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IHP 1001 > Ch.2 Acute Inflammation pt.2 > Flashcards

Ch.2 Acute Inflammation pt.2 Flashcards

1
Q

Derived from monocytes circulating in the blood

A

Macrophages

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2
Q

Macrophages injest organims via ____?

A

Phagocytosis

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3
Q

Phagocytosis in macrophages is faciliateted by what?

A

Opsinins

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4
Q

What helps destroy phagocytosed materials in macrophages?

A

Lysosyme & 2nd granuales

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5
Q

Macrophges can either 1. or 2.

A
  1. Promote resolution & healing if balance restored
  2. Recruit more help
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6
Q

Secretion of anti-inflmmatroy cytokines IL-10 and TGF-Beta by macrophages signales what?

A

Balance restored, promoting healing

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7
Q

What cytokiene is secreted by macrophages if there is continued inflamation and persistant pus formation

A

IL-8

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8
Q

What may follow acute inflammation if the issue is not resolved?

A

Abcess formation

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9
Q

Macrophages, active antigen presenters and activate + regulate what?

A

Chronic inflmation

CD4+ Helper T cells

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10
Q

Activation of what kind of cell via antigen prensentation from macrophages secrete cytokienes that promote chronic inflammation?

A

CD4+ Helper T cells

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11
Q

Macrophages are the link bewteen what?

A

Innate & adaptive immunity

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12
Q

_____ have the principle ligan Sialyl-Lewis X

A

Selectins

L-selectin, E-selectin, P-selectin

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13
Q

____ have the principle ligand ICAM-1 expressed

A

Integrings

LFA-1, MAC-1, VLA-4, a4b7

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14
Q

___ are important causes of injury to normal cells and tissues

Occures during normal defesne agaisnt microbs **esp those resistant*

Ex. Mycobacteria

A

Leukocytes

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15
Q

leukocyte-mediated tissue injury is release of the contents of ___ and ____

A

Lysozymes and Granules

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16
Q
A
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16
Q

Cells that secrete cytokienes like IL-17 that recruit neutrophils and stimulate production of antimicrobial peptides that directly kill microbes.

A

Th17 cells

Kind of T-cell

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17
Q

Cells that are mportant in reactions to helminthic parasites and in some allergic disorders

A

Eosinophills

(can cause cell damage)

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18
Q

critical cells of allergic reactions.

A

mast cells and basophils

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19
Q

What kind of inflmmatory mediator ?

Released from intracellular granules (e.g.,amines) or are synthesized de novo (e.g., prostaglandins and leukotrienes, cytokines) in response to a stimulus.

A

Cell-derived mediators

Produced locally by cells at site inflam. or derived from ciruclating

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20
Q

What are the three major cell types that produce mediators of acute inflammation?

A
  1. Tissue macrophages
  2. Dendritic cells
  3. Mast cells
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21
Q

What kind of inflmmatory mediator?

Complement protiens

A

Plasma-derived mediator

produced mainly in the liver and circulate as inactive precursors.

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22
Q

produced only in response to various stimuli, including microbial products and substances released from necrotic cells, which ensures that inflammation is triggered only when and where it is needed.

A

Acitve Mediators

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23
Q

Receptors found in innate immune system effectors (mac & dend) that detect foreign molecular patterns

A

Toll like receptors

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24
Q

Antigen presentors, cotrol what to process and send out necessary signals

Just the umbrella term

A

Regulators

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25
Q

They respond to stimulus

Just umbrella term

A

Effector

ex. Macrophages & Dendritic cells

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26
Q

Commo structural patterns found on many foreign microbs

A

Pathogen Associated Molecular patterns (PAMPS)

Ex. Cell membrane, dsRNA ssDNA, Proteins (flagella, techoic acid).

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27
Q

This is an example of what?

CD14 (a co-receptro fro TLR4) can identify a specific PAMP fond in LPS of gram (-) bacteria.

A

Toll Like receptors

Can be intra(combat injected nuclear material) or extracellular
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28
Q

TLR actiavtion results in upregulation of what?

A

Nuclear transcription Factor

NF-kB, activates immune response + promote inflmation

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29
Q

What gives TLR a link in mediation of both acute & chronic inflamation?

A

They are housed on lymphocytes

Which are adaptive immunity effector & regulators

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30
Q

What are the 2

lipid mediators produced from arachidonic acid (AA) present in membrane phospholipids that stimulate vascular and cellular reactions in acute inflammation

A

Prostaglandins & Leukotrienes

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31
Q

20-carbon polyunsaturated fatty acid that is released from membrane phospholipidsthrough the action of cellular phospholipases, mainly phospholipase A2

A

Arachindroic Acid

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32
Q

AA mediator is produced by what?

Generate prostaglandins

A

Cyclooxygenases

See left side
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33
Q

AA mediator is produced by what?

Produce leukotrienes and lipoxins

A

5- Lipooxgenanses

See right side
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34
Q

produced by mast cells, macrophages, endothelial cells, and many other cell types and are involved in the vascular and systemic reactions of inflammation.

A

Prostaglandins

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35
Q

What Cyclooxygenase?

produced in response to inflammatory stimuli and is also constitutively expressed in most tissues, where it may have homeostatic functions

A

COX-1

Cyclooxygenase

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36
Q

fluid and electrolyte balance in the kidneys, cytoprotection in the GI tract

Homeostatic function of tissues where ___ is found

A

COX-1

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37
Q

induced by **inflammatory stimuli **and thus generates prostaglandins in inflammatory reactions but is low or absent in most healthy tissues.

A

COX-2

Cyclooxygenase

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38
Q

Major Prostiglandins made by mast cells, cause vasilodation + increased membrane permability of post-cap venules.

(potentiant exduatio resulting in edema)

A

PGD2 and PGE2

PGDis a chemoattractant for neutrophuls.

39
Q

Platelets contain the enzyme thromboxane synthase, which produces _____ the major eicosanoid (AA mediator) in these cells.

A

TxA2

Potent platelet-aggregating agent and **vasoconstrictor.

40
Q

vascular endothelium lacks thromboxane synthase. Instead, it contains this enzyme____, which produces ____

A

prostacyclin synthase; produces Prostacyclin PGL2

*vasolidator, inhibitor of paltlet agregation, prevent thrombosis

41
Q

Prostoglandins are in invloved in the pathogenesis of ___ and ____

A

Pain & Fever

42
Q

Derived from Prostoglanding G2/H2

  • Induce platlet agregation
  • Potent vasoconstrictor
  • Induce vascular smooth muscle proliferation
  • Proatherogenic
A

Thromboxone A2

TXA2

43
Q

Derived from Prostoglanding G2/H2

  • Inhibit platlet agregation
  • Induce vasolidation
  • inhibit vascular smooth muscle proliferation
  • ANTI-athrerogenic
  • Gut protection
  • Renal blood flow regulation
A

Endothelial Prostacyclin

PGL2

44
Q

produced by leukocytes and mast cells by the action of lipoxygenase and are involved in vascular and smooth muscle reactions and leukocyte recruitment.

A

Leukotrienes

45
Q

Activation of ___ examples

  1. Prevent closure of ductus arteriosis in newborns with cyanoic heart defects
  2. Tx of NSAID induced gastric ulcers
  3. Reduction of pulmonary hypertension
  4. Induction of childbirth
  5. Vasodilation of digits for treatment of severe Raynaud disese or critical limb ischemia
  6. Management of glaucoma
  7. Tx of erectile dysfunction
A

Activation of Prostiglandins

46
Q

The ____ pathway yields hydroperoxyeicosatetraenoic acid (HPETE) and its derivatives

A

5-lipoxygenase pathway

47
Q

What does this do?

Zileuton

Used for tx of chronic asthma

A

Inhibit leukotriene synthesis

48
Q

LTC4, LTD4, LTE4

These leukotrienes do what?

A

Increase broncial tone
*intense vasoconstriction
* bronchospasm (important in asthma)
* increased permeability of venules.

49
Q

What does medicatio do?

Monetlukast & Zafirlukast

For allergic asthma & alergic rhinitis

A

Prevent action of leukotrienes responsible for increase in bronchial tone

LTC4, LTD4, LTE4

50
Q

What leukotriene?

produced by neutrophil and some macrophages and is a potent chemotactic agent and activator of neutrophils

A

LTB4

neutrophils arrive B4 others remember!

51
Q

In leukotriene synthesis

____ gives rise to leukotrienes

52
Q

Also generated by AA through lypoxygenase pathway.
supress inflamation; inhibit neutrophil chemotaxis, no recruitment of leukocytes

53
Q

Principle action of Arachidonic Acid Metabolites in Inflammation

Prostaglandins PGI2 (prostacyclin), PGE1, PGE2, PGD2

A

Vasodilation

Big blood vessles

54
Q

Principle action of Arachidonic Acid Metabolites in Inflammation

Thromboxane A2 (COO pathway) , leukotrienes C4, D4, E4

A

Vasoconsriction

Small vessels

55
Q

Principle action of Arachidonic Acid Metabolites in Inflammation

Leukotrienes C4, D4, E4

A

Increased vascular permeability

(exxudation & dev of edema in PG) ( Bronchospasm in leukotrienes)

56
Q

Principle action of Arachidonic Acid Metabolites in Inflammation

Leukotriene B4

A

Chemotaxis, leukocyte adhesion

Activate neutrophil, chemotaxis bring inmore.

57
Q

Aspirn & NSAIDs ex. Ibuprofen.

Inhibit COX-1 & COX-2

A

Cyclooxygenase inhibitors

= prostaglandin synthesis blocked

58
Q

Why are asprin and NSAIDs good at treating pain and fever?

A

They block COX-1 and COX-2 which prevents prostaglandin syntheis.

Aspringirreverisbly inactiavted COO

59
Q

What kind of inhibitiors:

may increase the risk of cardiovascular and cerebrovascular events:
Impairs PGL2 (antitrhombotic)
while ignoring COX-1 mediated production of TxA2 which promotes plate aggregation

*only used to treat arthritis & pre-op pain in pt. with zero cardio. ris

A

Selective COX-2 inhibitors

60
Q

Anti-inflammatory agents like glucocorticoids and corticosteroids are what?

A

Lipoxygenase inhibitors

61
Q

Broad spectrunm antiinflamatory drugs.
Reduce transcription of genes encoding COX-2, Phospholipase A2..

A

Corticosteroids

Contain Cortisol

62
Q

A major vasoactve amine that stored as a preformed molecule in the granules of mast cells, blood basophils, and platelets

Vasoacivte= affect diameter of blood vessles

A

Histamine

Rapidly released when cells are aitvated

63
Q

What kind of cell has the richest source of histamine?

A

Mast cells

normally found in connective tisssue next ot blood vessels

64
Q

What 5 things can activate Histamines?

A
  1. Trauma
  2. Complement C3a & C3b
  3. Cell surface IgE cross-linking by hapten/antigen (allergy)
  4. Cytokiene IL-1
  5. Neuropeptides
65
Q

What happnes when histamines are activated?

A

Degranulation of mast cell

histamine was already fromed

66
Q

What occurs if there is a mass degranulation of mast cells?

A

Anaphylactic SHOCK! Mass release of histamine; high vasodialation= hypotension

67
Q

What is the immeidte response of histamine?

A

Vasodialation of arterioles+ increased vascular permeability.

68
Q

What are the complement fragments C3a and C5a called?

They actiavte degranulation of mast cell; release histamine

A

Anaphylatoxins

69
Q

What kind of drug?

drugs that treat inflammatory reactions, such as allergies, bind to and block the H1 receptor

A

Antihistamines

71
Q

Vasodialation & increased vascular permeability causes what symptoms of inflmation?

What are their key-mediators?

A
  • Redness (rubor)
  • warmth (calor)
    Both caused by histamines, prostaglandins & bradykinins
72
Q

What symptom of inflmmation?

When fluids escape from post-capillary venules into interisital space

A

Swelling (tumor)

73
Q

What key mediator of inflmation will act on the integrity of the Blood vessel, which causes endothelial cell contraction and tissue damage, resulting in endothelial cell dissruption

A

Histamines

74
Q

Is congestive heart faliure inflmmatory?

Stagnation fo blood in heart

A

NO. b/c **permeability of vessels is not affected **. It is a transudate, fluid escaping due to pressure diffrences.

75
Q

How do prostogladinds like PGE2 affect pain?

What is a major player?

A

They** dont cause pain, **they lower threshold of pain i.e you feel more pain.
Bradykinin is major player in making action potential

Pain is peripheral!

76
Q

Lower concentrations of Bradykinn & histamine results in what?

A

Activation of nociception= more painful stimuli

77
Q

Substances that induce fever

A

Pyrogens

ex. Bacterial products like LPS

78
Q

Pyrogens stimulate leukocytes to release cytokienes ___ and ___

A

IL-1 & TNF

Acute Phase Response

79
Q

Following pyrogen stimulaton of leukocytes (macrophages 3-4 days post intial infection) to release IL1 & TNF the production of _____ is upregulated via increased cyclooxygenease acitvity.

Occurs in perivascular cells of hypothalamus

A

Prostaglandins, specifcally PGE2

80
Q

PGE2 does what to the body?

A

Fever!

Lowers threshold.

81
Q

WHere does temperature control occur?

A

Perivascular cells of the hypothalamus

Fever is CNS

82
Q

NSAIDS including aspring reduce fever how?

A

Inhbit cyclooxygense COX-1 and COX-2 therefor no prostoglandin syntheiss (no PGE2)

83
Q

proteins produced by many cell types (principally activated lymphocytes, macrophages, and dendritic cells, but also endothelial, epithelial, and connective tissue cells) that **mediate and regulate immune and inflammatory reactions

84
Q

What cytokienes?

serve critical roles in leukocyte recruitment by promoting adhesion of leukocytes to endothelium and their migration through vessels.

Mainly acitvated by macrophages & dendritic cells

A

TNF & IL-1

85
Q

Systemic effect of TNF & IL-1

A

Induce fever and Leukocytosis (send out lots of mature leukocytes, high leveles)

86
Q

sustained production of ____ contributes to cachexia, a pathologic state characterized by weight loss and anorexia that accompanies some chronic infections and cancers.

87
Q

What kinds of drugs? What is downside?

effective in the treatment of chronic inflammatory diseases, particularly rheumatoid arthritis, psoriasis, and some types of IBD

A

TNF antagonist.
Pt. more suseptible to mycobacterial infection b/c of reduced ability of macrophages to kill intracellular microbes

88
Q

Synthesis of acute pase protiens, induced by TNF & IL-1in the liver.

A

Hepatic Syntheis

89
Q

TNF & IL-1increase the expression of ____ molecules in the endothelium of blood vessels

A

Adhesion moleules

90
Q

IL-1 and TNF reduce the thromboresistant properties of endothelium, thus promoting ______

Vasodialation + increased permeability

A

Thrombosis

91
Q

This cytokinene raises hear rate, lower blood pressure due to vasodialation b/c of increased circulation of Neutrophils

92
Q

family of small (8 to 10 kD) proteins that act primarily as chemoattractants for specific types of leukocytes

A

Chemokines

93
Q

Chemokines bind to proteoglycans and are thus displayed at high concentrations on the ____ of endothelial cells and in the extracellular matrix

94
Q

What are 2 main function of Chemokines?

A
  1. Inflamtion; bind leukocyte receptors & stimulate inegrin dependent attachement to endothelium or migration (chemotaxis) of leukocyte to damaged tissue
  2. Maintain tissue architecture

IHP 1001 (18 decks)

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