All Musculoskeletal Pharm. Flashcards
(48 cards)
1
Q
Leukotrienes
A
The products of Lipoxygenase acting on arachidonic acid
2
Q
LTB4
A
- A leukotriene
- Acts as a neutrophil chemotactic factor
“Neutrophils arrive B4 the others”
3
Q
LTC4
A
- A leukotriene
- Bronchoconstriction
- Vasoconstriction
- Contraction of smooth muscle
- Increase vascular permeability
- Anaphylaxis?
4
Q
LTD4
A
- A leukotriene
- Bronchoconstriction
- Vasoconstriction
- Contraction of smooth muscle
- Increase vascular permeability
- Anaphylaxis?
5
Q
LTE4
A
- A leukotriene
- Bronchoconstriction
- Vasoconstriction
- Contraction of smooth muscle
- Increase vascular permeability
- Anaphylaxis?
6
Q
Prostaglandins
A
The products of cyclooxygenase acting on arachidonic acid
7
Q
PGI2
A
Prostacyclin - a prostaglandin
- A product of cyclooxygenase acting on arachadonic acid
- One location of production is the vascular endothelium –> Inhibits platelet aggregation and promotes vasodilation (Function opposes TXA2)
- Promotes relaxation of bronchial and uterine smooth muscle.
8
Q
TXA2
A
Thromboxane
- A product of cyclooxygenase acting on arachadonic acid
- One location of production is platelets –> Promote platelet aggregation and promote vasoconstriction (Function opposes TXA2)
- Also increase bronchial tone
9
Q
Aspirin - MOA
A
Irreversibly inhibit both Cox1 and Cox2 via acetylation
- A type of NSAID
- Lower synthesis of both Prostaglandins and TXA2
- Increase bleeding time
- Does not affect PT, PTT.
10
Q
Aspirin - Clinical Use
A
Low dose (
- Inhibit platelet aggregation
Intermediate dose (300-2400 mg/day)
- Antipyretic and analgesic
High dose (2400-4000 mg/day)
- Anti-inflammatory
11
Q
Aspirin - Toxicities
A
- Gastric ulceration
- Hyperventilation (note - this is a true hyperventilation toxicity, not a compensatory mechanism against the acidity caused by salicylates which are acids. An aspirin overdose can cause a mixed acid/base disorder - metabolic acidosis with respiratory alkalosis)
- Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding
- Reye’s syndrome in children with a viral infeciton
12
Q
NSAIDs - Available Drugs
A
- Ibuprofen
- Naproxen
- Indomethacin
- Ketorolac
13
Q
NSAIDs - MOA
A
Reversibly inhibit both Cox1 and Cox2
- Block prostaglandin synthesis
[Ibuprofen, Naproxen, Indomethacin, Ketorolac]
14
Q
NSAIDs - Clinical Use
A
- Antipyretic
- Analgesic
- Anti-inflammatory
- Indomethacin is used to close PDA’s
- Naproxen and Indomethacin used for acute gout.
[Ibuprofen, Naproxen, Indomethacin, Ketorolac]
15
Q
NSAIDs - Toxicities
A
- Renal damage
- Fluid retention
- Aplastic anemia
- GI distress
- Ulcers
[Ibuprofen, Naproxen, Indomethacin, Ketorolac]
16
Q
COX-2 Inhibitors - Available Drugs
A
Celecoxib
17
Q
Celecoxib - MOA
A
Reversibly inhibit specifically cyclooxygenase 2 (COX-2), which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain.
- Spares COX-1 which help maintain gastric mucosa
18
Q
Celecoxib - Clinical Use
A
- Rheumatoid arthritis
- Osteoarthritis
- Used for patients with gastritis or ulcers
19
Q
Celecoxib - Toxicities
A
- Risk of thrombosis
- Sulfa allergy
- Less toxic to GI mucosa than NSAIDs
20
Q
Acetaminophen - MOA
A
Reversibly inhibit cyclooxygenases
- Mostly in the CNS - Inactivated peripherally (in liver with Glutathione)
21
Q
Acetaminophen - Clinical Use
A
- Antipyretic
- Analgesic
- Used instead of aspirin in children with possible viral infection to prevent Reye’s
- No anti-inflammatory properties
22
Q
Acetaminophen - Toxicities
A
- Overdose produces hepatic necrosis - Acetaminophen metabolites deplete glutathione and form toxic tissue adducts in the liver
- Antidote is N-acetylcysteine - regenerates glutathione
23
Q
Bisphosphonates - Available Drugs
A
- Etidronate
- Pamidronate
- Alendronate
- Risedronate
- Zoledronate - IV
24
Q
Bisphosphonates - MOA
A
Inhibit osteoclastic activity - Reduce both formation and resorption of hydroxyapatite
[Etidronate, Pamidronate, Alendronate, Risecronate, Zoledronate]
25
**Bisphosphonates - Clinical Use**
* Malignancy associated hypercalcemia
* Paget's disease of the bone
* Post-menopausal osteoperosis
[Etidronate, Pamidronate, Alendronate, Risecronate, Zoledronate]
26
**Bisphosphonates - Toxicities**
* Corrosive esophagitis (not Zoledronate which is administered IV)
* Nausea, diarrhea
* Osteonecrosis of the jaw
27
**Chronic Gout Therapy - Available Drugs**
* Probenecid
* Allopurinol
* Febuxostat
28
**Probenecid - MOA**
Inhibit rabsorption of uric acid in the proximal convoluted tubule
* Also inhibits secretion of penicillin
29
**Probenecid - Clinical Use**
Lower urate in chronic gout
30
**Allopurinol - MOA**
Inhibit xanthine oxidase --\> reduce conversion of xanthine to uric acid
31
**Allopurinol - Clinical Use**
* Lower urate in chronic gout
* Also used in Lymphoma and leukemia to prevent tumor lysis associated urate nephropathy
32
**Allopurinol - Toxicities**
* Increases concentrations of Azothioprine and 6-MP which are both metabolized by xanthine oxidase
* Do not give with Salicylates --\> depress uric acid clearance
33
**Febuxostat - MOA**
Inhibit xanthine oxidase --\> reduce conversion of xanthine to uric acid
34
**Febuxostat - Clinical Use**
Lower urate in chronic gout
35
**Acute Gout Therapy - Available Drugs**
* Colchicine
* NSAIDs - Naproxen or Indomethacin
36
**Colchicine - MOA**
Binds and stabalizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation
37
**Colchicine - Clinical Use**
Treatment of acute gout
38
**Colchicine - Toxicities**
GI side effects if given orally
39
**TNF-a Inhibitors - Available Drugs**
* Etenercept
* Infliximab
* Adalimumab
40
**Etanercept - MOA**
Recombinant form of human TNF receptor
"Eten**ercept** is a decoy that int**ercept**s TNF before it can get to its normal target"
41
**Etanercept - Clinical Use**
* Rheumatoid arthritis
* Psoriasis
* Ankylosing spondylitis
42
**Etanercept - Toxicities**
All TNF-a inhibitors predispose to infection, including reactivation of latent TB. This is due to preventing activation of macrophages and subsequent destruction of phagocytosed microbes
43
**Infliximab - MOA**
Anti-TNF antibody
"**Inflix**imab **Inflix** pain on TNF
44
**Infliximab - Clinical Use**
* Crohn's disease
* Rheumatoid arthritis
* Ankylosing spondylitis
45
**Infliximab - Toxicities**
All TNF-a inhibitors predispose to infection, including reactivation of latent TB. This is due to preventing activation of macrophages and subsequent destruction of phagocytosed microbes
46
**Adalimumab - MOA**
Anti-TNF antibody
47
**Adalimumab - Clinical Use**
* Rheumatoid arthritis
* Psoriasis
* Ankylosing spondylitis
* Crohn's disease
48
**Adalimumab - Toxicities**
All TNF-a inhibitors predispose to infection, including reactivation of latent TB. This is due to preventing activation of macrophages and subsequent destruction of phagocytosed microbes
