Module 9 - Pain & Inflammation Flashcards
(72 cards)
1
Q
What type of drug is Acetaminophen and what is its MOA?
A
- Type: Analgesic & antipyretic
- MOA: Unclear MOA, possibly inhibits prostaglandin synthesis however it has little or no anti-inflammatory action and does not inhibit platelet aggregation. Acts within the CNS to reduce fever and pain.
2
Q
What are the indications for using acetaminophen?
A
Analgesic - for mild pain & antipyretic
- It is equal in effectiveness to aspirin and NSAIDs as an analgesic and antipyretic (325 - 500 mg qid) but lacks anti-inflammatory properties
3
Q
What are the s/x associated with acetaminophen?
A
- No remarkable SE.
- May cause elevated ALT levels in hispanic patients
4
Q
What are some toxicities that can occur with acetaminophen?
A
- Toxicity often occurs with acetaminophen overdoses, and 15g of it is fatal
- Often no early s/x, just mild GI cramping, nausea or vomiting.
- Later urine output decreases with hematuria and upper right abdominal pain. Liver enzymes (LDH, SGOT, SGPT) are increased and irreversible hepatic necrosis occurs with increased abdominal pain, jaundice, and anuria. The patient becomes hypoglycemia, goes into a coma and dies.
- Maximum FDA recommended dosage is 3g/day
5
Q
What is the antidote for an acetaminophen overdose?
A
- N-acetylcysteine (Mucomyst) given IV over 15minutes along with gastric lavage, cathartics, and activated charcoal.
6
Q
What are the drug interactions associated with acetaminophen?
A
- Acetaminophen can increase the anticoagulant effect of warfarin but it does so inconsistently. The mechanism is not established.
- The Medical letter suggests monitoring the INR in patients on chronic warfarin therapy more closely when they take more than 2 g per day of acetaminophen for more than a few days
7
Q
What are the indications for using Transdermal Fentanyl (Duragesic)?
A
Transdermal fentanyl [Duragesic] offers ease of dosing, consistent effects, and convenience for chronic pain control in patients with chronic or terminal cancer pain.
8
Q
Describe how Transdermal fentanyl [Duragesic] is used
A
- It is placed on nonirradiated skin of the upper torso (clip - do not shave- hair) for 72 hours (based on morphine equivalency dose) and makes repeated injection or continuous IV infusion unnecessary.
- After 72 h remove old system and apply new patch. Do not wash skin with soaps, alcohol, or lotions (may alter skin characteristics & absorption).
- Drug release is proportional to the surface area of the patch.
9
Q
What is the onset of action of Transdermal fentanyl [Duragesic]?
A
- Blood levels may be detected as early as 1-2 h after application but delays up to 17-48 h occur (due to accumulation of drug within the skin).
- Elimination half-life is 13-25 h, greater in elderly (43 vs. 20 h).
10
Q
What are the contraindications to using Transdermal fentanyl [Duragesic]?
A
It is contraindicated in patients with acute postoperative pain; deaths reported with the drug have usually been in patients treated for postoperative pain.
11
Q
What is the MOA of Opioids?
A
Opioid analgesics act on specific receptors (most importantly mu & kappa receptors) on neurons in the spinal cord and brain to raise pain threshold and reduce pain perception and the emotional reaction to pain.
12
Q
What is the MOA of NSAIDS?
A
In contrast, nonopioids (e.g., aspirin) act on peripheral nerves by blocking synthesis of substances that stimulate peripheral nerve endings in damaged tissue.
13
Q
Opioids are the DOC in which type of situations?
A
- Although opioids are usually considered the drugs of choice for severe acute pain and chronic cancer pain, the effectiveness of opioids overlaps that of the NSAIDs.
- Oral codeine, propoxyphene, tramadol, & pentazocine are no more effective when taken alone than aspirin or acetaminophen.
- Morphine & other full agonists, unlike NSAIDs, have no ceiling of their analgesic effectiveness, except that imposed by adverse effects.
14
Q
What are the adverse effects associated with opioid administration?
A
- Sedation, grogginess, dizziness, nausea, vomiting, and constipation are the most common adverse effects.
- Respiratory depression is the most serious.
- Even usual doses of opioids may decrease respiratory drive and cause apnea in patients with COPD, cor pulmonale, decreased respiratory reserve, or preexisting respiratory depression.
- May cause Hypotension & bradycardia
*
15
Q
What are the indications for using opioids?
A
- Relief of moderate to severe pain (affects both perception of & reaction to pain)
- Adjunctive treatment of acute CHF, pulmonary edema, or dyspnea (relief of pulmonary edema is remarkable but the mechanism of action is unclear. Opioids decrease the perception of shortness of breath & anxiety and decrease cardiac preload & afterload).
- Ventilator control
- Special anesthesia (fentanyl IV may be the primary anesthetic in cardiovascular & high risk surgery. Epidural and subarachnoid administration provides long-lasting effect with a minimum of side effects).
- Relief of cough (requires doses lower than needed for analgesia and there are effective non-analgesic nonaddictive synthetic compounds. Cough suppression may lead to accumulation of secretions).
- Pre- and post-operative analgesia
- Treatment of diarrhea (effective but do not substitute for chemotherapy if diarrhea is associated with infection).
16
Q
What happens when Mu receptors are activated in the CNS?
A
Activation of mu receptors produces analgesia, respiratory depression, sedation, euphoria, physical dependence and constipation.
17
Q
What are the signs of opioid toxicity?
A
- Cause of death is respiratory depression
- Triad symptoms include pin point pupils, respiratory depression, and loss of consciousness with decreased blood pressure.
- Treatment is naloxone or nalmefene, ventilatory support, parenteral fluids and/or sympathomimetics to support CV status.
18
Q
What are some drug interactions associated with opioids?
A
- Additive effect with other CNS depressants.
- Cimetidine may prolong and intensify effect.
- Prolongation of neuromuscular block.
- When given with MAO inhibitors, they may cause excessive CNS depression or hyperpyresis and hypertension. Death (due to serotonin syndrome) has been reported with meperidine & MAOI and serious reactions with dextromethorphan and MAOI.
- Change in urine pH has been reported to affect methadone excretion.
- Certain fluoroquinolones (levofloxacin, ofloxacin, perfloxacin and enoxacin) were shown to cause false-positive opiate results in urinary assays
- Alcohol: A Black Box Warning has been added to the labeling of extended-release morphine capsules (Avinza) regarding the potential for fatal dose dumping when the product is administered with alcoho
19
Q
How much stronger is oxycodone compared with codeine?
A
Oxycodone and oxycodone ER is 9.5 times more effective than codeine as an analgesic and more potent than oral morphine.
20
Q
What type of drug is Ketorolac and what is its MOA?
A
- Type: NSAID
- MOA: Act on peripheral nerves by blocking synthesis of substances that stimulate peripheral nerve endings in damaged tissue.
21
Q
What are the indications for using Ketorolac?
A
- When given as an IM injection in doses of 30-60 mg (followed by 15-30 mg q6h), it is an alternative to morphine or meperidine. It may also be given IV or orally
- It is indicated only for short-term (up to 5 days) management of moderately severe acute pain.
22
Q
What are some adverse effects of using Ketorolac?
A
- Causes peptic ulcers (with GI bleeding or perforation)
- Renal failure in patients who may be volume depleted or elderly subjects
- Because it inhibits platelet function, it is contraindicated in patients at risk of bleeding.
- Its use in labor and delivery is contraindicated because it may adversely affect fetal circulation and inhibit uterine contractions.
23
Q
What type of drug is Asprin and what is its MOA?
A
- Type: 1st generation NSAID / salicylate
- MOA: Aspirin irreversibly inhibits the cyclooxygenase enzymes which are responsible for vasodilation and platelet aggregation as well as for the formation of prostaglandins by injured or inflamed tissue. The duration of action depends on how quickly specific tissues can synthesize new molecules of COX-1 and COX-2. Aspirin inhibits synthesis of prostaglandins that have inflammatory effects and inhibits platelet thromboxane, which, having no nucleus, the platelet cannot replenish the cyclooxygenase.
This is the prototype drug
24
Q
What are the indications for using Asprin?
A
- Analgesia, anti-inflammatory (including rheumatoid arthritis; osteoarthritis), antipyretic, and antiplatelet (reduces recurrent strokes or MI).
- Aspirin is considered by many as the 1st line drug for both rheumatoid and osteoarthritis; others prefer a nonacetylated salicylate, NSAIDs or acetaminophen as the preferred drug for osteoarthritis.
25
How does Aspirin act as an antipyretic?
* Pyrogens in the blood (released by bacteria or trauma or found in fluids) cause release of prostaglandins that act on the temperature control center in the hypothalamus, setting it at a higher level. This causes shivering (muscle contraction) and an increase in body temperature.
* **Antipyresis occurs by inhibition of cyclooxygenase and the release of prostaglandins.** This resets the "thermostat" in the hypothalamus to a lower value. Salicylates (and NSAIDs) **do NOT lower normal body temperature or the increase in temperature caused by exercise or hot weather.**
* **The dose of aspirin to produce antipyresis (325-650 mg q4h) is less than that needed for anti-inflammatory action.** Toxic doses of salicylates may cause hyperpyrexia.
26
How does Aspirin produce analgesia?
Analgesia is qualitatively and quantitatively different from that produced with opioids and essentially the same as that produced by NSAIDs. These agents appear to reduce pain sensation by inhibiting cyclooxygenase that forms pain-producing prostaglandins. Salicylates (and NSAIDs) do NOT affect lipoxygenase enzymes, which form the leukotrienes.
27
How does aspirin produce an antiplatelet effect?
* The acetyl part of aspirin dissociates then binds irreversibly to platelet COX. This action prevents synthesis of thromboxane A2 Thromboxane (TXA2) is a prostaglandin that enhances platelet aggregation while prostacyclin (PGI2) decreases aggregation.
* L**ow doses (60-80 mg daily) of aspirin can irreversibly inhibit thromboxane production in platelets** (which have no nucleus to form additional thromboxane, hence the action of aspirin persists for the life of the platelet or 3-7 d) without markedly affecting prostacyclin in the endothelial cells of the blood vessels.
28
What are the s/x associated with Aspirin?
* **CNS:** Dizziness, confusion, tinnitus, drowsiness, and headache.
* **Blood:** Abnormal bruising or bleeding and increased bleeding time.
* **Respiratory:** Wheezing and bronchoconstriction. This can be fatal, especially in patients with nasal polyps.
* **CV:** Edema, hypertension, and premature closure of fetal ductus arteriosus.
* **GI:** Aspirin and NSAIDs prevent prostaglandins (COX-1) from being formed resulting in epigastric distress. Nausea and vomiting are most common with abdominal pain and bleeding occurring in some patients. Not only is salicylic acid irritating to the gastric mucosa, its antiprostaglandin effect reduces the cytoprotective mechanisms of the stomach.
* **Renal:** Certain prostaglandins, produced by the kidneys, are responsible for maintaining renal blood flow. Cyclooxygenase inhibitors prevent the synthesis of these prostaglandins, which may result in retention of sodium and water and, consequently, edema. Interstitial nephritis may occur with all NSAIDs.
* **Skin:** **A****spirin****& NSAIDs are cross allergenic.** Urticaria may occur. Hypersensitivity reactions occur especially in patients with rhinitis, nasal polyps and asthma.
* **Reproduction:** Prolonged labor. In the pregnant woman, salicylates (and NSAIDs) may delay gestation and cause premature closure of the ductus arteriosus in utero. Maternal use has been linked to low birth weight infants and hemorrhage in premature infants. Salicylates are excreted in breast milk
* **Acid-base balance:** Salicylates stimulate the respiratory center resulting in respiratory alkalosis
* **Reye syndrome:** Reye syndrome is characterized by encephalopathy, liver dysfunction and death. It occurs most often in children and teenagers **infected with influenza or chickenpox viruses (Box Warning). Administration of aspirin appears to increase the risk of its development.**
* **Otic:** There is a linear relationship between plasma concentration and intensity of tinnitus and degree of hearing loss.
29
What are some toxicities that can form with Aspirin use?
* Salicylism is the term for early signs of toxicity, characterized by dizziness, confusion, neuromuscular changes, vomiting, tinnitus, decreased hearing, headache, GI upset, and drowsiness. **People who react to aspirin are sensitive to most other NSAIDs.**
* Alterations of respiratory, fluid, & electrolyte balance with acid/base imbalance, shock & high fever occur. **Signs & symptoms include dyspnea, confusion, ataxia, hyperpyrexia, seizures, and oliguria.**
* Aspirin is Pregnancy Category D.
30
What are some drug interactions associated with aspirin?
* Aspirin (and NSAIDs) add to GI irritating effect of glucocorticoids, alcohol, and NSAIDs with increased potential for bleeding and ulcers.
* The antiplatelet effect of salicylates and NSAIDs increases the chance of bleeding in patients on anticoagulant therapy
* Aspirin may cause hypoglycemia or may increase the hypoglycemic effect of sulfonylurea antidiabetics.
* **Aspirin may displace phenytoin & valproic acid from albumin increasing anticonvulsant toxicity.**
* **Aspirin (and NSAIDs) interfere with excretion of methotrexate (via P-glycoprotein?), increasing its** **myelosuppressant** **effect**
* Asprin increases systolic and diastolic BP and counteracts the effect of ACE Inhibitors
* Studies suggest that Caffeine + aspirin enhances pain relief
* **Asprin should not be given to patients with gout as Asprin decreases uric acid secretion by the kidneys**
31
What type of drug is Gabapentin and what is its MOA?
* **Type:** Anticonvulsant
* **MOA:** Gabapentin's mechanism of action is unknown. The drug is an analog of GABA but does not directly affected GABA receptors. It provides fast and sustained relief of neuropathic pain
32
What are some adverse effects with Gabapentin?
Dizziness was the most commonly reported adverse effect. Other adverse effects include somnolence, dry mouth, & peripheral edema
33
What are the 1st line drugs for neuropathic pain?
TCAs, SNRIs (Selective serotonin/norepinephrine reuptake inhibitor) (duloxetine; milnacipran), certain anticonvulsants (gabapentin or pregabalin), and topical lidocaine
34
What type of drug is Celecoxib [Celebrex] and what are its effects?
. Celecoxib is a selective COX-2 inhibitor, providing relief of inflammation and pain of osteoarthritis and rheumatoid arthritis with fewer GI ulcers (than tNSAIDs) and theoretically no effect on platelet aggregation and bleeding time.
35
What are some blackbox warnings associated with Celecoxib [Celebrex]?
* increased risk of serious CV thrombotic events and of increases in prothrombin time and bleeding, **especially in elderly patients taking warfarin**
* risk of GI ulceration, bleeding and perforation
36
What are some reactions associated with Celecoxib [Celebrex]?
* Side effects are mainly GI in nature (e.g., abdominal pain, diarrhea, and dyspepsia).
* Celecoxib, a sulfonamide derivative, is contraindicated in patients who have demonstrated allergic-type reactions to sulfonamides, aspirin, or NSAIDs.
* **It is contraindicated for the treatment of peri-operative pain.**
37
What type of drug is Methotrexate and what is its MOA?
* **Type:** Immunosuppressant
* **MOA:** It inhibits Tetrahydrofloic acid production, and preventing folic acid activation leading to cells being unable to make DNA, RNA, or proteins.
38
What are the indications for using Methotrexate?
* It has been shown to be effective as an antiarthritic agent (indicated for severe, active, classical RA), possibly because arthritis may be an autoimmune disease.
* **It is the most widely used Disease Modifying Anti-arthritic Drug**
39
What are some s/x associated with Methotrexate administration?
* In low dosage, methotrexate is often well tolerated but may cause stomatitis, anorexia, nausea, and abdominal cramps.
* Larger doses cause hepatotoxicity.
40
What are the blackbox warnings associated with Methotrexate?
* Deaths have occurred; **use in arthritis only after failure of other agents**
* Methotrexate-induced lung disease is a potentially dangerous lesion, which may occur acutely at any time during therapy. It is not always fully reversible. A dry, nonproductive cough may require interruption of treatment.
* Pregnancy Category X
* **Hepatotoxicity, _bone marrow depression_, ulcerative colitis, severe skin reactions, and opportunistic infections.**
41
What are the signs of methotrexate toxicity?
**Anorexia, nausea, diarrhea & ulcerative stomatitis** may occur and are the most frequent symptoms of toxicity
42
What type of drug is Infliximab and what is its MOA?
* **Type:** TNF inhibitor
* **MOA:** Tissue necrosis factor (TNF-α) appears to be at the heart of the inflammatory process. **Infliximab is a monoclonal antibody that binds specifically to human TNF-α**.
43
What are the indications for using Infliximab [Remicade]?
* Infliximab is for IV injection in doses several weeks apart (half-life is 8-12 days) and is indicated for the treatment of rheumatoid arthritis in combination with methotrexate (1st line regimen).
* It is also indicated for the treatment of Crohn’s disease.
44
What are some s/x associated with Infliximab [Remicade]?
* There is a warning of increased risk of infection.
* 17% of patients had an infusion reaction (fever, chills, and pruritus) and a high incidence of mortality and hospitalization for worsening CHF.
* May cause acute liver failure and hepatitis
* **Increases the risk of activating latent TB in patients with rheumatoid arthritis,** some studies have suggested using methotrexate and isoniazid first before starting TNF inhibitors
45
What type of drug is Etanercept [Enbrel] and what is its MOA?
**Type:** TNF Inhibitor
**MOA:** Inhibits TNF alpha and has a rapid onset of action and a short half-life that makes toxicity relatively short-lived.
46
What are the indications for using Etanercept [Enbrel]?
* It is indicated **for** **reduction** **of signs and symptoms of moderately to severely active rheumatoid arthritis** in patients who have had an **inadequate response to disease-modifying antirheumatic drugs. (aka methotrexate)**
* It is approved for patients with **psoriatic arthritis**.
* Studies indicate the medication continued to inhibit joint destruction progression for 2 years.
47
What are some adverse effects associated with Etanercept [Enbrel]?
* Development of serious infections (due to **bone marrow suppression**)
* **Pancytopenia** may occur as early as two weeks after starting etanercept therapy.
* May cause CNS disorders, including multiple sclerosis. Other demyelinating disorders reported with the drug included myelitis and optic neuritis.
48
What type of drug is Probenecid and what is its MOA?
* **Type:** Uricosuric
* **MOA:** it inhibits tubular reabsorption, & it increases urinary excretion of uric acid; it is used in the treatment of hyperuricemia.
**Patients must have** **adequate** **renal function for an optimal response.**
49
What are the s/x associated with Probenecid?
* May cause GI upset
* Worsening of gout is a paradoxical effect on initiation of probenecid therapy (give colchicine [as probenecid and colchicine tablets 500/0.5 mg]).
* Mobilization of uric acid from tissues results in deposition of crystals in joints, causing pain.
* **The** **uricosuric effect also increases the risk of forming urate stones in the renal tubules, particularly in patients with poor renal function.**
* **Adverse effects of probenecid include anorexia, nausea, vomiting, and hypersensitivity reactions.**
* Advice to patient. Patients taking probenecid should be well hydrated (2L/d) (to minimize urate stone formation) and may require urinary alkalinization (sodium bicarbonate). **Avoid aspirin & salicylates** because they interfere with the uricosuric action of probenecid.
50
What is the MOA of Allopurinol?
It works by blocking the enzyme xanthine oxidase, the enzyme responsible for the formation of uric acid from the breakdown of cells.
51
What are the indications for using Allopurinol?
* Use. Like probenecid, allopurinol is **used in the treatment of hyperuricemia, but in patients who are excessive producers of uric acid**.
* lt is the **preferred** drug in **patients with impaired renal function**
* Allopurinol is especially useful in chronic gouty arthritis but the drug **has a slow onset (requires a week of treatment before uric acid blood levels fall)**
* It is also used in hyperuricemia associated with cancer chemotherapy
**Patients should be encouraged to drink enough fluids to produce 2L of urine per day**
52
What are some s/x associated with Allopurinol?
* The drug causes GI upset and skin rashes
* take once daily with food or milk
* It increases the incidence of skin rash in patients taking ampicillin.
* Peripheral neuritis and depression of bone marrow elements may occur.
* **Toxic doses may produce exfoliative dermatitis as well as hepatitis and renal toxicity.**
53
What are some drug interactions associated with allopurinol?
Other drugs are metabolized by xanthine oxidase (mercaptopurine; azathioprine), hence coadministration of allopurinol with these agents will result in increased blood levels and toxicity (bone marrow suppression).
54
What type of drug is Misoprostol [Cytotec] and what is its MOA?
* **Type:** Analog of prostaglandin E
* **MOA:** It serves as a replacement for endogenous prostaglandins.
55
What are some indications for using Misoprostol [Cytotec]?
* **Prevention of gastric ulcers caused by long-term therapy with** **NSAIDS**
* Used to promote cervical ripening
* Used in combination with Mifepristone (RU 486) to induce medical termination of pregnancy
56
What type of drug is Sumatriptan and what is its MOA?
* **Type:** Serotonin 5HT1 Receptor Agonists
* **MOA:** results in cranial vessel constriction and inhibition of pro-inflammatory neuropeptide release.
57
What are the indications for using Sumatriptan?
* indicated for the **acute treatment of** **migraine** **headache** with or without aura (1st line therapy)
* Sumatriptan injection is also indicated for **acute treatment of** **cluster** **headache**
* IV use is contraindicated because of the **potential to cause coronary vasospasm**. Can be given subQ or Orally
* Can lead to MI's
* **Relief of** **headache** **& associated symptoms (nausea, neck pain, and photophobia).**
## Footnote
**Sumatriptan injection and nasal spray often begin to produce relief in 10 to 15 minutes, compared to one to two hours with the tablets.**
58
What are the s/x associated with Sumatriptan?
* Unfortunately, with Sumatriptan, headache returns in about 40% of patients within 24 hours.
* tingling, chest tightness, warm sensation, dizziness, and injection site reaction.
* Paresthesias (“heavy arms”) and chest tightness are common
* **Maximum** **recommended dose is 12 mg (2-6 mg doses) subcutaneously in 24 h (avoid IV injection)**
* Additional doses are not likely to be of benefit if the first dose is ineffective
* Teratogenic & Pregnancy Category C
## Footnote
**Patients with ischemic heart disease, Prinzmetal’s angina, or uncontrolled hypertension should not use the triptans.**
59
What are the drug interactions associated with Sumatriptan?
* The triptans may cause serotonin syndrome when used in conjunction with other drugs that increase serotonin levels (antidepressants)
* Sumatriptan appears to be metabolized by MAO-A & MAO-A inhibitors increase the effects of sumatriptan
60
What type of drug is Colchicine and what is its MOA?
* **Type:** Anti-inflammatory agent
* **MOA:** Unknown but may alter the chemotactic response induced by phagocytosis of urate crystals
61
What are the indications for using Colchicine?
* Used to treat goat flare ups & acute gouty arthritis
* Also used in gout prophylaxis
* It can be used for patients with contraindications to NSAIDs.
* It has no effect on serum uric acid levels and has no effect on either uric acid formation or excretion
62
What are the s/x of using Colchicine?
* The drug can cause profound diarrhea, nausea, vomiting, dehydration, and shock.
* As little as 8 mg in 24 h can be fatal.
* When given prophylactically, the dose is 0.6 mg once or twice daily for 6 months.
* **Renal dysfunction reduces colchicine elimination (beware of its use in the elderly!).**
* Colchicine is **teratogenic.**
63
When and for what is leucovorin used for?
Helps to reduce methotrexate toxicity if given within 24 hours; also serves as a bladder protective
64
What are the indications for Hydroxychloroquine and what is its MOA?
* A derivative of the antimalarial, chloroquine (which caused retinal damage), hydroxychloroquine is **indicated in the treatment of chronic discoid and systemic lupus erythematosus and acute or chronic rheumatoid arthritis.**
* Its mechanism is unknown but it appears to stabilize lysosomal membranes and decrease chemotaxis.
## Footnote
**The drug’s effectiveness may require 3 to 6 months to become apparent**
65
What are the s/x associated with Hydroxychloroquine?
* Although less effective than other DMARDs, it has no life-threatening toxicity.
* Given orally, it causes GI and neurological toxicity.
* Retinal toxicity can be avoided if vision is monitored at 6 to 12 month intervals and the dosage is kept below 6.5 mg/kg/d.
66
What type of drug is Anakinra [Kineret] and what are the indications for using this drug?
* **Type:** interleukin-1 receptor antagonist that, in clinical trials in active and severe rheumatoid arthritis patients, slowed the rate of progressive joint erosion.
* **Indication:** i
* Indicated for reduction in signs and symptoms of moderately to severely active rheumatoid arthritis in adults who have failed more than 1 disease-modifying antirheumatic drug.
* It is also indicated for the treatment of neonatal onset multisystem inflammatory disease.
* It may be used alone or in combination with DMARDs except tumor necrosis factor blocking agents
67
What are some s/x associated with Anakinra [Kineret]?
* The most common adverse reactions were mild and transient dose-dependent injection site reactions. (from subQ injections)
* Other reactions reported included leukopenia, headache, infections, arthralgias, diarrhea
68
What are the DOC for treating Migraine headaches?
* **Mid:** Asprin, Tylenol + metoclopramide (Reglan) to aid in absorption and reduce nausea, may lessen pain
* Narcotic analgesics are NOT a choice. They are short-acting and may promote a headache
* **Severe:** Sumatriptan is quick and reliable in 50-60% of patients when given PO. Subcutaneous injection of 5 mg is effective in 88% of patients and acts in about 10 minutes
69
What is the MOA of Dihydroergotamine (DHE-45) and what are the indications for using it?
* **MOA:** It is an alpha-adrenergic-blocking agent that binds with 5-HT receptors and works as a serotonin agonist
* **Indications:** approved for acute treatment of migraine headaches with or without aura (single 2 mg dose)
70
What are the signs of toxicity when using Dihydroergotamine (DHE-45)?
* GI disturbances (NVD; 10% of patients).
* Numbness of fingers & toes, muscle pain, pulselessness, weakness in legs, precordial distress
* **Overdose or prolonged** **use** **causes vasospasm****, which may result in gangrene of the fingers and toes.**
71
Of what use is propranolol in associated with migraine headaches?
* **Propranolol [Inderal] is currently the preferred drug for prophylaxis of** **migraine**
* 70% of patients experience fewer or less intense attacks during propranolol therapy.
* Benefit remains constant for up to 12 mo. Mechanisms of action are unclear.
72
What are the first choice drugs for the treatment of acute gouty arthritis?
1. NSAIDs are considered agents of first choice for the treatment of acute gouty arthritis. **They suppress inflammation and most patients experience marked relief within 24 hours.**
2. The glucocorticoids are highly effective for relieving an acute gouty attack and may be used in patients who cannot take NSAIDs.
