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Pathology Midterm > Inflammation (part 1) > Flashcards

Inflammation (part 1) Flashcards

1
Q

define inflammation

A

a physiological response to cell injury

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2
Q

name the cardinal signs of inflammation

A

heat
pain
redness
swelling
loss of function

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3
Q

name 2 inflammatory mediators

A

bradykinin and prostaglandins

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4
Q

what causes redness in inflammation

A

dilation of small blood vessels and increased blood supply

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5
Q

hyperemia

A

increased blood supply

causes heat and redness in inflammation

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6
Q

inflammation is a ___ and ____ tissue response to injury

A

systemic and local

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7
Q

what is the goal of inflammation

A

to restore injured tissues to physical integrity and normal function

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8
Q

what are the 2 main components of acute inflammation

A

vascular changes and cellular events

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9
Q

the 2 main components of acute inflammation are vascular changes and cellular events

explain these

A

vascular changes - alterations in diameter/permeability of vessel wall, increased blood flow (vasodilation), EFFLUX OF PLASMA PROTEINS FROM CIRCULATION

cellular events - emigration of leukocytes from circulation to the site of injury

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10
Q

the 2 main components of inflammation are vascular changes and cellular events.

what are these components regulated by?

A

effector cascases

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11
Q

vascular changes and cellular events of inflammation are regulated by effector cascades.

name 3

A

3 activating cascades:

arachnoid acid (eisosanoids)
complement cascade
coagulation factors

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12
Q

these vascular changes and cellular events are driven by…

A

many molecular mediators – both plasma and cell associated

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13
Q

what is edema

A

the leakage of fluid into tissues

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14
Q

what leads to edema?

A

tissue injury results in vascular changes (vasodilation) which leads to the leakage of fluid into tissues (edema)

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15
Q

vascular changes due to tissue injury result in the activation of what

A

platelets to intitiate clot formation and hemostasis (stop bleeding) AND to increase vascular permeability via histamine release

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16
Q

histamine causes…

A

increased vascular permeability

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17
Q

What is the rule for nomenclature of an inflamed tissue?
any exceptions?

A

add itis to end of organ or tissue

exceptions:

pulmonary inflammation = pneumonia

pleural inflammation = pleurisy

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18
Q

inflammation of mammary tissue

A

mastitis

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19
Q

inflammation of colon

A

colitis

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20
Q

inflammation of joint

A

arthritis

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21
Q

how long does acute inflammation last

A

a few days or weeks

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22
Q

what is the central cell for acute inflammation

A

polymorphonuclear leukocyte (PMN)

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23
Q

what is the function of PMN leukocyte

A

-central to acute inflammation
-phagocytises microorganisms and tissue debris
-mediates tissue injury

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24
Q

explain the contents of PMN leukocytes

A

they contain primary inflammatory mediators such as ROS, lysosomal granules, primary, secondary, and tertiary granules

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25
Q

why are PMN leukocytes multi lobed?

A

helps them to squeeze between endothelial cells and get to the site of injury

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26
Q

explain the functions of the primary, secondary, and tertiary granules of PMN leukocytes

A

primary granules are responsible for killing and digesting ingested microorganisms

secondary and tertiary granule constituents may have REGULATORY functions outside of the cell - don’t participate in cell death

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27
Q

what produces superoxide radicals when oxidizing O2?

A

NADPH oxidase

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28
Q

true or false

neutrophils contain many receptors

A

TRUE

contain receptors that recognize PAMPS and DAMPS, antibodies, compliment components, amino acid metabolites, cytokines, and chemokines

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29
Q

what are PAMPS and DAMPS? what cell recognizes them?

A

PAMPS = pathogen associated molecular pattern molecules

DAMPS = damage associated molecular patterns

recognized by neutrophils receptors

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30
Q

what are NETs

A

neutrophil extracellular traps

31
Q

neutrophils can activate or suppress what cells?

A

T cells

32
Q

neutrophils can attract what cells

A

macrophages and dendritic cells

33
Q

name 4 inflammatory agents
what cells do they induce?

A

bradykinin
histamine
endotoxins
cytokines

induce endothelial cells

34
Q

what does nitric oxide do? when is it released?

A

relaxes smooth muscles and reacts with ROS to create highly active free radicals

released by activated endothelial cells

35
Q

what do endothelins do? when are they released

A

induce prolonged vasoconstriction of smooth muscle

released by activated endothelial cells

36
Q

inflammatory cytokines are generated by….

A

activated endothelial cells

37
Q

what cells regulate the acute and chronic inflammatory response, regulate coagulation, fibrinolytic pathway, and regulate the immune response?

A

monocytes/macrophages
** are also antigen presenting cells

38
Q

where are macrophoages/monocytes formed?

A

in the bone marrow and they migrate into tissues to become resident macrophages

39
Q

classify macrophages

A

classically activated (M1)
alternatively activated (M2)

40
Q

differentiate between M1 and M2 macrophages

A

M1 are classically activated and are driven by IFNY, TNFa, and LPS to support inflammatory repsonses and release ROS and cytokines

M2 are alternatively activated and respond to IL-4 and IL-13 to help clear PARASITIC INFECTIONS AND SUPPRESS INFLAMMATION

41
Q

which macrophages support inflammation - M1 or M2

A

M1 supports inflammation and M2 suppresses

M1 leads to cytotoxicity and tissue injury and M2 leads to immune SUPPRESSION and tissue REPAIR

42
Q

what cells have cell surface receptors for IGE?

A

mast cells(basophils)

43
Q

what cells are associated with allergy and asthma

A

mast cells and eosinophils

44
Q

what cells release inflammatory mediators including histamine when their receptors are stimulated?

A

mast cells

45
Q

what cells provide defense against parasites

A

eosinophils

46
Q

what cells are associated with chronic inflammation

A

eosinophils

47
Q

which type of cell has red granules

A

eosinophils

48
Q

what is thrombosis

A

clot formation

49
Q

true or false

platelets are small cells

A

FALSE - they are not cells. they are fragments of cells containing vacuoles, microtubules, and granules

50
Q

name 3 functions of platelets

A

-promote clot formation
-regulate permeability
-regulate proliferative response of mesenchymal cells

51
Q

true or false

platelets lack nuclei

A

true

52
Q

name 3 platelets inclusions

A

dense granules (serotonin, histamine, calcium, ADP)
a-granules (PDFG - platelet derived growth factor)
lysosomes - acid hydrolases

53
Q

serotonin has the same effects as ________

A

histamine
both increase vascular permeability

54
Q

what maintains vasodilation and vasoconstriction in balance

A

platelet derived TXA2
endothelial derived PGI2

55
Q

during inflammation, how is the balance of vasodilation and vasoconstriction shifted?

A

during inflammation, balance shifted to vasoconstriction, increased vascular permeability, platelet aggregation, and PMN responses

56
Q

which is proinflammatory and which is anti inflammatory – TXA2 and PGI2

A

TXA2 is proinflamm
PGI2 is anti

57
Q

during repair, which is predominately expressed – TXA2 or PGI2

A

PGI2 expressed during repair bc it inhibits platelet aggregation and the recruitment of PMNS

58
Q

what induces platelet aggregation? is it a vasoconstrictor or dilator?

A

TXA2 vasoconstrictor

59
Q

which enhances PMN responses – TXA2 or OGI1

A

TXA2

60
Q

What is a tissue’s first response after most forms of injury

A

acute inflammation

61
Q

what is the duration of acute inflammation

A

minutes to days

62
Q

true or false

normally (no injury or inflammation), platelets are unable to bind other platelets and cells, so there is no clotting

A

true

63
Q

what are the 2 types of edema

A

non-inflammatory edema and inflammatory edema

64
Q

oncotic pressure is dependent on….

A

proteins

65
Q

osmotic pressure is dependent on….

A

salt

66
Q

__________ is the earliest vascular response to mild skin injury

A

transient vasoconstriction of arterioles

67
Q

initially, fluid that forms edema is _____ and then it becomes _____

A

transudate - ultrafiltrate of blood plasma

as it becomes rich in protein and cells and vascular permeability increases, it becomes exudate

68
Q

what are the 2 sources of plasma derived mediators

A

hageman factor activation (fibrin split products, kinins (bradykinin))
complement system activation (C3a, C5a)

69
Q

What are 4 sources of cell derived mediators

A

mast cell degranulation (histamine)
platelets (serotonin)
inflammatory cells (platelet activating factor, prostaglandins, leukotrienes)
endothelium (nitric oxide, prostaglandins, platelet activating factor)

70
Q

both plasma and cell derived mediators ultimately lead to what

A

increased vascular permeability and edema

71
Q

differentiate between effusion, transudate, and exudate

A

effusion = excess fluid in body cavities (such as peritoneum and pleura)

transudate = edema fluid with a low protein content

exudate = edema fluid with high protein concentration and OFTEN CONTAINS INFLAMMATORY CELLS

72
Q

When are exudates seen and how are they produced?

A

early in acute inflammation.
produced by mild injuries such as sunburn or traumatic blisters

73
Q
A

Pathology Midterm (10 decks)

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