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Immunology > L18 > Flashcards

L18 Flashcards

1
Q

What is your first anti-inflam drug class choice for RA? Second choices?

A
  1. DMARDs
  2. Aspirin (salicylates)
    NSAIDs
    Steroids
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2
Q

What anti-inflams would you use for AS and psoriatic arthritic?

A

NSAIDs or aspirin (salicylates)

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3
Q

What is your first choice anti-inflams for osteoarthritis? Other options?

A
  1. Acetaminophen (Tylenol)
  2. NSAIDs
    Aspirin (salicylates)
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4
Q

What is your first choice anti-inflam for lupus and Crohn’s? Second choice?

A
  1. Steroids or DMARDs

2. Aspirin (salicylates)

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5
Q

What are the 3 main functions of NSAIDs? What don’t they do? Do they cure?

A
  1. Non-narcotic pain reduction (analgesic)
  2. Reduce fever (anti-pyretic)
  3. Anti-inflam
    NO immune suppression
    NO cure - suppress inflammation
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6
Q

Where do NSAIDs act?

A

Membrane phospholipids –> PLA2 –> arachidonic acid –> COX1/2 –> eicosanoids
= COX (cyclo-oxygenase) inhibitors

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7
Q

When COX1/2 breaks down eicosanoids (PGH2), what are the 3 main products?

A 
Thromboxane - makes TXA2 (thromboxane)
Prostacyclin - makes PGI2
Prostaglandins 
- from PGF & PGE synthase enzymes 
Which ones are made is due to cell specific enzymes
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8
Q

What are the 4 prostaglandins you should know?

A

PGE 1
2
PGD2
PGF alpha

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9
Q

Describe COX 1. Where is it found?

A 
ALWAYS on
- Can be induced 
@ platelets: thromboxane 
@ GI and to prevent clots: prostacyclin (PGI2)
@ Kidneys & fever: prostaglandin E2
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10
Q

Describe COX 2. What upregulates it? What is the main metabolite produced?

A

Inducible form
Upregulated by IL1, shear stress, own products (feed forward)
PGE2 = metabolite, feed forward (fever)

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11
Q

What are the 5 types of NSAIDS?

A
  1. Salicylates (aspirin - Bayer)
  2. Propionic acid derivatives (Advil, Aleve)
  3. Indole derivatives (indomethacin)
  4. Oxicams
  5. COX2 selective inhibitors
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12
Q

What is the active ingredient in aspirin? What is the natural source?

A

Acetyl-salicylic acid

Willow tree leaves/bark

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13
Q

How does aspirin interact with COX enzymes?

A

COVALENT - permanent inhibition
Low dose = preferential inhibit COX 1
High dose = inhibit both COX1/2
AKA dose-dependent mechanism for fever and inflammation reduction

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14
Q

Which COX enzymes is found on platelets? What does this enzyme prefer to make? What do you take for it?

A

COX1 –> thromboxaine
Take low dose aspirin - preferential inhibition
No platelet aggregation - no clots (baby aspirin prevents against heart attack, take 1 Bayer a day)

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15
Q

What are side-effects of aspirin use?

A

GI

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16
Q

What is the mechanism of propionic acid derivatives?

A

Non-specific, both COX1 & 2

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17
Q

What is Advil?

A 
Ibuprofen = propionic acid dervative
Shorter lasting, 3-4hrs
OTC - pain & fever
RX - anti-inflam
- \$\$$
- Slow to act because ti enters synovium slowly
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18
Q

What is Aleve?

A

Naproxen = propionic acid derivative

Longer lasting, 12 hrs

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19
Q

What is the use of indole derivatives (indomethacin)?

A

Delays labor
Used to close patent ductus arteriosis
Contra-indicated with GI disease - high side effect risk

20
Q

What are 3 common oxicams?

A
  1. Prioxicam (!!!!) - OA & RA
  2. Tenoxicam
    - Use only for chronic pain, NOT acute (post-op)
  3. Meloxicam
    COX2 selective (NOT specific)
    Arthritis
21
Q

What are phenyl acetic acid derivatives used for?

A

Rx - severe pain
Ketorlac
Tolmetin
Diclofenac

22
Q

What is the COX2 inhibitor you need to remember?
Mechanism
Contra-indications
Uses

A 
CELE-COX-IB
= Celebrex 
COX2 selective inhibitor 
Inhibits p450 enzymes 
Interacts with ACE inhibitors - monitor 
For RA
No GI - but watch for CARDIOVAS
- COX1 alone = sticky platelets, heart attacks (on the news!)
23
Q

What is Reye’s syndrome?

A 
KIDS!!! 
Virus host reaction 
Hepatic encephalopathy & steatosis 
May be due to taking aspirin/other NSAIDs - why don't give kids Advil
NOT seen with acetaminophen
24
Q

Can you be allergic to aspirin?

A

YES
Edema, skin rashes, bronchoconstriction & spasm
- B/c increases AA –> leutorienes –> spasm

25
Q

Why don’t you use aspirin (salicylates) for RA?

A

Helps the pain
Doesn’t help the inflammation
Side effects too great

26
Q

What is the major consequence of aspirin OD?

A

Uncouple oxidative phosphorylation

  • Accelerate glycotic and lipolytic pathways
  • More O2 consumed
  • More CO2 made
  • Use up all liver glycogen
27
Q

Why would you use NSAIDs for gout?

A

Creates dose-dependent excretion of ureic acid –> can’t form in joints

28
Q

What are unexpected benefits of NSAID use?

A

CVD protection if inhibit both COX1&2
↓Colon cancer risk
↓Alzheimer’s/dementia (neuroinflam)

29
Q

What is the mechanism by which NSAIDs protect against colon cancer?

A
  • X COX2 and/or thromboxane, TGF beta
  • NO PGE2
  • Remove angiogenesis, decreased apoptosis and cell proliferation associated with inflammation –> cancer
30
Q

Which NSAIDs do you use OTC for acute decrease inflam/pain?

A

Ibuprofen (Advil)

Naproxen (Aleve)

31
Q

Which NSAID do you use OTC for chronic pain?

A

Aspirin (Beyer)

32
Q

Which NSAIDs do you use Rx for acute inflam/pain?

A

Indomethacin
Phenyl acetic acid derivatives
- Ketolac
- Diclofenac

33
Q

Which NASIDs do you use Rx for chronic pain?

A

Meloxicam (oxicam for arthritis)
Celebrex (COX2 inhibitor)
Ibuprofen & naproxen (at higher doses)

34
Q

Which NSAIDs are selective for COX2 but still have COX1 affinity?

A

Meloxicam
Indomethacin
CV risk

35
Q

What are the benefits of aspirin, ibuprofen, and naproxen? Negatives?

A

↓CVD

↑GI side effects

36
Q

How are NSAIDs metabolized? Where?

A

p450 enzymes
No toxic metabolites
Often bound to albumin

37
Q

Why are there different ways to take aspirin - in water vs pill etc?

A

Changes how fast absorbed

38
Q

What are the big 5 negative side effects of NSAIDs?

A 
↑bleeding time b/c ↓TXA
Gastritis & ulceration b/x ↑PGI2
Liver toxic
Fluid retention ↓PGE2
Delayed labor ↓PGE2
39
Q

What is SCARS? What NSAID is most commonly associated?

A

Severe cutaneous adverse reactions
= Whole body blisters
Celecoxib - (Celebrex) suggests disease mechanism linked to COX2 inhibition

40
Q

What Stevens-Johnson syndrome?

A 
A type of SCAR
Life threatening! 
Epidermis separates from dermis
Why? medications (NSAIDs)
No trxt - ride it out
41
Q

Why don’t we give pregnant women NSAIDs?

A

Spontaneous abortion!!!

42
Q

What are the normal effect of thromboxane?

A

Platelet aggregation

Vasocontrict

43
Q

What are the normal effects of PGI2 (prostacyclin)?

A

Inhibit platelet aggregation
Vasodilator
GUT!!!!!

44
Q

What is the normal effect of PGF 2 alpha (prostaglandin)?

A

Contract uterus to induce delivery

45
Q

What is the normal effect of PGE2?

46
Q

What is the normal effect of PGDS?

A

Non-REM sleep

47
Q

What is common between all prostanoid receptors?

A

7 TM GCPR
- Lots of cross talk b/c similar structure
Prostanoids = molecules made from the membrane to act back on the membrane

Immunology (25 decks)

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