzyme activation
DNA/protein degradation
High Ca influx

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8
Q

Basics of Acute Inflammation (timing, histology, localization)

A

Fast response, TLR activation, chemical mediators released, vascular changes, leukocyte recruitment, local

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9
Q

Basics of Chronic Inflammation

A

slow, involves mononuclear infiltrate, tissue destruction and repair, local and systemic effects

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10
Q

Leukocyte Recruitment

A
  • IL-1 and histamine cause endothelial cells to express E and P selectins respectively.
  • Leukocytes in margins of blood flow interact via surface sugars and slow down
  • TNF and IL-1 stimulate leukocytes to express integrins and endothelials integrin ligands which causes adhesion
  • Diapedesis occurs as enzymes chew through basement membrane
  • Chemical gradient of chemokines draws leukocytes to inflammation site
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11
Q

Leukocyte Activation

A
  • Leukocyte surface Rs bind target directly or through opsonins, initiate phagocytosis
  • Lysosomes fuse w/ phagosome, myeloperoxidase creates ROS
  • enzymes and anti-microbial chemicals released into ECM (includes NETs)
  • Additional inflammatory mediators released (AA/cytokines)
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12
Q

Vascular Changes (3 causes)

A
  • Dilation of arterioles floods capillaries and causes stasis, occurs by 3 mechanisms….
  • Chemical (histamine or IL-1/TNF)
  • Injury
  • Transcytosis
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13
Q

Transudate vs. Exudate

A

Exudate is from increased vascular permeability, has high protein/WBC content
Transudate is from decreased colloid osmotic pressure, has minimal protein content.

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14
Q

Inflammasome (general info)

A

Variable composition of PRRs and DRRs that activate caspase-1 mediated IL-1B and IL-18 cytokines.

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15
Q

3 Outcomes of Inflammation/Tissue Damge

A

Resolution via regeneration
Scarring via fibrosis
Cell death

Can be combo of resolution/scarring

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16
Q

Different Morphologies of Acute Inflammation (5)

A

Serous: outpouring of water, protein-poor fluid
Fibrous: high vascular permeability releases fibrin that creates meshwork for scarring
Suppurative: lots of purulent exudate (PMN containing).
Ulcer: necrosis causing loss of suface tissue
Granulomatous: “walling off”

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17
Q

Common causes of leukocyte dysfunction (3)

A

Aplastic Anemia
Diabetes
Inborn defects

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18
Q

Main processes in chronic inflammaiton (3), are these sequential?

A

Non-seuqential
Mononuclear infiltrate
Tissue destruction
Tissue repair (neovascularization and fibrosis)

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19
Q

Granulomatous Inflammation (general)

A

Macrophages form nodule around organisms and promote fibrosis
Eosinophils are recruited

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20
Q

Acute-Phase Reaction

A
  • Pyrexia from IL-1, TNF, exogenous pyrogens acting on hypothallamus
  • IL-6 causes hepatocytes to release c-reactive protein and serum amyloid A
  • Fibrinogen causes stacking of RBCs to determine sedementation rate
  • IL-1/TNF causes increased and early release of WBCs from marrow
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21
Q

Tissue repair depends on…

A

proliferative capacity of damaged tissue

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22
Q

Tissue repair occurs when?

A

During chronic inflammation phase

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23
Q

ECM functions during inflammation (4)

A

Growth Factor Reservoir
Proliferation Regulation
Chemotaxis Assistance
Differentation/Adhesion

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24
Q

Cells involved in repair and their functions (4)

A

Macrophages: GF secretion
Fibroblasts: collagen deposition and collagen remodeling
Endothelial Cells: neovascularizaiton
Epithelial/Hepatocytes: regeneration

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25
Granulation Tissue Characteristics and Mediators
Pink, Soft, Angiogenesis (VEGF from Endothelials), loose ECM (MMPs from fibroblasts), Macrophages present Mediated by PDGF, FGF2, TGFb
26
Re-Epithelialization vs. Regeneration
Epithelials: w/ basement membrane intact, cells are replaced by stem cell proliferation. Regeneration: Cytokines/GFs from organ loss or inflammation cause replication/repopulation.
27
Pathologic Scarring
excessive collagen accumulation beyond injury area | Permanent = Keloid
28
Factors Reducing Repair/Regeneration
Infection, trauma, insult persistence | Nutritional/Metabolic issues
29
Edema
Fluid movement out of capillaries into tissues
30
Effusion
Fluid movement out of capillaries into body cavity
31
Hyperemeia
active increase in blood flow from arteriole dilation, increases oxygen and inflammatory cell delivery
32
Congestion
Pathologic accumulation of blood 2' to decreased venous outflow
33
What causes edema/effusion? (4)
Increased hydrostatic pressure (heart failure/venous obstruction) Decreased oncotic pressure (kidney/Gi issues or low protein production) Lymphatic Obstruction (inflammation, infection, neoplasm) Increased Vascular Permeability
34
Transudate Characteristics
``` Intact vessels walls Low specific gravity low Protein Low LDL High Glucose Low WBC ```
35
Exudate Characteristics
``` Broken vessles High specific gravity High protein content High LDL content Low glucose content High WBC content ```
36
Key Factors in Thrombosis (3)
Endothelial Injury Abnormal blood flow Hypercoaguability
37
Disseminated Intravascular Coagulation
Non-specific activation of clotting cascade leading to widespread thrombosis. Platelets/clotting factors are used up which increases risk of hemorrhage. Caused by global release of pro-coagulants, widespread endothelial injury. Symptoms: anemia, respiratory insufficiency, convulsions, acute renal failure, shock
38
Red Infarct
Venous blockage Dual blood supply Loose Tissue Lung/Liver/Intestine
39
White Infarct
Arterial Blockage Single Blood Supply Dense Tissue Heart/Kidney/Spleen
40
Types of Shock (3)
Cardiogenic: heart fails to pump enough blood for perfusion Hypvolemic: not enough blood for perfusion Septic: systemic inflammation causes widespread vessel dilation and vascular leakage
41
Features of Benign Tumors (7)
No invasion, circumscribed or encapsulated, no necrosis, uniform, well-differentiated, low rate of turnover, boundary w/ adjacent tissue
42
Features of Malignant Tumors (7)
Invade, Metastasize, necrosis, variable differentiation, high turnover, cytoplasmic pleomorphism, loss of boundaries
43
Causes of Neoplasia (4)
Genetic Mutation Gene Amplification/Deletion Promotor Methylation Chromosomal Translocations
44
Characteristics of Neoplasms (6)
``` Unlimited Replication Angiogenesis Tissue invasion/metastasis Insensitivity to anti-growth signals self-sufficiency of GFs Evasion of apoptosis ```
45
3 Types of Metastasis
Lymphatogenous Hematogenous Direct Cavity Seeding
46
What motivates a tumor to metastasize?
Crowding due to primary tumor growth produces hypoxia/starvation that creates selective pressure for invasion
47
Why do cancers metastasize to certain places?
Mechanical arrest: stop in first capillary bed encountered. | Seed-Soil: leave vessels based on endothelial marker expression, chemokine expression, overall habitability
48
Invasion Process
- Loss of cell-cell adherence: loss of E-cadherin expression via LOH, mutation, silencing, TFs SNAIL/TWIST/ZEB1-2 - Degradation of ECM: MMPs that release chemotactic, angiogenic, GFs from ECM - Loss of ECM attachment: loss of integrin expression and loss of death signals when detached
49
Intravasation Process
Tumor cells at risk of death in circulation through sheer stress, immune cell attack, lack of adhesion. Clumping together and attachment to cells improve survival.
50
Extravasation Process
Adhesion to endothelial cells through inegrins/laminin Rs
51
Colonization Process
dormancy of micrometastases is common, tumor cells release GFs/Cytokines
52
Direct effects of metastases
interfering with biological function at site
53
Indirect Effects of Metastases
paraneoplastic syndrome
54
Ultimate Effects of Metastases
Ulcers, Hemorrhage, pain, seizures, perforation, inflammation, edema.... Mortality from infection, organ failure, hemorrhage, thromboembolism, emaciation
55
Percent of cancers caused by environmental factors
80%
56
Chemical causes of cancer
Chemicals are carcinogenic if they damage/modify DNA/RNA. Most are benign until they are activated by metabolism into strong electrophiles
57
Ames Test
Chemical mixed w/ CYP450s is added to Hist- salmonella on Hist- agar. If mutation occurs, Hist+ reverted salmonella grow.
58
Principles of Carcinogenesis (6)
``` Dose Dependent Specific Cancers w/ Specific Chemical Requires Time Proliferating Cells at Risk Changes Stably Transmitted Stem Cells at Risk ```
59
Two Step Model of Carcinogenesis
Initiation: irreversible direct effect of carcinogen Promotion: repeated, reversible, effect of a non-carcinogen after initiation (usually irritant/inflammation)
60
Squamous Cell Lung Cancer
- Associated w/ smoking - 25-40% of lung cancers - Central growth - Starts w/ metaplasia - Causes hemorrhage/necrosis - Well-differentiated - Keratin Pearls - P53/ P16 mutations common
61
Adenocarcinoma Lung
- Non-smoker Cancer (25-40%) - central or peripheral origin (associated w/ scarring) - create glands that secrete mucin - K-Ras mutation common
62
Bronchioalveolar Subclass
Adencarcinoma w/ best prognosis, grows along alveolar septae
63
Large Cell Carcinoma Lung
- 10-15% - High grade and anaplastic - Likely no keratin or mucin - catch-all category
64
Small Cell Lung Cancer
- 20-25%, associated w/ smoking - origin throughout lung - High grade - No glandular/squamous differentiation - small dark clusters - endocrine cell origin, paraneoplastic syndrome
65
Pancreatic Cancer Pathology
Start w/ focal areas of non-invasive eptithelia that are well-differentiated, form mucin-secreting glands, poorly defined margins, rock-hard tumors that invade normal tissue
66
Pancreatic Cancer Prognosis
Poor, excision hard, symptoms usually post metastasis
67
Colon Cancer Pathology
well-differentiated, begin in mucosal layer of bowel, arise in adenomatous polyps (tubular or villous), risk incrases w/ poly size
68
Colon Cancer Clinical Features
Left-sided tumor is "apple core" and causes obstruction and constipation Right sided tumor creates polypoid mass
69
Germline Colon Cancer
FAP, HNPCC (mismatch repair), Loss of base excision repair (mutY)
70
Diseases w/ increase colon cancer risk
Inflammatory bowel diseases
71
Prostate Cancer vs BPH
Prostate cancer arises in periphery of gland, digital exam detection, no urinary effects BPH arises in center of gland, has urinary effects
72
Gleason Grading
1 is well differentiated w/ uniform glands. 5 has no glands and is high grade w/ tumor infiltration. Add grade of predominant and subordinate patterns.

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