Ellen - Pharmacology 2: Nsaids

Front 1

Prostaglandins chemical structure?

Back 1

Acidic lipids; unsaturated fatty acids with saturated cyclopentane ring and two aliphatic side chains; 20 carbon structures

Front 2

What converts phospholipid to arachidonic acid? What inhibits this?

Back 2

phospholipase A2
Inhib by glucocorticoids and mepacrine

Front 3

What does cyclooxygenase do and what's it inhibited by?

Back 3

Converts arachidonic acid to cyclic endoperoxides PGG2,PGH2. Inhib by salicylates, indomethacin, ibuprofen

Front 4

What inhibits the formation of thromboxane from prostaglandins?

Back 4

imidazole

Front 5

What does lipoxygenase do and what's it inhibited by?

Back 5

Converts acrachidonic acid to hydroperoxy-eicosatetrarnoic acid.
Inhib by Zileuton

Front 6

What inhibits the formation of CysLT from leukotrienes?

Back 6

montelukast

Front 7

What are Carboprost/ Dinoprostone and what are they used for?

Back 7

PGF2alpha
Induces abortion at 12-20 weeks
Promotes cervical dilation for delivery

Front 8

What is Alprostadil and what is it used for?

Back 8

PGE1
patent ductusarteriosis
ED

Front 9

What is Misoprostol and what is it used for?

Back 9

Me-PGE1
gastric ulceration

Front 10

What is Epoprostonol and what is it used for?

Back 10

PGI2
useful in hemodialysis to harvest platelets and in the treatment of pulmonary htn

Front 11

What stimulates the synthesis of PAF?

Back 11

antigen/antibody rx.
thrombin formation

Front 12

Action of PAF?

Back 12

Inc vascular permeability and platelet aggregation
Inc release of leukotrienes and free radical degranulation, chemotaxis ulcerogenic, neutrophil adhesion

Front 13

Where's PAF found?

Back 13

platelets, monocytes, neutrophils, mast cells, eosinophils, endothelial and renal mesangial cells

Front 14

What drugs function at PAF receptor antagonists?

Back 14

triazolobenzodiazepine derivatives
WEB 2086 (apafant) is being tested in asthma (Ph III), as an antithrombotic, and in allergic conjunctivitis

Front 15

Mechanism of gout?

Back 15

Hyperuricemia = uric acid xtals in the joint space (distal phalangial mostly, formation promoted by acidic enviro) =inflam rxn = Granulocytes phagacytose the xtals.

Front 16

What did Edmund Stone do?

Back 16

Rediscovered salicylate in willow bark in 1763.

Front 17

What's Pharmacognosy/Ethnobotany?

Back 17

Origin of medicinal agents in plants and animals

Front 18

What's Doctrine of Signatures?

Back 18

A cure for an endemic malady will be found in the plants of a region

Front 19

What are the phases of inflammation?

Back 19

I. Acute - vasodilation and capillary permeability.
II. Subacute or Delayed - infiltration of leukocytes and phagocytes (effects of chemokines).
III. Chronic proliferative - tissue degeneration and fibrosis

Front 20

What do prostaglandin's cause during inflammation?

Back 20

vasodilation of arterioles and venules = increased blood flow = erythema = REDNESS
Also edema = INDURATION

Front 21

What's the role of prostaglandins in pain?

Back 21

They directly sensitize pain fibers = hyperalgesia (respond to normally innocuous stimuli)

Front 22

What's the role of prostaglandins in fever?

Back 22

Pyrogens (released by neutrophils) stimulate release of prostaglandins in the preoptic hypothalamus = fever (due to inc heat production or decreased loss)

Front 23

How does prostaglandin inhibition decrease fever?

Back 23

Inhibition in the CNS = cutaneous vasodilation = increased heat loss. Also, decreased prostaglandin synthesis prob decreases the fever sxs.

Front 24

What type of antagonists are most NSAIDs (besides aspirin)?

Back 24

Competitive antagonists of cyclooxygenase

Front 25

What other actions may NSAIDs have (besides COX antag)?

Back 25

↓ leukocyte adherence
Block inflam cell degranulation
↓ reactive mediator production
↓PLA2 activity; chemokine binding.

Front 26

What type of pain are NSAIDs most effective against?

Back 26

Mild to moderate, particulary if it's due to inflammation.
Mylagias, arthralgias, and neuralgias (plus post-operative responds to aspirin)

Front 27

How are NSAIDs different from optiates with regards to pain management?

Back 27

Aren't addictive and don't alter sensory perception (except for cutaneous pain)

Front 28

What type of pain isn't relieved by NSAIDs?

Back 28

Hollow viscera pain

Front 29

What NSAIDs can be used for antipyresis (fever relief)?

Back 29

Less toxic agents like acetaminophen (Note: doesn't treat cause!)

Front 30

What's the drug of choice for newly diagnosed RA? What's of note with this treatment?

Back 30

aspirin
Relieves pain and inflammation but doesn't prevent progressive joint degeneration

Front 31

What inflammatory diseases are treated with NSAIDs? (major clinical use)

Back 31

RA, ankylosing spondylitis, OA

Front 32

What are the GI adverse effects of NSAIDs?

Back 32

Gastric and duodenal pain
Ulcer aggravation (esp elderly, may = anemia)
Bleeding

Front 33

What's important to know with doses of 650mg or more of aspirin?

Back 33

All patients will bleed (not significantly reduced by buffering but is diminished by enteric coating)

Front 34

What's the mechanism of NSAID toxicity?

Back 34

Loss of protective effect of PGE2 on gastric mucosa and direct corrosive effects of organic acids with table dissolution

Front 35

What is the effect of NSAIDs on the gastric mucosa?

Back 35

Increased permiability to H ions = impaired re-epithelialization
Decreased blood flow, delaying acid removal

Front 36

What can help to decrease mucosal damage from NSAIDs?

Back 36

PGE1 administration
Possibly indomethacin conjugated to NO (in clinical trials)

Front 37

What increases clotting time (with regards to COX and TXA2)?

Back 37

Inhibition of COX and decreased synthesis of TXA2.

Front 38

What dosage do you need to increase clotting time?

Back 38

Low dose is good enough in the prophylaxis of thromboembolic disease

Front 39

What is the effect of prostaglandin interference on gestation?

Back 39

Interference with the normal increase in prostaglandins just before birth may prolong delivery

Front 40

What's a renal complication in chronic users of OTC analgesics?

Back 40

Disruption of prostaglandin's regulatory function in renal blood flow can = papillary necrosis and secondary interstitial nephritis = irreversible renal insufficiency

Front 41

What NSAIDs are linked to nephropathy? Which aren't?

Back 41

Phenacetin
Probably acetaminophen
APCs (aspirin, phenacetin and caffeine combos)
Low dose aspirin is not.

Front 42

Name 4 important Salicylates.

Back 42

salicylic acid
sodium salicylate
methyl salicylate
acetylsalicylate (aspirin)

Front 43

What is the active moiety in all Salicylates? What's the exception to this?

Back 43

Salicylic acid

Exception = acetylation by aspirin

Front 44

Name 3 salicylates that are congeners of salicylic acid.

Back 44

1. Mesalamine: used as an enema for the treatment of proctosigmoiditis
2. Salsalate: metabolized to salicylic acid
3.Sulfasalazine: mesalamine covalently linked to sulfapyridine. (used for local tx of IBD - poorly absorbed orally)

Front 45

What's the first sign of acute salicylate toxicity?

Back 45

Oxidative phosphorylation uncoupled in skeletal muscle: ↑ O2 consumption and ↑ CO2, heat, and lactic acid production

Front 46

What's the second sign of acute salicylate toxicity?

Back 46

↑ CO2 = ↑ respirations = no significant change in pCO2.
If opioids/barbiturate = ↑ pCO2 + respiratory acidosis.

Front 47

What's the third sign of acute salicylate toxicity?

Back 47

Respiratory center in the medulla directly stimulated = hyperventilation = respiratory alkalosis compensated by loss of HCO3-, Na+ and K+ in kidney
Usually things do not progress further in adults

Front 48

What's the fourth sign of acute salicylate toxicity?

Back 48

Following longer periods of high-dose intoxication: Respiratory center's directly depressed = respiratory acidosis, respiratory paralysis, vasomotor collapse and death.

Front 49

What happens in kids with acute salicylate toxicity?

Back 49

Respiratory alkalosis → ↓ pH with low plasma HCO3- and near nl pCO2. Soon, ↓ ventilation = ↑ pCO2 and acidosis (uncompensated due to the loss of HCO3-)

Front 50

What causes the metabolic acidosis seen with acute salicylate toxicity?

Back 50

The salicylic acid itself, ↑ lactic acid and ↓ excretion of acids due to ↓kidney blood flow secondary to vasomotor depression

Front 51

What is the max therapeutic concentraion of plasma salicylate? What's the min lethal concentration

Back 51

50 mg/dL

160 mg/dL

Front 52

What's the respiratory effects of high dose salicylates? Acid-base effects?

Back 52

Respiratory = Uncouples oxidative phosphorylation
Acid-base = Metabolic acidosis and death in children

Front 53

What's of note about the GI effects of high dose salicylates? Uricosuric effects? Platelet effects?

Back 53

GI = very common and may interfere with Tx
Uricosuric = Can exacerbate gout?
Platelets = irreversible

Front 54

What's the absorption of salicylates?

Back 54

Rapidly absorbed from the stomach and upper intestine.
Salicylate and aspirin are highly bound to plasma proteins.

Front 55

How are salicylates distributed throughout the body?

Back 55

Widely distributed throughout fluids of the body including synovial fluid. Doesn't readily enter CSF due to the high ionized fraction in plasma.

Front 56

How are salicylates metabolized?

Back 56

metabolized by the liver primarily to glycine conjugates, and are excreted by the kidneys.

Front 57

What happens to aspirin after it's absorbed in the GI?

Back 57

Rapidly hydrolyzed to salicylate by enzymes circulating in the plasma, liver and erythrocytes

Front 58

What's the route for Salicylic acid and methyl salicylate?

Back 58

ointments, rapidly absorbed from the skin

Front 59

What's important about hypersensitivity reactions with salicylates?

Back 59

They're rare but there may be cross-sensitivity with other agents in this class so NSAIDs should be avoided in these patients.

Front 60

What happens with NSAID use in "aspirin-sensitive asthmatics"? Who are these patients?

Back 60

Aspirin and other NSAIDs can cause bronchoconstriction or anaphylaxis
Pts = asthma and nasal polyps

Front 61

What's of note with geriatric use of salicylates?

Back 61

No evidence that NSAIDs produce more GI toxicity but such events may be more likely to cause serious consequences.
Also watch metabolism since elderly pts are more likely to have renal insufficiency

Front 62

What's the dosing of NSAIDs for patients over 70?

Back 62

1/2 the amount you would dose to someone younger

Front 63

What's the concern with the use of NSAIDs in hypertensive patients? (which drugs in particular)?

Back 63

Indomethacin, ibuprofen, naproxen and piroxicam may counteract antihtns (esp diuretics) due to inhibition of renal PG synthesis and increased Na retention

Front 64

What are the symptoms of mild salicylate intoxication (salicylism)?

Back 64

Headache, dizziness, tinnitus and hearing impairment, thirst, sweating, hyper-ventilation, n&v

Front 65

What are the symptoms of severe salicylate intoxication?

Back 65

CNS disturbances, skin eruptions and serious acid-base imbalance

Front 66

What's Reye's syndrome?

Back 66

Rare but often fatal consequence (hepatic injury and encephalopathy) of giving aspirin to children with varicella or influenza virus infection

Front 67

What drug should be used as an antipyretic in children under 13.

Back 67

acetominophen. Administration of aspirin to children with chicken pox or any known viral infection is contraindicated.

Front 68

What's the treatment of salicylate intoxication?

Back 68

Depends on the sx: may include gastric lavage, reducing hyperthermia and reversal of metabolic acidosis with bicarbonate solution and glucose. Blood transfusion and vitamin K may reverse hemorrhage, and dialysis may be necessary to clear salicylates from the plasma.

Front 69

The use of NSAIDs is cautioned with the use of what "blood drugs"?

Back 69

anticoagulants (coumarin, heparin)
thrombolytic agents (tPa, streptokinase or urokinase)

Front 70

Why should NSAIDs be used with caution in patients who are on anticoagulants or thrombolytics?

Back 70

These drugs may be displaced by the very highly protein bound NSAIDs = risk of bleeding

Front 71

What NSAIDs are best to use patients who are on anticoagulants or thrombolytics? Why?

Back 71

The fenamates and the salicylate congener diflunisal (Dolobid) are less likely to cause antithrombotic effects

Front 72

What's the concern with the co-administration of Propionic acids (ibuprofen) and phenytoin?

Back 72

Propionic acids (ibuprofen et al.) can compete with phenytoin for protein binding leading to increased plasma levels of the anticonvulsant.

Front 73

Can you use 2 NSAIDs in combination?

Back 73

No - due to the increase incidence of gastric side effects.

Front 74

What's the concern with the co-administration of NSAIDs and cephalosporin antibiotics?

Back 74

may increase the risk of bleeding since several of these antibiotics produce hypoprothrombinemia.

Front 75

What's the concern with the co-administration of NSAIDs and lithium?

Back 75

Can result in increases in plasma lithium concentrations of as much as 50% due to decrease in clearance

Front 76

What's the concern with the co-administration of NSAIDs and methotrexate?

Back 76

Concurrent methotrexate (particularly high dose) therapy with diclofenac, indomethacin or ketoprofen has resulted in severe methotrexate toxicity including death. It is recommended that NSAIDs be withheld for 24 to 48 hours prior and for 12 hours following methotrexate dosing.

Front 77

What's the concern with the co-administration of NSAIDs and Probenecid?

Back 77

increases the plasma concentration of NSAIDs

Front 78

What's the concern with the co-administration of NSAIDs and zidovudine?

Back 78

Indomethacin completely inhibits the hepatic glucuronidation and clearance of zidovudine

Front 79

What types of patients should avoid indomethacin due to a possible worsening of their symptoms?

Back 79

Patients with depression, parkinsonism and epilepsy.

Front 80

Name 2 drugs included in the Para-aminophenol Derivatives.

Back 80

Acetaminophen
Phenacetin

Front 81

What are the actions of Acetaminophen?

Back 81

It has analgesic and antipyretic activity, but only weak anti-inflammatory activity

Front 82

Mechanism of action for Acetaminophen?

Back 82

Weak inhibition of PG synthesis
May be a better inhibitor of COX-3 in the CNS than in the periphery.

Front 83

What are the important differences in the pharmacological effects of acetaminophen and aspirin?

Back 83

Acetaminophen does not: effect the respiratory system, cause acid-base changes, cause gastric irritation, affect excretion of uric acid, block leukocyte adherence, or increase bleeding time.

Front 84

What's the absorption of acetaminophen?

Back 84

Well absorbed from the G.I. tract, and distributes evenly throughout bodily fluids.

Front 85

What's the metabolism of acetaminophen?

Back 85

Metabolized to a glucuronide conjugate by the liver, and excreted via the kidneys.

Front 86

What's the metabolism of acetaminophen in kids?

Back 86

Children do not metabolize efficiently, and at high doses a hepatotoxic metabolite, N-acetyl-p-benzoquinone is formed.

Front 87

What are the adverse effects of acetaminophen?

Back 87

Skin rash with drug fever and mucosal lesions
Dose-dependent potentially fatal hepatic necrosis (slowly reversible)

Front 88

What are the symptoms of acetaminophen-induced hepatic necrosis?

Back 88

gastrointestinal distress, increased activity of liver enzymes in the plasma, renal failure, jaundice, encephalopathy and coma.

Front 89

What's the treatment for acetaminophen toxicity?

Back 89

Gastric lavage followed by oral administration of charcoal. Sulfhydryl reagents (N-acetylcysteine) improve hepatic stores of glutathione which antagonizes the effects of the toxic metabolite.

Front 90

What is indomethacin/sulindac? Clinical uses?

Back 90

A potent and effective anti-inflamm agent used to tx RA, musculoskeletal pain and used IV to tx patent ductus arteriosus.

Front 91

What's the mechanism and effects of indomethacin/sulindac?

Back 91

highly effective inhibitor of COX
Analgesic (has peripheral and central components), antipyretic and anti-inflammatory

Front 92

indomethacin kinetics?

Back 92

orally effective, highly bound to plasma proteins and metabolized by the liver. Elimination is via renal and biliary mechanisms.

Front 93

Adverse effects of indomethacin?

Back 93

high incidence (35-50%) of effects including GI, hematopoietic and hypersensitivity reactions

Front 94

Can indomethacin be given to pregnant or breast-feeding mothers?

Back 94

Nope - crosses the placenta and is available in breast milk.

Front 95

What are the important drug interactions to consider with indomethacin?

Back 95

Avoid concurrent therapy with agents that cause hypoprothrombinemia, thrombocytopenia or gastric ulceration.
Aminoglycosides or digitalis: Indomethacin may cause the decreased renal excretion of these agents leading to increased plasma levels and potential toxicity.

Front 96

What is Sulindac?

Back 96

Originally developed as a substitute for indomethacin with reduced adverse effects. Sulindac is metabolized to a sulfide which is the active drug. There is less gastrointestinal toxicity probably because the active metabolite does not reach high levels in the gastric mucosa

Front 97

Clinical use of Sulindac?

Back 97

Treatment of rheumatoid arthritis and related diseases. Sulindac is about as effective as aspirin for these uses

Front 98

Name the 2 Fenamates.

Back 98

Mefanamic acid
Mecofenamate

Front 99

Pharmacologic effects of Mefanamic acid?

Back 99

inhibits cyclooxygenase and has analgesic, antipyretic and anti-inflammatory actions.

Front 100

Clinical uses of Mefanamic acid?

Back 100

Analgesic effect is the most important effect for clinical purposes but there's a high incidence of toxicity and lack of significant advantage over other drugs- not recommended as initial therapy, may be useful in primary dysmenorrhea

Front 101

Pharmacologic effects of Meclofenamate?

Back 101

inhibits cyclooxygenase and has analgesic, antipyretic and anti-inflammatory actions
may also block PG receptors.

Front 102

Clinical uses of Meclofenamate?

Back 102

Not recommended as initial therapy but is used in RA and osteoarthritis.

Front 103

Adverse effects of the Fenamates?

Back 103

potentially severe GI irritation leading to severe diarrhea. Decrease fertility in animals.
Should not be given to pregnant or breast feeding pts.

Front 104

What is Tolmetin? Primary use?

Back 104

A drug that has anti-inflammatory (more potent than aspirin, less than indomethacin), analgesic and antipyretic activity.
Primary use = RA tx

Front 105

What are the adverse effects of Tolmetin?

Back 105

GI (most common, limit use) and CNS effects, tinnitus and rashes.
Excreted in breast milk and should be avoided when nursing.

Front 106

What's of note with the interaction of Tolmetin and warfarin?

Back 106

Although Tolmetin binds extensively to plasma protein, it does not increase clotting time if given with warfarin

Front 107

What's Ibuprofen?

Back 107

Propionic Acid Derivatives- somewhat newer group of drugs with analgesic, antipyretic and anti-inflammatory effects.

Front 108

What's the advantage of ibuprofen over aspirin/indomethacin?

Back 108

Advantages in treating arthritis because side effects are less frequent and less severe

Front 109

Pharmacological actions of ibuprofen?

Back 109

inhibition of cyclooxygenase

Front 110

Adverse effects of ibuprofen?

Back 110

major = GI distress (less severe than with aspirin or indomethacin)
Increased bleeding time is also a potentially important side effect. Generally avoided in HTN.

Front 111

What drug interactions are of note when using propionic acid derivatives?

Back 111

The propionic acid derivatives are all highly bound to plasma proteins = potential for serious interaction with warfarin and possibly oral hypoglycemics.

Front 112

Name 6 propionic acid derivatives

Back 112

Ibuprofen, Naproxen, Ketoprofen = OTC;
Fenoprofen, Flurbiprofen, Oxaprozin

Front 113

What's Piroxicam? Main clinical use?

Back 113

Oxicams: Nonsteroidal anti-inflammatory, analgesic, antipyretic agent used to treat osteoarthritis

Front 114

Mechanism of action for the oxicams?

Back 114

inhibition of cyclooxygenase
Meloxicam is less selective for COX2 than COX1 inhibition but does block both.

Front 115

Kinetics notes for the oxicams?

Back 115

Long plasma half-life (50 hr) allows QD dosing for chronic arthritics. Very high plasma protein binding (99%).

Front 116

Side effects of the oxicams?

Back 116

G.I. distress is most common

Front 117

What is Diclofenac? Main clinical use?

Back 117

Phenylacetic acids: Nonsteroidal anti-inflammatory, analgesic, antipyretic agent used to tx RA, osteoarthritis and ankylosing spondylitis.

Front 118

Mechanism of action for Diclofenac?

Back 118

In addition to inhibition of COX1 and 2, it appears to block release of arachidonic acid in leukocytes which may participate in anti-inflammatory effects.

Front 119

Kinetics notes for Diclofenac?

Back 119

Diclofenac undergoes significant (50%) first-pass effect and exhibits very high plasma protein binding (99%).
Appears to accumulate in synovial fluid explaining its longer therapeutic effect than plasma T1/2.

Front 120

Side effects of Diclofenac?

Back 120

In addition to GI side effects, hepatic toxicity is known and hepatic transaminases should be followed. Embryotoxic in animal studies

Front 121

What is Zileuton? Clinical uses?

Back 121

5-lipoxigenase inhibitor developed for ulcerative colitis, asthma and allergic rhinitis. Indicated for the prophylaxis and chronic tx of asthma in adults and children 12+ years of age.

Front 122

Contraindications for Zileuton?

Back 122

Contraindicated in liver disease
Blocks warfarin and theophylline metabolism by blocking CYP1A2

Front 123

Side effects of Zileuton?

Back 123

Most common is headache

Front 124

What is Ketarolac? What's it related to?

Back 124

A potent agent with analgesic, antipyretic and anti-inflammatory activities.

Front 125

What's the strength of Ketarolac and what's it related it?

Back 125

It is chemically related to indomethacin and is 40 times as potent an anti-inflammatory as ibuprofen

Front 126

What's the major advantage of Ketarolac and what's a disadvantage?

Back 126

Can be give IM or orally for pain (may be useful in RA as a joint injection)
Not recommended for use beyond 1-2 weeks.

Front 127

What is important to note about the side effects of Ketarolac?

Back 127

side effects increase as the treatment period increases suggesting that it produces treatment duration-dependent toxicities

Front 128

Contraindications of Ketarolac?

Back 128

pregnant or breast-feeding women

Front 129

What is Etodolac?

Back 129

NSAID that be useful since it has less in the way of GI side effects compared to aspirin

Front 130

What additional side effects does Etodolac have?

Back 130

Caused decreased fertility in animal studies and not recommended for pregnant or lactating pts
Can cause thrombocytopenia

Front 131

What's important about Etodolac use in pts with liver disease?

Back 131

No dosage adjustment required

Front 132

What's Nabumetone?

Back 132

An NSAID that is not a very good cyclooxygenase inhibitor but it is a good anti-inflammatory

Front 133

Mechanism of action of Nabumetone?

Back 133

Better inhibitor of COX-2, the inducible form of cyclooxygenase than COX-1 at low doses but may work through other pathways

Front 134

Advantages of Nabumetone over other NSAIDs?

Back 134

Could be useful in combo w/ other NSAIDs.
Pro-drug activated by the liver = less direct stomach irritation
Doesn't undergo enterohepatic recycling and can be dosed once daily

Front 135

What's Celecoxib? Clinical uses?

Back 135

Orally effective COX-2 inhibitor. May be useful in the treatment of RA and osteoarthritis.

Front 136

Kinetics notes with Celecoxib?

Back 136

Complexes with food or co-administration of antacids. Highly protein bound.
60% eliminated in feces; 30% in urine.

Front 137

Side effects notes with Celecoxib?

Back 137

Significantly less GI damage is claimed

Front 138

What's of note with african americans and Celecoxib?

Back 138

They have higher blood levels of the drug on the same doses

Front 139

What's Rofecoxib?

Back 139

Selective COX-2 NSAID that lacks a sulfonamide and is not primarily dependent on CYP-450 enzymes for metabolism.

Front 140

Side effects of Rofecoxib?

Back 140

Risk of GI toxicity is not completely eliminated and increased risk of CV thrombotic events resulted in the drugs removal from the market

Front 141

Is it specifically COX1 antagonism that leads to the adverse renal effects of NSAIDs?

Back 141

People think so but COX2 selective inhibs have still shown similar adverse effects

Front 142

Why was rofecoxib removed from the market?

Back 142

The APPROVe trial observed increased risk for serious CV events, such as MIs and strokes, after 18 months of continuous treatment with rofecoxib as compared with placebo

Front 143

What are Dazoxiben, Primogrel and Ridogrel?

Back 143

thromboxane synthase inhibitors being developed for treatment of vascular ischemia and thrombosis

Front 144

Mechanism and clinical use of Ridogrel?

Back 144

Blocks TX receptor as well as the thromboxane synthase. May be useful for the prophylaxis of MI

Front 145

Clinical uses of Dazoxiben, Primogrel and Ridogrel?

Back 145

May be useful for unstable angina but are apparently not useful for Reynauds or pulmonary HTN. Have been studied with streptokinase as an adjunctive therapy to reduce the formation and size of blood clots.