Inflammation Flashcards

1
Q

I am characterized by local vasodilation and increased capillary permeability. What phase of inflammation am I?

A

Acute transient phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

I am characterized by infiltration of leukocytes and phagocytic cells. What phase of inflammation am I?

A

Delayed, subacute phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

I am characterized by tissue degeneration and necrosis. What phase of inflammation am I?

A

Chronic proliferative phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What type of allergic reaction is histamine a mediator in?

A

Type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the actions of histamine during inflammatory responses?

A

1) local increase of blood flow by capillary dilation
2) edema by increasing post capillary venule permeability
3) itching by sensitizing primary sensory neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the name of the two kinins and what effects do they have on injury and inflammation?

A

Bradykinin and kallidin. They acutely cause pain due to the excitation of primary sensory neurons and chronically cause capillary dilation, increase in pcv permeability, and stimulate PLA2 to activate arachidonic acid release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What releases IL-1 and what is IL-1’s role in inflammation?

A

Release by macrophages. Induces inflammatory response! Also regulates B and T cells and induces fever.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does IL-8 do in inflammation?

A

powerful chemotactic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does TNF do during inflammation?

A

regulates production of other cytokines, induces fibrosis and tissue catabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the potential products of arachidonic acid release?

A

leukotrienes or cyclooxygenases (prostaglandins, prostacyclins, thromboxanes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is COX-1 involved in and when is it produced?

A

Produced constitutively, and involved in
- gastric cytoprotection (PGE2)

  • platelet aggregation (TXA2)
  • renal blood flow autoregulation
  • initiation of parturition (PGF2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is COX-2 involved in and when is it produced?

A

Produced during inflammation, produces prostaglandins at site of inflammation or tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does aspirin do its thang? (MOA)

A

irreversibly acetylates COX-1 and COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Put these desired effects of aspirin in order from lowest dose to highest dose:

A) analgesic and antipyretic

B) antiplatelet

C) anti-inflammatory

A

B, A, C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name some side effects of aspirin

A

GI irritation, nephrotoxicity, bleeding and anemia, hepatotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the main differences when comparing aspirin with diflunisal?

A

Difunisal reversibly inhibits COX-1 and COX-2. Diflunisal is better tolerated due to fewer GI side effects and less effect on platelets. Diflunisal is great for anti inflammatory effects. However comma diflunisal is not a good antipyretic.

17
Q

Why does acetaminophen have poor anti-inflammatory properties?

A
  • poor ability to inhibit COX in the presence of high concentrations of peroxides, such that are found at sites of inflammation
18
Q

A patient comes into the ED after having taken a bottle of acetaminophen. What is happening in their liver and what do you give them to counteract those effects?

A

Glutathione stores are depleted and the quinone intermediate attacks hepatic cells. Administer acetylcysteine to detoxify the reactive metabolite.

19
Q

What are the drugs indomethacin and sulindac used for? Which is more potent?

A

Used for RA, ankylosing spondylitis, OA, and acute goat. Indomethacin is more potent.

20
Q

What do the drugs ibuprofen flurbiprofen, naproxen, and oxaprozin have in common?

A
  • Reversibly inhibit COX-1 and COX-2 but favors COX-1
  • Treat rheumatic disorders, OA, ankylosing spondylitis, postpartum pain, dysmenorrhelal pain
  • SE: GI irritation and hepatotoxicity
21
Q

Of the proprionic acid derivatives (ibuprofen, flurbiprofen, naproxen, and oxaprozin) which has the longest half life?

A

Oxaprozin (50 hrs)

Others:
Naproxen (13 hrs)
Ibuprofen, flurbiprofen (1-2 hrs)

22
Q

What is piroxicam especially useful for and why?

A

Long term treatment of RA or OA because of long half life (45 hrs)

23
Q

Your patient has a history of oxycodone abuse and just had an emergency appendectomy. What do you administer to relieve the pain while avoiding the temptation of opioids?

A

Ketorolac (injectable!)

24
Q

What’s the big deal about coxibs (celocoxib, etoricoxib) and how do they work?

A

Coxibs show greater selectivity for COX-2 inhibition, so could potentially have all of the anti-inflammatory, antipyretic, and analgesic effects without the GI toxicity. They are larger than traditional COX inhibitors and only fit into the larger COX-2 channel.

25
Q

What are the main and scariest side effects of coxibs?

A

Increased risk of MI, stroke, and thrombosis. Contraindicated in heart problems and pregnancy. In fact, coxibs have no impact on platelet aggregation so do not offer the cardioprotective effects of traditional NSAIDs.