Pharmacology Review (Week 8--Melega) Flashcards
Effects of cholinergic agonists
SLUDG (lots of secretions)
Salivation/sweating
Lacrimation
Urination (bladder constriction)
Defecation
Gastric acid secretion/peristaltic activity
(pupillary constriction, bradycardia, vasodilation, bronchoconstriction, penis/clitoris erection)
Where does arachidonic acid originate from?
Omega 6 (linoleic acid)
Essential fatty acid
Where do eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) originate from?
Omega 3 (alpha-linolenic acid)
EPA first, then DHA later in pathway (essential fatty acids)
Stomach/GI drugs
Erythromycin (motilin agonist)
Metoclopramide (5HT4 agonist and Dopamine antagonist –> prokinetic; 5HT –> anti-nausea)
Neostigmine (AChE inhibitor –> increased motility)
Atropine (decrease motility, in addition to other things)
Buspirone (5HT1A –> accommodation, tx dyspepsia, tx anxiety)
Sumatriptan (5TH1B/iD/1P –> vasoconstriction and accommodation agonist; tx dyspepsia/indigestion)
Octreotide (somatostatin analog –> decreased motility, acid, secretions)
Omeprazole (PPI)
Cimetidine, Ranitidine (H2 blocker)
Ondansetron (5HT3 blocker –> anti-vomit)
Sucralfate (cryoprotectant, mucus)
Misoprostol (PGE1 analog –> mucus and bicarb secretion)
Antacids
Drugs with bad GI side effects
Fluoxetine (SSRI antidepressant causes nausea b/c increased 5HT)
Oxybutynin (Ditropan) and Tolterodine (Detrol) (antimuscarinic so decrease GI motility)
Bladder and/or BPH drugs
Oxybutynin (Ditropan) (anticholinergic –> bladder relax –> tx urge incontinence)
Tolterodine (Detrol) (anticholinergic –> bladder relax –> tx urge incontinence)
Amitriptyline (Elavil) (TCA = NE and 5HT reuptake blocker AND antimuscarinic –> bladder relax –> tx overflow incontinence)
Allopurinol (xanthine oxidase inhibitor; anticolinergic –> relax detrusor)
Alpha adrenergic antagonists (terazosin, doxazosin, tamusolin (FloMax), alfuzosin (Uroxatral)) (relax smooth muscle of prostate and bladder neck –> tx BPH, allow bladder emptying)
5-alpha reductase inhibitors (finasteride (Proscar), dutasteride (Avodart)) (less DHT so less prostate growth; tx BPH)
Erectile Dysfunction drugs
Vasodilators/PDE5 inhibitors (Sildenafil (Viagra, Revatio), vardenafil (Levitra), tadalafil (Cialis)) (inhibit degradation of cGMP)
Gout drugs
Colchicine (binds MTs of neutrophils –> antiinflammatory response to urate crystals; tx acute gout)
Glucocorticoids (inhibit PLA2 –> antiinflammatory; tx acute gout)
NSAIDs (inhibit COX –> antiinflammatory; tx acute gout)
Allopurinol (xanthine oxidase inhibitor; anticolinergic –> relax detrusor; tx chronic gout)
Probenecid (inhibits reabsorption of uric acid at PCT; tx hyperuricemia w/gout; tx chronic gout)
Sulfinpyrazone (inhibits reabsorption of uric acid at PCT; tx gouty arthritis; tx chronic gout)
What does epinephrine do in terms of metabolism?
Epi is around when you’re fasting or stressed and need more glucose!
Epi acts to increase glucose in plasma: glycogenolysis, gluconeogenesis, lipolysis, inhibits glycogen synthesis
In the pancreas, epi binds alpha2 receptors to inhibit insulin secretion
In the liver, epi binds alpha receptors to activate IP3, PLC, phosphorylate insulin receptor so insulin can’t act on its receptors
In the liver and muscle, epi binds beta2 receptors to cause glycogenolysis
In fight or flight, why might you pee/poop yourself?
Fight or flight is sympathetic and pee/poop is symp–seems like paradox!
When we activate hypothalamic pituitary system, release CRF and have CRF receptors (both symp and parasymp side) IN the brain that control downput to organs, and these can cause an increase in GI motility causing defecation reflex and contraction of detrusor. Also, serotonin is released in GI tract which causes nausea and vomiting
“Centrally mediated CRF effect”
Why don’t we use muscarinic blockers to treat gastric acid over-secretion?
Because there are so many more things other than ACh that cause acid secretion!
(would still have histamine on H2, gastrin on CCK2)
Which drugs increase GI motility?
Fluoxetine (SSRI)
Erythromycin (motilin agonist)
Metoclopramide (5HT4 agonist)
Neostigmine (AChE inhibitor)
Which drugs decrease GI motility?
Atropine (decrease motility, in addition to other things)
Oxybutynin (Ditropan) and Tolterodine (Detrol) (antimuscarinic so decrease GI motility)
Buspirone (5HT1A –> accommodation, tx dyspepsia, tx anxiety)
Sumatriptan (5TH1B/iD/1P –> vasoconstriction and accommodation agonist; tx dyspepsia/indigestion)
Octreotide (somatostatin analog –> decreased motility, acid, secretions)
M2 vs. M3 effects on bladder
M2 is indirect but is everywhere (inhibits cAMP caused by NE on beta sympathetic)
M3 is direct (IP3 and PLC to contract detrusor)
Innervation of the bladder
Pelvic splanchnic parasympathetic ACh act on M3 receptor to contract bladder
Hypogastric nerve sympathetic NE acts on beta receptor to relax bladder and NE acts on alpha1 in urethra to constrict internal sphincter?
Pudendal nerve (somatic) ACh acts on Nicotinic receptor on external (skeletal muscle) sphincter
