Autacoids, Anti-Allergy, Inflammatory, Pain, Fever, Gout Drugs Flashcards
define autocoids
auto: self
Akos: medicinal remedy
- an endogenous substance produced by many tissues throughout the body
- are formed in the tissues on why they act:
histamine
serotonin
prostaglandins
leukotrienes
effects usually restricted to the tissue in which they are made (exception: anaphylactic reaction)
what are the 4 A properties of NSAIDs
- analgesic: work on nociceptor; relieve pain w/o sedation
- anti-inflam: inhibit prostaglandins
- anti-plate: inhibit thromboxane A2 to reduce clot formation in heart attack and stroke prevention (aspirin)
- anti-pyretic: fever treatment; decreases temp, but not below normal
aspirin
oral NSAID
MOA
- IRREVERSIBLY inhibits cox 1& 2
- reduces the production of thromboxane A2 (anti-plate effect)
- reduces the production of prostaglandins (anti-inflam., fever, pain effects)
- because irreversible, long anti-platelet effects = last life of platelet
* mainly used for anti-p therapy to reduce risk for blood clots that can lead to heart attack/ stroke (not used much for pain, fever, inflammation)
SE
- GI & nonGI bleeding
- dyspepsia
- peptic ulcers
- tinnitus
* contraindicated <18 can causes reyes syndrome (rare)
* contraindicated if allergy to aspirin (tylenol OK)
* triad increasing risk for aspirin anaphylaxis
- nasal polyps
- asthma
- chronic sinusitis/ urticaria (hives)
indomethacin
ibuprofen
flurbiprofen
naproxen
piroxicam
ketorolac
diclofenac
oral NSAID
MOA:
- REVERSIBLY inhibits COX 1 & 2
- reduces the production of thromboxane A2 (anti-plate effect)
- reduces the production of prostaglandins (anti-inflam., fever, pain effects)
* not as long-acting as aspirin
* not as strong anti-platelet effects (not used to prevent blood clots)
SE
*GI (take with meds and foods)
- cox 1 inhibition results in the inhibition of protective GI tract prostaglandins
- dyspepsia
- nausea, diarrhea
- peptic ulcers or bleeds (increased risk of H.pylori infection or heavy alcohol consumption, or taking steroids)
* increase non-GI bleeds (subconj heme, bruising
* kidney toxicity
- avoid using with other blood thinners
- contraindicated if allergy to aspirin or other NSAID, pregnancy, advances kidney or liver disease, after CABG surgery
INDOMETH ocular effects
1. whorl keratopathy
2. macula RPE
celecoxib
oral NSAID
MOA:
- a reversibly SELECTIVE inhibitor of cox 2
- reduces the production of prostaglandins (anti-inflam., fever, pain effects)
* developed to improve GI safety
* by avoiding cox 1 - helps protect gastric lining and limits bleeding adverse effects
* safer for patients with GI issues
SE: increased risk of cardiovascular problems (heart attack/ stroke)
- imbalance created overall
- predominately Cox 1 still present with less cox 2 in the body increases blood clots
- reserved for patients high risk for GI complications
- contraindicated in aspirin or other NSAID allergy, advance kidney or liver disease, pregnancy
acetaminophen
NOT NSAID
MOA
- inhibits prostaglandin synthesis in the CNS
- not much effect on COX enxyme
- full mechanism unknown
* good fever/ pain reducer, can be used in pt. who have an allergy to NSAID or aspirin, can be combined w/ NSAID or other pain med
* NO anti-imflamm effect
* No anti-platelet effect
SE
- irreversible liver damage
- leading cause of liver failure
- found in many OTC cold/ allergy meds
- contraindicated in liver disease and alcoholism
methylprednisolone
glucocorticoid
MOA1: inhibits phospholipase a2, reduces the production of leukotrienes prostaglandins and thromboxane
MOA2: helps stabilize mast cells + basophil membranes, decreasing histamine release (involved in allergy)
SE
- increase IOP
- cataracts (PSC)
- central serous chorioretinopathy
- decrease wound healing/ increased risk of infection (immunosuppression)
- altered mental status (depression, euphoria, insomnia)
- crushing syndrome (adipose redistribution collects in face/ neck)
- adrenal insufficiency
- osteoporosis
- HTN
- muscle atrophy
- increase blood sugar/ induce diabetes
- GI ulcers/ bleeds/ easy bruising
- weight gain
fluticasone nasal spray
glucocorticoid
SE:
- increase IOP
- cataracts
- central serous chorioretinopathy
- nosebleeds
hydrocortisone cream
glucocorticoid
SE:
- increase IOP
- cataracts
why do patients taking systemic steroids longer than ~ 7 days need a dose tapered?
first generation anti-histamine
- diphenhydramine
- chlorpheniramine
- brompheniramine
- promethazine
- meclizine
- diphenhydramine
- chlorpheniramine
- brompheniramine
- promethazine
- meclizine
first generation anti-histamine
MOA: block histamine from binding to H1 receptors (crosses BBB; lipid soluble)
AE
- sedation
- anti-cholinergic effects: mydriasis, dry eyes, decreased acc., increased IOP, tachycardia, dry mouth, constipation, urinary retention
- anti-cholinergic effects of these drugs don’t really cause enough bronchodilator or vasoconstriction to be helpful in severe anaphylaxis causing severe bronchoconstriction and vasodilation (severe hypotension)
PROMETH
1. whorl keratopathy
2. corneal endo pigment
3. cataracts
4. retinal pigment changes
second generation
- loratadine
- desloratadine
- fexofenadine
- cetirizine
- levocetirizine
- azelastine
- loratadine
- desloratadine
- fexofenadine
- cetirizine
- levocetirizine
- azelastine
second generation anti-histamine
MOA: block histamine from binding H1 receptors
- does not cross BBB
- not very lipid soluble
- much less sedation effects
- no anti-emetic effects
SE: dry eyes and mouth
CETIRIZINE
- some people do experience sedation
- oculogyric crisis: OU, involuntary turn/ gyrate upward and or up/out (usually) - can last seconds or hours
- disordered thinking
- restlessness, stiffening
- drug: rxn after anti-emetic (ex: prochlorperazine)
cromolyn sodium
nedocromil
mast cell stabliziers
* help prevent allergic rxn long term
MOA: reduce the release of histamine by preventing the breakdown of mast cells and basophils
SE: does nothing for acute symptoms
- not affecting histamine already released
what is the treatment for gout?
