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HLTH 341 - Pathobiology > Test 2 > Flashcards

Test 2 Flashcards

1
Q

what are the purposes of inflammation (3)?

A
  1. neutralize and destroy invading and harmful agents
  2. limit the spread of harmful agents to other tissue (localization)
  3. prepare damaged tissue for repair
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2
Q

during inflammation capillary permeability is increased. this results in _____, ____, and _____. The last of which allows for coagulation cascades to occur.

A
  • redness
  • increased viscosity (rbc and platelet accumulation)
  • slowed blood flow
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3
Q

what are the 3 major components of acute inflammation?

A
  1. dilation of small vessels
  2. increase permeabiltity of the microvasculature
  3. emigration of leukocytes from the microcirculation
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4
Q

what is the site of acute inflammation?

A

postcapillary vasculature: thin walled vessels that allow for passage of fluid and proteins

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5
Q

during inflammation there is efflux of 3 things from the vasculature. the two main ones are ____ and ____. the minority one is _____

A
  • proteins
  • fluid
  • rbcs
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6
Q

compare and contrast exudate and transudate. consider content and common times of occurrence.

A

exudate
* content: high protein, few cells
* time: inflammation, infection, injury

transudate
* content: low protein, few cells
* time: increased hydrostatic pressure and decreased colloid osmotic pressure - kidney and liver disease, protein malnutrition

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7
Q

what are the 5 cardinal signs of infection?

A
  1. redness (rubor)
  2. swelling (tumor)
  3. heat (calor)
  4. pain (dolor)
  5. loss of function (functio laesa)
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8
Q

what are the steps of inflammation?

A
  1. bradykinin release
  2. pain receptor activation via bradykinin
  3. histamine release from mast cells and basophils
  4. capillary dilation
  5. increased blood flow and capillary permeability
  6. bacteria enter tissue
  7. neutrophils and monocytes to injury site
  8. phagocytosis of bacteria by neutrophils
  9. macrophages leave bloodstream for phagocytosis
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9
Q

what is the process of inflammation from chemokines to extravasation?

A
  1. macrophage with microbes releases chemokines
  2. integrin on leukocyte goes from low to high affinity state
  3. selectins and integrin ligands allow for ‘rolling’ of the leukocyte
  4. leukocyte squeezes through endothelium
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10
Q

different interferons respond to different types of infection. ____ respond to bacterial infections, whereas ____ and respond to viral infections.

A
  • gamma
  • alpha
  • beta
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11
Q

what occurs with leukocyte activation via GPCRs?

A
  1. cytoskeletal changes and signal transduction
  2. increased integrin activity -> endothelial adhesion
  3. chemotaxis -> migration into tissues
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12
Q

what occurs with leukocyte activation via TLRs OR cytokine receptors?

A
  1. production of mediators -> inflammation amplification
  2. ROS production -> microbicidial leukocyte activity -> killing of microbes
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13
Q

what occurs with leukocyte activation via phagocytic receptors?

A
  1. ROS production -> microbicidial leukocyte activity - killing of microbes
  2. phagocytosis of microbe -> microbicidial leukocyte activity -> killing of microbes
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14
Q

what are the 4 types of exudates?

A
  1. serous
  2. fibrinous
  3. purulent
  4. hemorrhagic
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15
Q

describe serous exudate:
* texture
* contents
* location
* derivation
* cause

A
  • texture: water (serum like)
  • contents: mostly fluid, some proteins and white blood cells, sterile
  • location: within body cavities lined by the peritoneum, pleura, or pericardium
  • derivation: from plasma (via vascular permeability) or mesothelial secretions (irritation)
  • cause: tissue injury, irritation (friction), viral infection
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16
Q

describe fibrinous inflammation exudate:
* texture
* contents
* location
* cause
* resolution
* adverse outcomes

A
  • texture: thick and sticky
  • contents: lots of cells and fibrin
  • location: lining of body cavities - pericardium, meninges, pleura
  • cause: activation of coagulation cascade causing build-up of fibrin meshwork (increased vascular permeability)
  • resolution: fibrinolysis and macrophage activity
  • adverse outcome: scar tissue when sustained with vascularization
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17
Q

describe purulent inflammation exudate:
* texture
* colour
* contents
* cause

A
  • texture: thick
  • colour: yellow-green
  • contents: leukocytes, cell debris, microorganisms, edema fluid
  • cause: bacterial infection (staphylococcus, acute appendicitis)
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18
Q

the colour of a purulent exudate is indicative of different health levels. for example, white indicates —– , yellow-green indicates —–, and bright green indicates —–.

A
  • white: no infection
  • yellow-green: infection
  • bright green: pseudomonas infection (i.e. burn)
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19
Q

describe what an ulcer is an how it is formed

A
  • localized concave excavation of the surface of an organ or tissue
  • caused by shedding of inflamed necrotic tissue - extensive leukocyte infiltration in combination with vasodilation
  • late on it can inlcude scarring and chronic inflammation
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20
Q

what are the common sites of ulcers?

A
  • mouth
  • stomach
  • intestines
  • geniourinary tract
  • skin
  • subcutaneous tissues of lower extremities
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21
Q

describe abscess:
* what it is
* make-up
* cause
* type of exudate

A
  • what: localized collections of pus
  • make up: central mass (collection of neurotic leukocytes and tissue cells) with surrounding neutrophils
  • cause: bacterial infection
  • type of exudate: purulent
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22
Q

what are the 4 types of ulcers?

A
  1. venous leg ulcers
  2. arterial ulcers
  3. diabetic ulcers
  4. pressure sores
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23
Q

venous leg ulcers are common in elderly with —, but can also be caused by —— or ——-.

A
  1. chronic venous hypertension
  2. varicose veins
  3. congestive heart failure
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24
Q

aterial ulcers are common in those with what?

A

atherosclerosis of peripheral arteries

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25
Q

diabetic ulcers are of the —– extremeties and can be worsened by —–, —–, and —–.

A
  1. lower
  2. ichemia
  3. neuropathy
  4. secondary infections
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26
Q

what is the cause of pressure sores?

A

mechanical pressure and local ischemia

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27
Q

what are the 3 outcomes of acute inflammation?

A
  1. complete resolution
  2. tissue replacement
  3. chronic inflammation
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28
Q

in complete resolution there is complete removal of —–, —–, and —–. there is also the resorption of excess fluid through —-. this allows for regeneration of damaged host cells and regain of full and normal function.

A
  1. inflammatory cause
  2. offending/foreign agent
  3. cellular debris
  4. lymphatics
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28
Q
A
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29
Q

tissue replacement also includes healing of —– via —- or —–. this occurs due to what (3)?

A
  • healing of: connective tissue
  • via: scarring or fibrosis
    1. more substantive tissue destruction
    2. at sites where tissue cannot regenerate, or in serous cavities
    3. extensive fibrin deposits exudation in tissue
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30
Q

what are the potential causes of chronic inflammation?

A
  1. acute inflammatory response is sustained
  2. assaulting cause is presistent or recurring
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31
Q

where is complete resolution the easiest? provide an example

A

at sites where cells routinely proliferate
* i.e. epithelial tissue

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32
Q

provide an example of chronic inflammation due to:
1. assualt persistence
2. assault recurring

A
  1. hepatitis - liver damage
  2. asthma and Kohl’s disease
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33
Q

what type of cells/tissues are inherently more proliferative?

A
  1. stem cells
  2. epithelial skin cells (squamous epithelia)
  3. epithelial cells lining GI tract (columnar epithelium)
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34
Q

cells in the G0 phase can regenerate in response to what?

A

injury

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35
Q

quiescent cells can be stimulated to regenerate in response to what? give some examples of thesse cells

A

stimulated to regenerate in response to growth factors
* i.e. endothelial cells, fibroblasts, smooth muscle cells

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36
Q

explain the role of epidermal growth factor and what it is secreted by

A

secreted by: macrophages, salivary glands, keratinocytes
role: mitosis in keratinocytes and fibroblasts, stimulate keratinocyte migration, stimulate formation of granular tissue

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37
Q

explain the role of vascular endothelial growth factor and what it is secreted by

A

secreted by: mesencymal cells
role: stimulate proliferation in endothelial cells, increase vascular permeability, angiogenesis

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38
Q

describe collagen as an ECM component in tissue repair

A
  • main supportive protein of skin, tendons and scars
  • fibrous materials
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39
Q

describe fibronectin as an ECM component in tissue repair

A
  • fibrous glycoprotein
  • binding component of tissues
  • scaffold for ECM deposition, angiogenesis, re-epithelialization
  • made by fibroblasts, monocytes, and endothelium
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40
Q

describe fibrinogen as an ECM component in tissue repair

A
  • blood protein
  • forms clots in damaged vessels
  • key for blood clots and coagulation casacade
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41
Q

describe elastin as an ECM component in tissue repair

A
  • provide ability of tissues to recoil
  • important in cardiac valves and large blood vessels that have to accomodate recurrent pulsatile flow - also in uterus, skin, and ligaments
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42
Q

describe proteoglycans and hyaluronan as an ECM component in tissue repair

A
  • hydrated gels that cofner resistance to compressive forces
  • reservoirs for secreted growth factors
  • provide a layer of lubrication between bony surfaces
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43
Q

describe laminin as an ECM component in tissue repair

A
  • most abundant glycoprotein in the basement membrane
  • mediates attachment to the basement membrane, cell proliferation, differentiation, and motility
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44
Q

what are some of the cell (4) and fiber (3) components of ECM?

A

cells
1. fibroblasts
2. macrophages
3. lymphocytes
4. neutrophils

fibers
1. collagen
2. elastin
3. reticular

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45
Q

what is the mechanism of connective tissue deposition?

A
  • cytokines made by macrophages and leukocytes stimulate the migration and proliferation of fibroblasts and myofibroblasts
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46
Q

what are the stages of the tissue repair process?

A
  1. clot formation and inflammation
  2. cell proliferation - epithelial cells, vascularization, fibroblasts
  3. fibrous scar
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47
Q

what is the fundamental difference between healing by first intention and healing by second intention?

A

first intention : fibrous union where all edges fully close
second intention : concave nature of wound where there wasn’t full closure

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48
Q
A
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49
Q

abraisons occur when what layers of the skin is scraped off?

A

epidermis

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50
Q

what is a contusion?

A

skin wound when a blow that crushes the tissue occurs

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51
Q

the immune system from human physiological perspective is sometimes referred to as the ____ or ____ immune response

A

human OR host

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52
Q

what is the concept of immunity related to?

A

the ability of the human body to protect itself from foreign entities, invaders, pathogenic bacteria, viruses and disease causing agents

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53
Q

what are the 3 key functions of the immune system?

A
  1. protection against diseass causing agents
  2. removal of dead, dying or destroyed host cells
  3. recognition and removal of any abnormally functioning self cells
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54
Q

the immune system has three key functions. in order to perform these functions 2 things are needed:

A
  1. regular commmunication between immune cells via small chemical signaling molecules
  2. recruitment of additional immune cells
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55
Q

host defenses can be described in 3 lines. the first line of defense contains 3 things: ____. the second line of defense has four: ____. and the third line of defense has two subcomponents - ____ and ____ which lead to ____.

A
  • first line: physical barriers, chemical barriers, genetic components
  • second line: phagocytosis, inflammation, fever, antimicrobial proteins
  • third line: active (infection) or passive (maternal antibodies) that leads to B/T cells and their effects
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56
Q

in innate immunity recognition can occur via multiple traits, such as PAMP which stands for ____ and is recognized by PRRs or ____.

A
  • PAMP: pathogen associated molecular pattern
  • PPR: pattern recognition receptor
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57
Q

what are some mechanisms of innate immunity?

A
  • phagocytosis
  • complement cascade
  • inflammation and fever
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58
Q

what is innate immunity mediated by?

A

cells (whole cell response) and cytokines

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59
Q

what are the 5 types of receptors most utilized in innate immunity?

A
  1. TLRs: toll like receptors
  2. NLRs: NOD like receptors
  3. C-type lectin
  4. Kinase
  5. GPCRs
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60
Q

describe TLRs by their location and what they recognize

A
  • location: on cell surface or on membrane of an endosomal compartment
  • recognize: extracellular pathogens (i.e. pathogenic e. coli, cholera)
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61
Q

what are some examples of bacteria that are extracellular? intracellular?

A
  • intracellular: salmonella, mycobacterium Tb
  • extracellular: pathogenic e.coli, cholera
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62
Q

describe NLRs by their location and what they recognize

A
  • location: intracellular
  • recognize: internalized pathogens (i.e. viruses)
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63
Q

viruses are often recognized by NLRs (NOD-like receptors). why?

A

viruses are required to become internalized to replicate

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64
Q

kinases have what type of receptors?

A

type 1 IFN receptors

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65
Q

define antigen

A

any molecule that induces a specific immunity response

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66
Q

adaptive immunity is a specific response to target a given pathogen. this immunity is mediated by ____ and ____. it is composed of two branches - ____ and ____.

A
  • mediated by: B cells and T cells
  • branches: cell mediated (T cell), humoral (B cell)
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67
Q

t-lymphocytes are 60-70% of lymphocytes in peripheral blood. they mature in the thymus and respond to what?

A

respond to protein antigens on MHC

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68
Q

T helper cells have ____ protein markers and recognize antigens on ____ that are processed by APCs. they activate other cells via ____ and stimulate ____ and ____. have 3 subclasses, ____ that secrete pro-inflammatory cytokines

A

T helper cells have CD4+ protein markers and recognize antigens on MHC-II that are processed by APCs. they activate other cells via cytokine secretion and stimulate B cell proliferation and antibody production. have 3 subclasses, TH1, TH2, and TH17 that secrete pro-inflammatory cytokines

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69
Q

cytotoxic T cells have ____ protein markers and recognize antigen on ____ on viral-infected or cancer cells. they can also ____ these cells.

A

cytotoxic T cells have CD8+ protein markers and recognize antigen on MHC-I on viral-infected or cancer cells. they can also directly kill these cells.

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70
Q

what is the function of regulatory T lymphocytes?

A

supression of the immune/inflammatory response

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71
Q

what are the main classes of MHC?

A
  1. class 1: for CD8+ cells
  2. class II: for CD4+ cells
  3. class III: complement, cytokines, etc.
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72
Q

what is the broad function of MHC? (think in terms of it’s surface)

A

cell surface proteins display antigens on the surface of host cells

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73
Q

where is the human leukocyte antigen (HLA) encoded?

A

chromosome 6

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74
Q

what type of bonds are present in MHCs?

A

sulfide bonds (sulfur-sulfur)

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75
Q

in class I MHCs the alpha chain has ____ domains and is associated with ____ and the ____. the beta chain is a ____ polypeptide that is encoded by a separate gene on chromosome ____.

A

in class I MHCs the alpha chain has 3 domains and is associated with peptide/antigen binding and the cell membrane. the beta chain is a B2-microglobulin polypeptide that is encoded by a separate gene on chromosome 15.

76
Q

class II MHCs are ____ of ____ linked alpha and beta subunits. both of these subunits are associated with ____ and the ____, and have 3 subparts: ____.

A

class II MHCs are heterodimers of noncovalently linked alpha and beta subunits. both of these subunits are associated with peptide/antigen binding and the cell membrane, and have 3 subparts: DP, DQ, and DR.

77
Q

what are maternal and paternal HLA genes referred to as? what is the likelihood that siblings will inherit the same HLA alleles?

A
  • referred to as an HLA haplotype
  • 25% likelihood
78
Q

what types of diseases are associated with HLA alleles?

A

autoimmune diseases
* some may make people susceptible to allergic reactions

79
Q

what is the difference between the variable and constant regions of MHC-II’s protein chains?

A
  • variable - associated with peptide
  • constant - associated with cell membrane (through the membrane)
80
Q

what are the 3 portions of TCR (T-cell receptor complex) and their function?

A
  1. CD4
  2. CD3
  3. CD28 - facilitate signal transduction response
81
Q

explain MHC class I proteins based on:
* what they are recognized by
* where they are found
* what they display

A
  • recognized by cytotoxic T cells
  • found on the surface of nucleated cells
  • display intracellularly processed antigens
82
Q

explain class II MHC proteins based on:
* what they are recognized by
* where they are found
* what they display

A
  • recognized by helper T cells
  • found on the surface of dendritic cells, macrophages, and B cells
  • display extracellularly processed antigens
83
Q

how many antigenic epitopes will T cells recognize and respond to?

A

one

84
Q

what interleukin is required for cytotoxic T cells to proliferate into memory and effector cells?

A

IL-2

85
Q

how do cytotoxic T cell effector cells have their cytotoxic effects? (explain the process)

A
  • via perforins that are made in cytotoxic T cells
  • allow granzymes to enter the target cell
  • degrades DNA and triggers apoptosis
86
Q

____ releases IFN gamma which ____

A

TH1 releases IFN gamma which helps recruit macrophages

87
Q

____ releases IL-17 which is ____

A

TH17 releases IL-17 which is pro-inflammatory

88
Q

____ releases TGF-beta which helps ____

A

TREG releases TGF-beta which helps restrict tissue damage

89
Q

match the TH cell with the cytokines it releases:
TH cells:
* TH1
* TH2
* TH17
* TFH
* TREG

cytokines:
* TGF-beta, IL10
* IL4, IL5, IL13
* IL4, IL21
* IL17
* IFN-gamma

A
  • TH1 - IFN-gamma
  • TH2 - IL4, IL5, IL13
  • TH17 - IL17
  • TFH - IL4, IL21
  • TREG - TGF-beta, IL10
90
Q

what is the role of TH1 cells, what do they secrete, what do they provide defense against, what are their target cells?

A
  • role: autoimmunity and chronic inflammation
  • secretes: IFN-gamma
  • defense against: intracellular pathogens
  • target cell: macrophages
91
Q

what is the role of TH2 cells, what do they secrete, what do they provide defense against, what are their target cells?

A
  • role: allergies
  • secretes: IL4, IL5, IL13 (activates eosinophils)
  • defense against: helminths
  • target cell: eosinophils
92
Q

what is the role of TH17 cells, what do they secrete, what do they provide defense against, what are their target cells?

A
  • role: autoimmunity
  • secretes: IL17, IL22 (activates neutrophils)
  • defense against: extracellular pathogens
  • target cells: neutrophils
93
Q

a TH cell attracts macrophages to a site of infection by ____

A

secreting cytokines

94
Q

b-lymphocytes carry many copies of identical ____ and respond to ____ antigen epitope. however they form a reserve of cells that can mount an immune response and survive for ____

A

b-lymphocytes carry many copies of identical B-cell receptors and respond to one antigen epitope. however they form a reserve of cells that can mount an immune response and survive for months to years

95
Q

what are the 2 main types of B cells?

A
  1. memory B cells
  2. plasma B cells
96
Q

memory B cells ____ to respond ____ in the future. they have cell surface receptors that ____ recognize antigens

A

memory B cells retain memory of an antigen encounter to respond quickly in the future. they have cell surface receptors that directly recognize antigens

97
Q

plasma b cells are ____-lived but rapidly produce ____ in response to ____ .

A

plasma b cells are short-lived but rapidly produce multiple antibodies in response to antigen exposure

98
Q

antibodies are found in ____ to ____. they will continue to be produced until the ____ is cleared. once this happens ____ will die off

A

antibodies are found in secretions and bodily fluids to neutralize the effects of antigens. they will continue to be produced until the antigen is cleared. once this happens plasma cells will die off

99
Q
A
100
Q

what is an antibody liter?

A

the level of antibodies in one’s system

101
Q

describe the process in which B cell proliferation is dependent on activation by helper T cells

A
  • helper T cells recognize MHC-II-antigen complex on B cell surface
  • stimulation of clonal expansion and antibody production
  • T cells produce cytokines
102
Q

what is the molecular makeup of the constant regions of antibodies?

A

highly conserved amino acid sequence

103
Q

what is the molecular makeup of the variable regions of antibodies?

A

highly variable or different amino acide sequences

104
Q

what are the 5 types of heavy chains?

A

alpha
mu
gamma
delta
espilon

105
Q

what are the 2 kinds of light chains?

A

kappa
lambda

106
Q

what are the 5 Ig classes?

A

M, A, D, G, E

107
Q

what is valence in the context of antibodies?

A

number of antigen-binding sites on an antibody

108
Q

what is the Fab region of an antibody? is it heavy or light chain?

A
  • antigen binding end of an antibody
  • light chain
109
Q

what is the Fc end of an antibody? is it heavy or light chain?

A
  • fragment on stem that determines antibody class
  • heavy chain
110
Q

describe IgG and it’s key points

A
  • greatest antibody in circulation
  • the only antibody transferred across the placenta
  • works against anti-Rh infections
111
Q

describe IgM and it’s key points

A
  • located in mucous secretions and mucosal surfaces
  • sometimes ABO isoaggultinins
  • rheumatoid factor
112
Q

describe IgA and it’s key points

A
  • works against infections
113
Q

describe IgD and it’s key points

A
  • lowest concentration of Ig’s
  • not much known about it’s function
  • binds to B cells in the presence of IgM
114
Q

describe IgE and it’s key points

A
  • mast cell sensitization
  • cytophilic antibody
  • skin sensitizing antibody
  • allergic reactions
115
Q

compare and contrast good vs poor immunogens

A

good:
* variability in structure
* ability to ellicit a stronger immune response

poor:
* more repeating structure (less distinct molecular response)

116
Q

what are the (5) antibody-antigen interactions and outcomes?

A
  1. agglutination
  2. opsonization
  3. antibody-dependent cell-mediated cytotoxicity
  4. neutralization
  5. activation of complement system
117
Q

what is neutralization as an antibody outcome?

A

blocking of adhesion and attachment of the pathogen to our cells

118
Q

what is antibody-dependent cell-mediated cytotoxicity?

A

antibodies attached to target cell cause destruction by macrophages, eosinoohils, and NK cells
* perforin and lytic enzymes cause degradation

119
Q

what is the process of antibody mediated/ellicited response?

A
  1. antigen of pathogen detected
  2. APCs engulf cell and process contents
  3. macrophages release cytokines
  4. B cells detect antigen
  5. peptide displated on MHC-II
  6. T helper cell cytokines facilitate B cell activity
  7. B cell antibody production - neutralization and agglutination (in part facilitated by Fc receptors)
120
Q

what are some pediatric immunity considerations?

A
  1. thymus regression - quantity and function of T lymphocytes decreases
  2. slower B cell differentiation - specificity of IgM decreased, A/D/E produced slowly, maternal IgG decreases
  3. maternal antibodies passed on to newborn - vis placenta and milk, A in colostrum
    limited response to viral, fungal, and bacterial antigens
121
Q

what are geriatric considerations in immunity?

A
  • decreased ability to respond to antigenic stimulation
  • less able to respond to new antigens
  • decreased speed of repair of tissue damage
  • increased disease vulnerability
  • decreased T cell functionality
  • antibody production decreased
122
Q

what is the main difference between the primary and secondary immune response?

A
  • primary results in high amounts of antibody secreting plasma cells and is mediated by B cells
  • secondary is faster and more effective due to memory
123
Q

what are the generative (primary) lymphoid organs?

A

bone marrow and thymus

124
Q

what are the peripheral (secondary) lymphoid organs?

A

lymph nodes
spleen
tonsils
peyers patches

125
Q

what are the key traits of lymphatic capillaries?

A
  1. small and close-ended
  2. in direct contact with interstitial fluid
126
Q

what is lymphatic fluid?

A

excess interstitial fluid that flows into lymphatic vessels

127
Q

what are the flow dynamics of lymphatic fluid governed by?

A

pressure gradients

128
Q

where is lymphatic fluid filtered? what happens here if needed?

A

lymph nodes - B/T cells are activated if needed

129
Q

once fluid is filtered it is returned back into circulation via ____ and ____ ducts.

A
  • right lymphatic
  • thoracic
130
Q

where are lymph nodes primarily located?

A
  • neck
  • groin
  • axillae
  • thorax
  • abdomen
131
Q

if there is an active infection immune cells within lymph nodes will ____. this causes what to occur to lymph nodes?

A
  • detect and react to foreign material
  • become tender, palpable, enhance in size, most noticeable at back of throat
132
Q

within lymph nodes T-lymphocytes are within the ____ cortex which is ____, whereas B-lymphocytes are at ____ which is ____.

A
  • T-lymphocytes: parafollicular, deeper
  • B-lymphocytes: periphery/cortex, around edges
133
Q

what are germinal centers within the lymphoid system?

A

areas with B cells that have already responded to antigens

134
Q

describe the process of antigen delivery to the lymph node

A
  1. antigen carried in lymph directly inside
  2. antigen carried in on APC (dendritic cell) that enters too
  3. antigen within parafollicular cortex is presented to naive B and T cells
  4. effector T cells migrate to the site of injury
135
Q

what are the two types of bone marrow?

A

red - site of hematopoiesis/formation of erythrocytes, leukocytes, and platelets
yellow (fatty) - can be recruited to become red bone marrow

136
Q

where is red bone marrow typically found in adults?

A

pelvis
sternum
ribs
cranium
end of long bones
vertebral spine

137
Q

the spleen is located ____. it works to ____ by having red and white pulp. the red pulp contains ____ that filter out ____ and is highly vascular. the white pulp contains ____ that help ____.

A

the spleen is located under the diaphragm on the left side of the body. it works to filter by having red and white pulp. the red pulp contains macrophages that filter out foreign substances and old RBCs and is highly vascular. the white pulp contains lymphocytes that help detect antigens.

138
Q

where are tonsils located? what is their function?

A
  • located: back of mouth and pharynx
  • function: encounter microorganisms (respiratory pathogens)
139
Q

what is the cutaneous lymphoid system?

A

aggregated lymphoid tissue under skin epithelium

140
Q

what are mucosal lymphoid systems?

A
  • aggregated lymphoid tissue in GI, respiratory, and GU tracts
  • B cells make antibodies against microorganisms that have invaded mucosal tissue
  • aka - MALT/GALT
141
Q

define neoplasia

A

new growth

142
Q

define anaplasia

A

loss of distinct differential characteristics

143
Q

what causes normal cells to become cancerous?

A

genetic mutations in conjunction with the multi-step process

144
Q

what are some key traits of bengin growth?

A
  • doesn’t invade adjacent tissue or metastasize
  • many encapsulated in connective tissue
  • more closely resembles original tissue type
  • grows slowly (little vascularity)
  • rarely necrotic
  • often retains original function
145
Q

what are some key traits of malignant growth?

A
  • tissue-specific differentiation (does not resemble original tissue)
  • grows quickly
  • may initiate tumor vessel growth
  • often necrotic
  • dysfunctional
  • invasive/metastasizing
  • greater degree of anaplasia = aggressive
146
Q

what does the suffic -oma indicate?

A

bengin tumor

147
Q

what is fibroma?

A

bengin growth in fibrous tissue

148
Q

what is chondroma?

A

benign growth in cartilage

149
Q

what is adenoma?

A

benign tumor of epithelial tissue origin with/out glandular

150
Q

what is papilloma?

A

benign tumor of epithelial tissue that projects out from a surface

151
Q

what is cystadenoma?

A

cystic mass within ovaries

152
Q

what do the suffixes -carcinoma and -sarcoma indicate?

A

malignant tumors

153
Q

what is carcinoma?

A

malignancy of epithelial origin

154
Q

what does carcinoma in situ mean?

A

carcinoma in which the basement membrane is still intact

155
Q

what is sarcoma?

A

malignancy of mesenchymal origin

156
Q

what cell type is most likely to become cancerous?

A

epithelial - because it routinely undergoes growth/generation

157
Q

what portion of cancer related deaths may be attributable to lifestyle factors?

A

one third

158
Q

what are the major cancers in males? females?

A

males: lung and bronchus, prostate
females: lung and bronchus, breast

159
Q

what trait can make it harder to detect early stages of cancer in certain organs?

A

large reverse capacity - i.e. kidney and liver

160
Q
A
160
Q
A
161
Q

generally speaking, what are the 4 causes of cancers?

A
  1. genetic factors
  2. environmental factors
  3. lifestyle factors
  4. viruses
162
Q

what portion of cancers are related to preventable causes?

A

50%

163
Q

occupational cancers are caused by accumulative exposure to potential causative agents over time. what are some of these exposures and what are the most common types of occupational cancers?

A

exposures: arsenic, asbestoes, benzene, vinyl chloride, nickel
cancer types: lung, skin, prostate, myeloid leukemia, oropharyngeal

164
Q

provide the type of cancer associated with the following conditions and, if applicable, the etiologic agent:
* inflammatory bowel disease
* pancreatitis
* barrett esophagus
* gastritis/ulcers
* hepatitis

A
  • IBD - colorectal carcinoma
  • pancreatitis - pancreatic carcinoma, chronic alcohol use or germline mutations
  • barrett esophagus - esophageal adenocarcinoma - gastric acid
  • gastritis/ulcers - gastric adenocarcinoma or extranodal marginal zone lymphoma - H. Pylori
  • hepatitis - hepatocellular carcinoma - Hep B or C
165
Q

what autosomal dominant syndrome is associated with p53 linked predisposition to cancer?

A

li-fraumeni syndrome

166
Q

why are cancers considered different from other inherited ailments such as CF?

A

genetic mutations can be inherited or acquired through the life course

167
Q

what are 6 key characteristics of cancer cells?

A
  1. pleomorphic - abnormal cell shapes and sizes
  2. nuclear abnormalities
  3. abnormally sized cells
  4. irregular mitosis
  5. loss of differentiated features - anaplastic
  6. poorly defined tumor boundary
168
Q

cancer lacks many regulatory mechanisms present in typical cells. one of these is contact dependent growth inhibition. explain what this is and what it means for cancer cells.

A

what it is: once cells touch each other or other external boundaries they will stop growth (monolayer)
what it means for cancer cells: they will continue growth and layer on top of each other

169
Q

what are the 3 stages of the multi-step cancer process. briefly describe each one.

A
  1. initiation - few genetic mutations that result in uncontrollable growth
  2. promotion - mutant cell proliferates further activating oncogenes and deactivating tumor suppressor genes
  3. progression - mutant cells exhibit malignant behaviour providing a growth advantage. cells not deviate largely from regular tissue
170
Q

what is the alteration pathway leading to cancer. what progression does each of these losses result in?

A
  1. loss of apc - hyperplastic epithelium
  2. activation of K-Ras - intermediate adenoma
  3. loss of SMAD4/tumor suppressors - late adenoma
  4. loss of p53 - carcinoma
  5. other unknown alterations - invasion and metastasis
171
Q

what are the 4 malignant characteristics? what does each of these cause?

A
  1. laminin receptors - loss of cell-cell and cell to basement membrane contacts
  2. lytic enzymes - degradation of basement membrane to allow for invasion
  3. anchorage independent - loss of cell-cell contacts and basement membrane anchorage
  4. abnormal karyotype - variation in chromosomal # and or size
172
Q

what are the 10 hallmarks of cancer?

A
  1. sustaining proliferative signalling
  2. evading growth suppressors
  3. enabling replicative immortality
  4. activating invasion and metastasis
  5. inducing angiogenesis
  6. resisting cell death
  7. deregulated cellular energetics
  8. avoiding immune destruction
  9. tumor promoting inflammation
  10. genome instability and mutations
173
Q

describe the effects of cancer cells sustaining proliferative signaling and a key molecule.

A
  • key molecule - Ras
  • results in mutations of proto-oncogenes leading to excessive growth factor production that are autocrinely signaled
174
Q

describe the mechanisms of cancer cells evading growth suppressors and a key molecule.

A
  • p53
  • mutations in tumor suppressors
175
Q

describe the mechanisms by which cancer cells enable replicative immortality

A

increased telomerase activity

176
Q

describe how cancer cells activate invasion and metastasis and identify a key molecule.

A
  • MMP - Matrix metalloproteinases
  • degradation of ECM to destroy basement membrane contact and enable movement
177
Q

what size can cells grow to before requiring their own vascular supply?

A

2 mm

178
Q

describe how cancer cells resist cell death

A

excessive production of BCL2 to allow for resistance of pro-apoptotic signals

179
Q

describe the deregulated cellular energetics found in cancer cells

A
  • reliance of glycolysis independent of oxygen availability
  • use of intermediates as biosynthetic precursors
  • preferential uptake of glucose and glutamate use
  • no regulation of lactate buildup
180
Q

mutations in proto-oncogenes are often called what type of mutation?

A

gain of funciton

181
Q

describe how viruses contribute to cancer

A

can bring proto-oncogenes into a host-cell

182
Q

what are the 3 types of mutations that can result in cancer?

A
  • point mutation
  • gene amplification
  • chromosomal translocation
183
Q

describe how the amplification of MYCN results in a hyperproliferative state

A

excessive amounts in the chromosome results in double minutes (extra generated chromosome structure)

184
Q

describe how chronic myeloid leukemia can be enhanced with chromosomal translocation of genes 9 and 22

A
  • production of ABL-BCR hybrid gene
  • excessive production of tyrosine kinase
  • activation of growth factor signaling pathways
  • hyperproliferative state
185
Q

describe how chromosomal translocation in chromosome 8 and 14 can result in enhanced burkitt lymphoma

A
  • placement of IG and MYC gene beside each other
  • increased MYC protein
  • increased expresison of progrowth genes
186
Q

how does Ras mutation lead to increased transcription of progrowth genes?

A
  • constant bound to GTP - always active
  • stimulation of PI3K and RAF pathways
  • increased mTOR and MAPK (mitotic kinase factor)

HLTH 341 - Pathobiology (3 decks)

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