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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
Q

Granulation Tissue Characteristics and Mediators

A

Pink, Soft, Angiogenesis (VEGF from Endothelials), loose ECM (MMPs from fibroblasts), Macrophages present
Mediated by PDGF, FGF2, TGFb

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26
Q

Re-Epithelialization vs. Regeneration

A

Epithelials: w/ basement membrane intact, cells are replaced by stem cell proliferation.
Regeneration: Cytokines/GFs from organ loss or inflammation cause replication/repopulation.

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27
Q

Pathologic Scarring

A

excessive collagen accumulation beyond injury area

Permanent = Keloid

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28
Q

Factors Reducing Repair/Regeneration

A

Infection, trauma, insult persistence

Nutritional/Metabolic issues

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29
Q

Edema

A

Fluid movement out of capillaries into tissues

30
Q

Effusion

A

Fluid movement out of capillaries into body cavity

31
Q

Hyperemeia

A

active increase in blood flow from arteriole dilation, increases oxygen and inflammatory cell delivery

32
Q

Congestion

A

Pathologic accumulation of blood 2’ to decreased venous outflow

33
Q

What causes edema/effusion? (4)

A

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
Q

Transudate Characteristics

A 
Intact vessels walls
Low specific gravity
low Protein
Low LDL
High Glucose
Low WBC
35
Q

Exudate Characteristics

A 
Broken vessles
High specific gravity
High protein content
High LDL content
Low glucose content
High WBC content
36
Q

Key Factors in Thrombosis (3)

A

Endothelial Injury
Abnormal blood flow
Hypercoaguability

37
Q

Disseminated Intravascular Coagulation

A

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
Q

Red Infarct

A

Venous blockage
Dual blood supply
Loose Tissue
Lung/Liver/Intestine

39
Q

White Infarct

A

Arterial Blockage
Single Blood Supply
Dense Tissue
Heart/Kidney/Spleen

40
Q

Types of Shock (3)

A

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
Q

Features of Benign Tumors (7)

A

No invasion, circumscribed or encapsulated, no necrosis, uniform, well-differentiated, low rate of turnover, boundary w/ adjacent tissue

42
Q

Features of Malignant Tumors (7)

A

Invade, Metastasize, necrosis, variable differentiation, high turnover, cytoplasmic pleomorphism, loss of boundaries

43
Q

Causes of Neoplasia (4)

A

Genetic Mutation
Gene Amplification/Deletion
Promotor Methylation
Chromosomal Translocations

44
Q

Characteristics of Neoplasms (6)

A 
Unlimited Replication
Angiogenesis
Tissue invasion/metastasis
Insensitivity to anti-growth signals
self-sufficiency of GFs
Evasion of apoptosis
45
Q

3 Types of Metastasis

A

Lymphatogenous
Hematogenous
Direct Cavity Seeding

46
Q

What motivates a tumor to metastasize?

A

Crowding due to primary tumor growth produces hypoxia/starvation that creates selective pressure for invasion

47
Q

Why do cancers metastasize to certain places?

A

Mechanical arrest: stop in first capillary bed encountered.

Seed-Soil: leave vessels based on endothelial marker expression, chemokine expression, overall habitability

48
Q

Invasion Process

A
  • 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
Q

Intravasation Process

A

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
Q

Extravasation Process

A

Adhesion to endothelial cells through inegrins/laminin Rs

51
Q

Colonization Process

A

dormancy of micrometastases is common, tumor cells release GFs/Cytokines

52
Q

Direct effects of metastases

A

interfering with biological function at site

53
Q

Indirect Effects of Metastases

A

paraneoplastic syndrome

54
Q

Ultimate Effects of Metastases

A

Ulcers, Hemorrhage, pain, seizures, perforation, inflammation, edema….
Mortality from infection, organ failure, hemorrhage, thromboembolism, emaciation

55
Q

Percent of cancers caused by environmental factors

A

80%

56
Q

Chemical causes of cancer

A

Chemicals are carcinogenic if they damage/modify DNA/RNA. Most are benign until they are activated by metabolism into strong electrophiles

57
Q

Ames Test

A

Chemical mixed w/ CYP450s is added to Hist- salmonella on Hist- agar. If mutation occurs, Hist+ reverted salmonella grow.

58
Q

Principles of Carcinogenesis (6)

A 
Dose Dependent
Specific Cancers w/ Specific Chemical
Requires Time
Proliferating Cells at Risk
Changes Stably Transmitted
Stem Cells at Risk
59
Q

Two Step Model of Carcinogenesis

A

Initiation: irreversible direct effect of carcinogen
Promotion: repeated, reversible, effect of a non-carcinogen after initiation (usually irritant/inflammation)

60
Q

Squamous Cell Lung Cancer

A
  • 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
Q

Adenocarcinoma Lung

A
  • Non-smoker Cancer (25-40%)
  • central or peripheral origin (associated w/ scarring)
  • create glands that secrete mucin
  • K-Ras mutation common
62
Q

Bronchioalveolar Subclass

A

Adencarcinoma w/ best prognosis, grows along alveolar septae

63
Q

Large Cell Carcinoma Lung

A
  • 10-15%
  • High grade and anaplastic
  • Likely no keratin or mucin
  • catch-all category
64
Q

Small Cell Lung Cancer

A
  • 20-25%, associated w/ smoking
  • origin throughout lung
  • High grade
  • No glandular/squamous differentiation
  • small dark clusters
  • endocrine cell origin, paraneoplastic syndrome
65
Q

Pancreatic Cancer Pathology

A

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
Q

Pancreatic Cancer Prognosis

A

Poor, excision hard, symptoms usually post metastasis

67
Q

Colon Cancer Pathology

A

well-differentiated, begin in mucosal layer of bowel, arise in adenomatous polyps (tubular or villous), risk incrases w/ poly size

68
Q

Colon Cancer Clinical Features

A

Left-sided tumor is “apple core” and causes obstruction and constipation
Right sided tumor creates polypoid mass

69
Q

Germline Colon Cancer

A

FAP, HNPCC (mismatch repair), Loss of base excision repair (mutY)

70
Q

Diseases w/ increase colon cancer risk

A

Inflammatory bowel diseases

71
Q

Prostate Cancer vs BPH

A

Prostate cancer arises in periphery of gland, digital exam detection, no urinary effects
BPH arises in center of gland, has urinary effects

72
Q

Gleason Grading

A

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.

Disease and Defense (4 decks)

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