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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
Which lipoxygenase is predominant in neutrophils, and what conersion does it catalyze?
5-lipoxygenase; converts ArA to 5-HETE
26
5-HETE is the precursor for ____ and is chemotactic to ____.
leukotrienes; neutrophils
27
LT ___ is a potent chemotactic agent and activator of neutrophils,
B4
28
LTs __, __, and __ increase vascular permeability and bronchoconstriction even more powerfully than histamine, and also cause intense vasoconstriction.
C4, D4, E4
29
5-HPETE can be converted to what anti-inflammatory agents? (they are anti-inflammatory only if they interact with platelets)
lipoxins A4 and B4
30
Drugs that are useful in the treatment of asthma include inhibitors of what enzyme and what receptors?
the lipoxygenase enzyme and leukotriene receptors
31
NSAID drugs block ____ and subsequent production of ____. They usually block reversibly, except for ____.
cyclooxygenase (both 1 and 2); prostaglandins; aspirin
32
When a patient is on aspirin therapy, what happens to levels of COX, vessel diameter, and platelet activity?
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
Why were COX-2 inhibitors not as ideal as initially thought?
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
Corticosteroids block production of ___ and its metabolites.
arachidonic acid
35
In addition to ArA metabolism steroids have the effects of reducing transcription of genes for what 5 important products?
TNF, IL-1, inducible NOS, COX-2, and PLA2
36
What 2 complement components stimulate histamine release from mast cells?
C3a and C5a
37
Widespread histamine release causes what?
so much vasodilation and vascular permeability that blood volume becomes inadequate to maintain normal BP, leading to shock--total body hypoperfusion
38
A syndrome of vasodilatory shock, widespread edema, and bronchoconstriction due to an immunologic overreaction to environmental substance is called ____.
anaphylaxis
39
What are the clinical signs/symptoms of anaphylaxis?
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
In addition to stimulating release of histamine from mast cells, complement C5a is chemotactic for what 4 cells?
neutrophils, monocytes, eosinophils, and basophils
41
C5a activates what pathway of ArA metabolism in leukocytes?
lipoxygenase
42
What are leukocidins and what is their function?
leukocidins are exotoxins secreted by bacteria with the intended function of killing leukocytes to avoid opsonization
43
Encapsulated pathogens include what 3 important bacteria and 1 fungus?
1. pneumococcus 2. Klebsiella pneumonia 3. Haemophilus influenza Fungus - cryptococcus
44
The MAC is primarily important in the defense against one group of bacteria. What species is this?
Neisseria
45
C1 inhibitor blocks what?
activation of complement protein C1 in the classical pathway
46
CD59 inhibits what?
formation of MAC
47
DAF inhibits what?
formation of C3 convertases
48
Both DAF and CD59 share a glycophosphatidyl anchor. If missing that anchor, what disease results and why (general terms)?
paroxysmal nocturnal hemoglobinuria because of excessive complement activation and MAC formation, resulting in episodic RBC lysis and releases f Hgb into urine
49
How does turmeric act as an anti-inflammatory?
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
Bradykinin is a short-lived vasoactive peptide generated from ____ ____ by ____.
plasma kininogens by kallikreins
51
Bradykinin causes what?
pain, vasodilation, increased vascular permeability
52
What are the effects of platelet activating factor at high vs. low concentrations?
high: vasoconstriction, bronchoconstriction low: vasodilation, inc. vascular permeability
53
What factors cause vasodilation?
PGD2; PGE2; prostacyclin (increased COX activity which leads to increased prostacyclin); histamine; bradykinin; low concentrations of platelet activating factor
54
What factors cause vasoconstriction?
thromboxane A2; LTC4, LTD4, LTE4; high concentrations of platelet activating factor
55
What factors cause bronchoconstriction?
LTC4, LTD4, LTE4; high concentrations of platelet activating factor
56
What factors cause increased vascular permeability?
PGD2; PGE2; histamine; LTC4, LTD4, LTE4; bradykinin; low concentrations of platelet activating factor

CMOD- Block1 (36 decks)

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