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CMOD- Block1 > Path: Inflammation 3 > Flashcards

Path: Inflammation 3 Flashcards

1
Q

Inflammation of the bladder is called ____.

A

cystitis

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2
Q

____ is inflammation of the renal pelvis and is most commonly (not always) due to infection that ascends from the bladder.

A

pyelonephritis

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3
Q

What does DIC stand for?

A

disseminated intravascular coagulation

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4
Q

NETs, which stands for ___, consist of a viscous meshwork of ____ and ____ from ____.

A

neutrophil extracellular traps; nuclear chromatin and antimicrobial substances from neutrophils

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5
Q

NETs are formed where and serve what function?

A

they are formed in the interstitium and blood vessels; they serve to trap bacteria and fungi

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6
Q

How does “frustrated phagocytosis” contribute to adverse effects of inflammation?

A

if phagocytes can’t properly engulf a pathogen lysosomal degradative enzymes will be released into the tissue

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7
Q

Interleukin-__, produced by ___ lymphocytes, is important in recruiting ____ to sites of inflammation.

A

IL-17, produced by TH17 cells; leukocytes

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8
Q

Ineffective ___ leads to “cold abscesses”, lacking redness and warmth from skin infections with bacteria and fungi.

A

TH17

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9
Q

Chronic inflammation results in ___, and, in children, ____ ____.

A

anemia; retarded growth

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10
Q

Chronic excess stimulation of ___ release in advanced cancer results in ____ (a state of profound loss of lean body mass and fat due to cytokine-induced loss of appetite and prolonged catabolism).

A

TNF; cachexia

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11
Q

Chronically elevated serum ____ __ results in secondary amyloidosis in some patients.

A

amyloid A

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12
Q

3 main adverse effects of chronic inflammation include:

A
  1. anemia
  2. cachexia
  3. amyloidosis
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13
Q

Arachidonic acid, important for inflammation, has __ carbons and therefore its metabolites are sometimes called ____.

A

20; eicosanoids

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14
Q

The enzymes ____ generate eicosanoids from ArA, which can bind to ____s on many cell types.

A

COX and/or lipoxygenase; GPCRs

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15
Q

Phospholipase activity is blocked by what class of drugs?

A

corticosteroids (glucocorticoids), including prednisone and methylprednisone

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16
Q

COX converts ArA into ____ and lipoxygenase converts ArA into various ____.

A

prostaglandins; HPETEs

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17
Q

What is the difference in COX-1 and COX-2 expression?

A

COX-1 is expressed constitutively, whereas COX-2 is normally minimally expressed but induced by inflammation

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18
Q

Downstream of COX, vascular endothelial cells have the enzyme ____ ____, which converts prostaglandin H2 to prostaglandin ____ (aka prostacyclin), which dilates blood vessels and inhibits platelet aggregation.

A

prostacyclin synthetase

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19
Q

Platelets express the enzyme ____ ____, which converts ____ into ____.

A

thromboxane synthetase; PGH2 into thromboxane A2

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20
Q

Thromboxane A2 does what to blood vessels and platelets?

A

vasoconstricts; increases platelet aggregation

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21
Q

Prostacyclin does what to blood vessels and platelets?

A

vasodilates; inhibits platelet aggregation

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22
Q

Mast cells make PG D2, which causes what?

A

vasodilation and increased vascular permeability; is a chemoattractant for neutrophils

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23
Q

PG E2 causes ____ and ____.

A

vasodilation and increased vascular permeability

24
Q

PG ___ stimulates the contraction of smooth muscle in arterioles, bronchioles, and the uterus

A

PG F2 alpha

25
Q

Which lipoxygenase is predominant in neutrophils, and what conersion does it catalyze?

A

5-lipoxygenase; converts ArA to 5-HETE

26
Q

5-HETE is the precursor for ____ and is chemotactic to ____.

A

leukotrienes; neutrophils

27
Q

LT ___ is a potent chemotactic agent and activator of neutrophils,

A

B4

28
Q

LTs __, __, and __ increase vascular permeability and bronchoconstriction even more powerfully than histamine, and also cause intense vasoconstriction.

A

C4, D4, E4

29
Q

5-HPETE can be converted to what anti-inflammatory agents? (they are anti-inflammatory only if they interact with platelets)

A

lipoxins A4 and B4

30
Q

Drugs that are useful in the treatment of asthma include inhibitors of what enzyme and what receptors?

A

the lipoxygenase enzyme and leukotriene receptors

31
Q

NSAID drugs block ____ and subsequent production of ____. They usually block reversibly, except for ____.

A

cyclooxygenase (both 1 and 2); prostaglandins; aspirin

32
Q

When a patient is on aspirin therapy, what happens to levels of COX, vessel diameter, and platelet activity?

A

because COX is blocked, vascular endothelial cells make more COX which makes prostacyclin; this results in vasodilation and inhibited platelets; but because platelets lack DNA they can’t change their enzyme expression and therefore are prevented from making thromboxane as long as they live (about 10d)

33
Q

Why were COX-2 inhibitors not as ideal as initially thought?

A

through they avoided the ASA problem of causing gastric bleeding, they also caused MIs and strokes possibly due to inihibiting endothelial prostacyclin production more than platelet thromboxane

34
Q

Corticosteroids block production of ___ and its metabolites.

A

arachidonic acid

35
Q

In addition to ArA metabolism steroids have the effects of reducing transcription of genes for what 5 important products?

A

TNF, IL-1, inducible NOS, COX-2, and PLA2

36
Q

What 2 complement components stimulate histamine release from mast cells?

A

C3a and C5a

37
Q

Widespread histamine release causes what?

A

so much vasodilation and vascular permeability that blood volume becomes inadequate to maintain normal BP, leading to shock–total body hypoperfusion

38
Q

A syndrome of vasodilatory shock, widespread edema, and bronchoconstriction due to an immunologic overreaction to environmental substance is called ____.

A

anaphylaxis

39
Q

What are the clinical signs/symptoms of anaphylaxis?

A

lightheadedness as a result of hypotension; hoarseness due to laryngeal edema; N/V, abdominal cramps, and diarrhea; can be followed by rapidly declining mental status

40
Q

In addition to stimulating release of histamine from mast cells, complement C5a is chemotactic for what 4 cells?

A

neutrophils, monocytes, eosinophils, and basophils

41
Q

C5a activates what pathway of ArA metabolism in leukocytes?

A

lipoxygenase

42
Q

What are leukocidins and what is their function?

A

leukocidins are exotoxins secreted by bacteria with the intended function of killing leukocytes to avoid opsonization

43
Q

Encapsulated pathogens include what 3 important bacteria and 1 fungus?

A
  1. pneumococcus
  2. Klebsiella pneumonia
  3. Haemophilus influenza
    Fungus - cryptococcus
44
Q

The MAC is primarily important in the defense against one group of bacteria. What species is this?

A

Neisseria

45
Q

C1 inhibitor blocks what?

A

activation of complement protein C1 in the classical pathway

46
Q

CD59 inhibits what?

A

formation of MAC

47
Q

DAF inhibits what?

A

formation of C3 convertases

48
Q

Both DAF and CD59 share a glycophosphatidyl anchor. If missing that anchor, what disease results and why (general terms)?

A

paroxysmal nocturnal hemoglobinuria because of excessive complement activation and MAC formation, resulting in episodic RBC lysis and releases f Hgb into urine

49
Q

How does turmeric act as an anti-inflammatory?

A

contains curcumin, which inhibits COX and NF-kappa B, which decreases transcription of inflammatory proteins; also inhibits platelet aggregation, MPO, IFN-gamma, inducible NOS, and matrix metalloproteinases

50
Q

Bradykinin is a short-lived vasoactive peptide generated from ____ ____ by ____.

A

plasma kininogens by kallikreins

51
Q

Bradykinin causes what?

A

pain, vasodilation, increased vascular permeability

52
Q

What are the effects of platelet activating factor at high vs. low concentrations?

A

high: vasoconstriction, bronchoconstriction
low: vasodilation, inc. vascular permeability

53
Q

What factors cause vasodilation?

A

PGD2; PGE2; prostacyclin (increased COX activity which leads to increased prostacyclin); histamine; bradykinin; low concentrations of platelet activating factor

54
Q

What factors cause vasoconstriction?

A

thromboxane A2; LTC4, LTD4, LTE4; high concentrations of platelet activating factor

55
Q

What factors cause bronchoconstriction?

A

LTC4, LTD4, LTE4; high concentrations of platelet activating factor

56
Q

What factors cause increased vascular permeability?

A

PGD2; PGE2; histamine; LTC4, LTD4, LTE4; bradykinin; low concentrations of platelet activating factor

CMOD- Block1 (36 decks)

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