Sketchy Pharm

August 25, 2017 | Author: Laylee Ghafar | Category: Benzodiazepine, Selective Serotonin Reuptake Inhibitor, Opioid, Antidepressant
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1.1 Benzodiazepines, Flumazenil – L’Eggo my Benzo!  Ben’s diner: Benzodiazepines  PAM-cakes: “-pam” suffix of benzodiazepines (e.g. diazepam, lorazepam, oxazepam)  Fast ox: oxazepam (a short-acting benzodiazepine)  “All A.M.” = “-olam” suffix of short-acting benzodiazepines (trazolam, alprazotam, midazolam)  “Addictive flavor”: benzodiazepines have the potential to cause addiction (more common w/ short-acting agents)  Liver spot: benzodiazepines are metabolized by the liver (long acting agents form active metabolites)  Cab-A: benzodiazepines bind to an allosteric site on the GABA-A receptor  CNS light: benzodiazepines potentiate GABA-A transmission in the CNS  “Chlo-Rider”: the GABA-A receptor is a chloride channel  “Take it easy”: GABA (w/ glycine) is a major inhibitory NT in the CNS  “Open more frequently”: benzodiazepines increase the frequency of ion channel opening  Alcoholic on Cab-A: alcohol binds the GABA-A receptor at a separate allosteric site  Hangover special: benzodiazepines treat alcohol withdrawal  Alcohol withdrawal symptoms: o 8-12 hours: insomnia, tremulousness, anxiety, autonomic instability o 12-48 hours: seizures o 48-96 hours: delirium tremens (fever, disorientation, severe agitation)  Long tapering flag: long-acting benzodiazepines (e.g. diazepam, chlordiazepoxide) are useful in the treatment of alcohol withdrawal  Ivy: IV administration of benzos is useful for the management of alcohol withdrawal, seizures, and anesthesia  Unplugging jackhammer: benzodiazepines treat status epilepticus  Sedated customer: IV benzos can be used in general anesthesia (muscle relaxation, amnesia)  Lite: IV benzos can induce conscious sedation for minor procedures and surgeries  Sleeping customer: benzos treat insomnia (not first line due to side effect of physical dependence)  Crying kid in pajamas: benzos treat parasomnias in children (e.g. sleepwalking, night terrors)  Relaxing chair: benzos treat spasticity caused by upper motor neuron disorders (e.g. MS, stroke, spinal cord trauma, tetanus)  Anxious customer: benzos treat generalized anxiety disorder (SSRIs and SNRIs are first line)  The Scream: benzos treat panic disorder (SSRIs and SNRIs are first line)  Side Effects o All are welcome: benzos can cause tolerance (downregulation of GABA-A) o Sedation! o Question mark hat: benzos can cause anterograde amnesia (useful during conscious sedation) o Disoriented old man: elderly patients are more sensitive to the side effects of benzodiazepines (including somnolence, confusion, disorientation) o Unbalanced stack: benzos can cause central ataxia (causing falls in elderly) o Bee swatter smacking head: benzos should be avoided with other CNS depressants (e.g. 1st generation antihistamines, alcohol, barbs, neuroleptics)  Barbershop next to Cab-A: barbiturates bind the GABA-A receptor at a separate allosteric site

 Antagonizing fluffy muzzled dog: flumazenil (competitive antagonist at the BZD receptor) reverses benzo-induced sedation (but precipitates seizures)

1.2 Nonbenzodiazepine Hypnotics (Zolpidem, Zaleplon, esZopiclone), Melatonin, Ramelteon – Catching some Z’s  Cab-A: nonbenzos hypnotics (e.g. zolpidem) bind to an allosteric site on the GABA-A receptor  “Chlo-Rider”: the GABA-A receptor is a chloride channel  CNS light: benzos potentiate GABA-A transmission in the CNS  “Take it easy”: GABA (w/ glycine) is a major inhibitory NT in the CNS  Grabbing same cab handle: nonbenzo hypnotics and benzos bind to the same allosteric site on GABA-A  Alcoholic on Cab-A: alcohol binds the GABA-A receptor at a separate allosteric site  Barbershop next to Cab-A: barbiturates bind the GABA-A receptor at a separate allosteric site  “Fast”: zaleplon and zolpidem have a rapid onset of action  Quick jump and fall: nonbenzo hypnotics have a short duration of action  Liver spot: zaleplon and zolpidem are rapidly metabolized by the liver (CYP450)  Sleeping: nonbenzo hypnotics treat insomnia  “Fall asleep”: zaleplon and zolpidem treat sleep onset insomnia (eszopiclone has the longest half life and is effective for both sleep onset and sleep maintenance insomnia)  Disoriented old man: elderly patients are more sensitive to the SEs of nonbenzo hypnotics (cognitive impairment and delirium)  Unbalanced stack: nonbenzo hypnotics can cause central ataxia (causing falls in elderly)  “Cannot combine w/ other CoupoNS”: avoid use with other CNS depressants  Bee swatter smacking head: avoid use w/ other CNS depressants (e.g. 1st gen antihistamines, alcohol, benzos, barbs)  “Not tolerated”: nonbenzo hypnotics are less likely to cause tolerance  “Break bad habits”: nonbenzo hypnotics are less likely to cause withdrawal symptoms and dependence  Antagonizing fluffy muzzled dog: flumazenil (competitive antagonist at the BZD receptor) reverses the sedative actions of nonbenzo hypnotics (but precipitates seizures)  “Melt away”: melatonin and ramelteon (a melatonin receptor agonist) treat insomnia  Dark and light: melatonin receptors maintain circadian rhythm  Nucleus above “X”: MT1 and MT2 melatonin receptors are located in the suprachiasmatic nucleus of the hypothalamus (activated by ramelteon) 

Peacefully sleeping elderly: ramelteon has few side effects and is safe in geriatric patients

1.3 Barbiturates – Barb Shop             

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Cab-A: barbiturates bind to an allosteric site on the GABA-A receptor Ben’s diner next to Cab-A: benzos bind the GABA-A receptor at a separate allosteric site Alcoholic on Cab-A: alcohol binds the GABA-A receptor at a separate allosteric site “Chlo-Rider”: the GABA-A receptor is a chloride channel CNS light: barbiturates potentiate GABA-A transmission in the CNS “Take it easy”: GABA (w/ glycine) is a major inhibitory NT in the CNS Barbiturates work by prolonging the duration of channel opening in response to GABA, NOT the frequency of channel opening o Benzos enhance Cl conduction by increasing the frequency of ion channel opening “Open longer”: barbiturates increase the duration of opening of the GABA-A receptor Long tapering flag: barbiturates have long durations of action (“hangover” effects more common) Intubated customer: IV thiopental can be used for induction of anesthesia Ivy: IV administration of barbiturates is useful for induction of anesthesia (thiopental) and management of seizures (phenobarbital) “The ol’ quick shave”: thiopental has a rapid onset and short duration of action (highly lipid soluble) Hair “redistributed” onto arms and belly: plasma levels of thiopental decrease rapidly due to redistribution to skeletal muscle and adipose o Decay line: rapid decay of plasma thiopental levels (due to redistribution) o Brief peak: rapid accumulation of thiopental in brain tissue and rapid redistribution o Growth line: rapid accumulation of thiopental in skeletal muscle and adipose (recovery from anesthesia) Unplugging jackhammer: IV phenobarbital can be used to treat seizures Perm is done!: primidone (a barbiturate used to treat seizures and essential tremor) Tremulous hand: primidone treats essential tremor (first line w/ propanolol) Side Effects: o Fainting: barbiturates can cause hypotension o Collapsed heart and lungs: barbiturates can cause profound cardiac and respiratory depression o Brain hair dryer: barbiturates can cause severe CNS depression (e.g. coma) and should be avoided in the elderly o “All are welcome”: chronic barbiturate use leads to tolerance


“Addicted”: chronic barbiturate use leads to physical dependence


Activated chrome bumper: barbiturates (e.g. phenobarbital) are potent inducers of cytochrome P450 system

2.1 Propofol, Etomidate, Ketamine (IV anesthetics) – You’re Getting Sleepy… Very Sleepy ● ● ○ ○ ○ ○ ○ ○

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Climbing IV: IV anesthetics have replaced inhaled anesthetics. Also to provide minor anesthesia in ICU pts Propofol Prospero....Fall asleep! sign: propofol (IV anesthetic for induction and maintenance) “Introducing” on sign: propofol can be used for induction of anesthesia “Maintain” your sanity sign: allows continuous infusion so used for maintenance by itself or in combo with inhaled anesthetics, sedatives, and opioids Cab-A: MOA is potentiation of chloride current through GABA-A receptor complex Dilated sleeves and pants: causes profound decrease in systemic BP d/t vasodilation (arterial and venous) → hypotension Following bolus infusion, propofol is rapidly cleared from plasma & preferentially distributed to organs w/ high blood flow (e.g. brain) b/c its highly lipophilic and readily diffuses across membranes. Its rapid termination of drug action is accounted for by redistribution to organs receiving less blood flow (fat & adipose tissue) Etomidate “Intimidator” sign: etomidate (IV anesthetic for induction) “Introducing” sign: etomidate can be used for induction of anesthesia Cab-A: MOA is potentiation of chloride current through GABAA receptor complex Stabilized patient held above his head: etomidate preserves cardiovascular stability after bolus injection (minimal changes to CO, BP, HR → useful for pts with compromised cardiac contractility) Ketamine “snaKE TAMINg” sign: ketamine IV anesthetic for induction “Introducing” sign: can be used for induction of anesthesia “Nomad” sign and hitched nomadic camel: inhibition of NMDA receptor complex. Dissociative trance: ketamine causes “dissociative anesthesia” (eyes remain open w/ a slow nystagmic gaze) Unpleasant hallucinations: can cause unpleasant emergence reactions (e.g. vivid colorful dreams, hallucinations, out of body experiences). Stimulated heart cobra: ketamine causes CV stimulation (e.g. increased BP, HR, CO) Useful anesthetic for mentally challenged and uncooperative pediatrics patients Benzodiazepines also used perioperatively Bowel water pump: benzodiazepines are used for conscious sedation for minor procedures (colonoscopy) Midazolam and lorazepam Barbiturates used perioperatively Largely replaced by propofol “Introducing” sign” used for induction of anesthesia Thiopental (the ole quick shave) -- ultra short acting. Highly lipid soluble and enters CNS to take effect. Duration of action is just 5-10 minutes.

2.2 Inhaled Anesthetics, Dantrolene (“Laughing Gas” Ft. Nitrous Oxide and Volatile anesthetics) ● ● ○ ○ ● ● ● ○ ○ ● ○ ○ ○ ● ● ○ ● ○ ○ ○ ● ● ● ●

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May be administered to supplement IV anesthetic agents to deepen anesthesia. Mechanism not really known Drugs: N2O aka laughing gas – not enough to be used for anesthesia alone but helps potentiate other anesthetics Desflurane, Commonly used for wisdom teeth extraction Has low boiling point so gaseous at room temp Halothane, Enflurane, Air tank in water: volatile anesthetics (enflurane, isoflurane, halothane) are liquid @ room temp Isoflurane, Balloon flower: volatile anesthetics (e.g. enflurane, isoflurane, halothane) are fluorinated Sevoflurane, Moving freely in ball pit (kid in red shirt): highly soluble inhaled anesthetic (e.g. halothane) methoxyflurane, Passed out later: more soluble inhaled anesthetics have slower onset of action -- Saturation of CNS is delayed N2O Long tapering flag: more soluble inhaled anesthetics have a longer duration of action Impeded by ball pit (kid in blue shirt): less soluble inhaled anesthetic (e.g. N2O) Potency  MAC Solubility of gas in blood determines speed that blood becomes saturated with anesthetic Passed out earlier: less soluble inhaled anesthetic (N2O) have faster onset of action b/c brain takes it up faster Solubility  blood/gas Immediate rescue: less soluble inhaled anesthetics (e.g. N2O) have a faster recovery partition coefficient “Partition >>>>” sign on ball pit: Higher blood:gas partition coefficient (e.g. halothane) → higher solubility → slower onset of action Graph on the side of ball pit: Steeper arterial tension curve (e.g. N2O) → lower blood:gas partition coefficient → lower solubility → faster onset of action Less steep arterial tension curve (e.g. halothane) → higher blood:gas partition coefficient → higher solubility → slower onset of action Mac and Cheese: minimum alveolar concentration (MAC) 1 / 2 kids unresponsive: MAC corresponds to the dose of anesthetic that cz 50% of pts to become unresponsive to painful stimuli (ED50) Inverted bowl of potent mac and cheese: 1/MAC corresponds to the potency of inhaled anesthetic MAC and potency are inversely proportionate Deflating heart balloon: Inhaled anesthetics can cause myocardial depression (leading to decreased cardiac output and hypotension) Deflating lung balloons: inhaled anesthetics can cause respiratory depression (leading to decreased minute ventilation and hypercapnia) Red brain wig: fluorinated anesthetics  cerebral blood flow (decrease cerebral vascular resistance) Cracked liver on piñata: halothane (and the other halogenated inhaled anesthetics) can be hepatotoxic e.g. massive hepatic necrosis. LFT, liver tenderness, hepatomegaly and light microscopy of liver shows widespread centrilobular necrosis. 80% mortality rate Why halothane is rarely used in the states anymore. Still used worldwide Smacked in the flank: enflurane can be nephrotoxic Shaking piñata: enflurane can induce seizures Magnificent birthday: malignant hyperthermia*** (skeletal muscle hypersensitivity to volatile anesthetics). Doesn’t happen with N2O “Sucks” sign: succinylcholine (depolarizing muscle relaxant) can also causes malignant hyperthermia Defective RYAN: malignant hyperthermia a/w defect in ryanodine receptors (RyR) in the SR (act as Ca channels during m. contraction) Flame theme: Defective RyR release excess Ca2+ → excessive ATP dependent uptake by the SR → heat production Bite out of muscle: excessive heat production and consumption of ATP induces muscle damage (e.g. rhabdomyolysis) Trampoline: dantrolene (muscle relaxant) treats malignant hyperthermia. Blocking Ryan: dantrolene blocks ryanodine receptors

2.3 Opiates, Naloxone, Naltrexone – Utopia Resort  Utopia = opiates  μssage: μ-opioid receptor (mediates most clinical and adverse effects: e.g. analgesia, sedation, constipation, respiratory depression)  Open banana barrels: opiate receptors open K+ channels  Closed Calci-Yum ice cream cooler: opiate receptors close vg-Ca2+ channels  Disconnected presynaptic wire: closure presynaptic vg-Ca2+ channels prevents release of NTs (e.g. glutamate, ACh, NE, serotonin, substance P)  “Fantasy”: fentanyl (opioid analgesic) for post-op and chronic pain  “More fun”: morphine (opioid analgesic) for severe or chronic pain  Distant tram: tramadol (a weak μ-opioid receptor agonist used to manage chronic pain) o North-South: tramadol also inhibits reuptake of NE and serotonin  Colon μssage table: μ-opioid receptors are located in the GI tract (delay stool transit) o Removed muddy slippers: opioids (e.g. loperamide, diphenoxylate) can be used as antidiarrheals o Lop-eared rabbit: loperamide (opioid antidiarrheal) o Loping back and forth: loperamide increases colonic phasic segmentation (increase stool transit time) o Dolphins: diphenoxylate (opioid antidiarrheal)  Barcode: codeine (opioid antitussive)  Orphan: dextromethorphan (opioid antitussive) o Tethered nomadic camel: dextromethorphan antagonizes NMDA receptors  Side Effects: o Cerebral towel: opiates cause CNS depression (e.g. sedation) o Deflated lung vest: opiates can cause respiratory depression o Constricted hood: opiates cause miosis (constricted pupils) o Plunger: opiates can cause constipation o Biliary tree: opiates can cause biliary colic (contract biliary smooth muscle) o “All are welcome”: patients may develop tolerance to opiates o “Out of order”: tolerance does not develop for miosis or constipation!!!*** o Causing pain: opiate induced hyperalgesia can occur with chronic use  Withdrawal Symptoms: o Anxious, hot, and moist: opioid withdrawal (rhinorrhea, lacrimation, yawning, hyperventilation, hyperthermia, muscle aches, vomiting, diarrhea, anxiety) o DONE timer: methadone (long acting opioid used to attenuate withdrawal symptoms). Methadone = FULL-MU OPIOID RECEPTOR AGONIST o Long tapering flag: methadone and buprenorphine have long half lives (used in opioid detoxification). Methadone = LONG HALF-LIFE o Blueprint: buprenorphine (long acting partial μ-opioid agonist used to attenuate withdrawal sx) -- safer than methadone b/c partial agonist o Irritable, moist, tachypneic baby: neonatal abstinence syndrome (diarrhea, sweating, sneezing, crying, tachypnea, irritability)  Usually treated with methadone or morphine  Partial μssage: partial μ-opioid agonists (e.g. buprenorphine, nalbuphine, butorphanol) o Bluefin: “bu-phin” in names of partial μ-opioid agonists

o Falling into the withdrawal spa: partial μ-opioid agonists can induce withdrawals  No lax zone: naloxone (μ-opioid antagonist) used to reverse acute opioid toxicity (can precipitate withdrawals)  No tricks zone: naltrexone (μ-opioid antagonist) helps maintain abstinence in heroin addicts o Tempting alcohol: naltrexone helps reduce cravings for alcohol and nicotine o

Getting fit: naltrexone can help with weight loss

3.1 Serotonin Sitcom. SSRIs, SNRIs, Cyproheptadine ● ● ● ● ● ● ● ● ● ● ● ● ○ ○ ○ ○ ●

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expreSStRIps: selective serotonin reuptake inhibitors (SSRIs) Fly out: Fluoxetine Parrot: Paroxetine Desert Airline: Sertraline City: Citalopram Smiley face: serotonin (5-HT) Keeping post-it out of the drawer (Jim): SSRIs inhibit the presynaptic reuptake of serotonin (5-HT) North and South Map: SNRIs (venlafaxine, duloxetine) inhibit the presynaptic reuptake of norepinephrine and serotonin Fax machine: Venlafaxine Dual copier/scanner: Duloxetine Shared features of SSRIs or SNRIs Happy/sad masks: SSRIs and SNRIs are first line agents for treatment of depression 5H-TV logo: serotonin (aka 5-hydroxytryptamine, 5-HT) Anxious coworker (Andy): SSRIs and SNRIs are first line agents for tx of generalized anxiety disorder (GAD) The Scream on computer screen: SSRIs and SNRIs treat panic disorder Dogtags: SSRIs and SNRIs treat PTSD 2 month calendar: SSRIs and SNRIs take 1-2 months to achieve max effect (not for acute tx) Excessive smiley faces: SSRIs and SNRIs can cause serotonin syndrome -- potentially fatal syndrome. Hot and Hypertensive (Michael Scott): serotonin syndrome is characterized by hyperthermia and HTN. Hyperactive foot tap: s. syndrome is characterized by NM hyperactivity → hyperreflexia, clonus Tricycle and mouse traps: S. syndrome can occur if SSRIs/SNRIs are combined w/ drugs that increase serotonin levels (e.g. TCAs, MAO inhibitors) “Silly pranks prohibited” sign: cyproheptadine (5HT-2 blocker) treats serotonin syndrome Out [WIthdrawn] with the flu sign: withdrawal sx from SSRIs/SNRIs include flu-like sx. make sure to taper off  Meds inhibit reuptake released by neurons Features of SSRIs most likely apart of the  Raphe nuclei of Obsessively neat worker (Dwight): SSRIs are useful in management of OCD the brainstem Binge drawer (Angela): SSRIs are useful in the mgmt of bulimia  DOC for bulimia nervosa  fluoxetine Shy guy: SSRIs are useful in the management of social anxiety disorder Inappropriately wet head: SSRIs may cause hyponatremia (SIADH) Rejected advances (Pam): SSRIs can cause sexual dysfunction Fat belly: SSRIs can cause weight gain

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Sleeping on the job: SSRIs can cause drowsiness Features of SNRIs Pain in the diasweetes machine: SNRIs treat diabetic neuropathy Chronically frayed wire: SNRIs treat chronic pain - neuropathic pain (duloxetine for low back pain and OA) Fiber bars: SNRIs treat fibromyalgia Hypertensive coworker: SNRIs can cause HTN

3.2 Tricyclic Antidepressants

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● Tricycle: Tricyclic antidepressants (TCAs) ● Imprint: Imipramine (and derivatives desipramine, clomipramine -- TCAs) ● Tripping: Amitriptyline, Nortriptyline ● Prevented from picking up smiley face and compass balls: TCAs inhibit presynaptic uptake of serotonin and norepinephrine ● Happy and sad masks: TCAs can be useful in treatment resistant depression ● Resistant door: TCAs can be useful in treatment resistant depression ● Pain from diasweeties machine: TCAs treat diabetic neuropathy ● Chronically frayed wire: TCAs treat chronic pain (e.g. neuropathic pain) ● Pounding head bell: TCAs can be used for migraine prophylaxis ● Obsessively neat: Clomipramine (TCA) treats OCD (SSRIs are the first line though b/c less well tolerated) Adverse effects ● Rejected advances: TCAs can cause sexual dysfunction ● Anti-muscarinic tea party: TCAs inhibit muscarinic acetylcholine receptors → dry mouth, constipation, blurred vision, urinary retention ● Northside Prep: nortriptyline and desipramine (secondary amines) Protected by secondary sign: Secondary amines are a/w less cholinergic effects compared to amitriptyline ● Confused elderly: TCAs are relatively contraindicated in elderly pts d/t severe anticholinergic and antihistamine effects d/t increased risk of sedation, delirium, and falls ● Bee swatter: TCAs block H1 histamine receptors. Histamine blockade causes: Hefty kid: TCAs can cause increased appetite and weight gain Sleeping kid: TCAs can cause sedation Extinguished alpha flame: TCAs block alpha 1 receptors passed out: TCAs can cause orthostatic hypotension so watch for falls in elderly Broken hearts: TCAs induced cardiotoxicity (e.g. fatal cardiac arrhythmias) is the MCC of death in overdose Inactivated peanut butter jar: TCAs block the cardiac fast Na+ channels Wide QRS crack: TCAs can widen the QRS complex on ECG Twisted torsades streamer: TCAs can induce torsades Baking soda: Sodium bicarb treats widened QRS and ventricular arrhythmia caused by TCA overdose ● Remember 3 Cs for adverse effects of TCAs: Cardiac, Coma (anti-histamine effects), Convulsions ● Shaking kid: TCAs can induce seizures (likely due to TCAs effects on GABA-A receptor) ● Stack of smiley faces: TCAs can cause serotonin syndrome (esp with drugs used in combination)

3.3 MAO Inhibitors – of MIce and MAO ● ○ ○ ○ ● ● ● ○ ○ ○ ● ● ● ● ○ ○ ● ○ ■ ○ ○ ○ ○ ○

Albino Mouse: monoamine oxidase A (MAO-A) Albino mouse eating smiley face: MAO-A breaks down serotonin Albino mouse eating north compass: MAO-A breaks down NE Albino mouse eating rope: MAO-A breaks down dopamine Black Mouse: MAO-B. Metabolizes dopamine selectively. Mouse Trap: MAO Inhibitors Irreversible trap: MAO inhibitors are irreversible. The following are non-selective MAO inhibitors “Try a sip of wine”: tranylcypromine Funnel: phenelzine Boxed wine: isocarboxazid “Not typical”: MAO inhibitors may be useful in atypical depression (hyperphagia, hypersomnia, laden paralysis [limbs feel heavy], rejection sensitivity) **main distinguishing characteristic of atypical depression is  mood reactivity Happy and sad masks: MAO inhibitors can treat depression (but not first line tx) Resistant wine bottle: MAO Inhibitors can be useful in treatment resistant depression Sledge hammer: Selegiline (selective MAO-B inhibitor) Brain tied with rope: Selegiline increases dopamine levels in the CNS Cog wheels: Selegiline is useful in the management of Parkinson’s disease (increases DA levels in the CNS) Side effects Aged meats, wine, cheese: MAO inhibitors should be avoided with these tyramine containing foods Albino mouse eating GI meat: tyramine is normally broken down by MAO-A in the GI tract Trap releasing north compass cheeses: In the presence of MAO inhibitors, tyramine enters circulation and acts as a sympathomimetic agent Hypertensive and sweaty: Tyramine toxicity can precipitate a hypertensive crisis (e.g. HTN, blurry vision, diaphoresis). So pts must adhere to low tyramine diet Pile of smiley faces: MAO inhibitors can cause serotonin syndrome Tricycle: MAO inhibitors should be avoided with other drugs that increase serotonin levels (e.g. TCAs, SSRIs, SNRIs → cause serotonin syndrome) Phantom of the alpha: Phentolamine (alpha-1 and alpha-2 blocker) can be used to manage hypertensive symptoms of tyramine toxicity

3.4 Atypical Anti-Depressants Bupropion, Mirtazappine, Trazodone – March Sadness  

“NET DAT ball”: bupropion inhibits the NE transporter (NET) and the dopamine transporter (DAT) Pro ball player: bupropion (atypical antidepressant) o No effect on serotonin! o Aroused from sleep: bupropion exerts CNS activating effects o “Pros don’t smoke”: bupropion can be used to treat tobacco dependence o Shaking: bupropion can induce seizures  Shaking binge snacker: bupropion is contraindicated in bulimia (may induce seizures)  Shaking skinny player: bupropion is contraindicated in anorexia nervosa (may induce seizures) o Kissing couple: bupropion does NOT cause sexual dysfunction o “Lose weight”: bupropion is less likely to cause weight gain “Mirth and Misery”: mirtazapine (atypical antidepressant) o Happy and sad masks: atypical antidepressants can be used as first line agents to treat depression o Extinguished double alpha light: mirtazapine blocks alpha-2 receptors o Released smiley faces and north compasses: alpha-2 inhibition increases presynaptic release of serotonin and norepinephrine o Retired 52 and 53: mirtazapine blocks 5HT-2 and 5HT-3 receptors o Bee swatter: mirtazapine inhibits H1 histamine receptors  Sleeping fan: mirtazapine can cause sedation → this side effect can be used therapeutically and makes mirtazapine one of the first line options for major depression and insomnia  Also used as adjunctive treatment with more activating antidepressants like bupropion o Hefty fan: mirtazapine can cause weight gain o Kissing couple: mirtazapine does NOT cause sexual dysfunction Trombone: trazodone (serotonin modulator - antagonizes post-synaptic serotonin receptors while also weakly inhibiting serotonin reuptake) o Smiley face drummer: trazodone is a serotonin modulator (antagonizes 5-HT2 receptors and inhibits 5-HT2 reuptake) o Retired 52: trazodone inhibits 5-HT2 receptors o Extinguished alpha lighter: trazodone antagonizes alpha-1 receptors  Erect trombone: trazodone can cause priaprism  Fainting: trazodone can cause orthostatic hypotension

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Sleeping players: trazodone can cause sedation Bee swatter: trazodone blocks H1 histamine receptors Rejected advances: trazodone can cause sexuald dysfunction


Pile of smiley faces: trazodone can cause serotonin syndrome

4.1 Ski Mania ft. Lithium Stabilizing poles: Mood stabilizers (e.g. lithium, valproate, carbamazepine, lamotrigine, antipsychotics) Stabilizing chair lift: lithium treats bipolar disorder (acute mania and maintenance) Narrow window: lithium has a very narrow therapeutic index Early nausea: acute lithium toxicity causes GI sx (e.g. N/V/D) Late trembling: chronic lithium toxicity causes neurologic symptoms (e.g. tremor) Late falling: chronic lithium toxicity causes neurologic symptoms (e.g. ataxia) Undone bowtie: lithium therapy can cause hypothyroid Hefty snowboarder: signs of lithium induced hypothyroidism include weight gain, dry skin, hair loss and constipation Insipidus fountain: Lithium can cause nephrogenic diabetes insipidus (antagonize ADH in collecting tubules) Thighs on high dive: thiazide diuretics (increase lithium levels) “Low clearance” diuretics (e.g. thiazides) and NSAIDs decrease clearance of lithium (decrease GFR) NSAIDs block synthesis of prostaglandins in the kidney -- thus reduce GFR and reduce clearance of lithium (since Li a small positively charged molecule) Tarantula: Lithium is teratogenic (ebstein’s anomaly) Large right head: atrialization of the R ventricle (seen in ebstein’s anomaly with ASD and malformed tricuspid). Later in childhood these kids present with fatigue and avoidance of outside activity. Winter FestiVAL: valproate treats bipolar disorder (acute mania and maintenance) Classic car carving: carbamazepine treats bipolar disorder (acute mania and maintenance) Llama: Lamotrigine treats bipolar disorder (maintenance only) Psychotic painting on the high peak: first generation (e.g. haloperidol) and second generation (e.g. quetiapine) antipsychotics treat acute mania

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Haloperidol is med used in tx of schizophrenia; not indicated as monotherapy for maintenance tx of bipolar disorder First line medications for bipolar maintenance tx include: lithium, valproate, and quetiapine

4.2 Valproate, Topiramate, Lamotrigine, Levetiracetam – Seize the Land  “Seize the Land”: broad spectrum antiepileptic agents (e.g. valproate, topiramate, lamotrigine, levetiracetam)  Focal arm shaking: broad spectrum antiepileptic agents (e.g. valproate) treat focal seizures  Generalized body shaking: broad spectrum antiepileptic agents (e.g. valproate) treat generalized seizures  Juvenile shaking arms: broad spectrum antiepileptic agents (e.g. valproate) treat juvenile myoclonic epilepsy (a type of generalized seizure disorder)  Welcome festiVAL: valproate (broad spectrum antiepileptic) o Inactivated baskets of salty peanuts: valproate increases Na+ channel inactivation o Elevated cab: valproate increases GABA levels in CNS o Nauseated: valproate can cause GI distress (e.g. N/V) o Fat belly: valproate can cause increased appetite and weight gain o Trembling weapon: valproate can cause tremor at high levels o Liver spot: valproate can cause fatal hepatotoxicity o Squeezed pancreas sponge: valproate can cause pancreatitis o Tarantula: valproate is teratogenic o Tubes: valproate therapy during pregnancy can cause neural tube defects (e.g. spina bifida)  Toupee: topiramate (broad spectrum antiepileptic drug) o Inactivated baskets of salty peanuts: topiramate increases Na+ channel inactivation o Binding to cab driver: topiramate allosterically binds to the GABA-A receptor o Fatigued soldiers: topiramate can cause somnolence and fatigue o Scratching head: topiramate can cause confusion and cognitive slowing o Thin arm: topiramate can cause weight loss o High pressure eye kettle: topiramate can cause acute angle closure glaucoma  Llama: lamotrigine (broad spectrum antiepileptic drug) o Inactivated baskets of salty peanuts: lamotrigine increases Na+ channel inactivation o Sloughed off red mask: topiramate can cause Stevens-Johnson syndrome (SJS/TEN) o Cross-eyed: topiramate can cause diplopia

Elevator: levetiracetam (broad spectrum antiepileptic drug) o Sleeping on the job: levetiracetam can cause somnolence

Chrome CYP450 cannon: many antiepileptic drugs are metabolized by the hepatic cytochrome P450 system

4.3 Carbamazepine, Phenytoin, Gabapentin, Tiagabine, Vigabatrin – Seize the Night ● Seize the Night: Narrow spectrum antiepileptics (carbamazepine, phenytoin, phenobarbital, gabapentin). Not for treatment of Absence seizures ● Focal arm shaking: Narrow spectrum antiepileptics (carbamazepine, phenytoin) treat focal seizures (and generalized tonic-clonic) ● Classic car: Carbamazepine (narrow spectrum). ○ Inactivated salty sodium chip bags: carbamazepine increases Na+ channel inactivation ○ Three gems: carbamazepine is a first line therapy for trigeminal neuralgia ○ Unbalanced stack: carbamazepine can cause ataxia ○ Misaligned headlights: carbamazepine can cause diplopia and nystagmus ○ Inappropriate wet head: carbamazepine can cause SIADH (dose related over first few mo. of tx) ○ Sand timer: carbamazepine can cause agranulocytosis ○ Activated chrome bumper: carbamazepine induces cytochrome P450 ○ Eosinophilic dress: carbamazepine can cz drug rxn w/ eosinophilia and systemic sx (DRESS) syndrome ○ Tarantula: carbamazepine is teratogenic ○ brain exhaust tube: carbamazepine tx in pregnancy can cz

●Classic tow truck: phenytoin (narrow spectrum) ○ Inactivated salty sodium chip bags: Phenytoin increases Na+ channel inactivation ○ Unbalanced stack: phenytoin can cause ataxia ○ Misaligned headlights: phenytoin can cause diplopia and nystagmus ○ Spilled salad: phenytoin can cause folate deficiency → megaloblastic anemia ○ Expanding gum: phenytoin can cause gingival hyperplasia ○ Big bushy beard: phenytoin can cause hirsutism ○ Eosinophilic dress: phenytoin can cz drug rxn w/ eosinophilia and systemic sx (DRESS) syndrome ○ Lupus wolf: BOTH phenytoin and carbamazepine can cz druginduced lupus ○ Sloughed off red mask: phenytoin can cz Steven-Johnson Syndrome (SJS/TEN) (esp w/in first 8 weeks of therapy) ○ Tarantula: phenytoin is teratogenic ■ Cleft trucker hat: phenytoin therapy during pregnancy can cause cleft palate ○ Activated chrome bumper: phenytoin induces cytochrome P450 ○ Fractured osteoporotic axle: phenytoin can dec bone density ○ Order Status sign: status epilepticus (treat acutely w/ benzodiazepines and phenytoin for maintenance) ●Ben’s Diner: IV benzodiazepines (e.g. diazepam, lorazepam) acutely treat status epilepticus (give phenytoin for maintenance) ●Barbershop: IV phenobarbital (barbiturate) can be used in treatment refractory seizures ●“Grab a pint”: gabapentin (narrow spectrium) ○ Closed Calci-Yum ice cream cooler: gabapentin blocks voltage gated Ca2+ channels ■ DOES NOT BIND GABA RECEPTORS ○ Chronically frayed wire: gabapentin treats chronic pain (e.g. neuropathic pain) ○ Diasweeties: gabapentin treats painful diabetic neuropathy ○ Fiber bars: gabapentin treats fibromyalgia ○ Zeus: Gabapentin treats postherpetic neuralgia (reactivated VZV) ○ Unbalanced stack: gabapentin can cause ataxia ●Raised CAB: vigabatrin and tiagabine (narrow spectrum)

neural tube defects (spina bifida) ○ Sloughed off red mask: carbamazepine can cz Steven-Johnson Syndrome (SJS/TEN) ■ Mo re common in pts with HLA-B1502 which occurs almost exclusively in pts with Asian ancestry

○ V cab transmission: vigabatrin irreversibly inhibits GABA transaminase (decrease GABA degradation → inc GABA concentration) ○ Tied up cab driver: tiagabine inhibits GABA reuptake ○ Both meds increase GABA concentration in CNS -- adjunctive treatment for partial seizures

4.4 Ethosuximide, Valproate, Lamotrigine – Seize the Daydream  “Seize the day”: antiepileptic therapy for absence seizures (e.g. ethosuximide)  “Absences”: absence seizures (a type of generalized seizures)  Inattentive student: absence seizures are characterized by sudden momentary lapse in awareness accompanied by staring, blinking, or clonic jerks  “3 spikes”: absence seizure manifest as 3 Hz spike wave complexes on EEG  “Ethos”: ethosuximide (a narrow spectrum anti-epileptic drug used to treat absence seizures) o Closed Calci-Yum chocolate milk: ethosuximide blocks Ca2+ channels o CLosed T-thermos: ethosuximide blocks T-type Ca2+ channels in the thalamus o Punched in the stomach: ethosuximide can cause GI distress (e.g. pain, N/V) o Sleeping student: ethosuximide can cause lethargy or fatigue  FestiVAL banner: valproate is effective against absence seizures o Valproate is go to drug if you have a patient with absence seizures + tonic clonic seizures 

Llama: lamotrigine is effective against absence seizures

5.1 First Generation Antipsychotics (Typical antipsychotics) ● Typical post-impressionist: First generation (typical) antipsychotics (FGAs) ● Halo: Haloperidol (high potency FGA) ● “Gazing”: “-azine” suffix of FGAs (e.g. trifluoperazine, fluphenazine, chlorpromazine, thioridazine) ● Snapping double rope: FGAs block D2 receptors in the CNS ● Trying to fly: Trifluoperazine, fluphenazine (high potency FGAs) ● “Color Theory” wheel: thioridazine (low potency FGAs) ● “Color-Pro” paints: Chlorpromazine (low potency FGAs) lower incidence of extrapyramidal symptoms, high muscarinic activity w/ increased prevalence of sedation ● Blocking positive voices: FGAs treat the positive symptoms of schizophrenia ● Crazy peak: antipsychotics treat acute psychosis in many conditions (e.g. bipolar) ● Agitated peak: antipsych (e.g. haloperidol) treat acute agitation or aggression ● Marionette: FGAs can be useful for the management of Tourette syndrome ● Long tapering flag: FGAs have a long half life (highly lipophilic) ● Antimuscarinic tea party: FGAs (low potency > high potency) block muscarinic receptors → dry mouth, constipation, blurred vision, urinary retention ● Passed out: FGAs (low potency > high potency) can cause orthostatic hypotension ● Extinguished alpha flame: FGAs (low potency > high potency) block alpha 1 receptors ● Bee swatter: FGAs (low potency > high potency) block H1 histamine receptors ● Van Gogh’s bed: FGAs (low potency > high potency) can cause sedation ● EXTRA pyramid hat on the roof: FGAs (high potency > low potency) cz extrapyramidal sx (EPS) ○ Cocked head: Acute dystonia (EPS seen within minutes) ○ Falling chair: akathisia (irritable and can’t sit still) (EPS seen within days) ○ Cog wheels: Drug induced parkinsonism (EPS seen within weeks) ○ Sticking out tongue: FGAs (High potency > low potency) can cause tardive dyskinesia ● Elevated milk production: FGAs (high potency > low potency) can cz hyperprolactinemia → galactorrhea, amenorrhea, impotence ● “Now more spicy” label: FGAs (high potency > low potency) can cause neuroleptic malignant syndrome (NMS) ○ Rigidity holding pipe: NMS is characterized by generalized “lead-pipe” rigidity ○ Crazy sweaty and tachy: NMS is characterized by altered mental status, fever, autonomic instability ○ Eaten chicken: NMS is characterized by rhabdomyolysis ● Twisted streamer: FGAs can cause torsades de pointes ● Shaking: FGAs can cause lower the seizure threshold ● Corn Yellow paint: Chlorpromazine can cause corneal deposits ● Deposits on the retinal palette: thioridazine can cause retinal deposits (cause browning of vision and look like retinitis pigmentosa)

5.2 Second Generation Antipsychotics  Atypical surrealist: second gen (atypical) antipsychotics (SGAs)  Quiet please, only whispering is appropriate sign: Quietapine, olanzapine, risperidone, aripiprazole  Zipper: Ziprasidone  Closet: Clozapine (prototype)  Snapping double rope: SGAs block D2 receptors in the CNS  Cut smiley cake: SGAs block serotonin receptors (5-HT 2A)  Hearing positive and negative voices: SGAs treat schizophrenia (positive and negative. More negative than first gen) o Negative symptoms: apathy, flat affect, lack of energy  Happy and sad masks on wine bottle: SGAs can treat depression (treatment resistant)  Resisting opening: treatment resistant depression  Obsessively neat: SGAs (e.g. risperidone) can help manage OCD (adjunctive with SSRIs)  Marionette: risperidone can help manage Tourette syndrome  Bee swatter: SGAs block H1 histamine receptors  sedation (this effect most prominent in clozapine and quietapine)  Extinguished alpha candle: SGAs block alpha-1 receptors  orthostatic hypotension  Antimuscarinic tea party: SGAs (especially clozapine) block muscarinic receptors  dry mouth, constipation, blurred vision, urinary retention  Obscured tea party: SGAs have lower affinity for muscarinic receptors than FGAs (less antimuscarinic sx)  Passed out painting: SGAs can cause sedation and orthostatic hypotension (block H1 and alpha-1)  Metabolic syndrome that differentiates SGAs from FGAs o Fat face: SGAs (e.g. olanzapine, clozapine) can cause weight gain o Elevated butter: SGAs (e.g. olanzapine, clozapine) can cause dyslipidemia o Bunch of candy: SGAs (e.g. olanzapine, clozapine) can cause hyperglycemia  Side effects associated with clozapine o Melting sand timers: clozapine can cause agranulocytosis (must monitor neutrophil counts regularly) o Surreal heart: Clozapine can cause myocarditis or cardiomyopathy o Shaking clock: Clozapine reduces seizure threshold (all of these drugs carry risk for seizure though, clozapine the most)  EXTRA pyramid hat: extrapyramidal symptoms (e.g. acute dystonia, akasthisia, parkinsonism) d/t D2 blockade (FGA>SGA) o Whispering to the EXTRA hat: All antipsychotics (FGA/SGA) can cause extrapyramidal but risperidone has the highest risk of czing EPS among the SGAs o Can also cause prolactin secretion from anterior pituitary o “Now more spicy” bucket of chicken: neuroleptic malignant syndrome, NPS, (e.g. mental status changes, rigidity, autonomic instability, fever) (FGA>SGA) Key differences between FGA and SGA  life threatening neurologic syndrome  mental status changes,  SGA also 5H2 receptor blockade rigidity, autonomic instability, and fever  FGA – mostly tx positive sx of schizophrenia. SGA treat  Bite out of chicken: NMS is associated w/ rhabdomyolysis – can both positive and neg sx lead to elevation of serum creatinine kinase  SGA are also a/w metabolic syndrome  Twisted torsades streamer: SGAs can cause torsade de pointes  SGA a/w Agranulocytosis, myocarditis/cardiomyopathy and reduced seizure threshold risk

SGA – reduced risk of extrapyramidal sx

5.3 Levodopa/Carbidopa, Entacapone, Tolcapone, Selegiline, Ropinirole, Pramipexole, Amantadine – Money For Old Rope  

Cracked open cogwheels: parkinsonism therapy

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Bank vault threshold: BBB “L” rope crank inside vault: levodopa (L-DOPA) crosses the BBB o Unfurled rope in vault: levodopa is converted to dopamine by DOPA decarboxylase in the CNS o Unfurled rope in lobby: levodopa is converted to dopamine by DOPA decarboxylase in the periphery (can’t cross BBB) o Nauseated hostage: levodopa can cause GI distress (due to peripheral conversion into dopamine) o Arrhythmia rope: levodopa can cause cardiac arrhythmias (due to peripheral conversion into dopamine) o Passed out hostage: levodopa can cause orthostatic hypotension (due to peripheral conversion into dopamine) o Psychiatrically disturbed hostage: levodopa can cause neuropsychiatric symptoms e.g. anxiety, agitation, insomnia, confusion, hallucination (due to excess dopamine in CNS) o End of rope wearing-off: chronic levodopa therapy can cause a wearing-off reaction (akinesia and dyskinesia re-emerge at the end of each dose) o “Too long!”: chronic levodopa therapy can cause response fluctuations (wearing-off reaction, on-off phenomenon) and dyskinesias o Flashing on and off: chronic levodopa therapy can cause an onoff phenomenon (periods of akinesia alternate with periods of improved mobility, not related to dose) o Narrowing window: the therapeutic window of levodopa therapy narrows as Parkinson’s progresses (unpredictable response to therapy) o Writhing sneeze: chronic levodopa therapy can cause dyskinesias (choreoathetosis of the face and distal extremities) o

Damaged psychotic painting: levodopa is contraindicated in psychotic patients

Police car on periphery: carbidopa (peripheral DOPA decarboxylase inhibitor) o o

Scared into vault: carbidopa increases the bioavailability of levodopa (prevents peripheral conversion into dopamine) Pulling away from hostages: carbidopa decreases peripheral side effects of levodopa therapy (but exacerbates neuropsychiatric side effects - anxiety and agitation)

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InTerCOM guard shooting “L” crank: catechol-O-methyltransferase (COMT) converts levodopa to 3-O-methyldopa (3-OMD) in the periphery Tall Al Capone gangster: tolcapone (a peripheral and central COMT inhibitor) increases the bioavailability of levodopa Al Capone gangster at entrance: entacapone (a peripheral COMT inhibitor) increases the bioavailability of levodopa InTerCOM guard in vault: COMT converts dopamine to 3methoxytyramine (3-MT) in the CNS Tall gangster in vault: tolcapone (a peripheral and central COMT inhibitor) increases dopamine levels in CNS o Hepatic gun: tolcapone can cause hepatic failure Black mouse eating rope: monoamine oxidase B (MAO-B) selectively metabolizes dopamine o Sledge hammer: selegiline (a selective MAO-B inhibitor) increases dopamine levels in the CNS Rope in a roll: ropinirole (D2 dopamine receptor agonist) is an important initial treatment of Parkinson’s o Double rope ladder: D2 dopamine receptor Big pecs: pramipexole (D3 dopamine receptor agonist) is an important initial treatment of Parkinson’s Restless legs: dopamine receptor agonists (e.g. ropinirole, pramipexole) treat restless leg syndrome (RLS) “Rock and roll”: dopamine receptor agonists (e.g. ropinirole) may enhance impulse control disorders (e.g. gambling, shopping, hypersexuality) Manatee: amantadine can treat some motor symptoms of Parkinson’s o Breaking open rope: amantadine enhances the effect of endogenous dopamine (by increasing its synthesis/release and inhibiting its uptake) Tri-hex Benz car: trihexyphenidyl and benztropine (antimuscarinic agents used to treat parkinsonism) o Trembling getaway car: trihexyphenidyl and benztropine improve the tremor and rigidity of Parkinson’s with no effect on bradykinesia

3.1 Propylthiouracil, methimazole, levothyroxine – Iodine is Forever Outline of TH production (in follicular cell behind the bar) and action  Evil follicu-LAIR: thyroid follicular cell (site of iodine uptake and thyroid hormone production)  Salty sodium peanuts entering lair: sodium enters thyroid follicular cell through the sodium-iodide symporter (down Na [ ] gradient, against iodide [ ] gradient = energy dependent process)  Iodide vial smuggled in w/ salty peanuts: the sodium-iodide symporter concentrates iodide in the follicular cell  Follicu-LAIR truck lumen: thyroid follicle lumen (site of iodide storage as thyroglobulin)  TransPOrter: thyroid peroxidase. TPO – enzyme involved in iodide oxidation and organification o Rusty oxidized transport truck: TPO oxidizes iodide  iodine o “thyro-global” truck: thyroglobulin (tyrosine rich protein precursor to thyroid hormones located in the follicular lumen) o Coupled tires of transport truck: TPO facilitates coupling of iodinated tyrosine residues o Organic foods transporter truck TPO facilitates iodine organification (iodination of tyrosine residues on thyroglobulin)  Time bomb prep table in the follicular-LAIR: thyroid hormones (T4 and T3) are cleaved from thyroglobulin in the follicular cell (T4 in greater quantities) o T3 red time bomb: triiodothyronine (T3) is the more potent form of thyroid hormone o T4 green time bomb: tetraiodothyronine (thyroxine, T4)  T4 Detonator henchman in the periphery: 5’ deiodinase in the peripheral tissues converts T4 to T3. T3 binds intranuclear TH receptor leading to  transcription of several hormone responsive genes  Sensitive to catfish: thyroid hormone in the sensitivity of peripheral tissues to catecholamines (sympathetic stimulation; NE) by  transcription of beta-adrenergic receptors o Symptoms of hyperthyroidism resemble SNS overactivity  Anxious henchman w/ big bowtie: Hyperthyroidism is a/w hypermetabolic and hyperadrenergic sx (e.g. tachycardia, palpitations, insomnia, anxiety, tremor, heat intolerance, weight loss)

Tx of hyperthyroidism  Radioactive vial: hyperthyroidism d/t Grave’s dz can be tx w/ ablating doses of radioactive iodine (131-I) o Most direct and effective method. Destroying follicular cells by concentrating inside the cell o Undone bowtie: radioactive iodine tx can cz hypothyroidism o Bulging radioactive goggles: radioactive iodine tx can exacerbate Grave’s ophthalmopathy o Anxious radioactive henchman: radioactive iodine tx can exacerbate HYPERthyroidism  “PTU!” agent firing at the transporter: propylthiouracil (PTU – a thionamide) treats hyperthyroidism by directly inhibiting TPO o PTU agent firing at the bomb trigger: PTU also inhibits 5’ deiodinase   conversion of T4  T3 Broken liver beaker: PTU can cause severe hepatotoxicity & liver failure which is why its limited in use to PTU, 1st trimester pregnancy and those w/ reactions to methimazole o Chemical spots: PTU can cause a maculopapular rash  Evil math equations striking transporter: methimazole (thionamide) tx hyperthyroidism by inhibiting TPO o Does NOT inhibit peripheral conversion o Tarantula: methimazole is a 1st trimester teratogen (use PTU)  Self destruct sand timer: PTU and methimazole can cz agranulocytosis (absolute neutrophil count < 500)  Plastic chew bones: PTU/methimazole can cause aplastic anemia  Guard wolf: PTU/methimazole can cause drug induced lupus (rare) o Inflamed leash: PTU can cause ANCA-associated vasculitis  Silenced bugle gun pointed at catfish tank: -blockers treat the hyperadrenergic sx of hyperthyroidism  Silenced bugle gun pointed at trigger: -blockers treat hyperthyroidism by inhibiting the 5’ deiodinase   conversion of T4  T3. o -blockers should be started as soon as the dx of hyperthyroidism is made  Moon face death coaster blocking trigger: glucocorticoids inhibit the 5’ deiodinase   conversion of T4  T3. o Moon face death coaster hitting goggles: GC treat Grave’s o

o o

MCC = Graves. Bulging infrared goggles: Grave’s ophthalmopathy (vol of retroorbital connective tissue d/t cellular proliferation, inflammation, and the accumulation of hydrophilic glycosaminoglycans)  exophthalmos


ophthalmopathy. GCs are less effective than -blockers in controlling systemic sx of hyperTH but they do have anti-inflamm effects

3.1 – Iodine is Forever; Propylthiouracil, methimazole, levothyroxine  Thwarted Dr. Storm: tx thyroid storm by: o 1) blocking SNS effects (-blockers) o 2) blocking thyroid hormone synthesis (PTU); o

3) blocking conversion of T3T4 (-blockers, PTU, GCs)

Hypothyroidism and its treatment  Fat, cold, fatigued mixologist: hypothyroidism is a/w dry brittle hair, lethargy, fatigue, weakness,  BMR, cold intolerance, and myxedema  MCC: Hashimoto thyroiditis  Mixing cold drinks: untreated hypothyroidism can lead to myxedema coma (progressive weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia, death)  Synthetic T4 time bombs: levothyroxine (synthetic T4) treats hypothyroidism o Anxious agent taking cover: Levothyroxine tx can cause HYPERthyroidism  Obstructive box of anions: anions such as perchlorate, pertechnetate, and thiocyanate competitively inhibit the sodium-iodide transporter (treat accidental radioactive iodine exposure)

3.3 - Teriparatide, Vitamin D, Cinacalcet, Sevelamer – PthD in Paleontology  Osteo-builders: Osteoblasts (activated by teriparatide and vitamin D   bone mineral density)  Destructive classmates: Osteoclasts (indirectly activated by teriparatide and vitamin D   bone resorption/turnover)  Released P fossil: osteoclasts release phosphate from bone  Released calcified bones: osteoclasts release Ca2+ from bone  Pth. D lab: parathyroid gland  PthD paleontologist: parathyroid hormone (PTH)  PthD stuck behind bones: high serum Ca2+ levels inhibit PTH production and excretion  PthD convincing osteo-builder to give up crank-drill: PTH stimulates osteoblasts to release receptor activator of nuclear factor kappa-B ligand (RANKL)  activates osteoclasts  Classmate receiving crack drill: RANKL binds to RANK on osteoclast surface   differentiation and activity   bone resorption (net effect of PTH)  PthD teaching osteo-builders: PTH stimulates maturation of osteoblasts   bone formation  PthD gathering bones and dropping P fossils: PTH  Ca2+ resorption by the kidney (and  phosphate excretion)  PthD adding final piece to Calci-TRON: PTH  activity of 1-hydroxylase in the kidney   production of 1,25-dihydroxyvitamin D (calcitriol)  1-head added to calci-TRON: 1--hydroxylase in the kidney converts 25-hydroxyvitamin D into 1,25-dihydroxyvitamin D  PthD teaching assistant (TA) teriparatide (recombinant PTH) o Fresh piece of calcified chalk: teriparatide can be used to treat o

osteoporosis ( bone density) TA teaching osteo-builders: intermittent doses of teriparatide


stimulates maturation of osteoblasts   bone formation TA gathering bones and dropping P fossils: teriparatide  Ca2+


resorption by the kidney (and phosphate excretion) TA adding final piece to calci-TRON: teriparatide  activity of 1-hydroxylase in the kidney   production of 1,25dihydroxyvitamin D

 Calci-TRON gathering bones and fossils from dump site: calcitriol stimulates reabsorption of Ca2+ AND phosphate by the kidney  Calci-TRON gathering bones and fossils from GI truck: calcitriol stimulates intestinal reabsorption of Ca2+ AND phosphate  Calci-TRON delivering crank-drills: calcitriol stimulates osteoblasts to release RANKLactivates osteoclasts  Claci-TRON collapsing PthD lab: calcitriol inhibits PTH production by the parathyroid gland  Calci-TRON teaching osteo-builders: calcitriol stimulates maturation of osteoblasts   bone formation  Fresh piece of calcified chalk: calcitriol can be used to treat osteoporosis ( bone density)  Calci-TRON stabilizing rickety tower: Vitamin D (e.g. calcitriol) can be used to treat osteoporosis ( bone density)  Calci-TRON stabilizing broken kidney: calcitriol can be useful in chronic kidney disease (prevent hypocalcemia)  Scaly knee and elbow pads: topical vitamin D can be used to treat psoriasis (inhibit keratinocyte proliferation)  Calci-TRON saving falling calcified bones: calcitriol is useful in the long term management of hypocalcemia (e.g. hypoparathyroidism) Hypocalcemia  Falling PthD: hypocalcemia is commonly caused by hypoparathyroidism ( production of calcitriol by the kidney)  Undone bowtie on PthD: thyroid surgery can cause hypoparathyroidism and hypocalcemia  Tense fist: hypocalcemia can cause paresthesias, muscle cramps, trismus, tetany, and changes in mental status  Shaking structure: hypocalcemia can cause seizure  Raised calci-yum ice cream: Teriparatide and vitamin D therapy can cause hypercalcemia  Calculator at the calcified bone receptor: cinacalcet (a calcimimetic) activates the calcium sensing receptor on the parathyroid gland   production of PTH o Tricks parathyroid gland to think theres too much calcium in serum

 Solar D3 battery: vitamin D3 (cholecalciferol) is obtained via dairy products or UVB radiation in sunlight  Earth-friendly D2 battery: Vitamin D2 (ergocalciferol) is obtained via plants  Robot body added to D battery in liver-barrow: 25-hydroxylase in the liver converts vitamin D to 25-hydroxyvitamin D

 Calculating pile of calcified bones: cinacalcet is useful in the tx of hypercalcemia d/t hyperparathyroidism  Shoveling fossils in the GI truck: sevelamer (a phosphate binding polymer)  absorption of phosphate in the GI tract  Shoveling piles of fossils: sevelamer is useful in the tx of hyperphosphatemia d/t chronic kidney disease

3.4 Glucocorticoids – The Court of Sone Hendge  Stone: “-sone” suffix of glucocorticoids (GC) e.g. dexamethasone, fludrocortisone, prednisone  Adrenal Cap: Cortisol (an endogenous glucocorticoid) is released from the adrenal cortex  Moon face: glucocorticoids (GC)  Moon scepter in outer circle: the GC receptor is located in the cytoplasm  Activated scepter in inner circle: the activated GC receptor enters the nucleus and regulates gene transcription  Inhibited cataPuLt A2: GCs inhibit phospholipase A2 (PLA2 – the first step in arachidonic acid inflammatory pathway)  AA frame of catapult of A2: GCs prevent production of arachidonic acid (AA) by inhibiting PLA2  Inhibited pro-slugger bat: GCs prevent production of inflammatory prostaglandins by COX  Inhibited lacrosse stick: GCs prevent production of inflammatory leukotrienes by LOX  Inhibited N-Flame Krossbow: GCs inhibit NF-KB (transcription factor for proinflammatory cytokines, e.g. IL-2, TNF-) o Inhibited T-knight and antibody archer: GCs prevent activation of T-Cells and B-Cells (by inhibiting production of proinflammatory cytokines)  Blocked adhesion of first responders: GC prevent production of neutrophil adhesion molecules  demargination and  migration o Crowded 1st responders: demargination of neutrophils causes neutrophilia  Falling T-knight, helper T-squire, and antibody archer: glucocorticoids reduce T-Cell and B-cell counts o Helper T-squire lowest: GCs are most effective at reducing

 Locked welcome inside mat: GCs cause insulin resistance   hyperglycemia represented by statue holding up jar of candy  Liver bag producing candy: GCs stimulate gluconeogenesis  Sugar-filled liver jar: GCs  hepatic glycogen storage (by  glycogen synthase production in liver cells)  Cracked moon: Adrenal insufficiency (can be d/t Addison’s disease – primary adrenal insufficiency) o Fainted druid: acute adrenal insufficiency can manifest as circulatory shock and death o Falling candy: acute adrenal insufficiency can manifest as hypoglycemia o Exogenous moon face: exogenous GCs treat/prevent adrenal insufficiency  Shriveled adrenal hat: chronic exogenous GC use causes adrenal cortical atrophy (secondary adrenal insufficiency)  Adverse effects – to provide substrates for gluconeogenesis, your body promotes catabolism at peripheral tissues like skeletal muscle and adipose tissue o Falling meat: GCs promote proteolysis o Falling donut jar: GCs promote lipolysis o Cushion under moon statue: Cushing’s syndrome d/t chronic GC use – fat redistribution, muscle weakness, skin thinning, osteoporosis, immunosuppression o Moon face: moon facies (due to fat deposition o Fat belly: fat redistribution  central adiposity o Thin arms: myopathy, muscle wasting, proximal wasting o Thin striped fabric: GCs inhibit fibroblast proliferation  skin thinning, striae, impaired wound healing (even seen with topical GCs)

helper T-cell counts Falling eo-slingshot: GCs reduce peripheral eosinophil counts – treatment for asthma  Eclipsed inflammatory sun: GCs are useful for treating inflammatory disorders (e.g. gout, RA, asthma, IBD)  Cracked antibodies: GCs are useful for immunosuppressive tx (e.g. transplant rejection prevention, treatment of autoimmune disorders) o

o o o o

Fractured osteoporotic altar: GCs bone mass  osteoporosis, fractures. (give calcium and vitamin D supplementation) Cracked head and crossed eyes: GC induced psychosis (hypomania, confusion, hallucination Banana peel: GC can cz Hypokalemia d/t to mineralocorticoid effects of GC Cane: GC can cause immunosuppression  Pulmonary cacti: GCs can cause reactivation of latent infections (e.g. TB in upper lobes of lung)

4.1 – Water Hazard; ADH, DDAVP, ADH receptor antagonists (vaptans)

ADH aka Vasopressin  Collecting duct (CD) – the site of action of ADH (vasopressin)  Hydrating waterboy: antidiuretic hormone (ADH, vasopressin)  Posterior water jug: ADH is released from the posterior pituitary  V1 hole on the Q shaped green: ADH activates V1 receptors coupled to Gq (activates PLC  IP3 + DAG   intracellular Ca2+)  Constricted golfclub: ADH activation of V1 on vascular smooth muscle causes vasoconstriction and BP  V2 hole on the S shaped green: ADH activates V2 receptors coupled to Gs (activates adenylyl cyclase  cAMP)  Translocation of pure water: ADH activation of V2 on the basolateral membrane of the CD causes translocation of aquaporin 2 to the apical membrane and reabsorption of free water  Endothelial tile: extrarenal V2 receptors are located on the vascular endothelium o Von wille brand pool table: ADH activation of V2 on vascular endothelium causes release of von Willebrand factor (vWF) which increases platelet aggregation o 8-ball: ADH activation of V2 on vascular endothelium causes release of factor VIII o both vWF and factor VIII are stored and released from vascular endothelial cells  Insipidus fountain: polyuria diabetes insipidus (DI)  Dehydrating kidney sand trap: nephrogenic DI o Ignoring water boy: nephrogenic DI occurs when the nephron does not respond appropriately to ADH o Lift-ium balloons: lithium can cz drug-induced nephrogenic DI  Usually resolves with discontinuation of the drug o Chloro-thighs: thiazide diuretics treat nephrogenic DI (but remember pts on Li+  thiazides may reduce renal clearance of lithium and raise plasma lithium levels into toxic range) o Almond cart: amiloride (a K+ sparing diuretic) treats nephrogenic DI esp for pts on lithium  Falling lift-ium balloon man: Amiloride treats lithium


induced DI (blocks Li+ entry into CD cells   Li+ clearance) Fire extinguisher: NSAIDs (indomethacin) treat nephrogenic DI. They decrease production of the prostaglandins that antagonize the effects of ADH

Use for Exogenous ADH therapy (DDAVP)  Dehydrating brain sand trap: Central DI o Absent waterboys: central DI occurs when the pituitary does not release adequate amounts of ADH o Waterboy entering exogenously: exogenous administration of ADH treats central DI o Desert-mobile: desmopressin acetate (DDAVP – a long acting synthetic analog of ADH) treats central DI o V-2 engine: DDAVP has high specificity for the V2 receptor  Scratched von wille brand felt: DDAVP treats von Willebrand disease (releases vWF from vascular endothelium) o Bruised with mucosal bleeding: von willebrand disease (vWD – deficiency vWF) can be a/w  bruisability and mucosal bleeding (oropharyngeal, GI, uterine)  Missing 8-ball in “A” frame: DDAVP treats hemophilia A (releases factor VIII from vascular endothelium) o Bleeding knee joint: Hemophilia A (x-linked def of factor VIII) can be a/w hemarthrosis and prolonged bleeding after minor injuries  Wet mattress: DDAVP treats night enuresis ( urine production)  Falling salty peanut shells: DDAVP can cause hyponatremia  Bulging venous golf clubs: ADH is useful in the management of esophageal variceal bleeding (constricts mesenteric arterioles   portal pressure) ADH receptor antagonists  Inappropriate water hazard: Syndrome of inappropriate ADH (SIADH)  Over-hydrating waterboy: SIADH is caused by the overproduction ADH o Can be caused by ectopic ADH production by lung cancer, CNS disorders, trauma, or some drugs o Vaporizer: “-vaptan” suffix of V2 ADH receptor antagonists (e.g. conivaptan, tolvaptan) used to treat SIADH o Wet plants: vaptans promote free water excretion (correcting hyponatremia in conjunction with hypertonic saline and free water restriction o Elevated peanuts hitting head: vaptans may cause hypernatremia or central pontine myelinolysis (osmotic demyelination syndrome – d/t overly rapid correction of Na+) o Bicycle: demeclocycline treats SIADH (vaptans are first line)

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