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ASF Block 1, MUSC '13 > 8/27/13 > Flashcards

8/27/13 Flashcards

1
Q

3 of the 5 cardinal signs of inflammation that have to do with vascular changes

A

Redness, swelling, heat

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2
Q

What happens immediately following an injury?

A

transient vasoconstriction

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3
Q

Describe the two processes that occur after the transient vasoconstriction after an injury

A

vasodilation of the arteriolar side of the capillary bed, and as fluid moves into the interstitium stasis occurs in the blood flow

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4
Q

What is the threshold of the rate of amount of fluid into the interstitium above which edema occurs?

A

2ml/min

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5
Q

Describe the role of hydrostatic and oncotic pressure in acute inflammation?

A

The arteriolar dilates leading to increased blood flow and hydrostatic pressure. There is more fluid in the interstitium. As proteins start to enter the interstitium, the oncotic pressure on the venule side decreases leading to less fluid being taken up in the blood vessel

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6
Q

Watery ultrafiltrate of the plasma which is very low in protein content

A

transudate

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7
Q

Ultrafiltrate that contains protein

A

exudate

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8
Q

Where does most endothelial leakage occur (arterioles/capillary bed/venules)?

A

Venules

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9
Q

Stimulated by histamine, happens in the venule only immediately and is transient, and is a type of endothelial gap

A

endothelial contraction

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10
Q

Happens after hours but is long lasting, stimulated by TNF and IL-1, type of endothelial gap that happens in venules

A

endothelial retraction

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11
Q

Direct injury to endothelial by way of UV radiation, thermal injury, bacterial toxins leads to cell death by this process

A

Apoptosis

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12
Q

Direct injury by severe burns and infection in endothelial cells lead to cell death by this process

A

Necrosis

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13
Q

How do leukocytes contribute to endothelial injury?

A

They secrete reactive oxygen species and proteolytic enzymes

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14
Q

Name all 6 types of endothelial occurences that weaken the endothelial lining

A

endothelial contraction, endothelial retraction,direct endothelial injury, leukocyte-dependent endothelial injury, increased endothelial trancytosis, leakage due to angiogensis

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15
Q

migration of leukocytes from the blood into the tissue is called

A

extravastion

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16
Q

Leaukocytes are in the periphery/middle in normal blood flow

A

periphery

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17
Q

Selectins bind to what type of molecule?

A

Sugars on the glycoproteins

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18
Q

Name the three groups of interactions via selectins between leukocytes and endothelial cells

A

L-selectin–CD34
Sialyl-Lewis X GP– E selectin
Sialyl-Lewis X GP– P selectin

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19
Q

Histamine and thrombin stimulates this selectin to translocate to the surface

A

Selectin P from the Weibel-Palade body

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20
Q

TNF and IL-1 stimulate the translocation of this selectin to the surface

A

Selectin E

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21
Q

What increases integrin’s affinity to ICAM and VCAM

A

due to chemokines

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22
Q

TNF and IL-1 increase the expression of these endothelial adhesion molecules

A

ICAM and VCAM

23
Q

Diapedesis of leukocytes is mediated by what?

A

PECAM 1

24
Q

4 chemotatic agents for leukocytes and which type of receptor they bind too

A

soluble bacterial prodcuts, C5a, IL-8, arachidonic acid from membrane/ G-receptor

25
Q

Describe the G-protein receptor mechanism in leukocytes

A

Phospholipase cleaves PIP2–> IP3 and DAG–> IP3 signals the release of calcium which leads to the creation of pseudopods and modulates leukocyte adhesion factors–> DAG leads to the activation of PKC which leads to the degrnulation/secretion of lysosomal enzymes and oxidative burst–> DAG and high intracellular Ca2+ also leads to the activation of phospholipase A2 which metabolizes the membrane phospholipids into arachidonic acid

26
Q

What are the three molecules that are bound to the microbe that signal the leukocyte to engulf it

A

C3, collectin, IgG

27
Q

The lysosomes of neutrophils contribute what to the killing and degradation of microbes

A

MPO

28
Q

Describe the oxidative steps that lead to the destruction of the microbe

A

Cytoplasm and NADPH oxidases convert oxygen into superoxide anion–> superoxide anion is converted to hydrogen peroxide by dismutase–> MPO with Cl- converted hydrogen peroxide to hypochlorous radical

29
Q

Defects in leukocyte adhesion

A

LAD-1–> defect in the beta chain of integrin

LAD-2–> defect in the Sialyl-Lewis X GP (selectin problems)

30
Q

Defects in the microbicidial activity

A

CGD–> NADPH oxidase mutation, superoxide is not formed and granuloma formed
Che’diak-Higashi syndrome–> lysosomes do not meet with phagosome

31
Q

For the three systemic mediators, which include_____, this blood factor helps activate them

A

Complement, kinins, coagulation factors/Hageman factor (factor XII)

32
Q

What types of organelles activate factor XII in the presence of a cofactor

A

basement membrane, collagen, platelets

33
Q

Describe the kinin cascade

A

Activated factor XII converts prekallikrein to kallikrein–>Kallikrein converts HMWK to bradykinin–> Kallikrein also stimulates the increase of more active factor XII–> bradykinin increase vascular permeability, vasodilation, pain, and contract bronchial smooth muscle

34
Q

Describe the coagulation cascade

A

Factor XIIa activates factor XI–> factor XIa activates factor X–> factor Xa converts prothrombin to thrombin–> thrombin converts fibrinogen to fibrin the clotter

35
Q

Describe the effects of factor Xa

A

Increases vascular permeability and leukocyte emigration

36
Q

Describe the effects of thrombin

A

Increases the adhesion of leukocytes and cleaves Complement 5

37
Q

Describe the effects of fibrinopeptides

A

Increase vascular permeability and serve as chemotaxins for leukocytes

38
Q

Describe the fibrinolytic cascade

A

Kallikrein converts plasminogen to plasmin–> plasmin cleaves the fibrin clot–> plasmin also increases the factor XII activation–> fibrin degradation products increase vascular permeability and vasodilation–> plasmin also cleaves C3 to C3a

39
Q

Which complement proteins act as anaphylatoxins and what do they do?

A

C3a and C5a/ they signal mast cells to degranulate

40
Q

C5a proteins increase

A

Arachidonic acid metabolism, leukocyte integrin affinty, and chemotaxis

41
Q

How do C3b proteins function as inflammatory mediators?

A

They act as opsonin

42
Q

What results after histamine release?

A

Arteriolar dilation, vascular endothelial contraction, constricts large arteries, immediate permeability, quickly degraded by histaminase

43
Q

What stimulates serotonin release?

A

Platelet aggregation

44
Q

Where is substance P release?

A

By nerves in the lung and gut

45
Q

Describe the cyclooxygenase pathway

A

Phospolipase converts membrane into Arachidonic acid–> cycloxgenase converts AA to prostaglandins–> in endothelium prostacyclins are released which inhibit platelet aggregation and promotes vasodilation–> in platelets thromboxane are released which promote platelet aggregation and vasoconstriction

46
Q

What do leukotrienes from the lipoxygenase pathway promote?

A

Promote chemotaxis of neutrophils and vasocontriction

47
Q

What do lipoxins fromthe lipoxygenase pathway promote?

A

inhibit neutrophil chemotaxis and vasoduialtion, resolution of inflammation

48
Q

what part of arachidonic acid metabolism does steroids inhibit?

A

Inhibits phospholipase action, so AA formation prevents

49
Q

what part of arachidonic acid metabolism does aspirin and NSAIDS block?

A

They block COX-1 and COX-2 which are essential for prostaglandins and prostacyclins (COX-1 provides protection for gastric mucosa from acid)

50
Q

The problem with COX-2 inhibitors is that____

A

They block prostacyclins preferentially, so prostaglandins (thromboxane) promotes platelet aggregation leading to clots

51
Q

Besides making AA, phospholipase A2 also releases___

A

Platelet activating factor

52
Q

Which molecule stimulates hepatic synthesis of coagulation proteins, complement, and fibronogen in the acute phase reaction?

A

IL-6

53
Q

What are the two types of chemokines

A

CXC, CC (C represents cysteine)

ASF Block 1, MUSC '13 (9 decks)

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