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Pharmacology MTR
| Question | Answer |
|---|---|
| Routes of drug administration | ENTERAL: oral (PO), sublingual, rectal (PR); PARENTERAL: IV, IM, SC; OTHER: inhaled, intranasal, intathecal (spinal cord), intraventricular ("PIC" line), topical, transdermal |
| First-pass effect | the effect of liver metabolism prior to reaching systemic circulation |
| Effects of pH on drug absorption | (weakly) acidic drugs are best absorbed in an acidic environment (e.g. stomach: pH 1.5-2.0)). alkaline drugs are best absorbed in the SI (b/c it is slightly alkaline: pH of 8) |
| The two phases of drug metabolism | Phase I reactions (oxidized into more polar form, usually by p450 enzyme system), Phase II reactions (CONJUGATION of a polar group, typically glutathione) DRUGS CAN UNDERGO EITHER OR BOTH AND IN NO PARTICULAR ORDER. |
| Agonist (strong, weak, partial) | Promotes the natural, physiologic action ("alters physiology of the cell by binding to plasma membrane or intracellular receptors") |
| Antagonist (competitive, noncompetitive, physiologic, neutralization) | Inhibits or blocks natural, physiologic action ("inhibits or blocks responses caused by agonists") |
| Efficacy | (Lippincott definition is clumsy, but here we go): "the degree to which a drug is able to induce maximal effects" |
| Potency | (his definition seems a bit arbitrary, but it's straight from book!:) "the amount of drug required to produce 50% of the maximal response |
| Four types of drug-drug interactions | additive (1+1=2), synergistic (1+1=3), potentiating (1+1=1), antagonizing (1+1=0) |
| Tolerance | development, over time, of decreased response to a drug-- and thus the dose has to be increased to achieve same effect |
| Dependence | patient needs drug/drugs in question in order to functional "normally" |
| Withdrawal | (i don't quite understand the reasoning behind his definition. if you are taking a medication for a chronic condition, and that condition is not cured/eradicated, then OF COURSE you will begin experience symptoms again upon cessation of therapy!) |
| What happens when muscarinic receptors (on organs) are activated? | stimulate the parasympathetic response: pin point pupil (miosis), slower HT rate, bronchoconstriction, relaxed sphincters, increased secretions, UB detrusor contraction |
| Pilocarpine used for | treatment of glaucoma (direct-acting cholinergic agonist) |
| Donezpil used for | Alzheimer's (is an anticholinesterase, or indirect-acting cholinergic agonist) |
| INDIRECT cholinergic AGONISTS used for | Commonly used to prolong the "lifetime" of Ach (because they inhibit ACh-ase, the enzyme the "terminates the action of" ACh) |
| Used to treat organophosphate poisoning | Atropine (blocks the effects of excess ACh) + Pralidoxime (re-activates ACh by hydrolyzing the PO4 bond) |
| Effects of cholinergic antagonists | Dilated pupils (mydriasis) and thus blurry vision (cycloplegia), lack of sweat, flushing, reduced GI motility, reduced secretions, increased HT rate, BRONCHODILATION, urinary retention. "Drowsiness, hallucinations, coma!!" |
| Side-effects of cholinergic antagonists | DRYNESS (eyes, mouth, large intestine), urinary retention, (blurred vision) |
| Classification of cholinergic antagonists | muscarinic antagonists (EVERY DRUG BUT Succinylcholine), neuromuscular blockers (Succinylcholine), (ganglion blockers) |
| Atropine used for | (besides as part of antidote duo for poisoning with Irreversible ACh-ase inhibitors?) Treatment of Parkinson's, pre-anesthetic (prevents bronchial secretions), ENURESIS, severe bradycardia (very slow heart) |
| Scopolamine used for | as transdermal patch to prevent motion sickness |
| Ipratropium used for | for COPD (to produce bronchodilation) |
| Dicyclomine used for | for IBS (to decrease intestinal motility) |
| Succinylcholine used for | for rapid onset skeletal muscle relaxation, just before tracheal intubation (threatened respiratory failure, prep for surgery, brain injury) |
| What happens when you stimulate alpha-1 adrenoreceptor? | vasoconstriction, increased BP, mydriasis, bladder spinchter contraction |
| What happens when you stimulate beta-1 adrenoreceptor? | tachycardia, increased myocardial contractility, (increased lipolysis) |
| What happens when you stimulate beta-2 adrenoreceptor? | vasodilation, BRONCHODILATION, relaxed uterine smooth muscle |
| Epinephrine used for | OTC spray for "intense asthma," also anaphylactic shock (the only Direct Sympathomimetic that binds to ALL FOUR adrenoreceptors) |
| Dobutamine used for | "Drug of choice to stimulate heart" (beta-1 receptor) |
| Albuterol used for | (long-acting, slow onset) bronchodilator for chronic asthma (beta-2) |
| Methylphenidate used for | aka Ritalin, ADHD and narcolepsy (Along with amphetamine & dextroamphetamine (Dexedrine), methylphenidate is the only Indirect Acting Sympathomimetic on our list!) |
| Drug used to treat urinary problems in BPH | Tamsulosin (alpha-1a adrenergic antagonist) |
| Drug used to treat hypertensive episode of pheochromocytoma | Phenoxybenzamine (alpha-1 and alpha-2 adrenergic antagonist) |
| Non-selective beta blockers used for | HTN!! |
| Contraindication of non-selective beta blockers | ASTHMA (since they antagonize beta-2 as well as beta-1) |
| Example of selective beta blockers | Metoprolol, Atenolol |
| Uses of selective beta blockers | MI and AP as well as HTN |
| Example of using MIXED alpha and beta blockers in HTN | Labetalol + Carvedilol |
| Advantage of using MIXED alpha and beta blockers in HTN | no "reflex tachycardia" |
| Why beta-blockers "used with caution" in diabetic patients? | Beta receptors (esp. beta-2) are responsible for increasing glycogenolysis, "thereby increasing blood sugar in response to hypoglycemia. ("Reflex increase in HT rate," to lower blood sugar, is also blocked, so prompt dx can be delayed.) |
| Effect of botulism poison on ACh | Inhibits acetylcholine release, thus interferes with nerve impulses and causes flaccid (paralysis of) muscles-- and thus fewer wrinkles |
| Effect of spider venom on ACh | (once again, his answer seems simplistic. Only certain spiders' venom acts via ACh system:) Widow spider venom contains latrotoxins, which cause the release of ACh, stimulating muscle contractions, causing painful abdominal cramps, labored respiration. |
| Effect of reserpine on norepinephrine | depletes it from peripheral sympathetic nerve endings (thereby slowing heart rate, lessening force of cardiac contraction and peripheral resistance) |
| Effect of cocaine on norepinephrine | blocks reuptake of norepinephrine (as well as serotonin and dopamine, in "pre-synaptic terminals") |
| Effect of imipramine on norepinephrine | (so bizarre he's asking us about a tricyclic antidepressant. who uses them anymore??) The entire class (clumsily) blocks reuptake of norepinephrine as well as serotonin. |
| Carbidopa MOA (in Parkinson's) | (REPLACEMENT) used as adjunctive therapy (with L-dopa) b/c it slows the decarboxylation ("peripheral biotransformation") of L-dopa (in peripheral tissues), allowing for much lower dose of L-dopa |
| Selegiline MOA (in Parkinson's) | (REPLACEMENT) inhibits MAO-B (MAO-B "metabolizes" dopamine in the CNS, therefore inhibiting MAO-B would presumably help maintain levels of dopamine (in substantia nigra?) |
| Bromocyrptine MOA (in Parkinson's) | POWERFUL DOPAMINE RECEPTOR AGONIST |
| Amantidine MOA (in Parkinson's) | (REPLACEMENT) enhances the synthesis, release and reuptake (??) of dopamine |
| MOA of benzos | Bind to GABA receptor, resulting in MORE FREQUENT OPENING of Cl- channels |
| MOA of barbituates | Bind to GABA receptor, resulting in LONGER DURATION OF OPENING of Cl- channels |
| Withdrawal sx of benzos | "Confusion, anxiety (surprise), agitation, restlessness (surprise) |
| Diazepam used for | (LONGISH HALF-LIFE) Muscle spasms, spasticity from MS or cerebral palsy. And of course, anxiety. |
| Alprazolam used for | (SHORT HALF-LIFE, but faster to act) aka Xanax. PANIC ATTACKS (anxiolytic, "anti-depressant" but not really!) |
| Flumazenil used for | benzo OD (it is a competitive benzodiazepine receptor antagonist) |
| Buproprion (Wellbutrin) used for | Shahid says GAD (only the extended release, "XL," though!) It is more commonly used, in tiny doses to reduce sexual side-effects of SSRIs. As Zyban it is used, at 3x the antidepressant dose, for smoking cessation.) |
| MOA of local anesthetics | they block Na+ channels in the nerve membrane |
| What happens when epinephrine is added to local (topical) anesthetics? | Since epinephrine (an adrenergic agonist) causes VASOCONSTRICTION, the "loss" of the effect of topical anesthetic progresses more slowly into BV-- thereby prolonging anesthetic effect. |
| Therapeutic uses of lidocaine (give 2) | (other than skin/muscle anesthetic?) "Used IV for ventricular arrhythmia; also, for refractory cases of status epilepticus |
| Classes of antidepressant drugs. Which class is most often used today? | SSRI, tricyclic (TCA), MAO inhibitors, SNRIs. (SSRIs are still most commonly used, but SNRIs are quickly gaining ground!) |
| SSRI MOA | Duh. Blocks reuptake of serotonin (in synaptic cleft?) |
| Possible AE for Prozac (fluoxetine)? | suicidal ideation (This is actually a concern with ALL SSRIs/SNRIs. In 2004, FDA slapped a Black Box warning on them due to this risk-- most pronounced in persons <24 years of age—and during the first 2-3 weeks of treatment. |
| MOA for TCAs | they block reuptake of both serotonin and norepinephrine |
| Potential side-effects for TCAs | dry mouth, dry nose, blurry vision, lowered gastrointestinal motility or constipation, urinary retention, cognitive and/or memory impairment, and increased body temperature |
| Which TCA is used for OCD? | clomipramine |
| What is the danger of eating tyramine-rich foods while taking MAO inhibitors | People taking MAO inhibitors are unable to metabolize ("inactivate") tyramine. "This causes release of norepinephrine," which can lead to HYPERTENSIVE CRISIS and cardiac arrhythmia. |
| How does MAO inhibitor cause hypertensive crisis in presence of tyramine rich foods? | when the catabolism of exogenous tyramine is prevented, this amino acid is absorbed and DISPLACES norepinephrine from sympathetic nerve ending and epinephrine from the adrenal glands. |
| Lithium used for | (the mania side of) bi-polar disorder |
| Precautions for use of lithium | narrow therapeutic window (in his/the textbook's speak: LOW therapeutic index, which I find less helpful :) |
| Potential AEs of lithium | HYPOthyroidism, nephrogenic diabetes insipidus (KD fails to respond to ADH) |
| Classification of neuroleptics | Typical & Atypical |
| MOA for typical neuroleptics | Block dopamine, muscarinic cholinergic, alpha-adrenergic, and H1-histaminergic receptors. (ALL produce extrapyrimidal effects caused by the blocking of dopamine receptors in the basal ganglia (striatum).) |
| Extrapyrimidal effects of typical neuroleptics | DYSTONIA (muscle spasms), AKATHISIA (motor restlessness), TARDIVE DYSKINASIA (ip smacking, jaw movements, darting of tongue!!), PARKINSONISM (tremor, rigidity, shuffling gate!!) |
| Chlorpromazine used for | aka Thorazine, neuroleptic drug (schizophrenia/psychosis) "also used to treat nausea, vomiting, and hiccups" |
| Haloperidol used for | Tourette's, Huntington's |
| MOA of atypical antipsychotic meds (He says he asked "action" not MOA) | (Minimum of extrapyrimidal effects). They address the lows (negative symptoms: withdrawal, flat affect, anhedonia) as well as the high highs (positive symptoms: agitation, disordered thought, delusions, hallucinations) |
| Advantages of using atypical antipsychotic meds | (Minimum of extrapyrimidal side-effects ("EPS")). They address the lows (negative symptoms: withdrawal, flat affect, anhedonia) as well as the high highs (positive symptoms: agitation, disordered thought, delusions, hallucinations) |
| Potential side-effects of clozapine | severe agranulocytosis (weekly WBC indicated) |
| Precautions taken when administering clozapine | (didn't he just ask this?): severe agranulocytosis |
| Cause of neuroleptic malignant syndrome | NMS is a rare, potentially fatal neurologic side-effect of antipsychotic meds |
| Symptoms of neuroleptic malignant syndrome | F_A_L_T_E_R: fever, altered mental status/fluctuating BP, leukocytosis, tremor, elevated CPK, rigidity of muscles |
| Treatment of neuroleptic malignant syndrome | bromocryptine (dopamine AGonist) or dantrolene (MOA uncharacterized) |
| Narcotic (definition) | drugs that act on the Mu, Kappa, and/or Delta receptors in the CNS to reduce pain perception |
| Classification of narcotic drugs | 1) Full/strong agonist, 2) Moderate agonist, 3) Mixed agonist-antagonist, 4) Antagonist, ( 5) "Other" ) |
| Danger of using MIXED GROUP narcotics during withdrawal from a STRONG AGONIST | B/c mixed agonists-antagonists are PRIMARILY ANTAGONISTS, they may show "primarily blocking effects" in patients with opioid dependence, and produce withdrawal sx. |
| Example of opioid antagonists | Naloxone, Naltrexone. |
| Uses of opioid antagonists | Naloxone is the DRUG OF CHOICE for EMERGENCY CASES OF NARCOTIC OVERDOSE. (Naltrexone is used, oddly enough, more for ETOH dependence than for opiate dependency-- and is also used to counter the constipating effects of morphine and codeine.) |
| Actions of morphine on CNS | "drowsiness & sedation" and "reduction in awareness of pain" (initial doses may cause nausea, due to stimulation of the chemoreceptor trigger zone in the medulla oblongata & "an increase in vestibular sensitivity") |
| Actions of morphine on eye | pin point pupil (circular muscle contracts) |
| Actions of morphine on respiration | "respiratory suppression" (can be dramatic, can lead to death at high doses--and is used for this purpose in terminally ill patients) |
| Actions of morphine on CV system | "no major effect" |
| Actions of morphine on GI tract | constipation ("increased resting tone of smooth muscle"), less commonly, spasm |
| Actions of morphine on GU system | urinary retention (similar to GI: increased resting tone & spasm of smooth muscle) |
| Narcotic withdrawal symptoms | "autonomic hyperactivity"= diarrhea, vomiting, chills, fever, tearing, runny nose. ALSO: tremor, abdominal cramps, pain (may be severe) |
| MOA of phenytoin | blocks "voltage gated" Na+ channels (by selectively binding to the channel) |
| Possible AEs of phenytoin | gingival hypertrophy !!! and megaloblastic anemia (a macrocytic anemia with larger-than-normal red blood cells) |
| Drug(s) of choice in tonic-clonic seizure | Phenytoin, Carbamazepine, (three others not in bold) |
| Drug(s) of choice in "absence" seizure | Ethsuximide (good luck with that!) |
| Drug(s) of choice in myoclonic seizure | Valproic acid (actually has many uses: as an anticonvulsant and mood-stabilizing drug, primarily in the treatment of epilepsy, bipolar disorder, and, less commonly, major depression. It is also used to treat migraine headaches and schizophrenia) |
| Drug(s) of choice in febrile seizure (usually children <8 years old) | VALIUM!!!! (diazepam) Give the febrile seizing child some Valium!! |
| Drug(s) of choice in "status epilepticus" seizure | More Valium!!! (and Phenytoin-- which is also drug of choice, at least according to this 10-year old curriculum, for tonic-clonic (along with carbamazepine)) |
| MOA of H2-receptor antagonists | they block H2 receptors (responsible for acid secretion in stomach) (Remember for comps... H1 receptors govern "itchiness"; H2, acid secretion) |
| Examples of H2-receptor antagonists | All the old, wildly advertised antacid medications: Tagamet, Zantac, Pepcid: cimetidine, ranitidine, famotidine |
| MOA of PPI | They inhibit H+-K+-ATPase enzyme (the "proton pump" in the stomach) of the parietal lumen, thereby suppressing secretion of H+ ions into the gastric lumen. (Say that ten times fast.) |
| Examples of PPIs | The blockbusters of yore!!: Prilosec, Prevacid, NEXIUM, etc.: Omeprazole, Lansoprazole, Esomeprazole (respectively) |
| Misoprostol is used for what? (in GI tract) | used for prevention of ulcers in people who take alot of aspirin and other NSAIDS (increases HCO3 and mucin release; inhibits acid secretion) |
| Important potential AE of misoprostol | THREATENED MISCARRIAGE/expulsion of fetus (apparently can cause uterine contractions). Also diarrhea. |
| MOA of diphenoxylate (+ atropine) | Diphenoxylate is an agonist of opiate receptors (thus producing the constipation effects of opiates). Atropine blocks muscarinic receptors. (Which I guess means favoring the S over the PS response-- and thus intestinal immotility vs. motility.) |
| MOA of bismuth subsalicylate | aka Pepto-Bismol!! "Adsorbs [sic] toxins produced by bacteria and other GI irritants" |
| Drugs used for treatment of ulcerative colitis and Crohn's disease (he does not differentiate between the two, at least in terms of treatment) | Mesalamine, Sulfasalazine, INFLIXImAb |
| MOA for Infliximab | It binds to and thus blocks tumor necrosis factor-alpha (TNF-a), a proinflammatory cytokine |
| Infliximab used for? | severe Crohn's refractory to first- and second-line therapies |
| Names of important laxatives/cathartics | Dulcolax= bisacodyl (also cascara, senna, phenolphthalein (Ex Lax) |
| Anti-emetic drugs | He lists 3 classes: antihistamine antiemetics (who knew?), dopamine antagonist antiemetics (!!), and serotonin antagonists (not to be confused with SSRIs!): Meclizine is in 1st group. Chlorpromazine and Metoclopramide are in 2nd. Dolastetron is in 3rd. |
| MOA for serotonin antagonist anti-emetic agents | inhibits the action of serotonin (at the 5-HT3 receptor) in the small bowel, vagus nerve, and chemoreceptor trigger zone |
| Amphetamine, methamphetamine, dextroamphetamine (75% of Adderall), and methylphenidate (Ritalin) | Indirect-Acting Sympathetic Agonists (Sympathomimetics) used as recreational stimulants to induce euphoria and may be used as a study aid, social aid or party drug |
| Common side-effects of TCAs | Many antimuscarinic side effects are relatively common and may include dry mouth, dry nose, blurry vision, lowered gastrointestinal motility or constipation, urinary retention, cognitive and/or memory impairment, and increased body temperature. |
| Examples of anti-emetic drugs | Meclizine, Chlorpromazine and Metoclopramide, Dolastetron. |
| Competitive antagonism | 2 drugs compete for same receptor(s) |
| Non-competitive antagonism | 1 drug causes a change in shape of the binding site ("conformational change") so that the other drug cannot bind well or at all |
| Physiologic antagonism | 2 drugs ("agonists") with opposite effects canceling each other out |
| Antagonism by neutralization | 2 drugs fall in love & mate & forget what they were supposed to be doing. |
| What is resperine (class)? | inhibits the uptake of norepinephrine (into storage vesicles), "resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals" |
| What does resperine do/what is it used for ? | an antipsychotic and antihypertensive drug used for the control of high blood pressure and the relief of psychotic symptoms, although ... it is rarely used today |
| What is clomipramine (class)? | it is a TCA, developed in the 1960s!! |
| What is clomipramine and what is (or was) it used for? | it is useful in treating OCD, but is really only used 2nd or 3rd line these days-- after SSRIs have failed |
Created by:
mrbarr
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