Drugs - First Aid 2014 Flashcards

Question

What is Calcium carbonate?

Answer 1

Antacid. Causes hypercalcemia, rebound acid increase, constipation. Can chelate and decrease effectiveness of other drugs (e.g. tetracycline)

Answer 2

Antacid. Causes diarrhea, hyporeflexia, hypotension, cardiac arrest. Think magnesium and diarrhea. Magnesium salts will do this in general.

Answer 3

Provides osmotic load to draw water out. Lactulose also treats hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+. Clinical use: constipation Toxicity: diarrhea, dehydration; may be abused by bulimacs.

Answer 4

monoclonal antibody to TNFalpha. Clinical use: Crohn disease, ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis, psoriasis. Toxicity: infection (including reactivation of latent TB), fever, hypotension

Answer 5

A combination of sulfapyridine (anti-bacterial) and 5-aminosalicylic acid (anti-inflammatory). Activated by colonic bacteria. Clinical use: Ulcerative colitis, Crohn disease Toxicity: Malaise, nausea, sulfonamide toxicity, reversible oligospermia.

Answer 6

It is a 5-HT3 antagonist; decreased vagal stimulation. Powerful central-acting antiemetic. Clinical use: Control vomiting postoperatively and in patients undergoing cancer chemotherapy. Toxicity: Headache, constipation. Note: all -etron drugs are serotonin antagonists useful for anti-emetic purposes. e.g. granisetron and dolasetron.

Answer 7

It is a D2 receptor antagonist. Increased resting tone, contractility, LES tone, motility. Does not influence colon transport time. Clinical use: diabetic and post-surgery gastrparesis, antiemetic. Toxicity: increased parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea, diarrhea. Drug interaction with digoxin and diabetic agents. Contraindicated in patients with small bowel obstruction or Parkinson disease (D1-receptor blockade) Note: another prokinetic drug is erythromycin (that's why it has GI mobility side effects!)

Answer 8

Epinephrine (alpha-1): Decreased aqueous humor synthesis via vasoconstriction. Toxicity: Mydriasis and do not use in closed angle glaucoma. Brimonidine (alpha-2): Decreased aqueous humor synthesis (inhibit cAMP production and thus less secretion). Toxicity: Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis.

Answer 9

decrease IOP by decreasing amount of of aqueous humor. (by inhibiting synthesis/secretion or increasing drainage).

Answer 10

Timolol, betaxolol, carteolol. Decreased aqueous humor synthesis. Toxicity: no pupillary or vision changes.

Answer 11

Acetazolamide. Decreased aqueous humor synthesis via inhibition of carbonic anhydrase. Toxicity: no pupillary or vision changes.

Answer 12

Direct: pilocarpine, carbachol. Increased outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork. Toxicity: miosis, and cyclospasm (contraction of ciliary muscle). Use pilocarpine in emergencies- very effective at opening meshwork into canal of Schlemm. Indirect: physostigmine (reversible), echothiophate (irreversible).

Answer 13

Latanoprost (PGF2alpha). | Toxicity: darkens color of iris (browning).

Answer 14

Opioid analgesics. Act as agonists at opioid receptors (mu = morphine, delta = enkephaline, kappa = dynorphin) to modulate synaptic transmission - open K+ channels, close Ca+2 channels. Decreased synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P. Clinical use: pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (methadone). Toxicity: addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

Answer 15

Mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia. Clinical use: severe pain (migraine, labor, etc). Causes less respiratory depression than full opioid agonists. Toxicity: can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors). Overdose not easily reversed with naloxone.

Answer 16

Very weak opioid agonist; also inhibits serotonin and norepinephrine reuptake (works on multiple neurotransmitters). Clinical use: chronic pain Toxicity: similar to opioids. Decreases seizure threshold. Serotonin syndrome.

Answer 17

Treating generalized absence seizures. Mech: blacks thalamic T-type Ca+2 channels. Side effects: EFGHIJ Ethosouximide causes Fatigue, GI distress, Headache, Itching, Stevens-Johnson syndrome

Answer 18

Diazepam, Lorazepam. Used for first-line acute generalized status epilepticus. Increases GABA-A action. Side effects: Sedation, tolerance, dependence, respiratory depression. (Also for eclampsia seizures, but 1st line is MgSO4).

Answer 19

First line in generalized tonic-clonic and prophylaxis in status epilepticus. Also used for partial simple and complex seizures. Increased Na+ channel inactivation zero-order kinetics. Side effects: nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy (from B6 deficiency), megaloblastic anemia, teratogenesis (fetal hydantoin syndrome), SLE-like syndrome, induction of cytochrome P450, lymphadenopathy, Stevens-Johnson syndrome, osteopenia. Fosphenytoin for parenteral use. FLOG MASSH

Answer 20

First line for partial simple and complex seizures and generalized tonic-clonic seizures. Increased sodium channel inactivation. Side effects: diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P450, SIADH, Stevens-Johnson syndrome.

Answer 21

First line for generalized tonic-clonic. Otherwise used for partial simple and complex seizures and generalized absence. Increased sodium channel inactivation and increased GABA concentration by inhibiting GABA transaminase. Side effects: GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain, contraindicated in pregnancy. Also for myoclonic seizures and bipolar disorder.

Answer 22

Used for partial simple and complex seizures and generalized tonic-clonic seizures. Primarily inhibits high-voltage-activated Ca+2 channels; designed as GABA analog. Side effects: sedation, ataxia. Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder.

Answer 23

Used for partial simple and complex seizures and generalized tonic-clonic seizures. Increased GABA-A action. Side effects: sedation, tolerance, dependence, induction of cytochrome P450, cardiorespiratory depression. 1st line in neonates.

Answer 24

Used for partial simple and complex seizures and generalized tonic-clonic seizures. Blocks sodium channels, increased GABA action. Side effects: sedation, mental dulling, kidney stones, weight loss. Also used for migraine prevention.

Answer 25

Used for partial simple and complex seizures and generalized tonic-clonic and absence seizures. Blocks voltage-gated sodium channels. Side effects: Stevens-Johnson syndrome.

Answer 26

Used for partial simple and complex seizures and generalized tonic-clonic seizures. Unknown mech; may modulate GABA and glutamate and release.

Answer 27

Used in partial simple and complex seizures. | Increased GABA by inhibiting re-uptake.

Answer 28

Used in partial simple and complex seizures. | Increased GABA by irreversibly inhibiting GABA transaminase.

Answer 29

Prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital). Skin lesions progress to epidermal necrosis and sloughing.

Answer 30

``` Inducers: Chronic alcohol use Modafinil St. John's wort Phenytoin Phenobarbital Nevirapine Rifampin Griseofulvin Carbamazepine ``` Mnemonic: chronic alcohol Mona steals phen-phen and never refuses greasy carbs.

Answer 31

``` Inhibitors: Acute alcohol abuse Gemfibrozil Ciprofloxacin Isoniazid Grapefruit juice Quinidine Amiodarone Ketoconazole (all azoles: fluconazole, itraconazole, voriconazole) Macrolides Sulfonamides Cimetidine Ritonavir ``` A cute gentleman Cipped iced Grapefruit juice quickly and kept munching on soft cinammon rolls

Answer 32

Probenecid, Furosemide, Acetazolamide, Celecoxib, Thiazides, Sulfonamide antibiotics, Sulfasalazine, Sulfonylureas. Patients with sulfa allergies may develop: fever, urinary tract infection, Stevens-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis, and urticaria (hives).

Answer 33

Phenobarbital, pentobarbital, thiopental, secobarbital. Facilitate GABA-A action by increased duration of Cl- channel opening thus decreasing neuron firing (barbidurates increase duration). Contraindicated in porphyria. Clinical USE: Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental). Toxicity: respiratory and CV depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence; drug interactions (induces cytochrome P-450). Overdose treatment is supportive (assist respiration and maintain BP).

Answer 34

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chloridazepoxide, alprazolam. Facilitate GABA-a action by increased frequency of Cl- channel opening. Decreases REM sleep. Most have long half-lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting -> higher addictive potential). Clinical USE: Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia). Toxicity: Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzo receptor). Frenzodiazepines increased frequency. Benzos, barbs, and EtOH all bind GABA-a receptor

Answer 35

Zolpidem (Ambien), Zaleplon, esZopiclone. All ZZZs put you to sleep. Act via the BZ1 subtype of GABA receptor. Effects reversed by flumazenil (competitive antagonist at GABA benzo receptor). Clinical USE: Insomnia. Toxicity: Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Decreased dependence risk than benzodiazepines.

Answer 36

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide. Mechanism unknown Effects: myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand). Toxicity: Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas in a body cavity (nitrous oxide). Malignant hyperthermia: rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions. Tx: dantrolene.

Answer 37

Thiopental-high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue (i.e. skeletal muscle) and fat. Decreased cerebral blood flow.

Answer 38

Midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decreased BP (treat overdose with flumazenil), and anterograde amnesia.

Answer 39

PCP analog that act as dissociative anesthetics. Block NDMA receptors (non-competitive antagonist of glutamate binding). CV stimulants. Cause disorientation, hallucination, and bad dreams. Increased cerebral blood flow.

Answer 40

Morphine, fentanyl used with other CNS depressants during general anesthesia.

Answer 41

Used for sedation in ICU, rapid anesthesia induction, and short procedures. Less postoperative nausea than thiopental. Potentiates GABA-A.

Answer 42

Esters - procaine, cocaine, tetracaine

Answer 43

lidocaine, mepivacine, bupivacaine, (amides have two I's in them)

Answer 44

Mechanism: Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion chanels as charged form. Principle: can be given with vasoconstrictors (usually epinephrine) to enhance local action - decreased bleeding, increased anesthesia by decreased systemic concentration. In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively -> need more anesthetic. Order of nerve blockade: small-diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers. Order of loss: 1. pain 2. temperature 3. touch 4. pressure. Clinical use: minor surgical procedures, spinal anesthesia. If allergic to esters, give amides. Toxicity: CNS excitation, severe CV toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine).

Answer 45

Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

Answer 46

Succinylcholine - strong Ach receptor agonist; produces sustained depolarization and prevents muscle contraction. Reversal blockade: Phase 1 (prolonged depolarization): no antidote. Block potentiated by cholinesterase inhibitors. Phase 2 (repolarized but blocked; ACh receptors are available, but desensitized): antidote consists of cholinesterase inhibitors. Complications include hypercalcemia, hyperkalemia, and malignant hyperthermia.

Answer 47

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium - competitive antagonists - compete with ACh for receptors. Reversal of blockade: neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.

Answer 48

prevents the release of Ca+2 from the sarcoplasmic reticulum of skeletal muscle. Clinical use: used to treat malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).

Answer 49

Bromocriptine (ergot), pramipexole, ropinirole (non-ergot); non-ergots are preferred.

Answer 50

Amantadine (may increase dopamine release); also used as an antiviral against influenza A and rubella; toxicity = ataxia. L-dopa/carbidopa (converted to dopamine in CNS). Carbidopa is a peripheral decarboxylase inhibitor.

Answer 51

Selegiline (selective MAO type B inhibitor); entacopone, tolcapone (COMT inhibitors- prevent L-dopa degradation -> increased dopamine availability)

Answer 52

Benztropine (antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia.

Answer 53

increased level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine. Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa to increase the bioavailabity of L-dopa in the brain and to limit peripheral side effects. Clinical use: Parkinson disease. Toxicity: arrhythmias from increased peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration (on-off phenomonen), akinesia between doses.

Answer 54

Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, thereby increased availability of dopamine. Clinical use: adjunctive agent to L-dopa in treatment of Parkinson disease. Toxicity: may enhance adverse effects of L-dopa.

Answer 55

NDMA receptor antagonist; help prevent excitotoxicity (mediated by Ca+2 ) Toxicity: dizziness, confusion, hallucinations. ``` From wiki: The drug belongs to a class of drugs called NMDA receptor antagonists, which reduce certain types of brain activity by binding to NMDA receptors on brain cells and blocking the activity of the neurotransmitter glutamate. At normal levels, glutamate aids in memory and learning, but if levels are too high, glutamate appears to overstimulate nerve cells, killing them through excitotoxicity. ```

Answer 56

They are AChE inhibitors and are used for Alzheimer. | Toxicity: nausea, dizziness, insomnia.

Answer 57

Neurotransmitter changes in Huntington disease: decreased GABA, decreased ACh, increased dopamine. Tx: Tetrabenazine and reserpine: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release. Halperidol-dopamine receptor antagonist.

Answer 58

It's a 5-HT-1B/1D agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release (can result in vasodilation and headaches); induces vasoconstriction. Half-life <2 hours. Clinical USE: acute migraine, cluster headache attacks. Toxicity: coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild tingling.

Answer 59

Dimercaprol - Arsenic, Mercury, Lead Pencillamine - copper toxicity, (also gold, arsenic, lead) CaNA2 - EDTA - lead poisoning Dimercaptosuccinic acid - lead poisoning Deferoxamine/Deferasirox - acute iron poisoning and overload

Answer 60

BLock voltage-dependent L-type Calcium channels of cardiac/smooth muscle, thereby reducing contractility Toxicity: cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation.

Answer 61

Vascular smooth muscle: amlodipine = nifedipine > diltiazem > verapamil Except for Nimodipine the Dihydropyridines are used for hypertension, angina (including Prinzmetal), and Raynaud's Nimodipine used for Subarachnoid hemorrhage (prevents cerebral vasospasm).

Answer 62

Heart- verapamil > diltiazem > amlodipine = nifedipine | Non-dihydropyridine used for hypertension, angina, atrial fib/flutter.

Answer 63

increases cGMP -> smooth muscle relaxation -> Vasodilates arterioles more than veins. Reduces afterload. Clinical use: severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa. Frequently co-administered with a Beta-blocker to prevent reflex tachycardia. Toxicity: compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina. Lupus-like syndrome.

Answer 64

nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam,

Answer 65

short acting; increased cGMP via direct release of NO. can cause cyanide toxicity.

Answer 66

Dopamine D1 receptor agonist - coronary, peripheral, renal, and splanchnic vasodilation. Decreased BP and Increased natriuresis.

Answer 67

Vasodilate by increased NO in vascular smooth muscle by increased cGMP and smooth muscle relaxation. Dilates veins more than arteries so decreased preload. Clinical use: Angina, acute coronary syndrome, pulm edema. Toxicity: Reflex tachycardia (treat with Beta blockers), hypotension, flushing, headache. Monday disease is due to loss of tolerance over the weekend such that these toxic symptoms occur on Monday with tachycardia, dizziness, and headache on re-exposure.

Answer 68

Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin. Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor. Decreases LDL the most with slight decrease in TGs and slight increase in HDL. Toxicity: Hepatotoxicity (increased LFTs), rhabdomyolysis (esp when used with fibrates and niacin).

Answer 69

Vitamin B3. It inhibits lipolysis in adipose tissues and reduces hepatic VLDL synthesis. Decreases LDL and increases HDL and slightly decreases TG. Toxicity: Red, flushed face, which is decreased by aspirin or long-term use. Hyperglycemia (aconthosis nigricans). Hyperuricemia (exacerbates gout).

Answer 70

Cholestyramine, colestipol, colesevelam Decreased LDL and slightly increased HDL/TGs. Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more (thus increasing LDL receptors and taking LDL into the liver from the blood). Toxicity: Patients hate it - tastes bad, causes GI discomfort, decreased absorption of fat soluble vitamins.

Answer 71

Ezetimibe Decreased LDL and no effect on HDL/TGs. Prevent cholesterol absorption at small intestine brush border. Rare increased LFTs, diarrhea.

Answer 72

Gemifibrozil, clofibrate, bezafibrate, fenofibrate Bigg decrease in TGs and decrease in TGs and increase in HDL. Upregulate LPL -> increased TG clearance. Activates PPAR-alpha to induce HDL synthesis. Toxicity: Myositis (increased risk with concurrent statins), hepatotoxicity (increased LFTs), cholesterol gall stones (suppresses cholesterol 7alpha-hydroxylase, especially with concurrent bile acid resins).

Answer 73

Digoxin (75% bioavailabiity, 20-40% protein bound). Long half life at 40 hrs by urine. Direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger/antiport. Increased Ca+2 leads to positive inotropy. Stimulates vagus nerve leading to decreased HR. Uses: CHF (increased contractility); atrial fib (decreased conduction at AV node and depression of SA node). Toxicity: Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh). ECG - increased PR interval, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block. Can lead to hyperkalemia, which indicates poor prognosis. Factors predisposing to toxicity - renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+-binding site on Na/K ATPase), verapamil, amiodarone, quinidine (decreased digoxin clearance; displaces digoxin from tissue binding site). Antidote: slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg+2.

Answer 74

Slow conduction in depolarized cells, decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells. State dependent: affects most frequently depolarizing cells Hyperkalemia increases toxicity because it leaves cells partially depolarized and so more sodium channels will be inactivated. Putting a Class 1 on top of this will make the situation even worse.

Answer 75

Disopyramide, Quinidine, Procainamide, Double Quarter Pounder. Increases AP duration, Increases effective refractory period, increases QT interval. Uses: Atrial/ventricular arrhythmias, especially re-entrant and ectopic SVT and VT. Toxicity: heart failure (disopyramide), Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), thrombocytopenia, torsades de pointes due to increased QT interval.

Answer 76

Lidocaine, Phenytoin, Mexiletine Lettuce, Pickles, Mayo Decreased AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Uses: Acute ventricular arrhythmias (especially post MI), digitalis-induced arrhythmias. 1B is Best for post-MI. Toxicity: CNS stimulation/depression, CV depression.

Answer 77

Flecainide, Propafenone Fries with that Please. Significantly prolongs refractory period in AV node. Minimal effect on AP duration. Uses: SVTs, including A-fib, Last resort in refractory ventricular tachycardias. Toxicity: proarrhythmic, especially post MI (contraindicated). IC is Contraindicated post MI in structural and ischemic heart tissue.

Answer 78

Metoprolo, propranolol, esmolol, atenolol, timolol, carvedilol. Decrease SA/AV nodal activity by decreased cAMP, decreased Ca+2 activity. Suppresses abnormal pacemakers by decreased slope 4. AV node particularly sensitive. Increased PR interval. Esmolol very short acting. Uses: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter. Toxicity: Impotence, exacerbation of COPD and asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask signs of hypoglycemia. Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in Prinzmetal angina. Contraindicated in cocaine users (risk of unopposed alpha-adrenergic receptor agonist activity). Treat overdose with glucagon.

Answer 79

Amiodarone, Ibutilide, Dofetilide, Sotalol. AIDS K+ channel blockers Increased AP duration, increased effective refractory period. Used when other anti-arrhythmics fail. Increased QT interval. Uses: Atrial Fib, atrial flutter, ventricular tachycardia (amiodarone, sotalol). Toxicity: Sotalol - torsades de pointes, excessive Beta blockade. Ibutilide - torsades de pointes. Amiodarone - pulmonary fibrosis, hepatoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/grey) resulting in photodermatitis, neurologic defects, constipation, CV effects (bradycardia, heart block, CHF). ``` Must check PFTs, LFTs, TFTs, when using amiodarone. Amiodarone has class I, II, III, IV effects and alters lipid membrane. ```

Answer 80

Verapamil, diltiazem. Calcium channel blockers. Decreased conduction velocity, increased effective refractory period, increased PR interval. Uses: Prevention of nodal arrhythmias (e.g. SVT), rate control in atrial fib. Toxicity: Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression). Verapamil has gingival hyperplasia.

Answer 81

Increased K+ out of cells -> hyperpolarizing cells and decreasing Calcium current. Can be used for slowing HR in nodal cells. Drug of choice in diagnosing/abolishing SVT. Very short acting (15 seconds). Adverse effects include flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.

Answer 82

Effective in torsades de pointes and digoxin toxicity.

Answer 83

Reversible inhibitors of H1 histamine receptors Diphenhydramine, dimenhydrinate, chlorpheniramine. Names contain en/ine or en/ate Uses: allergy, motion sickness, sleep aid. Toxicity: Sedation, antimuscarinic, anti-alpha-adrenergic.

Answer 84

Loratadine, fexofenadine, desloratadine, cetirizine. Names usually end in "adine". Uses: allergy. Toxicity: far less sedating than 1st generation because of decreased entry into CNS.

Answer 85

Guaifenesin - Expectorant: thins respiratory secretions; does not suppress cough reflex. N-acetylcysteine - Mucolytic: can loosen mucous plugs in CF patients. Also used as an antidote for acetaminophen overdose.

Answer 86

Antitussive (suppresses cough by antagonizing NMDA glutamate receptors). Synthetic codeine analog. Has mild opioid effect when used in excess. Naloxone can be given for overdose. Mild abuse potential.

Answer 87

Sympathomimetic alpha-agonistic nonprescription nasal decongestants. Use: Reduce hyperemia, edema, and nasal congestion. open obstructed eustachian tubes. Pseudoephedrine also illicitly used to make methamphetamine. Toxicity: hypertension. can also cause CNS stimulation/anxiety (psuedophedrine).

Answer 88

Albuterol - relaxes bronchial smooth muscle (Beta-2). Use during acute exacerbation. Salmeterol, formoterol - long-acting agents for prophylaxis. Adverse effects are tremor and arrhythmia.

Answer 89

Theophylline - likely causes bronchodilation by inhibiting phosphodiesterase -> increases cAMP levels due to decreased cAMP hydrolysis. Usage limited because of narrow therapeutic index (cardiotoxicity, neurotoxicity); metabolised by cytochrome P-450. Blocks actions of adenosine.

Answer 90

Ipratropium - competitive block of muscarinic receptors, preventing bronchoconstriction. Also used for COPD, as is tiotropium, a long-acting muscarinic antagonist.

Answer 91

Beclomethasone, fluticasone - inhibit the synthesis of virtually all cytokines. Inactivate NF-kB, the TF that induces the production of TNF-alpha and other inflammatory agents. 1st line therapy for chronic asthma.

Answer 92

Montelukast, zafirlukast - block leukotriene receptors. Especially good for aspiring induced asthma. Zileuton - a 5-lipoxygenase pathway inhibitor. Blocks conversion of arachidonic acid to leukotrienes.

Answer 93

Monoclonal anti-IgE antibody. Binds mostly unbound serum IgE and blocks binding to FceRI. Used in allergic asthma resistant to inhaled steroids and long-acting B2 agonists.

Answer 94

Muscarinic receptor agonist. Used in bronchial provocation challange to help diagnose asthma.

Answer 95

Used to treat pulmonary arterial hypertension. Competitively antagonizes endothelin-1 receptors, decreased pulmonary vascular resistance.

Answer 96

Zafirlukast, montelukast. Receptor antagonists

Answer 97

LTB4: Neutrophil chemotaxis (neutrophils arive B4 others) LTC4/LTD4/LTE4: Increased bronchial tone, vasoconstriction, contraction of smooth muscle, and increased vascular permeability.

Answer 98

Decreases platelet aggregation, vascular tone, bronchial tone, uterine tone. Platelet Gathering Inhibitor (mnemonic)

Answer 99

Increased uterine tone and decreased bronchial tone

Answer 100

Increased platelet aggregation, vascular tone, and bronchial tone.

Answer 101

Irreversibly inhibits COX1/COX2 by covalent acetylation. Decreased TXA2 and prostaglandins and increased bleeding time until new platelets are produced (about 7 days). No effect on PT/PTT. Type of NSAID. With increasing doses you get, decreased platelet aggregation, antipyretic/analgesic, and antiinflammatory actions (in order of increasing dosage) Toxicity: gastric ulceration, tinnitus (CNVIII). Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Risk of Reye syndrome in children treated with aspirin for viral infection. Also stimulates respiratory centers, causing hyperventilation and respiratory alkalosis.

Answer 102

Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac. Reversibly inhibit COX1/COX2. Antipyretic, analgesic, anti-inflammatory. Indomethacin used to close a PDA. Toxicity: interstitial nephritis, gastric ulcer (PGs protect gastric mucosa), renal ischemia (PGs vasodilate afferent arteriole).

Answer 103

Reversible inhibition of COX2. Blocks pain/inflammation but spares platelet function (TXA2 dependent on COX1). Use: Rheumatoid arthritis, osteoarthritis; patients with gastric ulcers. Toxicity: increased risk of thrombosis. Sulfa allergy.

Answer 104

Reversibly inhibits COX, mostly in CNS. Inactivated peripherally. Use: antipyretic, analgesic, but not anti-inflammatory. Used instead of aspirin to avoid Reye syndrome in children with viral infection. Toxicity: overdose produces hepatic necrosis; acetominophen metabolite (NAPQI) depletes glutathione and forms toxic tissue adducts in liver. N-acetylcysteine is antidote - regenerates glutathione.

Answer 105

Alendronate, other -dronates. Mechanism: Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity (and induces apoptosis). Use: Osteoporosis, hypercalcemia, Paget disease of bone. Toxicity: Corrosive esophagitis (patients are advised to take with water and remain upright for 30 minutes), osteonecrosis of the jaw.

Answer 106

Allopurinol: inhibits xanthin oxidase, decreases xanthine to uric acid. Also used for tumor lysis syndrome. You see increase in azothioprine and 6-MP (before xanthine oxidase). Don't give salicylates because they depress uric acid clearance. Febuxostat: inhibits xanthine oxidase. Probenecid: Inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin).

Answer 107

NSAID: naproxen, indomethacin. Glucocorticoids: oral/intra-articular Colchicine: binds and stabilizes tubulin to inhibit microtubule polymerization, impairing leukocyte chemotaxis and degranulation. Acute and prophylactic value. GI side effects.

Answer 108

Etanercept: fusion protein of TNF-alpha receptor + IgG1 FC. Decoy receptor. Use: RA, psoriasis, ankylosing spondylitis. Inflixamab/adalimumab - anti-TNF-alpha monoclonal antibody. Use: IBD, RA, psoriasis, ankylosing spondylitis. All TNF-alpha inhibitors predispose to an infection, including re-activation of TB, since TNF blockade prevents activation of macrophages and destruction of phagocytosed microbes.

Answer 109

Mechanism: GnRH analog with agonist properties when used in pulsatile function; antagonist properties when used in continuous function (downregulates GnRH receptor in pituitary leading to decreased FSH/LH). Use: infertility (pulsatile), prostate cancer (continuous - use with flutamide), uterine fibroids (continuous), precocious puberty (continuous) Toxicity: antiandrogen, nausea, vomiting Leuprolide in Lieu of GnRH

Answer 110

Ethinyl estradiol, DES, mestranol Binds estrogen receptors Use: hypogonadism or ovarian failure, menstrual abnormalities, HRT postmenopausal women; use in men with androgen-dependent prostate cancer Toxicity: increased risk of endometrial cancer, bleeding in postmenopausal women, clear cell adenocarcinoma of vagina in females exposed to DES in utero, increased risk of thrombi. Contraindications- ER positive breast cancer or history of DVTs.

Answer 111

SERM. Antagonist at estrogen receptors in hypothalamus. Prevents normal feedback inhibition and increased release of LH/FSH from pituitary, which stimulates ovulation. Used to treat infertility due to anovulation (PCOS). Toxicity: may cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, and visual disturbances.

Answer 112

Antagonist on breast tissue; agonist at uterus, bone; Associated with endometrial cancer and thromboembolic events. Primarily used to treat and prevent recurrence of ER positive breast cancer.

Answer 113

Agonist on bone; antagonist at uterus. Causes decreased resorption of bone and so is used to treat osteoporosis. Toxicity: increased risk of thromboembolic events.

Answer 114

Used for relief or prevention of menopausal symptoms(e.g. hot flashes, vaginal atrophy) and osteoporosis (it increases estrogen and decreases osteoclast activity) Unopposed estrogen replacement therapy (ERT) increases the risk of endometrial cancer, so progesterone is added. Possible increased CV risk.

Answer 115

Aromatase inhibitors used in postmenopausal women with breast cancer. Decreases estrogen production.

Answer 116

Bind progesterone receptors, decreases growth and increased vascularization of endometrium. Use: used in oral contraceptives and in treatment of endometrial cancer and abnormal uterine bleeding.

Answer 117

RU-486. Competitive inhibitor of progestins at progesterone receptors. Use: termination of pregnancy. Administered with misoprostol (PGE1). Toxicity: heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain

Answer 118

Estrogen and progestins inhibit LH/FSH and thus prevent estrogen surge. No estrogen surge means no LH surge and no ovulation. Progestins cause thickening of the cervical mucus, thereby limiting access of sperm to uterus. Progestins also inhibit endometrial proliferation, thus making endometrium less suitable for the implantation of embryo. Contraindications: smokers > 35 yrs old (increased risk of CV events), patients with history of thromboembolism and stroke or history of estrogen-dependent tumor.

Answer 119

B2-agonist that relaxes the uterus; used to decrease contraction frequency in women during labor.

Answer 120

Synthetic androgen that acts as partial agonist at androgen receptors. Use: Endometriosis and hereditary angioedema. Toxicity: weight gain, edema, acne, hirsuitism, masculinization, decreased HDL levels, hepatotoxicity. From wiki: Danazol exhibits hypoestrogenic, hyperandrogenic effects that cause atrophy of the endometrium, which can alleviate the symptoms of endometriosis. Danazol prevents ovulation by suppressing the increase of luteinizing hormone during the middle of the menstrual cycle.[4][5] Danazol inhibits ovarian steroidogenesis resulting in decreased secretion of estradiol and may increase androgens. Danazol displaces testosterone from sex hormone-binding globulin (SHBG), displacing it and increasing serum testosterone levels.[4] Danazol also directly stimulates androgen and progesterone receptors.[4]

Answer 121

Agonist at androgen receptors Use: treats hypogonadism and promotes development of secondary sex characteristics; stimulation of anabolism to promote recovery after burn or injury. Toxicity: causes masculinization in females; decreased intratesticular testosterone in males by inhibiting release of LH (via neg feedback) and resultant gonadal atrophy. Premature closure of epiphyseal plates. Increased LDL and decreased HDL.

Answer 122

5-alpha reductase inhibitor (decreased conversion of testosterone to DHT). Used in BPH. Also promotes hair growth-used to treat male pattern baldness. To prevent male pattern hair loss, give a drug that will encourage female breast growth.

Answer 123

A nonsteroidal competitive inhibitor of androgens at the testosterone receptor. Used in prostate carcinoma

Answer 124

Inhibits steroid synthesis (inhibits 17,20 desmolase) Uses: Ketaconazole and spironolactone are used in the treatment of PCOS to prevent hirsutism. Both have side effects of gynecomastia and amenorrhea.

Answer 125

Inhibits steroid binding, 17-alpha hydroxylase, and 17,20 desmolase Uses: Ketaconazole and spironolactone are used in the treatment of PCOS to prevent hirsutism. Both have side effects of gynecomastia and amenorrhea.

Answer 126

alpha-1-antagonist used to treat BPH by inhibiting smooth muscle contraction. Selective for alpha1A,D receptors (found on prostate) vs. vascular alpha1B receptors.

Answer 127

Inhibit phosphodiesterase 5, causing increased cGMP, smooth muscle relaxation in the corpus cavernosum, increased blood flow, and penile erection. SildaneFIL and vardenaFIL fill the penis. Use: treatment of erectile dysfunction. Toxicity: headache, flushing, dyspepsia, impaired blue green color vision. Risk of life threatening hypotension in patients taking nitrates. "Hot and sweaty" but then Headache, Heartburn, and Hypotension. All the Hs.

Answer 128

Penicillin G (IV/IM forms), penicillin V (oral). Prototype B-lactam antibiotics. Mechanism: bind penicillin-binding proteins (transpeptidases). Block transpeptidase cross-linking of peptidoglycan. Activate autolytic enzymes. Use: mostly used for gram-pos organisms (S. pneumoniae, S. pyogenes, Actinomyces). Also used for N. meningitidis and T pallidum. Bactericidal for gram-pos cocci, gram-positive rods, gram-negative cocci, and sphirochetes. Penicillinase sensitive. Toxicity: hypersensitivity reactions, hemolytic anemia. Resistance: pencillinase in bacteria (a type of B-lactamase) cleaves B-lactam ring.

Answer 129

Amino penicillins, penicillinase-sensitive penicillins. Mechanism: Same as penicillin. Wider spectrum; penicillinase sensitive. Also combine with clavulanic acid to protect against B-lactamase. Use: Extended spectrum penicillin - Haemophilus influenzae, E. coli, Listeria Monocytogenes, Proteus, Salmonella, Shigella, enterococci. HELPSS mnemonic. Toxicity: Hypersensitivty reactions; rash; pseudomembranous colitis. Mechanism of Resistance: Penicillinase in bacteria (a type of B-lactamase) cleaves B-lactam ring.

Answer 130

Pencillinase-resistance penicillins Mech: same as penicillin. Narrow spectrum; pencillinase resistant because bulky R group blocks access of B-lactamase to B lactam ring. Use: Staph aureus (except MRSA; resistant because of altered penicillin-binding protein target site). Use NAFcillin for staph. Toxicity: Hypersensitivity reactions, interstitial nephritis.

Answer 131

Anti-pseudomonals. Mechanism: same as penicillin, extended spectrum. Use: Pseudomonas spp. and gram-neg rods; susceptible to penicillinase; use with B-lactamase inhibitors. Toxicity: hypersensitivity reactions.

Answer 132

CAST. Include clavulanic acid, sulbactam, tazobactam. Often added to penicillin antibiotics to protect the antibiotic from destruction by B-lactamase (penicillinase).

Answer 133

B-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal. Organisms typically not covered by cephalosporins are LAME: Listeria, Atypicals (Chlamydia, Mycoplasma), MRSA, and Enterococci. Exception: ceftaroline covers MRSA. Toxicity: Hypersensitivity reactions, vitamin K deficiency. Low cross-reactivity with penicillins. Increased nephrotoxicity of aminoglycosides.

Answer 134

1st generation cephalosporins Gram positive cocci: Proteus mirabilis, E. Coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections. PEcK.

Answer 135

2nd generation cephalosporins. Gram-positive cocci: Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens. HEN PEcKS.

Answer 136

3rd generation cephalosporins. Serious gram-negative infections resistant to other B-lactams. Ceftriaxone: meningitis and gonorrhea. Ceftazidime: Pseudomonas.

Answer 137

4th generation cephalosporin | Increased activity against Pseudomonas and gram-positive organisms.

Answer 138

5th Generation cephalosporin. | Broad gram-positive and gram-negative organism coverage, including MRSA; does not cover Pseudomonas.

Answer 139

Mechanism: a monobactam; resistant to B-lactamases. Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3. Synergistic with aminoglycosides. No cross-allergenicity with penicillins. Clinical use: gram negative rods only - no activity against gram positives or anaerobes. For penicillin allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides. Toxicity: Usually non toxic; occasional GI upset.

Answer 140

Carbapenems. Imipenem is a broad-spectrum, B-lactamase-resistant carbapenem. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules. With imipenem, "the kill is lastin' with cilastatin". Use: Gram-positive cocci, gram negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed. Meropenem has a decreased risk of seizures and is stable to dehydropeptidase I. Toxicity: GI Distress, skin rash, and CNS toxicity (seizures) at high plasma levels.

Answer 141

Mechanism: Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Use: gram positive only- serious, multidrug-resistant organisms, including MRSA, enterococci, and Clostridium difficile (oral dose for pseudomembranous colitis). Toxicity: well-tolerated in general, but NOT trouble free. Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing - red man syndrome (can largely prevent by pre-treatment with antihistamines and slow infusion rate). Resistance mechanism: Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac. Pay back 2 D-alas (dollars) for vandalizing (vancomycin).

Answer 142

30S Inhibitors: Aminoglycosides (bactericidal) -block Initiation complex formation (causes misreading of mRNA) Tetracyclines (bacteriostatic) - blocks A-site tRNA binding. 50S inhibitors: Chloramphenicol (bacteriostatic) - blocks peptidyl transferase Clindamycin (bacteriostatic) - blocks translocation Erythromycin (macrolides) (bacteriostatic) - blocks translocation Linezolid (variable) - blocks binding of everything to mRNA and initiation complex. buy AT 30, CCEL at 50

Answer 143

Aminoglycosides. Mean (aMINoglycoside) GNATS caNNOT kill anaerobes. Mechanism: Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Also block translocation. Require O2 for uptake; therefore ineffective against anaerobes. Use: severe gram-negative rod infections. Synergistic with Beta-lactam antibiotics. Neomycin for bowel surgery. Toxicity: Nephrotoxicity (especially with cephalosporins), Neuromuscular blockade, Ototoxicity (especially when used with loop diuretics). Teratogen. Resistance: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.

Answer 144

Mechanism: bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration. Doxycycline is fecally eliminated and can be used in patients with renal failure. Do not take with milk (Ca+2), antacids (Ca+2 or Mg+2) or iron containing preparations because divalent cations inhibit its absorption in the gut. Use: Borrelia Burgodorferi, M. pneumoniae. Drug's ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia. Also used to treat acne. Toxicity: GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy. Resistance: decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps.

Answer 145

Macrolides. Inhibit protein synthesis by blocking translocation (macroslides); bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic. Use: atypical pneumonias (mycoplasma, chlamydia, legionella), STDs (for Chlamydia), and gram-positive cocci (streptococcal infections in patients allergic to penicillin). Toxicity: MACRO: GI Motility issues (it's prokinetic), Arrhythmia caused by prolonged QT, acute Cholestatic hepatitis, Rash, eOsinophilia. Increases serum concentration of theophyllines, oral anti-coagulants. Resistance: methylation of 23S rRNA-binding site prevents binding of drug.

Answer 146

Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic. Use: Meningitis (H. influenzae, Neisseria meningitidis, Strep pneumoniae) and Rocky mountain spotted fever (rickettsia rickettsii). Limited use owing to toxicities but often still used in developing countries because of low cost. Toxicity: Anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (in premature infants because they lack liver UDP-glucoronyl transferase). Resistance: plasmid-encoded acetyltransferase inactivates the drug.

Answer 147

Blocks peptide transfer (translocation) at 50S ribosomal subunit. Bacteriostatic. Use: anaerobic infections (e.g. bacteroides spp. Clostridium perfringes) in aspiration pneumonia, lung abscesses, and oral infections. Also effective against invasive group A streptococcal (GAS) infection. Also can be used for acne. Treats anaerobes above the diaphragm vs. metronidazole (anaerobic infections below diaphragm). Toxicity: Pseudomembranous colitis (C. difficile overgrowth which should be treated with metronidazole or vancomycin), fever, diarrhea.

Answer 148

Inhibit folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic. Use: gram-pos, gram-neg, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI. Toxicity: Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g. warfarin). Resistance: altered enzyme (bacterial dihydropteroate synthase), decreased uptake, or increased PABA synthesis.

Answer 149

Inhibits bacterial dihydrofolate reductase. Bacteriostatic. Use: used in combo with sulfonamides (TMP-SMX), causing sequential block of folate synthesis. Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis. Toxicity: megaloblastic anemia, leukopenia, granulocytopenia, (may alleviate with folic acid supplementation). TMP: treats marrow poorly.

Answer 150

All are fluoroquinolones, except for nalidixic acid which is a quinalone. Mech: inhibit DNA gyrase (topoisomerase II) and topoisomerase IV. Bactericidal. Must not be taken with antacids. Use: gram neg rods of urinary and GI tracts (including pseudomonas), Neisseria, some gram pos organisms. Toxicity: GI upset, superinfections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnant women, nursing mothers, and children under 18 years old due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people > 60 years old and in patients taking prednisone. FluoroquinoLONES hurt attachments to your BONES. Resistance: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

Answer 151

Mechanism: Forms free radical toxic metabolites in the bacterial cell that damages DNA. bactericidal, antiprotozoal. Use: Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. difficile). Used with a proton pump inhibitor and clarithromycin for "triple therapy" against H. pylori. GET GAP on the Metro with METROnidazole! Treat anaerobic infection below the diaphragm vs clindamycin (which is anaerobic infections above the diaphragm). Toxicity: Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol; headache, metallic taste.

Answer 152

Prophlaxis: Isoniazid Treatment: Rifampin, Isoniazid, Pyrazinamide, Ethambutol RIPE for treatment.

Answer 153

Prophylaxis: Azithromycin, Rifabutin Treatment: More drug resistant than M. tuberculosis. Azithromycin or clarithromycin + ethambutol. Can add rifabutin or ciproflaxacin.

Answer 154

Long term treatment with dapsone and rifampin for tuberculoid form. Add clofazimine for lepromatous form.

Answer 155

Mech: decreased synthesis of mycolic acids. Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolite. Use: Mycobacterium tuberculosis. The only agent as solo prophylaxis against TB. Different INH half-lives in fast vs. slow acetylators. Toxicity: Neurotoxicity, hepatotoxicity. Pyridoxine (B6) can prevent neurotoxicity, lupus. INH injures Neurons and Hepatocytes.

Answer 156

Rifamycins Mech: inhibits DNA-dependent RNA polymerase Use: M. tuberculosis; delays resistance to dapsone when used fro leprosy. Used for menigococcal prophylaxis and chemoprophylaxis in contacts of children with H. influenzae type B. Rifampin's four Rs: RNA polymerase inhibitor, Ramps up microsomal cytochrome P450, Red/orange body fluids, Rapid resistance if used alone, Rifampin ramps up cytochrome P-450, but rifabutin does not.

Answer 157

Mechanism uncertain. Thought to acidify intracellular environment via conversion to pyrazinoic acid. Effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found. Use: Mycobacterium tuberculosis. Toxicity: Hyperuricemia, hepatotoxicity.

Answer 158

Decreased carbohydrate polymerization of mycobacterium cell wall by blocking arbinosyltransferase. Use: mycobacterium tuberculosis. Toxicity: optic neuropathy (red-green color blindness).

Answer 159

200: Pneumocystis pneumoniae with TMP-SMX 100: Pneumocystis pneumonia and toxoplasmosis with TMP-SMX 50: Mycobacterium avium complex with Azithromycin

Answer 160

1) Penicillins 2) Ceftriaxone 3) TMP-SMX 4) Ciprofloxacin (drug of choice), rifampin for children 5) Ampicillin 6) Erythromycin ointment 7) Cefazolin 8) Oral penicillin 9) Benzathine penicillin G

Answer 161

MRSA - vancomycin, daptomycin, linezolid (can cause serotonin syndrome, optic neuritis, thrombocytopenia), tigecycline, ceftaroline VRSA - linezolid and streptogramins (quinupristin/dalfopristin) Note: according to wikipedia regarding action of streptogramins -> Quinupristin and dalfopristin are protein synthesis inhibitors in a synergistic manner. While each of the two is only a bacteriostatic agent, the combination shows bactericidal activity. Dalfopristin binds to the 23S portion of the 50S ribosomal subunit, and changes the conformation of it, enhancing the binding of quinupristin by a factor of about 100. In addition, it inhibits peptidyl transfer. Quinupristin binds to a nearby site on the 50S ribosomal subunit and prevents elongation of the polypeptide, as well as causing incomplete chains to be released.

Answer 162

Mechanism: binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes. AmphoTERicin "tears" holes in the fungal membrane by forming pores. Use: serious, systemic mycoses. Cryptococcus (amphotericin B with/without flucytosine for cryptococcal meningitis), Blastomyces, Coccidioides, Histoplasma, Candida, Mucor. Intrathecally for fungal meningitis. Supplement K+ and Mg+2 because of altered renal tubule permeability. Toxicity: Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis ("amphoterrible"). Hydration decreases nephrotoxicity. Liposomal amphotericin decreases toxicity. Phlebitis means inflammation of vessel walls.

Answer 163

Mech: same as amphotericin B. Topical form because too toxic for systemic use. Use: "swish and swallow" for oral candidiasis (thrush); topical for diaper rash or vaginal candiasis.

Answer 164

Mech: Inhibit fungal sterol (ergosterol) synthesis, by inhibiting the cytochrome P-450 enzyme (14-alpha-demehtylase) that converts lanosterol to ergosterol. Use: local and less serious systemic mycoses. Fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections. Toxicity: Testosterone synthesis inhibition (gynecomastia, esp. with ketoconazole), liver dysfunction (inhibits cytochrome P-450).

Answer 165

Mech: inhibits DNA and RNA biosynthesis by conversion to 5-flurouracil by cytosine deaminase. Use: Systemic fungal infections (esp. meningitis caused by Cryptococcus) in combination with amphotericin B. Toxicity: Bone marrow suppression.

Answer 166

mech: inhibits cell wall synthesis by inhibiting synthesis of B-glucan. Use: invasive aspergillosis, Candida. Toxicity: GI upset, flushing (by histamine release).

Answer 167

Mech: inhibits the fungal enzyme squalene epoxidase. Use: dermatophytoses (especially onychomycosis - fungal infection of finger or toe nails). Toxicity: GI upset, headaches, hepatotoxicity, taste disturbance.

Answer 168

Mech: interferes with microtubule function: disrupts mitosis. Deposits in keratin-containing tissues (e.g. nails). Use: Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm). Toxicity: teratogenic, carcinogenic, confusion, headaches, increased P-450, and warfarin metabolism.

Answer 169

Pyrimethamine - toxoplasmosis Suramin and melarsoprol - Trypanosoma brucei Nifurtimox - T. cruzi Sodium stibogluconate - leishmaniasis

Answer 170

Mech: blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia. Use: Treatment of plasmodial species other than P. falciparum (frequency of resistance in P. falciparum is too high). Resistance due to membrane pump that decreases intracellular concentration of drug. Treat P. falciparum with artemether/lumefantrine or atovaquone/proguanil. For life-threatening malaria, use quinidine in U.S. (quinine elsewhere) or artesunate. Primaquine is used for dormant hypnozoites. Toxicity: retinopathy; pruritis (especially in dark-skinned individuals).

Answer 171

mebendazole, pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel...immobilize helminths. Use praziquantel against flukes (trematodes) such as Schistosoma.

Answer 172

Nematodes (roundworms): Enterobius vermicularis (pinworm), ascaris lumbricoides (giant roundworms), Ancylostoma duodenale/Necator Americanus (hookworms). Also albendazole/mebendazole used for Toxocara canis. Albendazole used in Echniococcus granulosus.

Answer 173

Strongyloides stercoralis Onchocerca volvulus Both nematodes (roundworms)

Answer 174

``` Loa loa and Wuchereria bancrofti Both Nematodes (roundworms) ```

Answer 175

Cestodes (tapeworms) Taenia solium (although albendazole for neurocysticercosis) Diphyllobothrium latum Tramatodes (flukes) Schistosoma Clonorchis sinensis

Answer 176

Inhibit influenza neuraminidase -> decreases the release of progeny virus. Use: treatment and prevention of both influenza A and B.

Answer 177

Mech: inhibit synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate. Use: RSV, chronic hepatitis C. Toxicity: Hemolytic anemia. Severe teratogen.

Answer 178

Mechanism: monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells -> few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination. Use: HSV and ZVZ. weak activity against EBV and no activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyvlovir, a prodrug of acyclovir, has better oral bioavailability. For herpes zoster, use a related agent, famciclovir. Toxicity: obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. Resistance: mutated viral thymidine kinase

Answer 179

Mechanism: 5'-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibit viral DNA polymerase. Use: CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability. Toxicity: leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir. Mech of resistance: mutated CMV DNA polymerase or lack of viral kinase.

Answer 180

Mech: Viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does not require activation by viral kinase. FOScarnet = pyroFOSphate analog. Use: CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV. Toxicity: nephrotoxicity Mech of resistance: mutated DNA polymerase.

Answer 181

Mech: preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase. Use: CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. long-half life. Toxicity: nephrotoxicity (co-administer with probenecid -decreases excretion- and IV saline to decrease toxicity)

Answer 182

carotid massage

Answer 183

Highly active antiretroviral therapy (HAART): initiated when patients present with AIDS-defining illness, low CD4 cell counts (<500cells/mm3), or high viral load. Regimen consists of 3 drugs to prevent resistance: [2 NRTIs] + [1 NNRTI or 1 protease inhibitor or 1 integrase inhibitor]

Answer 184

Protease inhibitors. Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses. Ritonavir can "boost" other drug concentrations by inhibiting cytochrome P-450. All protease inhibitors end in -navir. Navir (never) tease a protease. Toxicity: Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy. Nephropathy, hematuria (indinavir).

Answer 185

NRTIs. Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3' OH group). Tenofovir is a nucleoTide; the others are nucleosides and need to be phosphorylated to be active. ZDV is used for general prophylaxis and during pregnancy to decrease risk of fetal transmission. Have you dined (vudine) with my nuclear (nucleosides) family? Toxicity: bone marrow suppression ( can be reversed with granulocyte colony-stimulating factor [G-CSF] and EPO), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), anemia (ZDV), pancreatitis (didanosine).

Answer 186

NNRTIs. Bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides. Toxicity: Rash and hepatotoxicity are common to all NNRTIs. Vivid dreams and CNS symptoms are common with efavirenz. Delavirdine and efavirenz are contraindicated in pregnancy. SJS and toxic epidermal necrolysis with efavirenz and nevirapine.

Answer 187

Integrase inhibitor. Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase. Toxicity: Hypercholesteremia

Answer 188

Fusion inhibitor. Binds gp41 and inhibits viral entry. Toxicity: Skin reaction at injection sites

Answer 189

Fusion inhibitor | Binds CCR-5 on surface of T cells/monocytes inhibiting interaction with gp120.

Answer 190

Mech: Glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumoral properties. Clinical use: IFN-alpha - chronic hepatitis B and C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma. IFN-beta - multiple sclerosis IFN-gamma - chronic granulomatous disease. Toxicity: neutropenia, myopathy.

Answer 191

Sulfonamides (kernicterus), Aminioglycosides (ototoxicity), fluoroquinolones (cartilage damage), clarithromycin (embryotoxic), tetracyclines (discolored teeth/inhibition of bone growth), Ribavirin (anti-viral and teratogenic), Griseofulvin (anti-fungal and teratogenic), Chloramphenicol ("gray baby") SAFe Children Take Really Good Care.

Answer 192

Mech: osmotic diuretic, increased tubular fluid osmolarity, producing increased urine flow, decreased intracranial/intraocular pressure. Use: drug overdose, increased intracranial/intraocular pressure Toxicity: pulmonary edema, dehydration. Contraindicated in anuria, CHF.

Answer 193

Mech: Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and decreased total-body HCO3- stores. Use: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri. Toxicity: hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy.

Answer 194

Sulfonamide loop diuretic. Inhibits cotransport system (Na+/K+/2 Cl-) of thick ascending limb of loop of Henle. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs. Increased Ca+2 excretion. Loops Lose calcium. Use: Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia. Toxicity: Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout. OH DANG.

Answer 195

Loop diuretics Mech: Phenoxyacetic acid derivative (not a sulfonamide). Essentially same action as furosemide. Use: Diuresis in patients allergic to sulfa drugs. Toxicity: Similar to furosemide; can cause hyperuricemia; never use to treat gout.

Answer 196

Mech: thiazide diuretic. Inhibits NaCl reabsorption in early distal tubule. Decreased diluting capacity of the nephron. Decreased Ca+2 excretion. Use: Hypertension, CHF, idiopathic hypercalcuria, nephrogenic diabetes insipidus, osteoporosis. Toxicity: Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, and hyperCalcemia. Sulfa allergy. HyperGLUC

Answer 197

K+ sparing diuretics. The K+ STAys. Mech: spironolactone and eplerenone are competitive aldosterone receptor antagonists in the cortical collecting tubule. Triamterene and amiloride act at the same part of the tubule by blocking Na+ channels in the CCT. Clinical use: hyperaldosteronism, K+ depletion, CHF. Toxicity: Hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (e.g. gynecomastia, antiandrogen effects).

Answer 198

Increased by all diuretics except acetazolamide. Serum NaCl may decrease too.

Answer 199

increased with loop and thiazide diuretics. Serum K+ may decrease as a result.

Answer 200

decreased (acidemia) by carbonic anyhydrase inhibitors- > decreased HCO3- reabsorption. K+ sparing-aldosterone blockade prevents K+ secretion and H+ secretion. Additionally, hyperkalemia leads to K+ entering all cells (via H/K exchange) in exchange for H+ exiting cells. Increased (alkaemia) by loop diuretics and thiazides cause alkalemia through several mechanisms: 1) volume contraction -> increased ATII -> increased Na/H+ exchange in proximal tubules -> increased HCO3- reabsorption (contraction alkalosis) 2) K+ loss leads to K+ exiting all cells (via H/K exchanger) in exchange for H+ entering cells. 3) in low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule -> alkalosis and "paradoxical aciduria"

Answer 201

Increased with loop diuretics: decreased paracellular Ca+2 reabsorption leading to hypocalcemia. Decreased with thiazides: enchanced paracellular Ca+2 reabsorption in distal tubule.

Answer 202

ACE inhibitors Mech: inhibit ACE leads to decreased angiotensin II and then decreased GFR by preventing constriction of efferent arterioles. Levels of renin increased as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator. Use: hypertension, CHF, proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a result of chronic hypertension. Toxicity: Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), Increased Creatinine (decreased GFR), Hyperkalemia, and Hypotension. Avoid in bilateral renal artery stenosis, because ACE inhibitors will further decrease GFR leading to renal failure. Captopril's CATCHH.

Answer 203

methylphenidate

Answer 204

benzodiazepines

Answer 205

SSRIs, SNRIs, buspirone

Answer 206

"Mood stabilizers" (e.g. lithium, valproic acid, carbamazepine), atypical antipsychotics.

Answer 207

SSRIs, SNRIs, TCA, bupropion, mirtazapine (especially with insomnia)

Answer 208

SSRIs, clomipramine

Answer 209

SSRIs, venlafaxine, benzodiazepines.

Answer 210

SSRIs note: prazosin also (according to pharm section in FA)

Answer 211

Antipsychotics

Answer 212

SSRIs, Beta-blockers

Answer 213

Antipsychotics

Answer 214

CNS stimulants Increased catecholamines at the synaptic cleft, especially norepinephrine and dopamine (by promoting vesicular release, also some reuptake inhibition). USE: ADHD, narcolepsy, appetite control.

Answer 215

Typical Antipsychotics. All typical antipsychotics block Dopamine D2 receptors (increased cAMP). Use: Schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette syndrome. Toxicity: Highly lipid soluble and stored in body fat; thus, very slow to be removed from body. Extrapyramidal symptoms side effects (e.g. dyskinesias). Treatment: benztropine or diphenhydramine. Endocrine side effects (e.g. dopamine receptor antagonism -> hyperprolactinemia -> galactorrhea). Side effects arising from blocking muscarinic (dry mouth, constipation), alpha-1 (hypotension), and histamine (sedation) receptors.

Answer 216

Trifluoperazine, Fluphenazine, Haloperidol (Try to Fly High) - neurologic side effects (EPS symptoms). Haloperidal - NMS, tardive dyskinesia.

Answer 217

Chlorpromazine, Thioridazine (Cheating Thieves are low) - non-neurologic side effects (anticholinergic, antihistamine, and alpha-1-blockade effects) - non-neurologic side effects (anticholinergic, antihistamine, and alpha-1-blockade effects) Chlorpromazine- Corneal deposits Thioridazine - reTinal deposits;

Answer 218

4 hr acute dystonia (muscle spasm, stiffness, oculogyric crisis) 4 day akathisia (restlessness) 4 week bradykinesia (parkinsonism) 4 month tardive dyskinesia

Answer 219

caused by typical antipsychotics Rigidity, myoglobinuria, autonomic instability, hyperpyrexia. Treatment: dantrolene, D2 agonists (e.g. bromocriptine) For NMS, think FEVER Fever, Encephalopathy, Vitals unstable, Enzymes increased, Rigidity of muscles.

Answer 220

stereotypic oral-facial movements as a result of long term anti-psychotic use. Potentially irreversible.

Answer 221

Atypical antipsychotics Mech: not completely understood. Varied effects on 5-HT2, dopamine, and alpha and H1-receptors. Use: Schizophrenia - both positive and negative symptoms. Also used for bipolar disorder, OCD, anxiety disorder, depression, mania, Tourette syndrome. Toxicity: Fewer EPS and anticholinergic side effects than traditional antipsychotics. Olanzapine/clozapine may cause significant weight gain. Clozapine may cause agranulocytosis (requires weekly WBC monitoring) and seizure. Risperidone may increase prolactin (causing lactation and gynecomastia) decrease GnRH, LH, and FSH (causing irregular menstruation and fertility issues). Ziprasidone may prolong the QT interval.

Answer 222

Mech: not established; possibly related to inhibition of phosphoinositol cascade. Use: mood stabilizer for bipolar disorder; blocks relapse and acute manic events. Also SIADH. Toxicity: Tremor, sedation, edema, heart block, hypothyroidism, polyuria (ADH antagonist causing nephrogenic diabetes insipidus), teratogenesis. Fetal cardiac defects include Ebstein anomaly and malformation of the great vessels. Narrow therapeutic window requires close monitoring of serum levels. Almost exclusively excreted by the kidneys; most is reabsorbed at the proximal convoluted tubules following Na+ reabsorption. LMNOP - Lithium side effects - Movement (tremor), Nephrogenic diabetes insipidus, hypOthyroidism, Pregnancy problems.

Answer 223

Mech: Stimulates 5-HT1A receptors. Use: Generalized anxiety disorders. Does not cause sedation, addiction, or tolerance. Takes 1-2 weeks to take effect. Does not interact with alcohol (vs. barbiturates, benzodiazepines). I'm alway anxious if the BUS will be ON time, so I take BUSpirONe.

Answer 224

Flashbacks paralyze senior citizens. Mech: 5-HT specific reuptake inhibitors Use: Depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSD. Toxicity: Fewer than TCAs. GI distress, sexual dysfunction (anorgasmia and decreased libido). Serotonin syndrome with any drug that increases 5-HT (e.g. MAO inhibitors, SNRIs, TCAs) - hyperthermia, confusion, myoclonus, cardiovascular collapse, flushing, diarrhea, seizures. Treatment is cyproheptadine (5-HT2 receptor antagonist).

Answer 225

SNRIs. Mech: inhibit 5-HT and norepinephrine reuptake. Use: Depression. Venlafaxine is also used in generalized anxiety disorder and panic disorders; duloxetine is also indicated for diabetic peripheral neuropathy. Toxicity: increased BP most common; also stimulant effects, sedation, nausea.

Answer 226

TCAs. Mech: Block re-uptake of norepinephrine and 5-HT. Use: Major depression, OCD (clomipramine), fibromyalgia. Toxicity: Sedation, alpha-1-blocking effects, including postural hypotension, and atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). Tertiary TCAs (amitriptyline) have more anti-cholinergic effects than secondary TCAs (nortriptyline) have. Desipramine is less sedating, but has a higher seizure incidence. Tri-C's: Convulsions, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects (use nortriptyline). Treatment: NaHCO3 for cardiovascular toxicity.

Answer 227

MAO Takes Pride In Shanghai. (Selegiline is a selective MAO-B inhibitor) Mech: Nonselective MAO inhibition increases levels of amine neurotransmitters (norepinephrine, 5-HT, dopamine). Use: atypical depression, anxiety, hypochondriasis. Toxicity: Hypertensive crisis (most notably with ingestion of tyramine, which is found in many foods such as wine and cheese); CNS stimulation. Contraindicated with SSRIs, TCAs, St. John's wort, meperidine, and dextromethorphan (to prevent serotonin syndrome).

Answer 228

Atypical antidepressant. Also used for smoking cessation. Increased norepinephrine and dopamine via unknown mechanism. Toxicity: stimulant effects (tachycardia, insomnia), headache, seizure in bulimic patients. No sexual side effects.

Answer 229

Atypical antidepressants. alpha-2-antagonist (increased release of norepinephrine and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist. Toxicity: sedation (which may be desirable in depressed patients with insomnia), increased appetite, weight gain (which may be desirable in elderly or anorexic patients), dry mouth.

Answer 230

Primarily blocks 5-HT2 and alpha-1-adrenergic receptors. Used primarily for insomnia as high doses are needed for antidepressant effects. Toxicity: sedation, nausea, priapism, postural hypotension. called trazoBONE due to male-specific side effects.

Answer 231

Sympathomimetic drug with direct stimulation of B1 receptors of the sympathetic nervous system. Positive inotropic action. Weak B2 and alpha 1 activity. Uses: heart failure and cardiogenic shock. Side effects: hypertension, angina, arrhythmia, and tachycardia. Less likely to induce hypertension than dopamine is (dopamine acts on dopamine receptors to also release norepinephrine which is alpha-1-agonist)

Answer 232

Stops them in G1. activates nuclear receptor that goes and degrades DNA. Antagonist in breast and bone and activator in endometrium.

Answer 233

Mech: Calcineurin inhibitor; binds cyclophilin. Blocks T cell activation by preventing IL-2 transcription. Use: transplant rejection prophylaxis, psoriasis, rheumatoid arthritis. Toxicity: nephrotoxicity, hypertension, hyperlipidemia, hyperglycemia, tremor, hirsutism, gingival hyperplasia. Notes: both calcineurin inhibitors are very nephrotoxic.

Answer 234

Mech: Calcineurin inhibitor; binds FK506 binding protein (FKBP). Blocks T cell activation by preventing IL-2 transcription. Use: transplant rejection prophylaxis. Toxicity: similar to cyclosporine, increased risk of diabetes and neurotoxicity; no gingival hyperplasia or hirsuitism. -limus drugs binds FKBP.

Answer 235

mTOR inhibitor; binds FKBP. Blocks T cell activation and B cell differentiation by preventing IL-2 signal transduction. Use: kidney transplant rejection prophylaxis. Toxicity: anemia, thrombocytopenia, leukopenia, insulin resistance, hyperlipidemia, non-nephrotoxic. Notes: Kidney "sir-vives". Synergistic with cyclosporine. Also used in drug-eluting stents.

Answer 236

Mech: monoclonal antibody; blocks IL-2R. Use: Kidney transplant rejection prophylaxis. Toxicity: edema, hypertension, tremor.

Answer 237

Antimetabolite precursor of 6-mercaptopurine. Inhibits lymphocyte proliferation by blocking nucleotide synthesis. Use: Transplant rejection prophylaxis, rheumatoid arthritis, Crohn disease, glomerulonephritis, other autoimmune conditions. Toxicity: leukopenia, anemia, thrombocytopenia. Note: 6-MP degrade by xanthine oxidase; toxicity increased by allopurinol. Pronounce azathio-PURINE.

Answer 238

Mech: Inhibit NF-kB and suppress both B and T cell function by decreased transcription of many cytokines. Use: Transplant rejection prophylaxis (immune suppression), many autoimmune disorders, inflammation. Toxicity: hyperglycemia, osteoporosis, central obesity, muscle breakdown, psychosis, acne, hypertension, cataracts, peptic ulcers.

Answer 239

thrombocytopenia. Thrombopoitetin stimulates platelet production and is mainly produced in liver and kidney. Stimulates production and differentiation of megakaryocytes.

Answer 240

recovery of bone marrow

Answer 241

Renal cell carcinoma, metastatic melanoma

Answer 242

Chronic Hep B and C; kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma.

Answer 243

Multiple sclerosis

Answer 244

chronic granulomatous disease

Answer 245

CD52 is target. Use is CLL | aLYMtuzumab - chronic LYMphocytic leukemia

Answer 246

VEGF is target. | Colorectal cancer, renal cell carcinoma

Answer 247

EGFR is target | Stage IV colorectal cancer, head and neck cancer

Answer 248

CD20 is target. | B-cell non-Hodgkin lymphoma, rheumatoid arthritis (with MTX), ITP

Answer 249

HER2/neu is target. | Breast cancer, gastric cancer.

Answer 250

TNF-alpha is target IBD, rheumatoid arthritis, ankylosing spondylitis, psoriasis. RA "inflix" pain in "DA LIMbs"

Answer 251

alpha-4-integrin is target. MS, crohn disease. Alpha-4-integrin is involved in leukocyte adhesion. Risk of PML in patients with JC virus.

Answer 252

Glycoprotein IIb/IIIa is the target. Anti-platelet agent for prevention of ischemic complications in patients undergoing percutaneous coronary intervention. IIb times IIIa equals "abSIXimab"

Answer 253

RANKL is the target. Osteoporosis; inhibits osteoclast maturation (mimics osteoprotegrin). DenOSumab affects OSteoclasts.

Answer 254

Digoxin is the target | Antidote for digoxin toxicity

Answer 255

IgE is the target. | Allergic asthma; prevents IgE binding to FceRI

Answer 256

RSV F protein is target RSV prophylaxis for high-risk infants. PaliVIzumab - VIrus.

Answer 257

propranolol - nonspecific Beta blocker

Answer 258

Mech: Depolarization of membrane. Can only penetrate gram positive membranes and causes the creation of transmembrane channels that depolarize it and inhibit cellular function causing death. Use: invasive MRSA infections Adverse actions: Myopathy and CPK elevation. Inactivated by pulmonary surfactant.

Answer 259

Used for preventing mast cell degranulation in asthma prophylaxis.

Answer 260

LEAD - Lead lines on gingivae and on metaphyses of long bones on xray Encephalopathy and Erythrocyte basophilic stipling (rRNA degradation blocked) Abdominal colic and sideroblastic anemia Drops - wrist and foot drop. Dimercaprol and eDta are first line of treatment. Succimer used for chelation in kids. lead inhibits ferrochelatase and ALA dehydratase.

Answer 261

5-FU, zidovudine, hydroxyurea Also liver disease, alcoholism (vacuolization), and reticulocytosis

Answer 262

Enoxaparin, dalteparin Act more on factor Xa. They have better bioavailability and 2-4 times longer half-life. Can be administered subcu and without lab monitoring. Not easily reversible.

Answer 263

development of IgG antibodies against heparin bound to platelet factor (PF4). Antibody-heparin-PF4 complex activates platelets -> thrombosis and thrombocytopenia.

Answer 264

Derivatives of hirudin, the anti-coagulant used by leeches; inhibit thrombin directly. Used instead of Heparin for anti-coagulating patients with HIT.

Answer 265

Mech: blocks normal synthesis and gamma carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X and proteins C and S. Metabolized by the cytochrome P-450 pathway. Increases PT...long half-life. Use: Chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation). Not used in pregnant women (because warfarin, unlike heparin, can cross the placenta). Follow PT/INR values. Toxicity: Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions.

Answer 266

Direct factor Xa inhibitors Bind and directly inhibit the activity of factor Xa. Use: treatment and prophylaxis of DVT and PE (rivaroxaban), stroke prophylaxis in patients with atrial fibrillation. Oral agents do not usually require coagulation monitoring. Toxicity: bleeding (no specific reversal agent available).

Answer 267

Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions. For rapid reversal (antidote), use protamine sulfate (positively charged molecule that binds negatively charged heparin).

Answer 268

Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increased PT, PTT, no change in platelet count. Use: Early MI, early ischemic stroke, direct thrombolysis of severe PE. Toxicity: Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis. Fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies.

Answer 269

Mech: irreversibly inhibits cyclooxygenase (both COX1 and COX2) enzyme by covalent acetylation. Platelets cannot synthesize new enzyme, so effect lasts until new platelets are produced. Increased bleeding time, decreased thromboxane and prostaglandins. No effect on PT or PTT. Clinical use: antipyretic, analgesic, anti-inflammatory, antiplatelet (decreased aggregation) Toxicity: Gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Reye syndrome in children with viral infection Overdose causes respiratory alkalosis initially, which is then superimposed by metabolic acidosis.

Answer 270

Mech: Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen (through the mechanism of reduced glycoprotein receptors) Use: acute coronary syndrome; coronary stenting. Decreased incidence or recurrence of thrombotic stroke. Toxicity: neutropenia (ticlopidine). TTP/HUS may be seen.

Answer 271

Mech: Phosphodiesterase III inhibitor; cAMP increased in platelets, thus inhibiting platelet aggregation. Use: intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis. Toxicity: Nausea, headache, facial flushing, hypotension, abdominal pain. CORONARY STEAL PHENOMENON a

Answer 272

Mech: bind to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation (blocks binding of fibrinogen). Abciximab is made from monoclonal antibody Fab fragments. Use: Unstable angina, percutaneous transluminal coronary angioplasty. Toxicity: bleeding, thrombocytopenia.

Answer 273

Mech: folic acid analog that inhibits dihydrofolate reductase -> decreased dTMP -> decreased DNA and decreased protein synthesis. Use: cancers: leukemias, lymphomas, choriocarcinoma, sarcomas. Non-neoplastic: abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis, IBD. Toxicity: myelosuppression, which is reversible with leucovorin (folinic acid) "rescue" Macrovesicular fatty change in liver. Mucositis. Teratogenic.

Answer 274

Mech: Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. This complex inhibits thymidylate synthase -> decreased dTMP -> decreased DNA and decreased protein synthesis. Use: colon cancer, pancreatic cancer, basal cell carcinoma (topical) Toxicity: myelosuppression, which is not reversible with leucovorin. Overdose: "rescue" with uridine. Photosensitivity.

Answer 275

Pyrimidine analog -> inhibition of DNA polymerase Use: leukemias, lymphomas Toxicity: leukopenia, thrombocytopenia, megaloblastic anemia, CYTarabine causes panCYTopenia.

Answer 276

Purine (thiol) analogs -> decreased de novo purine synthesis. Activated by HGPRT. Use: preventing organ rejection, RA, SLE (azathioprine). Leukemia, IBD (6-MP, 6-TG). Toxicity: bone marrow, GI, liver. Azathioprine and 6-MP are metabolized by xanthine oxidase; thus both have increased toxicity with allopurinol, which inhibits their metabolism.

Answer 277

Intercalates in DNA Use: Wilms tumor, Ewing sarcoma, rhabdomyosarcoma. Used for childhood tumors (children ACT out). Toxicity: myelosuppression

Answer 278

Generate free radicals. Intercalate in DNA -> breaks in DNA -> decreased replication. Use: solid tumors, leukemias, lymphomas. Toxicity: Cardiotoxicity (dilated cardiomyopathy), myelosuppression, alopecia. Toxic to tissues following extravasation. Dexrazoxane (iron chelating agent), used to prevent cardiotoxicity.

Answer 279

Induces free radical formation, which causes breaks in DNA strands. Use; testicular cancer, Hodgkin lymphoma Toxicity: pulmonary fibrosis, skin changes, mucositis. Minimal myelosuppression.

Answer 280

covalently X-link (interstrand) DNA at guanine N-7. Require bioactivation by liver. Use: solid tumors, leukemia, lymphomas, and some brain cancers. Toxicity: Myelosuppression; hemorrhagic cystitis, partially prevented with mesna (thiol group of mesna binds toxic metabolites).

Answer 281

Require bioactivation. Cross blood brain barrier into CNS and cross link DNA. Use: brain tumors (including glioblastoma multiforme) Toxicity: CNS toxicity (convulsions, dizziness, ataxia)

Answer 282

Cross links DNA. USed for: CML. Also used to ablate patient's bone marrow before bone marrow transplantation. Toxicity: severe myelosuppression (in almost all cases), pulmonary fibrosis, hyperpigmentation.

Answer 283

Vinca alkaloids that bind Beta-tubulin, inhibit its polymerization into microtubules, thereby preventing mitotic spindle formation (M-phase arrest) Use: solid tumors, leukemias, and lymphomas. Toxicity: vincristine - neurotoxicity (areflexia, peripheral neuritis), paralytic ileus. Vinblastine blasts bone marrow (suppression).

Answer 284

Hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down (anaphase cannot occur). It is TAXing to stay polymerized. Use: ovarian and breast carcinomas. Toxicity: myelosuppression, alopecia, hypersensitivity.

Answer 285

mech: cross-link DNA Use: testicular, bladder, ovary, and lung carcinomas. Toxicity: nephrotoxicity, and acoustic nerve damage. Prevent nephrotoxicity with amifostine (free radical scavenger) and chloride diuresis.

Answer 286

Mech: eTOPOside inhibits TOPOisomerase II -> DNA degradation Use: solid tumors (particularly testicular and small cell lung cancer), leukemias, lymphomas Toxicity: myelosuppression, GI irritation, alopecia

Answer 287

mech: inhibit topoisomerase I and prevent DNA unwinding and replication Use: colon cancer (irinotecan); ovarian and small cell lung cancers (troptecan) Toxicity: severe myelosuppression, diarrhea.

Answer 288

Inhibits ribnoucleotide reductase -> DNA synthesis decreased (S-phase specific) Use: Melanoma, CML, sickle cell disease (by increasing HbF) Toxicity: Bone marrow suppression, GI upset.

Answer 289

May trigger apoptosis. May even work on nondividing cells Most commonly used glucocorticoids in cancer chemotherapy. Used in CLL, non-hodgkin lymphomas (part of combo therapy), also used as immunosuppressants in autoimmune diseases and others. Toxicity: Cushing like symptoms; weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis, water retention, hypernatremia, hypokalemia, hypocalcemia.

Answer 290

Mech: SERMs - receptor antagonists in breast and agonists in bones. Block the binding of estrogen to ER + cells. Use: breast cancer treatment (tamoxifen only) and prevention. Raloxifene is also used to prevent osteoporosis. Toxicity: tamoxifen - partial agonist in endometrium, which has the increased risk of endometrial cancer. "hot flashes". Raloxifene - no increase in endometrial carcinoma because it is an endometrial antagonist.

Answer 291

Herceptin. Monoclonal antibody against HER-2 (e-erbB2), a tyrosine kinase receptor. Helps kill breast cancer cells that overexpress HER-2, through inhibition of HER2-initiated cellular signaling and antibody-dependent cytotoxicity. Use: HER-2 positive breast cancer and gastric cancer (tras2zumab). Toxicity: cardiotoxicity. "HEARTceptin" damages the HEART.

Answer 292

Gleevec. Tyrosine kinase inhibitor of bcr-abl (Philadelphia chromosome fusion gene in CML) and c-Kit (common in GI stromal tumors). Use: CML, GI stromal tumors. Toxicity: fluid retention

Answer 293

Monoclonal antibody against CD20, which is found on most B-cell neoplasms. Use: non-hodgkin lymphoma, rheumatoid arthritis (with MTX), ITP. Toxicity: increased risk of progressive multifocal leukoencephalopathy.

Answer 294

Small molecular inhibitor of forms of the B-raf kinase with the V600E mutation Use; Metastatic melanoma

Answer 295

Mech: monoclonal antibody against VEGF. Inhibits angiogenesis. Use: solid tumors (colorectal cancer, renal cell carcinoma) Toxicity: hemorrhage and impaired wound healing.

Answer 296

Baclofen is a muscle relaxant that affects GABAb receptors at the level of the spinal cord.

Answer 297

It's a selective norepinephrine reuptake inhibitor for ADHD. Good because there is little abuse potential.

Answer 298

Intoxication: emotional lability, slurred speech, ataxia, coma, blackouts. Serum gamma-glutamyltransferase (GGT) - sensitive indicator of alcohol use. Lab AST value is twice ALT level. Withdrawal: symptoms similar to other depressants. Severe alcohol withdrawal can cause autonomic hyperactivity and DTs (5-15% mortality rate). Treatment for DTs: benzodiazepines.

Answer 299

Intoxication: euphoria, respiratory and CNS depression, decreased gag reflex, pupillary constriction (pinpoint pupils), seizures (overdose). Constipation too. Treatment: naloxone, naltrexone. Withdrawal: Sweating, dilated pupils, piloerection ("cold turkey" from pilae erector muscle), fever, rinorrhea, yawning, nausea, stomach cramps, diarrhea (flu like symptoms). Treatment: long-term support, methadone, buprenorphine.

Answer 300

Low safety margin, marked respiratory depression. Treatment: symptom management (assist respiration, increased BP). Withdrawal: delirium, life-threatening cardiovascular collapse.

Answer 301

Intox: greater safety margin. Ataxia, minor respiratory depression. Tx: supportive care; consider flumazenil (competitive benzodiazepine antagonist). Withdrawal: sleep disturbance, depression, rebound anxiety, seizure (can be triggered by reversal with flumazenil).

Answer 302

Intoxication: Euphoria, grandiosity, pupillary dilation, prolonged wakefulness and attention, hypertension, tachycardia, anorexia, paranoia, fever. Severe: cardiac arrest, seizure. Withdrawal: anhedonia, increased appetite, hypersomnolence, existential crisis.

Answer 303

Intox: impaired judgement, pupillary dilation, hallucinations (including tactile), paranoid ideations, angina, sudden cardiac death. Tx: benzodiazepines Withdrawal: hypersomnolence, malaise, severe psychological craving, depression/suicidality.

Answer 304

Intoxication: Restlessness, increased diuresis, muscle twitching Withdrawal: lack of concentration, headache.

Answer 305

Intox: restlessness. Withdrawal: irritability, anxiety, craving. Tx: nicotine patch, gum, or lozenges. bupropion (norepi/dopamine reuptake inhibitor and nicotinic antagonist)/varenicline (partial agonist of nicotinic receptors)

Answer 306

Intox: belligerence, impulsiveness, fever, psychomotor agitation, analgesia, vertical and horizontal nystagmus, tachycardia, homicidality, psychosis, delirium, seizures. Tx: benzodiazepines, rapid-acting antipsychotic. Withdrawal: Depression, anxiety, irritability, restlessness, anergia, disturbances of thought and sleep.

Answer 307

Intox: perceptual distortion (visual, auditory), depersonalization, anxiety, paranoia, psychosis, possible flashbacks.

Answer 308

Intox: euphoria, anxiety, paranoid delusions, perception of slowed time, impaired judgement, social withdrawal, increased appetite, dry mouth, conjunctival injection, hallucinations. Prescription form is dronabinol (tetrahydrocannabinol isomer): used as anti-emetic (chemotherapy) and appetite stimulant (in AIDS). used when conventional therapies have failed. Withdrawal: irritability, depression, insomnia, nausea, anorexia. Most symptoms peak in 48 hours and last for 5-7 days. Generally detectable in urine for 4-10 days.

Answer 309

Users at increased risk for hepatitis, abscesses, overdose, hemorrhoids, AIDS, and right-sided endocarditis. Look for track marks (needle sticks in veins). Treatments: Methadone: long acting oral opiate; used for heroin detox or long term maintenance Naloxone and buprenorphine: Partial agonist; long acting with fewer withdrawal symptoms than methadone. Naloxone is not active when taken orally, so withdrawal symptoms occur only if injected (lower abuse potential). Naltrexone: long-acting opioid antagonist used for relapse prevention once detoxified.

Answer 310

Complications: alcoholic cirrhosis, hepatitis, pancreatitis, peripheral neuropathy, testicular atrophy. Treatment: disulfiram (inhibitor of acetylaldehyde...to condition the patient to abstain from alcohol use), naltrexone, supportive care. AA and peer support groups are helpful too. Delirium tremens: life-threatening and peaks 2-5 days after last drink. Symptoms in order of apperance: autonomic system hyperactivity (tachycardia, tremors, anxiety, seizures), psychotic symptoms (hallucinations, delusions), confusion. Treatment is benzodiazepines.

Answer 311

hypertension that is high after 20th week of gestation (no existing hypertension and no proteinuria or organ damage) Treat with anti-hypertensives (alpha-methyldopa, labetalol, hydralazine, nifedipine), deliver at 39 weeks.

Answer 312

it's an irreversible competitive antagonist on alpha receptors.

Answer 313

Inhibits uptake of choline into pre-synaptic cholinergic terminal. Remember: choline is taken up and then converted with Acetyl-CoA to ACh by ChAT.

Answer 314

It inhibits the uptake of ACh into pre-synpatic vesicles.

Answer 315

It inhibits the release of pre-synaptic ACh vesicles.

Answer 316

Choline and acetate.

Answer 317

it inhibits the conversion of tyrosine to DOPA in the pre-synaptic nor-adrenergic receptor. This step is carried out by tyrosine hydroxylase with co-factor BH4

Answer 318

It blocks the uptake of dopamine into pre-synaptic storage vesicles.

Answer 319

They block pre-synaptic release of nor-epinephrine.

Answer 320

It promotes the pre-synpatic release of nor-epinephrine.

Answer 321

they prevent reuptake of the nor-epinephrine into the pre-synaptic terminal.

Answer 322

Nor-epinpehrine modulates itself by binding to alpha-2 receptors which prevent further vesicle release. Angiotensin II acts to promote release of nor-epinephrine presynaptic vesicles.

Answer 323

Cholinomimetic agent - direct agonist Gq mechanism so increases phosphoinositide turnover. Uses: Postoperative ileus, neurogenic ileus, urinary retention Action: Activates Bowel and Bladder smooth muscle; resistant to AChE. "Bethany, call (bethanechol) me, maybe if you want to activate your Bowels and Bladder" Think all the B's for this drug.

Answer 324

Cholinomimetic agent - direct agonist Uses: glaucoma, pupillary constriction, and relief of intraocular pressure. CARBon copy of of AcetylCHOLine.

Answer 325

Cholinomimetic agent - direct agonist Uses: Potent stimulator of sweat, tears, and saliva. Open angle and closed angle glaucoma. Action: Contracts ciliary muscle of eye (open angle glaucoma), pupillary sphincter (closed angle glaucoma); resistant to AChE. "You cry, drool, and sweat on your "pilow".

Answer 326

Cholinomimetic agent - direct agonist Use: Challenge test for diagnosis of asthma. Action: stimulates muscarinic receptors in airway when inhaled.

Answer 327

Cholinomimetic agent - indirect agonist (anticholinesterases) Uses: postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative). Action: Increases endogenous ACh. Neo CNS = NO CNS Penetration.

Answer 328

Cholinomimetic agent - indirect agonist (anticholinesterases) Uses: Myasthenia gravis (long acting); does not penetrate CNS. Action: Increased endogenous ACh, increased strength. PyRIDostiGMine gets RID of Myasthenia Gravis.

Answer 329

Cholinomimetic agent - indirect agonist (anticholinesterases) Uses: Anti-cholinergic toxicity (crosses blood brain barrier -> CNS). Action: increased endogenous ACh. PHYsostigmine "PHYxes" atropine overdose.

Answer 330

Cholinomimetic agent - indirect agonist (anticholinesterases) Uses: Alzheimer disease Action: Increased endogenous ACh.

Answer 331

Cholinomimetic agent - indirect agonist (anticholinesterases) Uses: Historically diagnosis of myasthenia gravis (extremely short acting); Myasthenia now diagnosed by anti-AChR Ab (anti-acetylcholine receptor antibody) test.

Answer 332

Watch for exacerbation of COPD, asthma, and peptic ulcers when giving to susceptible patients. M3 causes smooth muscle contraction (so bronchoconstriction, stimulation of acid secretion).

Answer 333

Often due to organophosphates, such as parathion, that irreversibly inhibit AChE. Causes Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, and Salivation. DUMBBELSS. Organophosphates are a component of insecticides; poisoning usually seen in farmers. Antidote is atropine (competitive inhibitor) + pralidoxime (regenerates AChE if given early enough).

Answer 334

Muscarinic antagonist | Acts at eyes. Produces mydriasis and cycloplegia. Atropine used as antidote for AChE inhibitor poisoning.

Answer 335

Muscarinic antagonist. Used to treat bradycardia and for ophthalmic applications. Action: Increases pupil dilation, cycloplegia (Eye), decreased secretions (Airway), decreased acid secretion (stomach), decreased motility (gut), decreased urgency in cystitis (bladder). Blocks DUMBBeLSS. Note it does not affect the E, excitation of Skeletal muscles and CNS. Those are mediated by nicotinic receptors NOT muscarinic. This is relevant because you can treat myasthenia gravis with AChE inhibitor and give atropine to block unwanted muscarnic side effects, without taking away the therapeutic effect on muscles. Toxicity: Increased body temperature (due to decreased sweating); rapid pulse; dry mouth; dry flushed skin; cycloplegia; constipation; disorientation. Can cause acute angle-closure glaucoma in elderly (due to mydriasis), urinary retention in men with prostatic hyperplasia, and hyperthermia in infants. Hot as a Hare, Dry as a Bone, Red as a Beet, Blind as a Bat, Mad as a Hatter. Also Jimson weed (Datura)...causes gardeners pupil (mydriasis due to plant alkaloids). It's made of atropine and scopolamine.

Answer 336

Muscarinic antagonist | Acts in the CNS system and used for Parkinson disease - "PARK my BENZ"

Answer 337

Muscarinic antagonist | Motion sickness

Answer 338

Muscarinic antagonist In respiratory system for COPD, asthma (I PRAy I can breathe soon). Ipratropium (short), tiotropium (long)

Answer 339

Muscarinic antagonist In genitourinary system for reducing urgency in mild cystitis and reducing bladder spasms. Other agents: tolterodine, fesoterodine, trospium.

Answer 340

Muscarinic antagonist Used in Gastrointestinal and respiratory systems for preoperative use to reduce airway secretions (parenteral) and for drooling and peptic ulcers (orally).

Answer 341

Direct sympathomimetic Beta greater than alpha Uses: anaphylaxis, open angle glaucoma, asthma, hypotension; alpha effects predominate at high doses

Answer 342

Direct sympathomimetic alpha1 > alpha2 > Beta1 Uses: hypotension (but decreased renal perfusion).

Answer 343

Direct sympathomimetic Beta1 = Beta2 uses: electrophysiologic evaluation of tachyarrhythmias. Can worsen ischemia.

Answer 344

Direct sympathomimetic D1 = D2 > Beta > alpha Uses: unstable bradycardia, heart failure, shock; inotropic and chronotropic alpha effects predominate at high doses.

Answer 345

Direct sympathomimetic B1 > B2, alpha. Uses: Heart failure (inotropic > chronotropic), cardiac stress testing.

Answer 346

Direct sympathomimetic alpha1 > alpha 2. Uses: Hypotension (vasoconstrictor), ocular procedures (mydriatic), rhinitis (decongestant) .

Answer 347

Direct sympathomimetic B2 > B1. Uses: Albuterol for acute asthma; salmeterol for long-term asthma or COPD control; terbutaline to reduce premature uterine contractions.

Answer 348

Indirect sympathomimetic. Action: indirect general agonist, reuptake inhibitor, also released stored catecholamines. Uses: narcolepsy, obesity, attention deficit disorder.

Answer 349

Indirect sympathomimetic Action: Indirect general agonist, released stored catecholamines. Uses: nasal decongestion, urinary incontinence, hypotension.

Answer 350

indirect sympathomimetic Action: Indirect general agonist, reuptake inhibitor. Uses: causes vasoconstriction and local anesthesia; never give B-blockers if cocaine intoxication is suspected ( can lead to unopposed alpha1 activation and extreme hypertension).

Answer 351

Sympatholytic (alpha2- agonist) Uses: Hypertensive urgency (limited siutations); does not decrease renal blood flow. ADHD, severe pain, and a variety of off-label indications (e.g. ethanol and opioid withdrawal). Toxicity: CNS depression, bradycardia, hypotension, respiratory depression, and small pupil size.

Answer 352

Sympatholytic (alpha2- agonist) Uses: Hypertension in pregnancy. Safe in pregnancy. Toxicity: Direct Coombs + hemolytic anemia, SLE-like syndrome.

Answer 353

nonselective alpha blocker. Irreversible. Uses: pheochromocytoma (used preoperatively) to prevent catecholamine (hypertensive) crisis. Toxicity: orthostatic hypotension, reflex tachycardia.

Answer 354

nonselective alpha blocker. Reversible. Uses: Give to patients on MAO inhibitors who eat tyramine containing foods.

Answer 355

alpha-1 selective blocker. Think all the -osin endings. Uses: urinary symptoms of BPH; PTSD (prazosin); hypertension (except tamsulosin). Toxicity: 1st dose orthostatic hypotension, dizziness, headache.

Answer 356

Alpha-2 selective inhibitor. Uses: depression. Toxicity: sedation, increased serum cholesterol, increased appetite.

Answer 357

Epinephrine: Before it has an increase in blood pressure because of the high dose effects on alpha receptors. After alpha blockade, the Beta effects win out and you get a drop in blood pressure (primarily B2). Phenylephrine: Before it has an increase in blood pressure because it is alpha 1 agonist (more than alpha 2). After there is a suppressed change (i.e. the pressure does not change), because it is only an alpha 1 agonist and nothing else.

Answer 358

Beta blockers. Angina pectoris: decreased heart rate and contractility, result in decreased O2 consumption MI: B-blockers (metoprolol, carvedilol, bisoprolol) decreased mortality SVT: Metoprolol, esmolol. Decreased AV conduction velocitiy (class 2 antiarrhythmic). Hypertension: decreased cardiac output, decreased renin secretion (Beta 1 blockade on JGA cells). CHF: slows progression of chronic failure Glaucoma: Timolol. decreased secretion of aqueous humor. Toxicity: Impotence, cardiovascular effects (bradycardia, AV block, CHF), CNS adverse effects (seizures, sedation, sleep alterations), dyslipidemia (metoprolol), and asthmatics/COPDers (may cause exacerbation). Avoid in cocaine users due to risk of unopposed alpha adrenergic receptor agonist activity. Despite theoretical concern of masking hypoglycemia in diabetics, benefits likely outweigh risks; not contraindicated.

Answer 359

They mask the effects in diabetics taking insulin. When a person becomes hypoglycemia they begin experience sympathetic symptoms (tremors, sweating, palpitations). Beta blockers (specifcally through B1) will block these effects and a person will not be aware their blood glucose is dropping. Also, through effects on blocking B2 on muscle and liver (which is normally stimulated by epinephrine), there will be decreased glycogenolysis and gluconeogenesis and it will be harder to correct for hypoglycemia.

Answer 360

B1 selective antagonists (B1 > B2): acebutolol (partial agonist), atenolol, betaxolol, esmolol, metoprolol. Selective antagonists mostly go from A to M (B1 with first half of alphabet).

Answer 361

``` nonselective antagonists (B1 = B2): nadolol, pindolol (partial agonist), propranolol, timolol. Non-selective antagonists mostly go from N to Z (Beta 2 with second half of the alphabet). ```

Answer 362

nonselective alpha and beta antagonists: carvedilol, labetalol. Nonselective alpha- and beta-antagonists have modified suffixes (instead of -"olol").

Answer 363

Combines cardiac-selective B1-adrenergic blockade with stimulation of B3 receptors, which activate NO synthase in vasculature.

Answer 364

Growth hormone receptor antagonist. Used for treating acromegaly.

Answer 365

HCTZ, indomethacin, amiloride (the diuretics work by causing diuresis and promoting reabsorption at the proximal tubule) Hydration

Answer 366

Treatment: fluid restriction, IV hypertonic saline, conivaptan, tolvaptan, demeclocycline (these last three drugs are ADH antagonists).

Answer 367

oxytocin has been shown to help by inducing uterine contraction. If not available, misoprostol can be used to (PGE analog)

Answer 368

``` Sotalol Risperidone (anti-psychotics) Macrolides Chloroquine Protease inhibitors (-navir) Quinidine (class Ia..also class III) Thiazides ``` Some Risky Meds Can Prolong QT Treatment is with Magnesium Sulfate. Remember: torasdes de pointes can progress to VT. Decrease K+ or Mg+ can also prolong QT.

Answer 369

a recombinant form of B-type natriuretic peptide for heart failure. Remember: this is normally released from ventricular myocytes (vs ANP which is released from atrial myocytes) in response to increased tension. Similar physiological action as ANP but with longer half life: it causes vasodilation, decreased Na+ absorption in the collecting tubule, and constriction of efferent arterioles and dilation of afferent arterioles via cGMP. thus promotes diuresis and contributes to aldosterone escape. BNP is also used for diagnosing heart failure (has very good negative predictive value).

Answer 370

methyldopa hyralazine nifedipine Labetol My Hypertension No Likey

Answer 371

SSRIs like paroxetine.

Answer 372

oral desmopressin acetate (DDAVP). Can also be used for central nephrogenic insipidus and von willebrands disease or hemophilia A (because of its effect on vasculature V2 to increase von willebrand factor release and consequently factor VIII).

Answer 373

lactulose to acidify GI tract and trap NH4+ for excretion. Benzoate or phenylbutrate bind amino acids and lead to excretion, decreasing ammonia levels. Note: this happens usually because of liver disease or hereditary urea cycle enzyme deficiencies. Results in excess NH4+ which depletes alpha ketoglutarate and blocks TCA cycle.

Answer 374

TMP-SMX and pentamidine are used for both. | Dapsone and atovaquone are used for prophylaxis only.

Answer 375

Cyproheptadine (5-HT2 receptor antagonist)

Answer 376

Trimetaphan camsilate (INN) or trimethaphan camsylate (USAN), trade name Arfonad, is a drug that counteracts cholinergic transmission at the ganglion type of nicotinic receptors of the autonomic ganglia and therefore blocks both the sympathetic nervous system and the parasympathetic nervous system. It acts as a non-depolarizing competitive antagonist at the nicotinic acetylcholine receptor, is short-acting, and is given intravenously. Uses: It is occasionally used to treat a hypertensive crisis and dissecting aortic aneurysm, to treat pulmonary edema, and to reduce bleeding during neurosurgery

Answer 377

mesalamine (5-ASA compound)

Answer 378

Phenobarbital which increases enzyme synthesis. | Note: Type 2 is already a milder form.

Answer 379

Phenothiazine antiemetic that acts by blocking dopamine receptors in the chemoreceptor trigger zone (floor of the fourth ventricle in the medulla). Helps with severe nausea and vomiting as well as nonpsychotic anxiety. Side effects: tardive dyskinesia, neuroleptic malignant syndrome, blood dsycrasias, lupus. Basically one of the high potency antipsychotics.

Drugs - First Aid 2014 Flashcards

(405 cards)