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Patho 1 > Chap 3- Inflammation and repair > Flashcards

Chap 3- Inflammation and repair Flashcards

1
Q

inflammation

A

response of vascular tissue to infection and damage

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2
Q

causes of inflammation

A
  • infections
  • tissue necrosis
  • foreign bodies
  • immune reactions
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3
Q

inflammatory cells

A
  • neutrophils
  • eosinophils
  • basophils
  • mast cells
  • phagocytes
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4
Q

neutrophils

A
  • main fn is phagocytosis
  • internalize pathogen and destroy it
  • has antimicrobial factors
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5
Q

eosinophils

A
  • eradicate parasites
  • mainly found in GI tract
  • trigger mast cells which releases histamines
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6
Q

basophils

A

-circulating cells
- involved in allergic rxn
- have IgE receptors
release histamine and prostaglandins

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7
Q

mast cells

A
  • live in connective tissue close to blood vessels
  • involved in immediate allergic rxn
  • main source of histamines
  • receptors for IgE
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8
Q

monocyte

A
  • type of phagocyte
  • precursor for macrophages
  • found in blood cell
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9
Q

macrophage

A
  • once monocyte reaches target tissue is called macrophage
  • type of phagocyte
  • derived from hematopoietic stem cells in bone marrow
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10
Q

steps of phagocytosis

A
  1. recognition and attachment-
    pathogen attaches to receptor
  2. engulfment
  3. killing by ROS or degradation by lysosomes
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11
Q

How are ROS derived?

A
  • can be from leukocytes after phagocytosis

- exposure to chemokines, immune complexes, or microbial products

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12
Q

Effect of ROS

A
  • endothelial cell damage -> increased vascular permeability

- injury to multiple cell types by oxidative stress

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13
Q

mediators of inflammation

A
  • “middle man”
  • initiate and regulate inflammation
  • either secreted by cells or made from plasma proteins
  • short lived
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14
Q

Histamine

A
  • inflammatory mediatior
  • main source= mast cells
  • cause vasodilation, increased vascular permeability
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15
Q

prostaglandins

A
  • inflammatory mediator
  • main source= mast cells
  • cause vasodilation, pain, fever
  • generated by COX
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16
Q

leukotrienes

A
  • inflammatory mediator
  • main source= mast cells
  • cause increased vascular permeability, involved in vascular/smooth muscle response, leukocyte recruitment
  • generated by lipoxygenase
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17
Q

Cytokines (TNF, IL-1)

A
  • inflammatory mediator
  • mains source= macrophages, helper t cells
  • local action= endothelial activation
  • systemic action= fever
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18
Q

chemokines

A
  • inflammatory mediator
  • main source= leukocytes, activated macrophages
  • cause chemotaxis
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19
Q

Platelet- activating factor (PAF)

A
  • inflammatory mediator
  • main source= leukocytes, mast cells
  • cause platelet aggregation and degranulation
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20
Q

complement system

A
  • inflammatory mediator
  • main source= plasma produced in liver
  • action- direct target killing (via membrane attack complex)
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21
Q

3 functions of histamine

A
  • vasodilation in arterioles
  • increased permeability of venules
  • smooth muscle contraction
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22
Q

serotonin

A
  • same effect as histamines

- comes from platelets

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23
Q

arachidonic acid metabolites

A
  • lipid mediators produced from phospholipid bilayer of plasma membrane
  • types: prostaglandins, leukotrienes, lipoxins
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24
Q

lipoxins

A
  • generated by lipoxygenase

- suppress inflammation by inhibiting recruitment of leukocytes

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25
Q

cytokine

A

-broad umbrella term for proteins that mediate and regulate inflammatory response

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26
Q

role of chemokines

A
  • type of cytokine
  • chemotaxis
  • guide neutrophil to move towards invader
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27
Q

inflammatory reaction’s sequence of events

A
  1. recognition by receptors
  2. recruit leukocytes and plasma proteins
  3. remove dead cells/ bacteria/ pathogen etc.
  4. regulate inflammatory response
  5. resolution/repair
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28
Q

TLRs

A
  • toll like receptors
  • recognize pathogen in or outside of cell
    recognize pathogen-associated molecular patterns (PAMPs) which stim release of inflammatory mediators
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29
Q

DAMPS

A
  • damage-associated molecular patterns

- recognize endogenous stimuli

30
Q

Function of complement system

A
  • opsonization and phagocytosis
  • inflammation
  • cell lysis by forming membrane attack complex (MAC)
31
Q

what are the complement proteins involved in inflammation?

A

C3a and C5a

32
Q

What does C3b do?

A

it is like a flag, marks pathogen to be eaten

33
Q

types of pathways that the complement system can join together to function

A
  • classical pathway- binds to antibody, used in adaptive immunity
  • lectin pathway- mannose that binds to lectin, used innate immunity
  • alternative pathway- used in innate immunity
34
Q

major components of acute inflammation

A
  • vasodilation and increased blood flow
  • increased permeability and leukocyte migration
  • emigration and activation of leukocytes
35
Q

what is blood caliber?

A

diameter of blood vessel gets increased by vasodilation

36
Q

what is stasis of blood flow?

A

movement of RBC slows down

37
Q

what are vascular reactions to acute inflammation?

A
  • vasodilation via histamines
  • stasis of blood flow
  • neutrophils accumulate along epithelium
  • increased permeability of vessels
38
Q

what do lymphatic vessels and lymph nodes do during inflammation?

A
  • filter extravascular fluids, become engorged

- want to direct this extra fluid towards the circulation and out of extracellular space

39
Q

reactions of leukocytes in inflammation

A
  1. rolling and adhesion to endothelium (selectins and integrins)
  2. diapedesis- get out of blood vessel, results in vascular congestion
  3. migration in the tissues toward a chemotactic stimulus
40
Q

allergy

A

excessive inflammatory response

41
Q

autoimmune disease

A

misdirected inflammatory response against body’s own tissues

42
Q

possible outcomes of acute inflammation

A
  • resolution- not too much damage so tissues regenerate/repair
  • fibrosis- loss of function
  • chronic inflammation- occurs when injury persists and cannot heal properly
43
Q

chronic inflammation

A
  • inflammation lasting longer than a few weeks
  • caused by persistent infection, hypersensitivity diseases, prolonged exposure to toxic substance
  • phagocytes and lymphocytes found with chronic inflammation
44
Q

role of macrophages in chronic inflammation

A
  • phagocytic function
  • initiate tissue repair
  • participate in scar formation and fibrosis
  • secrete TNF, IL-1 and ROS causing inflammation and tissue injury
  • present antigen to T lymphocyte
45
Q

role of lymphocytes in chronic inflammation

A
  • when lymphocytes activated inflammation is persistent and severe
46
Q

relationship of lymphocytes and macrophages

A
  • macrophages activate lymphocytes
  • lymphocytes activate macrophages
    both cause chronic inflammation
47
Q

granulomatous inflammation

A
  • form of chronic inflammation

- necrosis in center, lymphocytes, macrophages, epithelioid cells, macrophages that have fused together

48
Q

types of granulomas

A
  • foreign body granulomas

- immune granulomas

49
Q

systemic effect of inflammation

A
  • fever caused by pyrogens
  • acute- phase proteins made in liver
  • leukocytosis- increased WBCs
50
Q

what are acute-phase proteins?

A
  • synthesized in liver
  • c- reactive proteins attach to microbial cell wall, act like flag for complement system
  • fibrinogen- attach to RBC and makes stack of RBC
51
Q

what is tissue repair?

A

rebuilding of tissue architecture and function after injury

52
Q

mechanisms of tissue repair in mild tissue injury

A
  • proliferation of surviving cells

- maturation of tissue stem cells

53
Q

tissue repair in severe injury

A
  • results in scar formation

- excessive amount of collagen and extracellular material deposited

54
Q

labile tissues

A

cells proliferate throughout life

i.e. skin

55
Q

stable tissues

A

proliferation capacity is limited, if enough stimulation then they can go through the cell cycle i.e. the liver

56
Q

permanent tissues

A

tissue cannot divide in postnatal life so damage is permanent i.e. brain

57
Q

cell proliferation

A

tissue goes through cell cycle, makes copies of itself

58
Q

fibroblasts

A

make collagen

59
Q

what are the steps in scar formation?

A
  1. inflammation for 6-48 hours, macrophages are major players
  2. cell proliferation for up to 10 days- epithelial cells respond to GF, angiogenesis occurs, fibroblasts function
  3. remodeling of connective tissue starts 2-3 weeks after injury- scar tissue
60
Q

what is the difference between fibrosis and scarring?

A
  • fibrosis- better used for internal organs

- scarring- usually for skin or wound healing

61
Q

Systemic factors effecting tissue repair

A
  • nutritional status
  • metabolic status
  • circulatory status
  • hormones
62
Q

Local factors effecting tissue repair

A
  • size, location, and type of wound
  • infection**
  • mechanical forces
  • foreign bodies
63
Q

venous leg ulcer

A
  • chronic wound

- due to lack of oxygen and nutrients to extremities

64
Q

arterial ulcer

A
  • chronic wound

- usually caused by atherosclerosis, reduced blood supply

65
Q

pressure sore

A
  • chronic wound

- mechanical force of tissue against bone, area becomes ischedmic

66
Q

hypertrophic scars

A

excessive collagen accumulation forms raised scar

67
Q

keloid

A

progression beyond original area of injury

68
Q

exuberant granulation

A

blocks reepithelization, excessive amount of granulation tissue

69
Q

contractures

A

is an exaggerated process that results in wound deformity (common in burn victims)

70
Q

fibrosis

A
  • excessive deposition of collagen
  • pathologic process
  • cytokines stim fibroblasts -> collagen and othe ECM protein deposition

Patho 1 (12 decks)

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