Pharm Flashcards

Question

Metyrapone

Answer 1

11-beta-hydroxylase inhibitor. Blocks cortisol synthesis.

Answer 2

Dopamine agonist. Decreases pituitary release of prolactin, useful in patients with infertility due to hyperprolactinemia or in patients with pituitary prolactinoma.

Answer 3

Dopamine agonist. Decreases pituitary release of prolactin, useful in patients with infertility due to hyperprolactinemia or in patients with pituitary prolactinoma.

Answer 4

Relaxes skeletal muscle by reducing the release of Ca++ from the sarcoplasmic reticulum. Used to tx malignant hyperthermia and neuroleptic malignant syndrome.

Answer 5

1. Vecuronium, rocuronium, pancuronium, tubocurarine. 2. Competitively inhibit postsynaptic ACh receptors at motor endplate as well as presynaptic ACh receptors, leading to progressively less ACh release at the NMJ. 3. Competitive inhibition of postsynaptic receptors prevents activation of some muscle fibers, decreasing strength of twitch compared to normal muscle twitch. 4. TOF stimulation displays progressive reduction in each of 4 responses (fading pattern) as result of less Ach being released with each subsequent impulse 2/2 the additional effect of presynaptic Ach receptor blockade. * ********************

Answer 6

1. Reversible acetylcholinesterase inhibitor. 2. Tx myasthenia gravis 3. Used routinely in anesthesia to reverse nondepolarizing muscle relaxants (rocuronium, vecuronium) at the end of an operation. 3. Tx postoperative or neurogenic ileus and urinary retention. 4. As quaternary amine, does not penetrate CNS like physostigmine does. NEOstigmine = NO CNS. * *********************

Answer 7

1. Used during anesthesia to assess degree of paralysis induced by NMJ-blocking agents. 2. Peripheral nerve stimulated 4 times in quick succession and muscular response recorded. 3. Height of each bar represents the strength of each twitch, with higher bars indicating the activation of increasing numbers of individual myocytes. 4. Nondepolarizing blockade always shows a fading pattern, depolarizing blockade always has a constant but diminished phase I and later a phase II fading pattern. * ******************

Answer 8

1. Succinylcholine. 2. Initially functions by preventing repolarization of motor endplate, causing equal reduction of all 4 twitches during TOF stimulation (phase I blockade). 3. Responses remain equal b/c presynaptic ACh receptor stimulation mobilizes presynaptic Ach vesicles for release. 4. Persistent exposure to succinylcholine results in eventual transition to phase II blockade as ACh receptors become desensitized and inactivated. * ******************

Answer 9

Potassium channel blockers. Inhibit outward potassium currents during phase 3 of cardiac AP, prolonging repolarization and total action potential duration (APD), with no effect on AP conduction velocity. Prolong QT interval. Eg, amiodarone, dronedarone, dofetilide, sotalol (also class II).

Answer 10

1. QT interval represents time required for ventricular depolarization and repolarization; can be thought of as a rough estimate of the APD. 2. Drugs that prolong cardiac APD (eg, class IA and III antiarrhythmics) will cause QT prolongation. 3. Prolonged QT is associated with torsades de pointes (polymorphic VT). 4. However, unlike other drugs that cause QT prolongation, AMIODARONE has very little risk of inducing torsades de pointes. 2/2 more homogenous effect on ventricular repolarization than other drugs (ie, less QT dispersion). * ******************

Answer 11

1. Sodium channel blockers. 2. Inhibit sodium-dependent depolarization (phase 0) causing slowed AP conduction velocity. 3. Moderate potassium channel blocking activity (phase 3) leading to prolongation of APD, and therefore the QT interval. 4. Increased risk of torsades de pointes. 5. Eg, Disopyramide, procainamide, quinidine. * ******************

Answer 12

1. Sodium channel blockers. 2. Inhibit sodium-dependent depolarization (phase 0). 3. Shortens APD (and therefore does not prolong the QT interval). No effect on AP conduction velocity. 4. Eg, Lidocaine, phenytoin, mexiletine. * ******************

Answer 13

1. Sodium channel blockers. 2. Inhibit sodium-dependent depolarization (phase 0) causing slowed AP conduction velocity. Minimal effect on APD and QT interval. 3. Eg, Flecainide, propafenone. * ******************

Answer 14

1. Beta receptor blockers. 2. Slow sinus node discharge rate. Slow AV nodal conduction and prolong refractoriness. 3. Eg, Atenolol, metoprolol, esmolol, carvedilol. * ******************

Answer 15

1. Non-dihydropyridine calcium channel blockers. 2. Slow sinus node discharge rate. Slow AV nodal conduction and prolong refractoriness. 3. Eg, Verapamil, diltiazem. * ******************

Answer 16

1. Interacts with A1 receptors on cardiac cells and activates K+ channels, increasing K+ conductance. 2. Causes transient conduction delay through AV node 3. Used for acute termination of paroxysmal supraventricular tachycardia (PSVT). 4. Rapidly metabolized in blood and tissues, with very brief duration of action (must be flushed with saline when administered to ensure reaching the AV node before degradation). * ******************

Answer 17

Rapidly-acting, short-duration beta-blocker (class II antiarrhythmic) that slows the rate of discharge of sinus node or ectopic pacemakers and increases refractory period of AV node. No effect on QT interval prolongation.

Answer 18

1. Fast-acting (less than 1 min), depolarizing neuromuscular blocking agent (muscle relaxant) used for rapid-sequence intubation that causes equal reduction of all 4 twitches during TOF stimulation (phase I blockade). 2. Cholinesterase metabolism determines duration of action, typically less than 10 mins. 3. Prolonged administration or use in patients with atypical cholinesterase activity (homozygous mutation that causes slowed metabolism of succinylcholine) causes transition to phase II blockade with progressive reduction in each of 4 twitches. 4. Paralysis can last for hours in these patients and they must be maintained on mechanical ventilation until spontaneous respiration resumes. * ******************

Answer 19

1. MAO, type B inhibitor. 2. Prevents MPTP-induced damage of dopaminergic neurons in substantia nigra (MPTP is a toxin that is converted to MPP+ by MAO-B. ) 3. MPP+ metabolite causes a Parkinsonism-like syndrome by destroying CNS dopaminergic neurons, and can be inhibited by Selegiline if given beforehand. 4. Used clinically to delay progression of Parkinson disease (PD). 5. Many neurologists favor use of combinations of selegiline, anticholinergics, and amantadine until they no longer provide control of symptoms, then starting levodopa/carbidopa. * ******************

Answer 20

1. Dopamine absent in the nigrostriatum of patients with Parkinson disease. 2. Levodopa is immediate precursor of DA and can cross blood brain barrier. 3. Levodopa absorbed in small intestine and converted to DA by DOPA-decarboxylase. 4. Peripheral conversion of L-dopa responsible for N/V 5. Carbidopa is a DOPA-decarboxylase inhibitor that doesn't cross BBB, therefore decreasing peripheral formation of DA, causing less side effects and allowing more levodopa to reach brain. * ******************

Answer 21

Dopamine agonist at D2 receptors. Shows only modest improvement in Parkinson symptoms as monotherapy but may delay introduction of levodopa by months to years.

Answer 22

May provide moderate improvement in patients with Parkinson disease. Initially designed as an antiviral influenza agent and found to have dopaminergic activity and possible anticholinergic action as well. Mechanism of action not well known. Side effects: dry mouth, N/V, visual blurring, mental changes, use with caution in the elderly.

Answer 23

Class III antiarrhythmic used to maintain sinus rhythm is patients with atrial fibrillation or other SVTs. Risks include serious ventricular arrhythmias (2/2 QT prolongation) and conduction disturbances. Prolongs APD and therefore QT interval by blocking outward potassium currents during phase 3 of AP, prolonging repolarization.

Answer 24

A newer, more selective aldosterone antagonist with fewer endocrine side effects than spironolactone. By competitively inhibiting aldosterone, eplerenone blocks aldosterone's detrimental cardiac remodeling and fibrosis effects.

Answer 25

Inhibits lipoic acid. Sx. vomiting, rice water stools, garlic breath.

Answer 26

Inhibits alcohol dehydrogenase, acting as an antidote for methanol or ethylene glycol poisoning

Answer 27

"Antabuse". Inhibits acetaldehyde dehydrogenase. An increase in acetaldehyde after drinking alcohol leads to an increase in hangover symptoms, which theoretically should make someone less likely to continue abusing alcohol.

Answer 28

1. Synthetic IFN-alpha is used in the tx of hairy cell leukemia, condyloma acuminata, hepatitis B and C infection, Kaposi sarcoma, renal cell carcinoma, malignant melanoma. 2. IFN-alpha is part of the innate host defense against both RNA and DNA viruses. Interferons alpha and beta are glycoproteins synthesized by virus-infected cells. 3. IFN-alpha and -beta act locally on uninfected cells to prime them for viral defense by helping to selectively degrade viral nucleic acid and protein. "Interfere" with viruses. * ******************

Answer 29

1. 2 NRTIs (or NtRTIs) "backbone" plus a 3rd drug (protease inhibitor, NNRTI, or integrase inhibitor) "base": eg, Atripla = [efavirenz + tenofovir + emtricitabine]. 2. Current US DHHS preferred initial regimens for adults and adolescents: 3. tenofovir/emtricitabine + raltegravir (integrase inhibitor) 4. tenofovir/emtricitabine + dolutegravir (integrase inhibitor) 5. abacavir/lamivudine (2 NRTIs) + dolutegravir for patients tested negative for HLA-B*5701 gene allele 6. tenofovir/emtricitabine + elvitegravir (integrase inhibitor) + cobicistat (inhibiting hepatic metabolism of elvitegravir) in patients with good kidney function (gfr > 70); Genvoya = [elvitegravir + cobicistat + emtricitabine + tenofovir] 7. tenofovir/emtricitabine + ritonavir + darunavir (both protease inhibitors) 8. In protease inhibitor based regimens, ritonavir is used at low doses to inhibit cytochrome p450 enzymes and "boost" levels of other protease inhibitors, rather than for direct antiviral effect. 9. Cobicistat used with elvitegravir for similar effect but has no direct antiviral effect itself. * ******************

Answer 30

Change in peptide precursor structure that alters vancomycin-binding site from D-alanyl-D-alanine terminus to a D-alanine-D-lactate terminus, preventing vancomycin from binding to its usual site.

Answer 31

1. Bacteria that produce beta-lactamase (penicillinase) are able to destroy beta-lactam ring of penicillins and render them ineffective. 2. Cephalosporins, carbapenems, and penicillinase-resistant penicillins (nafcillin, methicillin) are not susceptible to beta-lactamase. 3. Some bacteria (MRSA) have modified the penicillin binding proteins (PBPs) in their peptidoglycan cell walls so that beta-lactam antibiotics are unable to bind and interfere with cell wall synthesis. * ******************

Answer 32

Antibiotic that binds to, disrupts, and interferes with the permeability of the cytoplasmic membrane.

Answer 33

Mechanisms of tetracycline resistance include an increased efflux of the drug from within the bacterial cell via an active efflux pump or production of a protein that allows translation to take place even with tetracycline present.

Answer 34

1. Sulfonamides (sulfamethoxazole, sulfadiazine) are structural analogues of PABA, a precursor for dihydrofolic acid. 2. High levels of PABA analogue competitively inhibit dihydropteroate synthase (DHPS), an enzyme needed to form dihydrofolic acid and therefore folic acid synthesis. 3. Trimethoprim inhibits bacterial dihydrofolate reductase, the enzyme needed to create THF. (MTX inhibits DHFR in humans, pyrimethamine in protozoa). 4. Inhibition of folic acid synthesis results in disruption of DNA synthesis and inhibition of bacterial growth. * ******************

Answer 35

1. zidovudine (AZT or ZDV) - thymidine analog 2. didanosine (ddI) - adenosine analog 3. zalcitabine (ddC) - cytidine analog, d/c'd by drug company 4. lamivudine (3TC) - cytidine analog, also used in chronic hepatitis B tx 5. stavudine (d4T) - thymidine analog 6. emtricitabine (FTC) - cytidine analong 7. abacavir (ABC) - guanosine analog 8. entecavir (ETV) - guanosine analog, only approved for hepatitis B tx not HIV * ******************

Answer 36

1. Competitively inhibit HIV reverse transcriptase. 2. Compete with nucleotide triphosphates (eg, dATP, dCTP) to be added to newly synthesized viral DNA strand. 3. Prior to incorporation into viral DNA, NRTIs must be phosphorylated to form NRTI triphosphates. Phosphorylation carried out by cellular kinase enzymes. 4. Unlike natural deoxynucleotides, NRTIs and NtRTIs lack a 3′-hydroxyl group on deoxyribose moiety. 5. After incorporation of NRTI or NtRTI, next incoming deoxynucleotide cannot form a 5′–3′ phosphodiester bond needed to extend the DNA chain. 6. Thus, incorporation of NRTI or NtRTI halts viral DNA synthesis in a process known as chain termination. * ******************

Answer 37

1. All NRTIs- neutropenia (bone marrow suppression that can be reversed with granuloctye colony-stimulating factor G-CSF and erythropoietin), hypersensitivity reactions (rash), GI upset, lactic acidosis 2. zidovudine (AZT/ZDV)- megaloblastic anemia 3. didanosine (ddI)- pancreatitis 4. zalcitabine (ddC), stavudine (d4T)- peripheral neuropathy 5. abacavir (ABC)- lactic acidosis, contraindicated if patient has HLA-B5701 mutation * ******************

Answer 38

Use of AZT during pregnancy and in neonates with HIV+ mothers has been shown to significantly reduce the risk of viral transmission from mother to child. Can be used as general prophylaxis. Side effects of AZT- neutropenia, rash, GI upset, megaloblastic anemia.

Answer 39

1. Tenofovir (TDF) - adenosine analog, approved for HIV and HBV tx 2. Adefovir - adenosine analog, lower dose approved for chronic Hepatitis B tx, not approved for HIV 2/2 to toxicity issues with high dose * *****

Answer 40

1. Efavirenz 2. Nevirapine 3. Delavirdine 4. Etravirine (new) 5. Rilpivirine (new) * *******

Answer 41

1. NNRTIs block HIV reverse transcriptase by binding directly at a specific site. 2. Not incorporated into viral DNA like NRTIs and do not require phosphorylation to be active. 3. Inhibit movement of protein domains of reverse transcriptase needed to carry out the process of DNA synthesis. 4. NNRTIs are therefore classified as non-competitive inhibitors of reverse transcriptase. * ******************

Answer 42

1. Efavirenz- CNS disturbances (insomnia, dizziness, delusions, vivid nightmares), rash, hepatotoxicity, teratogenic (contraindicated in pregnancy) 2. Nevirapine - SJS (rash), fulminant hepatitis (hepatotoxicity), induction of cytochrome P450 resulting in increased metabolism of several drugs (OCPs, warfarin, metronidazole, ketoconazole, some protease inhibitors) 3. Delaviridine - headache, fatigue, nausea, rash, elevated LFTs, teratogenic (contraindicated in pregnancy) * ******************

Answer 43

1. Inhibit HIV protease enzyme, responsible for cleaving precursor proteins into mature proteins involved in forming core of viral particle. 2. Assembly of virions depends on HIV-1 protease (pol gene), which cleaves polypeptide products of HIV mRNA into their functional parts. 3. Thus, protease inhibitors prevent maturation of new viruses and the virus is UNABLE TO REPLICATE. 4. All protease inhibitor names end in -navir. 5. Rifampin is a potent CYP/UGT inducer and is contraindicated with protease inhibitors as it can decrease their concentration. * ******************

Answer 44

1. Atazanavir 2. Darunavir 3. Fosamprenavir- superceded Amprenavir 4. Indinavir - "Crix belly" 5. Lopinavir - combo with ritonavir 6. Ritonavir - can boost other drug concentrations by inhibiting cytochrome P450. 7. Saquinavir - first approved ever 8. Nelfinavir 9. Tipranavir * ******************

Answer 45

1. Raltegravir 2. Elvitegravir 3. Dolutegravir * *****

Answer 46

Inhibit HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase. Side effects: increase in creatine kinase

Answer 47

1. All protease inhibitors - lipodystrophy (Cushing-like syndrome of altered distribution of body fat causing a buffalo hump or truncal obesity), insulin resistance, hyperglycemia, hyperlipidemia, GI intolerance (nausea, diarrhea). 2. Ritonavir, nelfinavir- paresthesias 3. Indinavir- elevated bilirubin, kidney stones, nephropathy, hematuria 4. Ritonavir- inhibits cyt P450 leading to increased serum levels of drugs (eg, other protease inhibitors, ketoconazole, rifampin, erythromycin, some anti-arrhythmics, benzodiazepines, slozapine, fluoxetine, haloperidol.) * ******************

Answer 48

Highly active antiretroviral therapy often initiated at time of HIV diagnosis. Strongest indication for patients presenting with AIDS-defining illness, low CD4+ cell counts (less than 500) or high viral load. Regimen consists of 3 drugs to prevent resistance: 2 NRTIs and preferably an integrase inhibitor.

Answer 49

1. Enfuvirtide- binds gp41, inhibiting viral entry/penetration into the cell. Skin reaction at injection sites. 2. Maraviroc- binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120 and thus inhibiting attachment of the virion. * ***********

Answer 50

1. Acyclovir, famciclovir, valacyclovir, penciclovir. 2. Guanosine analogs that are monophosphorylated by viral thymidine kinase. Not phosphorylated in uninfected cells, causing few adverse effects. Triphosphate formed by cellular enzymes. Once phosphorylated, dGTP analogs preferentially inhibit viral DNA polymerase by chain termination. 3. Active against HSV-1, HSV-2, VZV (famciclovir), weakly against EBV. 4. Not active against CMV. 5. Tx mucocutaneous/genital herpes, herpes encephalitis, acute VZV infection, and oral hairy leukoplakia (assoc with EBV infection). Prophylaxis in immunocompromised patients. 6. No effect on latent HSV/VZV. 7. Valacyclovir (prodrug of acyclovir) has better oral bioavailability. 8. Resistance to acyclovir if virus has mutated viral thymidine kinase. * ******************

Answer 51

1. Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. 2. GI upset. 3. Neurotoxicity (tremor, delirium) * ************

Answer 52

1. Oseltamivir, zanamivir 2. Inhibit influenza neuraminidase (viral enzyme necessary for viral replication and release of viral particles from infected cells), thus decreasing release of progeny virus. 3. Tx and prevention (prophylaxis) of both influenza A and B. * *********

Answer 53

1. Similar drug: Rimantadine 2. Binds to the M2 surface protein proton channel ion on influenza A viral particles, blocking the uncoating of the viral RNA within host cells, and thus inhibiting intracellular viral replication. 3. Amantadine has also been shown to stimulate release of dopamine from neurons of the nigrostriatum. Used in the treatment of early Parkinson disease. 4. Previously used to reduce duration of influenza A symptoms and prophylaxis in elderly/immunocompromised, but no longer used 2/2 increased resistance. 5. Side effects: CNS symptoms such as ataxia, slurred speech, dizziness, and GI upset. * ******************

Answer 54

1. Ganciclovir, valganciclovir (prodrug of ganciclovir with better oral bioavailability) 2. Guanosine analog. Phosphorylation by CMV viral kinase into monophosphate. Triphosphate formed by cellular kinases. Once phosphorylated, ganciclovir preferentially inhibits CMV DNA polymerase, leading to inhibition of viral DNA synthesis. 3. Used to treat CMV infections, especially CMV retinitis (often seen in HIV infected patients) 4. Mechanism of resistance is mutated viral kinase. * ******************

Answer 55

Pancytopenia (bone marrow suppression), nephrotoxicity, seizures, headache. More toxic to host enzymes than acyclovir.

Answer 56

1. Viral DNA polymerase inhibitor: 2. Pyrophosphate analogue that inhibits viral DNA/RNA polymerase without requiring activation by viral kinase. Binds to pyrophosphate-binding site of enzyme. 3. Used as second-line tx in CMV retinitis and other infections (when ganciclovir fails). 4. Also used in treatment of acyclovir-resistant HSV and VZV infections. 5. Major side effect is nephrotoxicity. Also electrolyte abnormalities (hypo/hypercalcemia, hypo/hyperphosphatemia, hypokalemia, hypomagnesemia) can lead to seizures. 6. Mechanism of resistance is mutated DNA polymerase. 7. FOScarnet = pyroFOSphate analog * ******************

Answer 57

1. Viral DNA polymerase inhibitor: 2. Preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase. 3. Tx CMV retinitis in immunocompromised patients; tx acyclovir-resistant HSV. 4. Long half-life. 5. Nephrotoxicity- coadminister with probenecid and IV saline to reduce toxicity. * ***********

Answer 58

1. Inhibits synthesis of guanine nucleotides (GMP) by competitively inhibiting inosine monophosphate dehydrogenase and also is a guanosine analog that inhibits viral RNA polymerase, resulting in inhibition of viral replication. 2. Tx for chronic HCV infection 3. Tx for severe RSV bronchiolitis (palivizumab preferred in children) 4. Adverse effects include hemolytic anemia, elevated bilirubin, and severe teratogenicity. Contraindicated in pregnancy and in patients with renal insufficiency. * ************

Answer 59

1. Guanosine nucleoside analog (like HIV NRTI but only for HBV infection). 2. Preferentially inhibits hepatitis B viral polymerase. * ********

Answer 60

1. Entecavir (guanosine nulceoside analog) 2. Lamivudine (3TC) - cytidine analog, used in HIV tx 3. Tenofovir (TDF) - adenosine analog, used in HIV tx 4. Adefovir - adenosine analog, lower dose approved for chronic Hepatitis B tx, not approved for HIV 2/2 to toxicity issues with high dose. 5. Interferon-alpha * **********

Answer 61

1. Glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumor properties. 2. IFN-alpha: chronic hepatitis B and C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma. The pegylated types are pegylated interferon alfa-2a and pegylated interferon alfa-2b. 3. IFN-beta: multiple sclerosis, reduces relapse rate. IFN-β1 is not an appropriate treatment for patients with progressive, non-relapsing forms of multiple sclerosis. 4. IFN-gamma: chronic granulomatous disease (CGD) 5. Side effects: flu-like symptoms, depression, neutropenia, myopathy. * ******************

Answer 62

IFN-gamma is a type II interferon produced mainly by T cells and NK cells. It promotes Th1 differentiation, increases expression of class II MHC molecules on APCs, and improves the intracellular killing ability of macrophages. Virally-infected respiratory epithelial cells would secret IFN alpha and beta, not IFN gamma. Synthetic IFN-gamma is used to treat CGD, an AR disorder characterized by NADPH oxidase deficiency.

Answer 63

IFN-alpha and IFN-beta are synthesized and secreted by most human cells in response to VIRAL infections. These IFNs bind to type I interferon receptors found on infected and neighboring cells (autocrine/paracrine signaling), resulting in transcription of antiviral enzymes capable of stopping protein synthesis: RNase L (endonuclease that degrades all cellular RNA), protein kinase R (inactivates elF-2, inhibiting translation initiation). However, these enzymes only become active in the presence of dsRNA, which forms in virally-infected cells. Thus, normal metabolism and protein synthesis can continue in uninfected cells but is selectively inhibited in virally-infected cells. IFN-alpha and beta also induce MHC class I expression on all cells and stimulate the activity of NK and cytotoxic T cells, increasing the proportion of virally infected cells that undergo apoptosis.

Answer 64

A metalloprotease that inactivates several peptide hormones: bradykinin, glucagon, enkephalins, natriuretic peptides (ANP and BNP).

Answer 65

1. Inhibits HCV RNA-dependent RNA polymerase by acting as a chain terminator. 2. Chronic HCV tx in combination with ribavirin, +/- peginterferon alfa 3. Do not use as monotherapy. 4. Adverse effects: fatigue, headache, nausea * ********

Answer 66

1. HCV protease inhibitor, prevents viral replication. 2. Chronic HCV tx in combination with ledipasvir (NS5A inhibitor) 3. Do not use as monotherapy. 4. Adverse effects: photosensitivity, rash. * ********

Answer 67

1. Ribavirin 2. Sofosbuvir (not monotherapy) 3. Simeprevir (not monotherapy) 4. Peginterferon alfa-2a or -2b * ******

Answer 68

1. Autoclave- pressurized steam at 120C. May be sporicidal. 2. Alcohols- denature proteins and disrupt cell membranes, not sporicidal. 3. Chlorhexidine- denature proteins and disrupt cell membranes, not sporicidal. 4. Hydrogen peroxide- free radical oxidation. Sporicidal. 5. Iodine/iodophors- halogenation of DNA, RNA, proteins. May be sporicidal. * *******

Answer 69

1. SAFE Children Take Really Good Care: 2. Sulfonamides - kernicterus (sulfasalazine, SMX-TMP, sulfadiazine) 3. Aminoglycosides - ototoxicity 4. Fluoroquinolones - cartilage damage 5. Efavirenz/Delavirdine (HIV meds) 6. Clarithromycin - embryotoxic 7. Tetracyclines - discolored teeth, inhibition of bone growth 8. Ribavirin - teratogenic 9. Griseofulvin - teratogenic 10. Chloramphenicol - gray baby syndrome * **********

Answer 70

Ceftriaxone

Answer 71

Ceftriaxone, ciprofloxacin, or rifampin

Answer 72

Intrapartum penicillin G or ampicillin

Answer 73

Erythromycin ointment in eyes

Answer 74

Benzathine penicillin G or oral penicillin V

Answer 75

Benzathine penicillin G

Answer 76

1. CD4 less than 200- TMP-SMX prophylaxis against PCP 2. CD4 less than 100- TMP-SMX prophylaxis against PCP and toxoplasmosis (+ pyrimethamine) 3. CD4 less than 50- azithromycin/clarithromycin prophylaxis against MAC * **********

Answer 77

1. Vancomycin 2. Daptomycin 3. Linezolid 4. Tigecycline 5. Ceftaroline * ******

Answer 78

1. Linezolid 2. Streptogramins (quinupristin, dalfopristin) * *******

Answer 79

1. Polymyxin B 2. Polymyxin E (colistin) * *******

Answer 80

1. Antifungal tx 2. Inhibits fungal enzyme squalene epoxidase, inhibits synthesis of lanosterol in fungus 3. Tx dermatophytoses, especially onychomycosis 4. Adverse effects: GI upset, headaches, hepatoxicity, taste disturbance. * *******

Answer 81

1. Anidulafungin, caspofungin, micafungin 2. Inhibit cell wall synthesis by inhibiting synthesis of beta-glucan 3. Tx invasive aspergillosis, Candida. 4. Adverse effects: GI upset, flushing (by histamine release) * *******

Answer 82

1. Binds ergosterol (unique to fungi) and forms membrane pores that allow leakage of electrolytes. 2. "AmphoTEARicin B tears holes in the fungal membrane by forming pores." 3. Tx serious systemic mycoses: cryptococcus (amphotericin B +/- flucytosine for cryptococcal meningitis), Blastomyces, Coccidioides, Histoplasma, Candida, Mucor 5. Intrathecal tx for fungal meningitis 6. Supplement K+ and Mg2+ due to altered renal tubule permeability 7. Adverse effects "amphoterrible": fever/chills (shake and bake), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis. 8. Hydration to decrease nephrotoxicity 9. Liposomal amphotericin decreases toxicity. * ******************

Answer 83

1. Binds ergosterol (unique to fungi) and forms membrane pores that allow leakage of electrolytes. 2. Topical use only as too toxic for systemic use. 3. "Swish and swallow" for oral candidiasis (trush) 4. Topical for diaper rash or vaginal candidiasis. * ******

Answer 84

1. Inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase. 2. Tx systemic fungal infections (especially meningitis caused by Cryptococcus) in combination with amphotericin B. 3. Bone marrow suppression. * *******

Answer 85

1. Fluconazole (itraconazole, voriconazole), ketoconazole (clotrimazole, miconazole) 2. Inhibit ergosterol synthesis by inhibiting 14-alpha-demethylase (fungal cytochrome P-450 that converts lanosterol to ergosterol). 3. Tx local and less serious systemic mycoses. 4. Fluconazole- chronic suppression of cryptococcal meningitis and candidal infections in AIDS patients. 5. Itraconazole- Blastomyces, Coccidioides, Histoplasma 6. Clotrimazole and miconazole- cutaneous fungal infections only (2/2 toxicity) such as vulvovaginal candidiasis, tinea pedis, tinea cruris) 7. Adverse effects: testosterone synthesis inhibition (gynecomastia, decreased libido, menstrual irregularities, esp ketoconazole), liver dysfunction (inhibits cytochrome P-450). 8. Ketoconazole also used in treatment of patients with Cushing syndrome and prostate cancer 2/2 its disruption of gonadal and adrenal steroid synthesis. * ******************

Answer 86

1. Interferes with microtubule function, thereby disrupting mitosis and fungal replication. 2. Deposits in keratin-containing tissues (eg, nails, hair) 3. Oral tx of superficial infections; inhibits growth of superficial dermatophyte infections (tinea, ringworm) 4. Adverse effects: teratogenic, carcinogenic, confusion, headaches, GI upset, hepatitis, increases cyt P-450 and therefore warfarin metabolism. * ************

Answer 87

1. Interferes with THF synthesis from folic acid by inhibiting dihydrofolate reductase (DHFR) in protozoans. THF is needed for DNA and RNA synthesis. 2. Tx of Toxoplasmosis (Toxoplasma gondii) when combined with sulfadiazine. 3. Tx and prophylaxis of P falciparum (in combo with sulfadiazine). 4. Adverse effects: bone marrow suppression, can give folinic acid to prevent. * ***********

Answer 88

1. Tx of early Trypanosoma brucei infections (before CNS involvement). 2. Also used to treat Onchocerca volvulus infections (river blindness). 3. Adverse effects: GI upset, neurologic disturbances, renal abnormalities. 4. Thought to inhibit parasitic enzymes involved in energy metabolism. * ***********

Answer 89

1. Tx Trypanosoma cruzi infection (Chagas disease) 2. Adverse effects: GI upset, neuropathy, seizures, hypersensitivity reactions. 3. Breakdown of drug generates oxygen free radicals that damage the parasite. * **********

Answer 90

1. Tx of Leishmaniasis 2. Adverse effects: GI upset, ECG changes, cardiac arrhythmias. 3. Thought to inhibit parasitic glycolysis. * ********

Answer 91

1. Tx of late Trypanosoma brucei infections (after CNS involvement) 2. Adverse effects: encephalopathy, hypersensitivity reactions, GI upset, renal damage. 3. Thought to inhibit multiple parasitic enzymes. * *********

Answer 92

1. Alternative tx of Trypanosoma brucei infection (African trypanosomiasis) and leishmaniasis. 2. Alternative tx and prophylaxis for PCP pneumonia 3. Thought to inhibit parasitic RNA synthesis. 4. Adverse effects: nephrotoxicity, pancreatic damage, cardiac arrhythmias. * ********

Answer 93

1. Permethrin - blocks Na+ channels leading to neurotoxicity 2. Malathion - acetylcholinesterase inhibitor 3. Lindane - blocks GABA channels leading to neurotoxicity 4. Used to treat scabies (Sarcoptes scabiei) and lice (Pediculus and Pthirus). 5. "Treat PML (Pesty Mites and Lice) with PML (Permethrin, Malathion, Lindane) b/c they NAG you (Na+, AChE, GABA blockade). * ********

Answer 94

1. Concentrates in parasite food vacuoles and prevents metabolism of heme into hemozoin. Heme accumulates and is toxic to plasmodia, causing cell death. 2. Tx and chemoprophylaxis for erythrocytic forms of P vivax and P ovale. 3. Frequency of resistance in P falciparum too high 2/2 mutation that codes for membrane pump that decreases intracellular concentration of chloroquine. 4. Tx P falciparum with artemether/lumefantrine or atovaquone/proguanil. For life-threatening malaria, use quinidine (quinine) or artesunate. 5. Adverse effects: GI upset, pruritis (especially in dark-skinned individuals), retinopathy/visual disturbances, ECG changes. * ******************

Answer 95

1. MOA unknown 2. Tx of drug-resistant P falciparum malaria 3. Also used to tx Babesia microti infection 4. Adverse effects: Cinchonism (tinnitus, headache, dizziness, nausea); Coombs positive hemolytic anemia; fetal toxicity. * *********

Answer 96

1. MOA unknown 2. Tx of drug-resistant P falciparum malaria 3. Chemoprophylaxis for malaria 4. Adverse effects: GI upset, mental status changes, cardiac abnormalities. * ********

Answer 97

1. MOA unknown, thought that metabolites of primaquine act as oxidizing agents, causing parasitic and host cell damage and death. 2. Tx hepatic forms of P vivax and P ovale malaria. 3. Adverse effects: hemolytic anemia in G6PD patients, abdominal pain. 4. Contraindicated in pregnancy as can cause hemolytic anemia in fetus. * ********

Answer 98

1. TB prophylaxis: Isoniazid 2. TB tx: RIPE 3. Rifampin, Isoniazid, Pyrazinamide, Ethambutol * ********

Answer 99

1. MAI prophylaxis: azithromycin/clarithromycin, rifabutin 2. MAI tx: azithromycin or clarithromycin + ethambutol 3. Can add rifabutin or ciprofloxacin. 4. More drug resistant than M tuberculosis * ********

Answer 100

1. Long-term treatment with dapsone and rifampin for tuberculoid form. 2. Add clofazimine for lepromatous form. * ********

Answer 101

1. MOA: Inhibit DNA-dependent RNA polymerase 2. Rifampin's 4 Rs: 3. RNA polymerase inhibitor 4. Ramps up microsomal cytochrome P-450 5. Red/orange body fluids 6. Rapid resistance if used alone 7. RifAMPin RAMPs up cytochrome P-450, BUT rifaBUTin does not. 8. Tx for TB (RIPE), delays resistance to dapsone when used to tx leprosy 9. Prophylaxis for meningococcus and Haemophilus influenzae type B. 10. Minor hepatotoxicity and drug interactions; orange body fluids (nonhazardous); rifabutin favored over rifampin in patients with HIV infection due to less cyt P-450 stimulaiotn. 11. Mutations reduce drug binding to RNA polymerase, so monotherapy rapidly leads to resistance. * ******************

Answer 102

1. MOA: decreased synthesis of mycolic acids required for cell wall. Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolite. 2. Mutations leading to underexpression of KatG cause resistance. 3. Only agent used as solo prophylaxis against TB. 4. Used as monotherapy for latent TB. 5. Different INH half-lives in fast vs. slow acetylators. 6. INH Injures Neurons and Hepatocytes. 7. Hepatotoxicity, P-450 inhibition, drug-induced SLE, vitamin B6 deficiency leading to peripheral neuropathy and sideroblastic anemia. 8. Administer with pyridoxine (vitamin B6) * ******************

Answer 103

1. MOA uncertain. 2. Prodrug converted to active compound pyrazinoic acid. 3. Works best at acidic pH (eg, in host phagolysosomes). 4. Tx for TB (RIPE) 5. Hyperuricemia, hepatotoxicity. * ******

Answer 104

1. MOA: decreased carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase (enzyme required to make arabinogalactan component of mycobacterial cell wall). 2. Tx for TB (RIPE) 3. Optic neuropathy (red-green color blindness), think "EYEthambutol" * *******

Answer 105

1. MOA: interferes with 30s component of ribosome. 2. 2nd line tx for TB. 3. Tinnitus, vertigo, ataxia, nephrotoxicity. * ********

Answer 106

1. Penicillin G (IV and IM) 2. Penicillin V (oral) 3. Amoxicillin (aminopenicillin) 4. Ampicillin (aminopenicillin) 5. Amoxicillin/Clavulanate (Augmentin) 6. Ampicillin/Sulbactam (Unasyn) 7. Must be used with beta-lactamase inhibitors * **********

Answer 107

1. Dicloxacillin 2. Nafcillin 3. Oxacillin * ******

Answer 108

1. Piperacillin 2. Ticarcillin 3. Extended spectrum penicillin. Tx Pseudomonas spp. and gram - rods. Use with beta-lactamase inhibitors as susceptible. Eg, Piperacillin-Tazobactam (Zosyn), Ticarcillin/Clavulanate (Timentin) 4. Hypersensitivity reactions * *******

Answer 109

1. 1st generation - Cefazolin 2. 2nd generation - Cefoxitin 3. 3rd generation - Ceftriaxone 4. 4th generation - Cefepime 5. 5th generation - Ceftaroline * ********

Answer 110

1. Imipenem- broad-spectrum, beta-lactamase resistant, always administer with cilastatin (inhibitor of dehydropeptidase I) to decrease inactivation of drug in renal tubules. 2. Meropenem - decreased risk of seizures, stable to dehydropeptidase I 3. Ertapenem - limited Pseudomonas coverage 4. Doripenem 5. Wide spectrum (gram + cocci, gram - rods, anaerobes) but significant side effects. Limit use to life-threatening infections or after other drugs have failed. 6. Adverse effects: GI distress, skin rash, CNS toxicity (seizures) at high plasma levels. * ********

Answer 111

1. Aztreonam 2. Less susceptible to beta-lactamases. 3. Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3. 4. Synergistic with aminoglycosides. 5. No cross-allergenicity with penicillins. 6. Tx Gram - rods only, no activity against gram + rods or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides. 7. Usually nontoxic; occasional GI upset. * ********

Answer 112

1. D-Ala-D-Ala structural analog. Bind PBPs (transpeptidases), preventing peptidoglycan cross-linking of bacterial cell wall. Activates autolytic enzymes. Penicillinase sensitive, cleaves Beta-lactam ring rendering penicillin ineffective. 2. Mostly used for gram + organisms (S pneumoniae, S pyogenes, Actinomyces). 3. Also used for gram - cocci (mainly N meningitidis) and spirochetes (T pallidum) 4. Bactericidal for gram + cocci, gram + rods, gram - cocci, and spirochetes. 5. Hypersensitivity reactions, direct Coombs + hemolytic anemia. * ***********

Answer 113

1. Amoxicillin, ampicillin; penicillinase-sensitive penicillins 2. MOA: bind PBPs, inhibiting cell wall formation. 3. Wider spectrum than penicillin - H influenzae, H pylori, E coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci. (HHELPSS kill) 4. Adverse effects: hypersensitivity reactions, rash, pseudomembranous colitis. 5. AmOxicillin has greater Oral bioavailability than ampicillin. * **********

Answer 114

1. Dicloxacillin, nafcillin, oxacillin 2. Narrow spectrum. "Use naf for staph." Staph aureus, except MRSA, resistant 2/2 altered PBP target site. 3. Hypersensitivity reactions, interstitial nephritis. 4. Penicillinase resistant b/c bulky R group blocks access of beta-lactamase to beta-lactam ring. * *********

Answer 115

1. Beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal. 2. Organisms not covered by 1st-4th generation cephalosporins are LAME. Listeria, Atypicals (Chlamydia, Mycoplasma), MRSA, Enterococci. 3. Ceftaroline (5th gen) covers MRSA. 4. Adverse effects: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency. Exhibit some cross-reactivity with penicillins. Increase nephrotoxicity of aminoglycosides. 5. Mechanism of resistance = structural changes in PBPs. * *********

Answer 116

1. Cefazolin, cephalexin 2. Tx gram + cocci, Proteus mirabilis, E coli, Klebsiella pneumoniae. (PEcK) 3. Cefazolin used prior to surgery to prevent S aureus wound infections. * **********

Answer 117

1. Cefaclor, cefoxitin, cefuroxime 2. Tx gram + cocci, H influenzae, Enterobacter aerogenes, Neisseria spp., Serratia marcescens, Proteus mirabilis, E coli, Klebsiella pneumoniae. (HENS PEcK) * *********

Answer 118

1. Ceftriaxone, cefotaxime, ceftazidime 2. Tx serious gram - infections resistant to other beta lactams 3. Ceftriaxone- meningitis, gonorrhea, disseminated Lyme 4. Ceftazidime- Pseudomonas * *********

Answer 119

1. Cefepime 2. Tx gram - organisms, with increased activity against Pseudomonas and gram + organisms * ***********

Answer 120

1. Ceftaroline 2. Broad gram + and gram - coverage, including MRSA 3. Does not cover Pseudomonas * *********

Answer 121

1. Prevents formation of peptidoglycan cell wall by binding D-alanyl-D-alanine termini of cell wall peptide precursors. 2. Bactericidal against most bacteria (bacteriostatic against C difficile). Not susceptible to beta lactamases. 3. Tx Gram + bugs only: serious, MDR organisms, including MRSA, S epidermidis, sensitive Enterococcus species, Clostridium difficile (oral dose). 4. Well tolerated in general- but NOT trouble free: Nephrotoxicity, Ototoxicity, Thrombophlebitis 5. Red man syndrome- diffuse flushing, can largely prevent with pretreatment with antihistamines and slow infusion rate 6. Mechanism of resistance occurs via amino acid modification of D-ala-D-ala to D-ala-D-lac, so vancomycin cannot bind. * ******************

Answer 122

1. Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin (GNATS) 2. Bactericidal- irreversible inhibition of initiation complex through binding of 30s subunit. Can cause misreading of mRNA. Also block translocation. Require oxygen for uptake into bacterial cells and therefore ineffective against anaerobes. 3. Tx severe gram - rod infections. Synergistic with b-lactams. 4. Neomycin for bowel surgery. 5. Adverse effects: Nephrotoxicity, Neuromuscular blockade, Ototoxicity (esp when used with loop diuretics), Teratogen. (NNOT) 6. Mechanisms of resistance include bacterial transferase enzymes inactivating the drugs by acetylation, phosphorylation, or adenylation. 7. Pseudomonas species have been found to have another resistance mechanism to aminoglycosides in which there is decreased antibiotic entry into the bacterium. * ******************

Answer 123

1. Competitive muscarinic (M1, M2, M3) antagonist (inhibits parasympathetic nervous system) 2. Causes sedation (M1), disorientation (M1), psychosis (M1), tachycardia (M2), flushing (M2), constipation (M3, urinary retention (M3), cycloplegia (M3), mydriasis, hyperthermia (2/2 decreased sweating), dry mouth (2/2 decreased salivation) (M3). 3. Atropine can cause acute angle-closure glaucoma in elderly (due to mydriasis), urinary retention in men with BPH, and hyperthermia in infants. 4. Used to tx bradycardia in cardiac emergencies or as antidote for cholinesterase inhibitor poisoning (eg "nerve gas", insecticide). Does not block excitation of skeletal muscle and CNS as mediated by NAChR. 6. Occurs naturally in some plants- deadly nightshade, mandrake, Jimson weed 8. Atropine poisoning treated with cholinesterase inhibitors (eg, physostigmine can cross BBB). * ******************

Answer 124

1. Atropine, Jimson weed (garderner's pupil, mydriasis due to plant alkaloids), scopolamine, diphenhydramine, phenothiazine, benztropine 2. Pilocarpine/physostigmine are antidotes 3. Hyperthermia, flushing, decreased sweating, pupil dilation (cycloplegia), dry mouth (decreased salivation), urinary retention, tachycardia, psychosis. 4. "Hot as a hare, red as a beet, blind as a bat, mad as a hatter, dry as a bone, and the heart runs alone." * ******************

Answer 125

1. Used in conjunction with atropine as an antidote to organophosphate poisoning (nerve gases/insecticides) by organophosphate compounds that inhibit cholinesterases through phosphorylation. 2. Pralidoxime reactivates phosphorylated cholinesterases by removing phosphate group, thus allowing cholinesterases to function normally again and breakdown of ACh at neuronal synapse. 3. Side effects: flushing, tachycardia, dry mouth, blurry vision, sedation. * ******************

Answer 126

1. M1 receptor: CNS (including sympathetic ganglia) --- PLC activated by Gq, causing increased IP3 and DAG, causing increased intracellular Ca2+ --- CNS stimulation. 2. M2 receptor: Heart --- AC inhibited by Gi leading to decreased cAMP and increased K+ conductance --- decreased heart rate and contractility. 3. M3 receptor: smooth muscle of GI and GU tracts, smooth muscle of bronchi, sphincter and ciliary muscle of eyes --- PLC activated by Gq, causing increased IP3 and DAG, causing increased intracellular Ca2+ --- increased gut peristalsis and exocrine secretions, increased bladder contraction and relaxed bladder sphincter, bronchoconstriction and increased respiratory secretions, contracted sphincter muscle leading to pupil constriction and contracted ciliary muscle, leading to loss of far vision (accommodation). * ******************

Answer 127

1. Hexamethonium, mecamylamine, trimethaphan 2. Used to tx hypertensive emergencies in the past, but much greater side effects than drugs used today 3. Competitively inhibit activation of Nn-receptors on postsynaptic neuron of autonomic ganglia, blocking autonomic outflow to both sympathetic and parasympathetic nervous systems. Hypotension produced by decreased in PVR and cardiac output mediated by blockade of sympathetic nervous system. 4. Nicotine acts as an agonist at Nn (autonomic ganglia, CNS, adrenal medulla) and Nm (NMJ) nicotinic receptors. Nicotine promotes muscle contraction at NmRs and vasodilation of renal blood vessels and stims epinephrine release at NnRs. * ******************

Answer 128

1. Muscarinic receptor agonist (M1, M2, M3), resistant to AChE 2. Tx Open-angle and narrow-angle glaucoma, xerostomia (Sjogren syndrome) 3. Potent stimulator of sweat, tears, saliva 4. Stimulates M3-->contraction of pupillary sphincter muscle and opening canal of Schlemm (tx narrow-angle glaucoma). Also opens trabecular mesh-work of eye by contracting ciliary muscle, increasing outflow of aqueous humor (tx open-angle glaucoma). * ******************

Answer 129

1. Muscarinic and nicotinic R agonist 2. Used to constrict pupil and relieve intraocular pressure in open-angle glaucoma or to produce pupillary constriction during ophthalmic surgery. 3. "CARBon copy of AcetylCHOLine." * *******

Answer 130

1. Muscarinic receptor agonist administered in the inhaled form, acting primarily at the M3-receptor to produce smooth muscle contraction of the bronchi 2. Primarily used as a bronchial challenge test for diagnosis of reactive airways disease (eg, asthma) 3. If given in high doses can cause bradycardia/hypotension. Contraindicated in pts with recent MI or stroke ot in pts with known severe asthma or COPD. * ********

Answer 131

1. Muscarinic M2 and M3 agonist - activates Bowel and Bladder smooth muscle, resistant to AChE. 2. Tx postoperative ileus, neurogenic ileus, urinary retention postpartum or postoperatively. 3. Side effects 2/2 M2 agonism: bradycardia/hypotension 4. Side effects 2/2 M3 agonism: sweating, salivation, diarrhea 5. Doesn't cross BBB, no effect on CNS M1 receptors 6. Atropine given preoperatively to prevent voiding of the bowel/bladder during surgery, Bethanechol is given postoperatively to revert this action. * ********

Answer 132

1. Plant derivative similar to atropine. 2. Competitive muscarininc receptor antagonist at M1, M2, M3 receptors 3. Crosses BBB and blocks M1-receptors, thought to interfere with neuronal communication between vestibular ear and vomiting center of brain, preventing motion sickness 4. Blocks M3 receptors causing decreased GI motility, urinary retention, cycloplegia with mydriasis. 5. Also used to decrease respiratory secretions and salivation in patients at end of life or with ALS. 6. Side effects include sedation, blurred vision, psychosis, urinary retention, tachycardia. * ******************

Answer 133

bethanechol (PO), carbachol (eye drops), methacholine (inhaled), pilocarpine (usually eye drops)

Answer 134

Donepezil, rivastigmine, galantamine, edrophonium, neostigmine, physostigmine, pyridostigmine.

Answer 135

1. Reversibly inhibit AChE at synaptic junctions 2. Increased stimulation of both nicotinic and muscarinic receptors 2/2 elevated levels of ACh in synaptic junction. 3. Used to tx Alzheimer disease, has been shown to slow progression of disease by about 6 months. 4. Side effects: nausea, hepatotoxicity * ******

Answer 136

1. Historically used to diagnose myasthenia gravis- "Tensilon test"- if patient's sx improve transiently after drug given, test is positive. Now dx by anti-AChR antibodies. 2. Extremely short acting reversible inhibitor of AChE 3. Sx of muscle weakness and fatigability are similar in MG patients who are either overmedicated with pyridostigmine or MG patients who are undermedicated and still experiencing sx. Edrophonium is given to these patients to differentiate etiology of sx. After administration, sx should worsen in patients who are overmedicated and improved in patients who are undereducated. * ******************

Answer 137

1. Reversibly inhibits AChE, does not penetrate CNS as quaternary amine. Long acting. 2. In pts with Myasthenia Gravis elevated levels of ACh are able to overcome anti-AChR antibodies, leading to stimulation at NMJ 3. Increased ACh = increased muscle strength. 4. Side effects: bradycardia, diarrhea, bronchoconstriction, salivation, flushing, and nausea. 5. Overdose tx'd with atropine. * ******************

Answer 138

1. Reversibly inhibits acetylcholinesterase 2. Able to cross BBB (tertiary amine), thus can treat atropine poisoning (anticholinergic toxicity) 3. Also ophthalmic solution in tx of glaucoma as can produce miosis and stimulate outflow of aqueous humor from eye, decreasing intraocular pressure. 4. "Physostigmine phyxes atropine overdose." * ******************

Answer 139

1. Irreversibly inhibit acetylcholinesterase 2. Used in ophthalmic ointments to treat open-angle glaucoma by contracting the ciliary muscle of the eye (M3 receptor) and improving outflow of aqueous humor. * ******

Answer 140

1. Irreversibly inhibit AChE 2. Systemically cause widespread muscarinic activation resulting in seizures, psychosis, GI upset, salivation, blurry vision, bradycardia. 3. Persistent nicotinic activation results in neuromuscular blockade that can lead to flaccid paralysis. 4. DUMBBELSS= Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation (skeletal muscle, seizures), Lacrimation, Sweating, Salivation. 5. Respiratory failure if untreated. 6. Antidote- atropine (competitive inhibitor at AChR) + pralidoxime (regenerates AChE by cleaving covalent bond if given early). * ******************

Answer 141

Atropine (IV, eye drops), homatropine (eye drops), tropicamide (eye drops), benztropine (CNS), glycopyrrolate (GI, respiratory), hyoscyamine/dicyclomine (GI), ipratropium/tiotropium (inhalers), oxybutynin/solifenacin, tolterodine (urinary incontinence), scopolamine (CNS)

Answer 142

1. Analogues of atropine used in ophthalmic solutions to produce mydriasis and cycloplegia for retinal examination. 2. Competitive muscarinic receptor antagonists. * *******

Answer 143

1. Muscarinic receptor antagonist, also trihexyphenidyl 2. Crosses BBB, acting on M1- receptors in basal ganglia to treat Parkinson's disease. 3. DA neurons (which are lost from the SN pars compacta in PD) inhibit GABA-ergic outflow, while cholinergic neurons stimulate GABA-ergic outflow from the putamen. The unopposed excitatory cholinergic activity leads to increased GABA-ergic outflow from the putamen to the GP leading to inhibition of motor centers in the hypothalamus and hypokinetic movement. 4. By inhibiting M1-receptors, benztropine acts to restore dopaminergic-cholinergic balance in basal ganglia. 5. Adjuvant treatment in PD, or to tx acute dystonia 6. Side effects: dry mouth, irritability and confusion, constipation, pupillary dilation and blurred vision, urinary retention, hyperthermia, sedation. 7. Benztropine CONTRAINDICATED in patients with narrow-angle glaucoma. * ******************

Answer 144

1. Muscarinic receptor antagonist, competitive 2. Given IV preoperatively to reduce airway secretions 3. Given PO for excessive salivation (drooling) or peptic ulcer disease (2/2 gastric secretions). * *********

Answer 145

1. Muscarinic receptor antagonist, acts on M3 receptors in GI tract 2. Antispasmodics for irritable bowel syndrome * ***********

Answer 146

1. Ipratropium, tiotropium (inhaled) 2. Muscarinic receptor antagonist, acts on M3 receptors in lungs to bronchodilate 3. Tx COPD, asthma 4. Side effects: tachycardia, dry mouth, sedation possible although inhaled so not much systemic absorption. * **********

Answer 147

1. Muscarinic receptor antagonist, acts on M3 receptors in GU system and M3 receptors on sweat glands 2. Reduces bladder spasms of detrusor muscle contractions and increases bladder sphincter tone thereby reducing urge urinary incontinence (overactive bladder) 3. Other similar drugs: solifenacin, tolterodine 4. Can also cause decreased sweating, and used to tx hyperhidrosis * ******************

Answer 148

1. Muscarinic receptor antagonist that acts primarily at M3-receptor 2. Increases bladder sphincter tone and decreases GI tract motility and secretions of gastric acid thus used to tx urinary incontinence and duodenal ulcers. * *********

Answer 149

1. Beta-adrenergic agonist 2. Beta-2 more than Beta-1 * ********

Answer 150

1. Long-acting beta-adrenergic agonist 2. Beta-2 more than Beta-1 * *********

Answer 151

1. Albuterol, salmeterol: beta-2 >> beta-1 2. Phenylephrine: alpha-1 3. Midodrine: alpha-1 4. Clonidine: alpha-2 5. Isoproterenol: beta-1 and beta-2 6. Terbutaline: beta-2 7. alpha-methyldopa: alpha-2 8. Guanfacine: alpha-2 * *****************************

Answer 152

1. Epinephrine: beta > alpha 2. Norepinephrine (NE): alpha-1 > alpha-2 > beta-1 3. Dopamine: D1 = D2 > beta > alpha 4. Dobutamine: beta-1 > beta-2 > alpha * *****************************

Answer 153

1. Ephedrine - releases stored catecholamines 2. Cocaine - reuptake inhibitor 3. Amphetamines - reuptake inhibitor and releases stored catecholamines * *****************************

Answer 154

1. Blocks T-type Ca++ channels that trigger and sustain rhythmic pulsed discharges from thalamic neurons. 2. Tx absence seizures. 3. Adverse reactions: Pancytopenia * *****************************

Answer 155

1. Blocks fast v-gated Na+ channels at presynaptic neuron, causing decreased release of glutamate and aspartate (excitatory NTs) 2. Tx simple and complex partial seizures, generalized tonic-clonic seizures, bipolar disorder, depression. 3. Adverse reactions: SJS, toxic epidermal necrolysis * *****************************

Answer 156

1. Mechanism of action unclear. May inhibit enzymes that metabolize GABA leading to overall greater inhibition. Also may affect Na+ and K+ conductance. 2. Tx patients with combined absence and generalized tonic-clonic seizures, myoclonic seizures, mania associated with bipolar disorders, migraine prevention. 3. Adverse reactions: hepatotoxic, thrombocytopenia, teratogen, weight gain. * *****************************

Answer 157

1. Barbiturate. Indirectly potentiates GABA-A receptor activity in brain, increasing flow of Cl- through adjacent Cl- channels, leading to cell membrane hyper polarization and decreased activity of CNS neurons. 2. Tx generalize tonic-clonic seizures, neonatal hyperbilirubinemia as induces cytochrome P450 enzymes. * *****************************

Answer 158

1. Decreases flow of Na+ and Ca++ across the cell membrane, therefore inhibiting neuronal high frequency firing of APs by blocking Na++ channels and prolonging the recovery rate. 2. Tx tonic-clonic seizures, status epilepticus, simple/complex partial seizures. 3. Side effects: nystagmus, gingival hyperplasia, megaloblastic anemia, drug-induced lupus. 4. Teratogen leading to fetal hydantoin syndrome * *****************************

Answer 159

1. Inhibits flow of Na+ ions through Na+ channels 2. Tx complex partial seizures and generalized tonic-clonic, also tx for trigeminal neuralgia. 3. Adverse reactions: aplastic anemia, agranulocytosis, hepatotoxicity * *****************************

Pharm Flashcards

(185 cards)