FINAL Flashcards

Question

indications, MOA and SE of amitriptyline?

Answer 1

* Indications: migraine/tension H/A, chronic pain, bipolar d/o, depression, tricyclic antidepressant * MOA: CNS modulation of both serotonin and norepinephrine; acts primarily as a serotonin-NE reuptake inhibitor * SE: dizziness, marked drowsiness, anticholinergic effects (anti-SLUD) * DO NOT USE WITH MAOIS

Answer 2

* Indications: anticonvulsant used in treating epilepsy, prophylaxis of migraine H/A, off-label use for bipolar d/o * MOA: blocks voltage dependent sodium channels in the CNS which augments the activity of neurotransmitter gamma-amino butyrate (GABA) at some subtypes of GABA-A receptor, MOA as anti-migraine med is not fully known * SE: fatigue, dizziness, vision changes, acute angle glaucoma, nausea, constipation

Answer 3

* Indications: prophylaxis of migraine and cluster H/As; reserved for cases refractory to other medications and tx modalities * MOA: not fully known, yet it appears to be a serotonin 2 receptor antagonist which results in vasoconstrictor effect * SE: HTN, thrombophlebitis, N/V, pulmonary fibrosis and retroperitoneal fibrosis are severe and potentially life-threatening occurrences, heart valve thickening * PG category X * DO NO USE W/IN 24 HRS OF A TRIPTAN B/C CAN CAUSE VASOCONSTRICTIVE SPASM

Answer 4

* Indications: migraine and cluster H/As * MOA: serotonin agonist; serotonin agonist at 5-HT 1D and 1B receptors, found in small, peripheral nerves that innervate the intracranial vasculature * SE: dizziness, tingling, facial flushing, weakness, chest tightness or pain, arrhythmias, HTN, use in caution in pts w/HTN and in pts w/angina; serotonin syndrome, frequent use can result in rebound H/As * PG category C

Answer 5

* Indications: pain relief, antitussive * MOA: opioid agonist, converted to morphine in the body but mg per mg codeine is a much weaker analgesic than morphine * SE: sedation, constipation * DEA category CII to CV depending on dose of codeine * PG category C

Answer 6

* Indications: inflammation, pain, fever * MOA: Reversible inhibition of COX-1 and COX-2 enzymes, blockage of PG synthesis at target tissues; NSAID * SE: no increased risk for Reye’s syndrome

Answer 7

* Indications: migraine H/A that is refractory to triptans and other agents as well as less potent analgesics * MOA: mixed agonist-antagonist of opioid receptors * SE: nasal irritation, drowsiness, dysphoria, N/V, withdrawal sxs in those w/underlying addiction to opiates b/c of agonist-antagonist effects

Answer 8

* Indications: anti-emetic particularly when associated w/migraine H/A, vertigo, anti-psychotic * MOA: primarily H1 histamine receptor antagonist, also D2 dopaminergic receptor antagonist and an alpha-adrenergic receptor antagonist * SE: drowsiness, dry mouth, constipation, urinary retention, lowers seizure threshold, extrapyramidal SEs generally only seen when given at high doses over a long period of time

Answer 9

* Indications: severe nausea * MOA: blockade of serotonin (5HT3) receptor sites results in significant anti-nausea effect * SE: generally well tolerated but can cause dizziness and headaches

Answer 10

* Indications: gout, arthritis, bursitis, migraine H/As, hemicraina, pain and swelling * MOA: COX-I and COX-II inhibitors * SE: bleeding, gastritis, PUD, may exacerbate HTN or CHF, use with caution in pts w/preexisting renal and/or liver dz, avoid use in those w/NSAID, aspirin or indomethacin allergy, avoid use in pts w/hx of asthma and nasal or sinus polyps

Answer 11

* Indications: to give short-term pain relief and reduce swelling from inflammation of a joint, tendon or bursa as well as for marked allergic reaction or post-epi tx of anaphylaxis * MOA: decreases inflammation by inhibiting pro-inflammatory proteins * SE: hyperglycemia, insulin resistance, DM, osteoporosis, anxiety, depression, amenorrhea, cataracts, glaucoma

Answer 12

* Indications: gout – both for acute flares and for prophylaxis ; relative low therapeutic index; Behçet’s dz * MOA: colchicine inhibits microtubule polymerization by binding to tubulin (one of main constituents of microtubules) ; inhibits neutrophil motility and neutrophil activity resulting in anti-inflammatory effects * SE: GI upset, anemia, neutropenia, hair loss, peripheral neuropathy * Overdose sxs: vomiting, diarrhea, acute renal failure, possible hypovolemic shock, NO ANTIDOTES KNOWN

Answer 13

* Indications: hyperuricemia, gout, prophylaxis against tumor lysis syndrome * MOA: xanthine oxidase inhibitor (enzyme responsible for end product formation of purines) * SE: N/V, skin rash, SJS, hypersensitivity syndrome: fever, rash, eosinophilia, hepatitis, decreased renal fxn

Answer 14

* Indications: hyperuricemia, gout * MOA: increase excretion of uric acid in the urine = less of a concentration of uric acid in blood plasma = decrease crystals but can lead to KD stones * SE: N/V, rash, SJS, hypersensitivity syndrome: fever, rash, eosinophilia, hepatitis, decreased renal fxn, KD stones; anemia, leukopenia, possible hemolytic anemia in pts w/G6PD deficiency, dizziness, hepatitis, exacerbation of gout following therapy w/probenecid may occur (switch to colchicine or another at this point) * Was used during WWII to extend limited supplies of penicillin

Answer 15

* Indications: CA, AI dzs: RA, psoriasis, psoritatic arthritis, lupus, Crohn’s dz, abortifacient, has also been used for MS but not FDA approved * MOA: anti-metabolite and anti-folate * SE: myelopathies, leucoencephalopathies, nausea, abd pn, fatigue, fever, dizziness, ulcerative stomatitis, low WBC count (predisposition to infxns), pulmonary fibrosis (but also used to treat pulmonary fibrosis…) * PG category X

Answer 16

* Indications: prevention of transplant rejection, IBD, SLE, RA * MOA: metabolic breakdown products of azathioprine act to inhibit purine synthesis which will block protein synthesis, particularly in cells that experience rapid turnover; purine anti-metabolite, immunosuppressant * SE: rapidly growing cells are most readily affected (hair loss, bone marrow suppression, GI toxicity, leukopenia, thrombocytopenia), decreased ability to fight infections, pancreatitis, known to cause birth defects * PG category X

Answer 17

* Indications: prevent rejection of KD, liver and heart transplants as well as for the tx of RA and other AI dzs such as severe psoriasis * MOA: T-cell inhibition, blocks the signal to lymphocytes to produce IL-1, IL-2, IL-3, IL-4 and interferon gamma; immunosuppressant drug derived from soil fungus * SE: N/V, diarrhea, loss of appetite, HTN, KD damage, tremors, H/As, seizures, excessive hair growth, excessive gum growth, confusion, coma, gout, increased risk of infxn leading to sepsis

Answer 18

* Indications: protection against rejection of organ transplantation, topical tx for severe eczema * MOA: T-cell inhibition similar to that of cyclosporine; immunosuppressant drug related to macrolide class of abx extracted from soil microorganism * SE: very similar to cyclosporine w/N/V, diarrhea, loss of appetite, HTN, KD damage, increased risk for infxn * ~100x more potent in its immunosuppressive effects than equal volume of cyclosporine

Answer 19

* Indications: moderate to severe RA, moderate to severe polyarticular JA, psoriatic arthritis, ankylosing spondylitis, moderate to severe plaque psoriasis * MOA: DMARD, recombinant DNA drug; reduction of inflammatory response via TNF-a therapy (human soluble TNF-a receptor to the Fc component of human immunoglobulin) * SE: very broad SE profile w/notable decreased resistance to infxn, increasing # of reports of potential for increased leukemia, lymphoma, solid tumors, as well as increasing #s of serious liver injury, CHF, demyelinating CNS d/os * #1 prescribed TNF-a blocker in field of rheumatology

Answer 20

* Indications: anti-malaria, RA, SLE, Sjögren’s Syndrome, post-Lyme arthritis * MOA: increases lysosomal pH in antigen presenting cells, blocks the activation of TLRs (TLR 9) on plasmacytoid dendritic cells which reduces inflammatory process; may also possess anti-spirochete activity * SE: corneal and macular damage, abd cramps, diarrhea, reduced appetite, H/A, N/V, vision difficulties, tinnitus, hearing loss, diminished reflexes, hives, itching, rash, loss of hair, weakness, anemia, in pts w/G6PD deficiency can develop severe anemia

Answer 21

* Indications: reduce inflammation esp related to RA, IBD, psoriatic arthritis, membranous nephritis, SLE, juvenile rheumatoid arthritis, kids w/progressive poly-arthritis who are unresponsive to NSAIDs, methotrexate and other meds such as DMARDs * MOA: according to product labeling, neutralizes biological activity of TNF-a by binding w/high affinity to the soluble TNF-a and trans-membrane forms of TNF-a thus preventing the effective binding of TNF-a w/its receptors * SE: decreased appetite, nausea, hair thinning, diarrhea, rash, thrombocytopenia, renal toxicity is generally the most severe complication * Need to regularly check urine for protein and blood tests for liver or KD damage

Answer 22

* Indications: depression * MOA: prevent the breakdown of neurotransmitters * SE: weakness, dizziness, H/A, tremors, potential for marked HTN, can potentiate the effects of sympathomimetics such as NE, hypertensive emergency, fatal accelerated HTN * Less often used b/c can have serious side effects * Need to avoid foods high in tyramine when using b/c MAO is essential for tyramine breakdown

Answer 23

* Indications: obsessive compulsive disorders, enuresis, panic attacks, chronic pain, migraine H/A as well as depression * MOA: not exactly known, diminishing the reuptake of monoamine neurotransmitters is clearly one of the chief effects or may be dt subsequent down regulation of postsynaptic receptors; inhibits reuptake of both serotonin and NE which increases amount of neurotransmitter left in postsynaptic cleft * SE: need to take medication as prescribed as opposed to as-needed; remission may not occur until 4 or more wks; anti-cholinergic symptoms such as dry mouth, constipation, urinary hesitancy, orthostatic hypotension, sedation; potentially cardiotoxic (avoid in those w/heart dz), can slow intra-cardiac conduction, arrhythmias, ECG changes may occur, benign or otherwise (toxicity usually due to prolongation of QT interval)

Answer 24

* Indications: tricyclic antidepressant, major depression, bipolar d/o, migraine and tension H/A, chronic pain * MOA: CNS modulation of both serotonin and NE, increasing levels of each of these neurotransmitters; primarily acts as a serotonin-NE reuptake inhibitor * SE: dizziness, marked drowsiness, anticholinergic effects such as dry mouth, constipation, urinary hesitancy, blurred vision, stopping tx abruptly can cause withdrawal-like sxs: nausea, H/A, dizziness, lethargy, flu-like symptoms, QT prolongation

Answer 25

* Indications: depression * MOA: tetracyclic antidepressant; potent antagonist of 5-TH2 and 5-HT3 receptors, as well as histamine (H1) receptors and is a moderate antagonist of peripheral a-1 adrenergic receptors * SE: sedation, wt gain

Answer 26

* Indications: depression, anti-anxiety, sleep-inducing effects, fibromyalgia, complex regional pain syndrome, control of nightmares, panic d/o, diabetic neuropathy, bulimia nervosa, OCD, EtOH withdrawal, erectile dysfxn * MOA: tetracyclic antidepressant of the serotonin antagonist and reuptake inhibitor (SARI ) class * SE: sedation, orthostatic hypotension, fatigue, cardiac dysrhythmias, mania in pts w/bipolar d/o, increased risk of suicidality, in overdose scenarios can lead to torsades des pointes, complete AV block and organ failure (but it is very rare to overdose on trazodone) * Appears to be relatively safer than TCAs, MAOIs

Answer 27

* Indications: major depressive d/o, OCD, bulimia, panic d/o * MOA: decreased serotonin reuptake at presynaptic cleft = more left in synapse and increased serotonin made available at post-synaptic receptor sites * SE: serotonin syndrome: fever, agitation, diarrhea, elevated BP, sexual dysfxn (lack of interest, impotency, anorgasmia) * NSAIDs may decrease efficacy and may compound risk of GI bleeds

Answer 28

* Indications: depression, neuropathic pain, major depressive disorder, generalized anxiety disorder, chronic MS pain including chronic osteoarthritis pain and chronic low back pain (one of only three meds approved for fibromyalgia) * MOA: serotonin and NE reuptake inhibitors (leave it in the synapse) * SE: H/A, somnolence, fatigue, nausea, xerostomia, insomnia, ED, increased risk of suicidal thinking and behavior in children, adolescents and young adults w/ major depressive d/o and other psychiatric d/os * C/I in those w/heavy EtOH use or chronic liver dz as it can increase levels of certain liver enzymes that can lead to acute hepatitis

Answer 29

* Indications: major depression, bipolar d/o, ADD, aid in smoking cessation (called Zyban when used for this purpose) * MOA: NE and dopamine reuptake inhibitor and nicotine receptor antagonist * SE: H/A, insomnia, dry mouth, tremors, restlessness, agitation, anxiety, sweating and dizziness, possible risk of increased thoughts of suicide

Answer 30

* Indications: smoking cessation * MOA: partial nicotine agonist * SE: serious neuropsychiatric events including depression, suicidal thoughts, suicide, nicotine withdrawal sxs * Chamby’s recommendation: DON’T USE

Answer 31

* Indications: suboptimal folate levels in depressed patients (usu have MTHF gene mutation) * MOA: active form of folate (prescription variety)

Answer 32

* Indications: anxiety, calming effects, sedation at higher doses; nervous system depression * MOA: bind to specific high affinity sites on the cell membrane of neurons in the CNS which are adjacent to but separate from gamma-aminobutyric acid (GABA) receptor sites * SE: can result in coma and death if given at too high of a dose * Do not raise pain threshold and no analgesic properties

Answer 33

* Ultra-short acting: Thiopental – “truth serum” * Short acting: Pentobarbital – insomnia, pre-operative sedation; Schedule II drugs; Also used in physician-assisted suicide * Intermediate acting: Butalbital – insomnia, pre-operative sedation as well as added to aspirin or acetaminophen for migraine and cluster H/A. Most commonly used now b/c less drug tolerance, less psychological and physical dependence, less severe withdrawal sxs, less potential for coma and respiratory failure. Schedule II drugs * Long-acting: Phenobarbital – most widely used anticonvulsant worldwide, also sedative and hypnotic properties (superseded by benzos now though)

Answer 34

* Indications: anxiety, seizures, severe muscle spasms * MOA: bind to specific high affinity sites on the cell membrane of neurons in the CNS which are adjacent to but separate from gamma-aminobutyric acid (GABA) receptor sites, leads to opening of chloride channels = hyperpolarization of the cell which makes it more difficult for excitatory neurotransmitters to subsequently depolarize the nerve cell

Answer 35

* Indications: sedative, hypnotic, anxiolytic, anticonvulsant, skeletal muscle relaxant, amnestic properties, acute management of aggressive, violent or delirious pts, acute seizure tx, moderate to severe insomnia, sedation and amnesia before medical procedures * MOA: benzodiazepine; bind to specific high affinity sites on the cell membrane of neurons in the CNS which are adjacent to but separate from gamma-aminobutyric acid (GABA) receptor sites, leads to opening of chloride channels = hyperpolarization of the cell which makes it more difficult for excitatory neurotransmitters to subsequently depolarize the nerve cell * SE: upon discontinuation can cause withdrawal syndrome, including rebound insomnia

Answer 36

* Indications: anxiolytic, sedative, muscle relaxant, seizure control * MOA: binds to benzodiazepine receptors in the CNS to enhance GABA activity * SE: drowsiness, impaired mentation, tolerance and addiction, rebound insomnia after drug discontinuation, withdrawal can be severe (similar to that of barbiturates esp when chronically used)

Answer 37

* Indications: initiating sleep | * MOA: short-acting non-benzo hypnotic that potentiates GABA by binding to GABAa receptors at same location as benzos

Answer 38

* Indications: tx insomnia * MOA: potentiation of GABA effect on chloride ion channels by binding to a specific receptor site not involved w/the binding of benzos * SE: Impaired mentation prior to sedation, minimal drowsiness upon waking and minimal change in mentation relative to all other benzos

Answer 39

* Indications: suboptimal folate levels in depressed patients (usu have MTHF gene mutation) * MOA: melatonin agonist; high binding affinity at melatonin MT1 and MT2 receptors – by binding these the drug mimics and enhances the action of endogenous melatonin which has been associated w/maintenance of circadian sleep rhythm through inhibitory activity of MT1 and MT2 systems * SE: no studies have showed if it is more or less effective than melatonin you can take w/o a rx

Answer 40

* Indications: benzo overdose, IV administration only * MOA: benzo receptor antagonist that can rapidly reverse the effects of benzos * Very effective at reversing CNS depression associated w/benzos but is less effective at reversing respiratory depression

Answer 41

sodium channel blockade calcium channel blockade potentiate GABA decrease glutamate

Answer 42

* Carbamazepine/Tegretol * Phenytoin/Dilantin * Diazepam/Valium * Primidone/Mysoline * Valproic acid/Depakote * Lamotrigine/Lamactil

Answer 43

• Ethosuzimide/Zarontin

Answer 44

* Valproic acid/Depakote * Lamotrigine/Lamactil * Levetriacetam/Keppra * Topiramate/Topamax

Answer 45

* Diazepam/Valiujm | * IV Lorazepam/Ativan

Answer 46

* Valproic acid/Depakote | * Clonazepam

Answer 47

* Indications: generalized seizures * MOA: barbiturate anticonvulsant - enhanced GABA activity * SE: CNS depression, drowsiness, associated w/lower IQ scores in children undergoing chronic tx * Now rarely used to tx seizures * Sodium injection can be used to stop acute convulsions or status epilepticus but Lorazepam or Diazepam is usu tried first

Answer 48

* Indications: all types of seizure d/o except absence seizures * MOA: barbiturate anticonvulsant – exact MOA unknown but pehnobarb is a known metabolite of primidone so GABA mediated inhibition is considered as chief MOA * SE: nausea, anorexia, H/A, vertigo, ataxia * PG category D (don’t use unless lifethreatening condition)

Answer 49

* Indications: grand mal seizures, status epilepticus, seldom if ever used as a chronic tx choice for seizures, anxiety, panic d/o * MOA: benzodiazepine; increased sensitivity of GABA w/subsequent increased chloride influx which serves to inhibit CNS synaptic transmission * SE: drowsiness, impaired mentation, tolerance and addiction, rebound insomnia after drug discontinuation, withdrawal can be severe (similar to that of barbiturates esp when chronically used)

Answer 50

* Indications: alt to ethosuximide or valproic acid for absence seizures, status epilepticus tx * MOA: similar to diazepam; enhanced GABA activity * SE: drowsiness, altered mentation, additive w/CNS depressants, marked abuse potential, tolerance develops

Answer 51

* Indications: prophylaxis for all types of seizures except absence seizures * MOA: reduces Na2+ and Ca2+ and currents across neuronal membranes * SE: nystagmus, ataxia, gingival hyperplasia, possible hepatotoxicity, possible bone marrow suppression, IV admin can cause hypotension and arrhythmias

Answer 52

* Indications: prophylaxis against all types of seizures except absence seizures, chronic pain such as trigeminal neuralgia, post-herpetic neuralgia, schizophrenia, bipolar d/o * MOA: similar to phenytoin in the reduction of sodium and calcium across neuronal membranes * SE: vertigo, N/V, possible bone marrow suppression and aplastic anemia so need to follow blood counts * NEVER COMBINE WITH MAOIs!!

Answer 53

* Indications: all seizure types, esp in absence seizures and combined seizure conditions, also to tx bipolar d/o, chronic pain syndromes, can add to another agent if can’t get away w/monotherapy * MOA: unknown, possible enhancement of GABA transmissions * SE: nausea, insomnia, anxiety, potential for severe hepatotoxicity, known to be an antagonist of folic acid, birth defects such as anencephaly

Answer 54

* Indications: absence seizures (drug of choice for this kind of seizure) * MOA: unknown, possibly affects T-type calcium ion channels * SE: increases phenytoin levels, H/A, N/V, fatigue, ataxia, blurred vision, confusion, skin rashes, insomnia, gingival hyperplasia (not as severe as dilantin), notable for possible hepatotoxicity and lupus-like syndrome, intractable hiccoughs

Answer 55

* Indications: adjunctive tx of partial seizures, also used in chronic pain syndromes such as post-herpetic neuralgia, migraine H/As; anticonvulsant, atypical analgesic, can add to monotherapy if one drug isn’t producing desired effects, 1200 mg at bedtime for 40-60 has been effective in reducing withdrawal sxs and diminishes desire to meth and/or cocaine (one of only drugs to tx meth, cocaine and EtOH addiction) * MOA: appears to potentiate GABA and also affect N-type calcium channels or may halt the formation of new synapses * SE: somnolence, dizziness, ataxia, H/A and other CNS effects

Answer 56

* Indications: tonic-clonic (grand mal) seizures, complex partial seizures and seizures resistant to other drugs; type I bipolar d/o * MOA: unknown, may stabilize neurons by decreasing sensitivity to excitatory effects of glutamate and aspartate * SE: dizziness, H/A, rashes, diplopia, somnolence, ataxia

Answer 57

* Indications: tonic-clonic seizures, complex partial seizures, seizures resistant to other drug txs, neuropathic pain * MOA: anticonvulsant - unknown, may stabilize neurons by inhibition of calcium movement through presynaptic calcium channels * SE: generally well tolerated by can cause drowsiness, weakness, unsteady gait, coordination problems, H/A, mood changes, nervousness, loss of appetite, vomiting, diarrhea, constipation and rare reports of possible changes in skin pigmentation

Answer 58

* Indications: psychosis, mania, schizophrenia, N/V, intractable hiccoughs * MOA: typical neuroleptic, chiefly D2 dopaminergic receptor site blockade, also alpha-adrenergic blockade and H1 blockade (anti-histamine effects, anti-nausea effects) * SE: Parkinsonian sxs and extrapyramidal signs such as tardive dyskinesia

Answer 59

* Indications: psychosis as well as vertigo and N/V, particularly when associated with migraine H/As * MOA: typical neuroleptic, primarily H1-histamine receptor antagonist as well as alpha-adrenergic receptor antagonist and D2 dopaminergic receptor antagonist * SE: significant drowsiness, dry mouth, constipation, urinary retention, extrapyramidal sxs only seen when given in high doses over a long period of time * Prochlorperazine is perhaps 10-20x’s more potent than chlorpromazine in terms of antipsychotic effects

Answer 60

* Indications: psychosis, Tourette’s syndrome, Huntington’s disease, acute agitated behavior * MOA: typical neuroleptics, chiefly D2 dopaminergic receptor site blockade * SE: chiefly Parkinsonian-like sxs and extrapyramidal effects which can be very dramatic, tremors, potentially fatal neuroleptic malignant syndrome

Answer 61

* Indications: schizophrenia, esp when other anti-psychotic agents have failed or have produced undesirable side effects * MOA: multiple receptor site blockade yet greatest effects at D2 and 5HT2 receptor sites * SE: relatively diminished extrapyramidal sxs compared to other neuroleptic drugs but agranulocytosis and myocarditis are two bigs * B/c of side effects need to do weekly blood draws for 5 months then four weekly tests after that

Answer 62

* Indications: psychosis * MOA: atypical neuroleptic, exact MOA is unknown yet presumed to be combination of dopamine and serotonin receptor blockade * SE: extrapyramidal effects, tardive dyskinesia, constipation, sedation, slow withdrawal is recommended to reduce incidence of acute psychosis, wt gain, hyperglycemia and DM, increased risk for stroke in elderly pts

Answer 63

* Indications: schizophrenia, esp when other antipsychotic agents have failed or have produced undesirable effects * MOA: atypical neuroleptic, multiple receptor site blockade yet greatest effects at D2 and 5HT2 receptor sites (higher affinity for 5HT2 receptors) * SE: relatively diminished extra-pyramidal SEs compared to other neuroleptics; wt gain, hyperglycemia, DM, increased risk for stroke in elderly

Answer 64

* Indications: psychosis, depression, schizophrenia, bipolar d/o, clinical depression * MOA: partial dopamine agonist of 2nd generation class of atypical antipsychotics

Answer 65

* Indications: bipolar d/o, manic episodes, schizophrenia * MOA: lithium salt, widely distributed in CNS and interacts w/# of neurotransmitters and receptors, decreases NE release and increases serotonin synthesis; exact MOA unknown but may serve to dampen transmission by NE as well as acting to diminish response to gluatamate * SE: lack of compliance esp dt wt gain, cognitive impairment and short-term memory deficits that come with taking the drug; renal impairment in the essence that concentration capacity is decreased dt reduced renal response to ADH, polyuria dt nephrogenic diabetes insipidus, polydyspia, hypothyroidism, leukocytosis, tremor, as levels increase seizures and cardiotoxicity can occur

Answer 66

* Indications: parkinson’s dz * MOA: replacing the dopamine that is missing, levodopa is a dopamine precursor that is transformed by dopa-decarboxylase to dopamine * SE: N/V, anorexia induced by stimulation of dopamine receptors in the GI tract and chemotrigger receptor zone in the brain, hypotension, choreiform movements, insomnia, anxiety * Long term complications: motor fluctuations with wearing off and on-off phenomenon, dyskinesias, mental status changes * NEVER COMBINE WITH A MAOI B/C CAN LEAD TO HYPERTENSIVE CRISIS, also do not give to schizophrenic pts as can lead to worsening of psychotic sxs and do not give with dopamine blocking antipsychotic agent (duh)

Answer 67

* Indications: Parkinson’s dz * MOA: increases dopamine levels in the brain, esp in the substantia nigra * SE: prior to addition of Carbidopa nausea was the MC SE, nausea can still occur but significantly reduced; hallucinations, nightmares, dyskinesias, serpentine-like movements

Answer 68

* Indications: used early in tx of PD to delay initiation of L-dopa, can also use with L-dopa so as to keep the L-dopa dose lower * MOA: bind to D1, D2, D3, D4 dopamine receptor sites

Answer 69

* Indications: PD, tx of prolactin secreting adenomas and acromegaly * MOA: mimic dopamine in stimulation of dopamine receptor sites * SE: nausea, HTN, hypotension, confusion, hallucinations, H/A, depression, dyskinesia, possible seizures, pulmonary fibrosis, inhibits release of glutamate by reversing GLT1 transporter, stroke, MI, can cause insulin resistance; to reduce SEs, start at very low dose and slowly increase over 4-6 wks

Answer 70

* Indications: to decrease SLUD (not very useful to tx bradykinesia and rigidity associated with PD) that can be associated with PD; decrease secretions from throat, lungs or GI tract; can also be used in surgical and emergency procedures; antidote to organophosphate poisoning (too much Ach) * MOA: increase breakdown of Ach * SE: anti-SLUD effects

Answer 71

* Indications: PD esp when tremor or drooling are prominent sxs, appear to help w/cognitive sxs dt PD as well, used to diminish SE of antipsychotic drugs * MOA: anticholinergic antagonist at muscarinic receptor sites * SE: dry mouth, blurred vision, urinary retention, constipation, confusion, drowsiness, disorientation, memory impairment, visual hallucinations, possible exacerbation of pre-existing psychotic sxs, CNS depression, confusion, nervousness, listlessness, intensification of mental sxs * TX W/PHYSOSTIGMINE (cholinergic drug) if overdose or intoxication

Answer 72

* Indications: anti-PD and influenza A * MOA: unknown but appears to be related to antagonism of NMDA receptors; antagonism of NMDA appears to result in diminished dopamine reuptake which may be the chief mech that accounts for beneficial effects in tx of PD; can be used alone to tx early PD or as an adjunct in later stages of PD (usu in pts w/L-dopa related dyskinesias) * SE: lightheadedness, confusion, drowsiness, nightmares, dry mouth, constipation, urinary retention, N/V, benefits of therapy are short lived w/diminished or absent response occurring in 6 mos or less

Answer 73

* Indications: AD (increases cortical Ach), off-label use to tx other cognitive d/o such as DLB and vascular dementia, improve sleep apnea in those with AD * MOA: centrally acting reversible AchE inhibitor * SE: MC SEs are bradycardia, nausea, diarrhea, anoriexia, abn pn, vivid dreams; can potentially increase and improve vocabulary and expressive language in children w/autism

Answer 74

* Indications: mild to moderate dementia dt AD and mild to moderate dementia dt PD; very useful in those w/aggressive dz course * MOA: centrally acting reversible AchE inhibitor * SE: N/V, dizziness, diarrhea, H/A, anorexia, abd pn

Answer 75

• Indications: mild to moderate AD and mild to moderate vascular dementia • MOA: AchE inhibitor, stimulate nicotinic acetylcholine receptors • SE: SLUDGEM • Overdose of AchE inhibitors may cause N/V, salivation, sweating, bradycardia, hypotension, convulsions, circulatory collapse o Antidote is anti-cholinergic drug such as atropine

Answer 76

* Indications: dementia, AD * MOA: blocks NMDA glutamate receptors (excitatory pathway); antagonist of glutamanergic NMDA receptor sites – inhibits influx of Ca2+ which plays a role in neuronal excitotoxicity; also acts as non-competitive antagonist at 5HT3 receptor; also acts as D2 agonist * SE: confusion, dizziness, drowsiness, insomnia, H/A, agitation, and/or hallucinations, vomiting, anxiety, increased libido

Answer 77

o Biguanides:) inhibits glucose production by the liver and decreases insulin resistance o Sulfonylureas: increase secretion of insulin o Meglitinides: increase secretion of insulin o Alpha-glucosidase inhibitors: delay absorption of glucose by the intestine o Thiazolidinediones (Glitazones): decrease insulin resistance o Dipeptidyl peptidase-4 inhibitors (DPP-4): promote release of insulin from the pancreas after eating a meal o Insulin may be given in conjunction w/any of the aforementioned drugs

Answer 78

* Indications: DMT2 * MOA: decreases hepatic glucose production and to a lesser extent enhances insulin sensitivity in skeletal muscle * SE: when used alone generally does not cause hypoglycemia; can cause modest wt reduction in pts taking; MC SEs are abd cramping and nausea; metallic taste; most serious SE is development of lactic acidosis which can be fatal (don’t use in pts w/impaired renal fxn as this can cause lactic acidosis) * Need to supplement with B12 or B complex when on

Answer 79

• Indications: DMT2 • MOA: stimulate intact beta cells of the pancreas to release more insulin – occurs as a result of interaction of a sulfonylurea w/the ATP sensitive K+ channels in the beta cell membrane, by partially blocking K+ channels the time the beta cell spends in the Ca2+ release stage is increased which means more insulin release • SE: most concerning SE is hypoglycemia, particularly in pts w/impaired renal or hepatic fxn; wt gain; total beta cell fxn generally declines with prolonged use (will need to switch after 5-10 years of use) • Cause fetal hypoxemia as a direct result of hyper-insulinemia (causes increased extraction of O2 from fetal blood supply by baby and this exceeds the placenta’s ability to supply O2= fetal hypoxemia) • DO NOT GIVE TO PTS W/SULFA ALLERGY o Gyburide, Gimepiride, Glipizide • Will be ineffective in pts where there is an absolute deficiency of insulin production such as in DMT1 pts or post-pancreatectomy

Answer 80

* Indications: DMT2 * MOA: stimulate beta cells to release insulin (non-sulfonylurea secretagogues); closes K+ channels on beta cell plasma membranes = more insulin release * SE: wt gain, hypoglycemia, have to take with meals = frequent dosing * Repaglinide is most efficacious in achieving blood glucose control and lowering HgA1c levels

Answer 81

* Indications: DMT2 * MOA: improve insulin sensitivity in skeletal muscle cells, fat cells and liver cells and decrease hepatic glucose production * SE: CVD events (MI) as well as CHF; hepatic damage (need to perform LFTs before starting tx and re-measure at 1 mo and again at 3 mo to assess for any rise in ALT), reduced bone density and increased incidence of bone fxs, wt gain from 5-10 lbs * TAKE 6-14 WKS TO ACHIEVE MAXIMUM DOSE * Can use alone or in combo w/metformin or a sulfonylurea * ACTOS is currently approved for concurrent use with insulin

Answer 82

* Indications: DMT2 * MOA: inhibit the alpha-glucosidase enzymes that line the brush border of the SI which interferes w/hydrolysis of carbs and delays the absorption of glucose and other monosaccharides * SE: b/c leaving carbs in the lumen of the SI/LI can cause abd pn, diarrhea, flatulence (osmotic effects + bacterial fermentation); Acarbose in high doses has been assoc w/moderately elevated transaminase levels and rare fatal hepatic failure has been reported * Need to be taken with each meal in order to lower postprandial glucose levels; will not cause hypoglycemia on their own but can cause hypoglycemia when given with a sulfonylurea or insulin – in case of hypoglycemia give glucose * PG category B

Answer 83

* Indications: DMT2 * MOA: DPP-4 enzyme normally breaks down incretins GLP-1 and GIP that are released following a meal so by inhibiting its activity in the periphery you get augmented insulin secretion and inhibits glucagon secretion which all together increases glucose utilization and diminishes hepatic glucose production which leads to reduced postprandial and fasting glucose and a reduced HgA1c * SE: increased risk of pancreatitis, potentially increases risk for pancreatic cancer * Can be used as monotherapy or in combo with metformin or TZD

Answer 84

* Indications: DMT1, DMT2 * MOA: synthetic form of amylin which is produced along w/insulin by beta cells, amylin plays a role in glycemic regulation by slowing gastric emptying and promoting satiety thereby preventing post-prandial spikes in blood glucose levels * SE: promote modest wt los, primary SE is nausea, tends to improve over time * Injectable; CANNOT combine pramlintide with insulin in same vial or syringe!

Answer 85

* Indications: DMT1, DMT2 * MOA: incretin mimetic; increase insulin secretion; only has effects when blood glucose is raised = no increased risk of hypoglycemia on it’ sown (can occur if taken with another hypoglycemic such as a sulfonylurea) * SE: nausea which tends to improve over time; modest wt loss * Inject with meals

Answer 86

* Indications: DMT1, DMT2 * MOA: anabolic hormone, analogue to endogenously produced insulin, made through recombinant DNA technology * SE: wt gain, hypoglycemia if inject too much, seizures, coma and death can result from hypoglycemia, hypokalemia; fibrosis at injection site, muscle or fat atrophy at injection site * First inhaled insulin: Exubera

Answer 87

* Indications: hypothyroidism, TSH suppression in select cases of thyroid nodules and thyroid CA * MOA: replaces normal levels of T4 and T3 (if able to convert) * SE: toxicity directly related to thyroxine levels and manifests as palpitations, tachycardia, intolerance to heat and anxiety; long term elevation of serum T4 may accelerate cardiac dz and osteoporosis; hold or reduce if any complaints of angina * Takes 6-8 wks to achieve steady state, tx is usu life long, follow pts clinical response and serum TSH * IN PTS W/ADDISON’S DZ AND HYPOTHYROIDSM NEED TO REPLACE CORTICOL FIRST – can be fatal if don’t do this (applies to any med you’re going to use to tx hypothyroidism with concomitant Addison’s dz)

Answer 88

* Indications: hypothyroidism (use in those who can’t convert T4 to T3 peripherally) * MOA: replaces both T4 and T3 * SE: toxicity directly related to thyroxine levels and manifests as palpitations, tachycardia, intolerance to heat and anxiety; long term elevation of serum T4 may accelerate cardiac dz and osteoporosis * Begin at low dose and advance slowly in those over 65 yo or hx of CAD; hold or reduce if any complaints of angina

Answer 89

* Indications: hypothyroidism, intolerance to T4 replacement therapy or not improvement on T4 replacement therapy, myxedema coma, Wilson’s syndrome * MOA: replaces T3 * SE: toxicity directly related to thyroxine levels and manifests as palpitations, tachycardia, intolerance to heat and anxiety; long term elevation of serum T4 may accelerate cardiac dz and osteoporosis; higher peaks and troughs of T3 may increase risk of CAD and osteoporosis

Answer 90

* Indications: hyperthyroidism dt Grave’s dz, toxic nodular or toxic multinodular dz and thyroid storm (give IV) * MOA: inhibits transformation of inorganic iodine to organic iodine therefore blocking the production of thyroxine, also inhibits the coupling of iodotyrosine to form T3 and T4 * SE: may cause hypothyroidism, rash, edema, arthralgias; agranulocytosis is feared SE * DO NOT GIVE BEYOND 6-12 MO PERIOD, do not give during PG

Answer 91

* Indications: hyperthyroidism dt Grave’s dz, toxic nodular or toxic multinodular dz, thyroid storm (give IV) * MOA: inhibits transformation of inorganic iodine to organic iodine, blocking the production of thyroxine and inhibits the coupling of iodotyrosine to form T3 and T4, notable effect of blocking the peripheral conversion of T4 to T3 * SE: may cause hypothyroidism, rash, edema, arthralgias; agranulocytosis is the most feared SE * DO NOT GIVE BEYOND 6-12 MO PERIOD * PG category D, give PTU over methimazole w/PG * Pts usually achieve euthryoid state after tx is discontinued

Answer 92

* Indications: blockade of adrenergic sxs of hyperthyroidism, emergent tx of thyroid storms * MOA: non-specific B1 and B2 blocker * SE: fatigue, sedation, impotency or depression

Answer 93

* Indications: hyperthyroidism, thyroid storm * MOA: large doses of iodine inhibits the release of thyroxine from the thyroid gland * SE: rash, fever, beneficial effects generally last no more than 2-3 wks as thyroid gland appears to adapt and resumes secretion of thyroxine

Answer 94

* Indications: definitive tx of hyperthyroidism and in selected cases of thyroid cancer; thyroid gland ablation in cases of Grave’s dz, thyroid nodules and in some cases of thyroid ca * MOA: while in thyroid gland, disrupts fxn of thyroid cells, eventually they cease functioning and thus excessive amounts of thyroid hormones are no longer produced and ssxs of hyperthyroidism disappear; radioactive emission of beta particles results in destruction of thyroid tissue * SE: tenderness, swelling during initial week of therapy; N/V, extremely high doses can cause bone marrow depression, sore throat, rarely salivary glands may swell * PG category X * After tx may need lifelong hypothyroidism tx

Answer 95

``` o Bisphosphonates (Alendronate) o SERMs ```

Answer 96

``` o Calcitonin o Teriparatide (synthetic PTH – postmenopausal women and in men who are at high risk for fracture) o Denosumab (human monoclonal ab) ```

Answer 97

``` o Calcium o Vitamin D o Magnesium o Strontium o Estrogen/HRT (postmenopausal osteoporosis) ```

Answer 98

* Indications: prevention and tx of osteoporosis, osteitis deformans, bone METS, multiple myeloma, primary hyperparathyroidism, osteogenesis imperfect, conditions w/bone fragility * MOA: inhibit osteoclast activity by causing apoptosis of osteoclasts = increase in bone mass * SE: when taken orally can cause upset stomach and inflammation and erosions of the esophagus – this SE can be mitigated by not taking with food (only water) and remaining upright for at least 30 mins after taking * Reduce the risk of osteoporotic fx in those w/previous fx (not dt osteoporosis itself)

Answer 99

* Indications: prevention and tx of osteoporosis * MOA: inhibition of osteoclast activity * SE: GI upset – esp stomach ache, heartburn, nausea, possible erosive esophagitis; rarely causes osteonecrosis of the jaw and atypical femur fractures as well as myalgias * Hypocalcemia needs to be corrected before starting therapy

Answer 100

* Indications: increases bone mass and reduces the risk of vertebral fx, has been shown to significantly reduce the incidence of breast CA * MOA: binding to select E receptor sites, developed to maintain beneficial estrogenic activity on bone and lipids and “anti-estrogenic” activity on endometrial and breast tissue * SE: uterine cancer, blood clots, hot flashes, arthrlagias, myalgias, edema, pruritis, small but definite increased risk for DVT * C/I during breast feeding, PG and women w/PMHx of venous thromboembolic events including DVT, PE and retinal vein thrombosis

Answer 101

* Indications: treatment of osteoporosis, reduce risk of spinal fractures and possibly reduce the risk of developing hip fractures * MOA: calcium regulation and bone metabolism and diminishes osteoclast activity * SE: nose bleeds and sinusitis, H/A, dizziness, edema, anorexia, diarrhea, skin rashes * Give as a nasal spray!

Answer 102

* Indications: treatment of osteoporosis in postmenopausal women and men w/osteoporosis at high risk for fx, shown to reduce risk of vertebral and non-vertebral fx in postmenopausal women * MOA: daily injections of low and intermittent doses of PTH stimulates osteoblasts; enhances release of calcium from large reservoir contained in bones; OPG binds to RANKL and blocks it from interacting with RANK so no bone destruction (greater osteoblast activation than osteoclast) * SE: nausea, leg cramps, dizziness

Answer 103

* Indications: reduce bone loss, increase bone density in spine and hip and reduce risk of hip and spine fx in postmenopausal women; prevention of osteoporosis * MOA: * SE: if given alone in a woman w/a uterus (don’t do, give progestin along with E), can lead to endometrial CA; vaginal bleeding, breast tenderness, venous blood clots, increased risk for GB dz, breast CA, stroke, MI, ovarian CA * May have a protective factor against atherosclerosis, may lower LDL and TGs and raise HDL and cause vasodilation plus have an anti-inflammatory component

Answer 104

* Indications: treatment of osteoporosis in postmenopausal women, bone METS, RA, multiple myeloma, giant cell tumor of boen * MOA: targets RANKL (a protein that acts as the primary signal to promote bone removal) and thereby inhibits osteoclasts * SE: increased susceptibility to infxn (urinary, respiratory tract), cataracts, constipation, rashes, joint pain, slightly increased risk for CA and severe infections

Answer 105

studies have reported a lower risk of hip and other fxs in ppl who have taken statin drugs

Answer 106

* Indications: prevention of osteoporosis? | * MOA: synthetic isoflavone, conserve bone in postmenopausal women

Answer 107

* Indications: menopause ssxs (hot flashes, night sweats, atrophy of tissues [urogenital tract, vulva, vagina, urethra], improve quality of sleep, prevent osteoporosis) * MOA: estradiol, acts as endogenous estrogen does * SE: increases risk for stroke, blood clots, ovarian cancer, endometrial cancer, breast cancer

Answer 108

* Indications: birth control, can reduce fertility for 10 mos, endometriosis, primary dysmenorrhea, ovulation pain, functional ovarian cysts * MOA: progestin inhibits follicular development and prevents ovulation as primary mechanism of action – decreases GnRH release by the hypothalamus which decreases the release of FSH and LH by anterior pituitary * SE: when combined w/CEEs has been assoc w/greater incidence of breast CA, dementia and thrombus in the eye, in combo w/E increases risk of CVD; delayed return of fertility for 9-10 mos after last injection, increases bone loss and increases the risk for the development of osteoporosis = can’t take for longer than 2 years * Reduces risk of endometrial CA, no risk for DVT, PE, stroke or MI b/c no E

Answer 109

* Indications: prevention and tx of osteoporosis, postmenopausal sx relief * MOA: acts as endogenous E and P * SE: increased risk of MI, stroke, DVT, PE, breast cancer * Decreased risk of colorectal CA, fewer fxs * CEE and MPA are no longer given to women in order to prevent CVD in older women, but younger women seeking relief of menopause sxs are still candidates for HRT

Answer 110

* Indications: prevention and tx of osteoporosis and of postmenopausal sxs such as hot flashes, vaginal dryness and itching * MOA: acts as HRT * SE: vaginal bleeding, breast tenderness, increased risk of DVT, atherosclerosis and CAD, uterine and breast CA

Answer 111

* Indications: hormonal contraception (either alone or with an estrogen) and to prevent endometrial hyperplasia from unopposed E in HRT * MOA: synthetic progesterone that has effects similar to endogenous progesterone

Answer 112

* Indications: contraceptive, hormone replacement therapy, dysfunctional uterine bleeding and tx of endometriosis; HRT for male-to-female transsexuals; chemical castration in convicted sex offenders * MOA: alters gene transcription * SE: increase the ratio of LDL to HDL and increases risk for DVT, breast tenderness, increased facial hair, decreased scalp hair, difficulty falling or remaining asleep, stomach pain, painful urination, anxiety, H/A, N/V, cervicitis; at high doses when used to tx breast CA can cause wt gain, worsen DM, edema; when used to tx BPH can reduce libido, cause impotence, reduce ejaculate volume, chemically castrate w/in 3 days * C/I if prior hx of DVT, breast, ovarian or uterine CA * PG category X

Answer 113

* Indications: birth control, at low doses in men and women it may slightly reduce HDL and increase LDL * MOA: combo of E and progestin, or just progestin - inhibits fertility in females by inhibiting GnRH which prevents ovarian follicle maturation and ovulation plus it thins the endometrium * SE: may affect libido, failure rate (PG), increased vaginal lubrication, depression (switch to just progestin-containing pill); DVT, CVD, HTN, stroke (esp if over 35 yo and/or smoke), acne, H/A, edema, nausea, breast tenderness * Mini-ill is just progestin * Use of OCPs for five or more years decrease risk of ovarian cancer later in life, COCPs reduce risk of ovarian and endometrial cancer

Answer 114

* Indications: birth control * MOA: synthetic progestin; anti-mineralcorticoid properties, counteracts E-stimulated activity of RAS and is not androgenic * SE: 6-7x risk of developing thromboembolism compared to women who don’t take any OCPs and 2x risk of women taking OCP containing levonorgestrel * C/I in women with hepatic failure, renal insufficiency or adrenal insufficiency * FIRST AND ONLY HORMONAL CONTRACEPTIVE SHOWN TO EFFECTIVELY TX PMDD

Answer 115

* Indications: birth control * MOA: low dose of progestin and E over 3 weeks * SE: vaginitis, H/A, leucorrhea, nausea, wt gain

Answer 116

* Indications: birth control * MOA: either hormonal which diminishes the frequency of ovulation and changes the consistency of cervical mucous and causes inflammation which decreases implantation plausibility or ParaGuard w/copper may immobilize sperm or cause ongoing inflammation of the uterine lining therefore decreasing the likelihood of a fertilized ovum attaching to the uterine wall * SE: cramping, bleeding, spontaneous ejection * ParaGuard – only non-hormonal, contains copper – thought to immobilize sperm * Mirena, Sklya, Kiara – hormone containing (progestin, levonorgestrel in varying amounts)

Answer 117

* Indications: prevent ovulation or fertilization and prevent post-fertilization implantation of a blastocyst * MOA: progestin or progestin-levonorgestrel methods * SE: abd pain, vaginal bleeding, N/V, H/A, dizziness * EllaOne: selective progesterone receptor modulator, can be given w/in 5 days after unprotected intercourse or contraceptive failure; able to prevent ~60% of expected pregnancies

Answer 118

* Indications: abortifacient (can be used in first 2 mos of PG) and in smaller doses as an emergency contraceptive * MOA: synthetic steroid compound; blockade of progesterone receptors as well as causing a decline in GnRH which decreases production of progesterone by the corpus luteum as well as endometrial degeneration, cervical softening and dilation and increases sensitivity of myometrium to contractile effects of prostaglandins * SE: abd pain, uterine cramping, vaginal bleeding for 9-16 d, some experienced bleeding for 30 days or more, N/V, diarrhea, dizziness, fatigue, fever * Results in abortion in ~85% of cases in 1st TM of PG * Often used in conjunction w/Misoprostol to encourage uterine contractions and cervical dilation

Answer 119

* Indications: SERM, infertility, amenorrhea * MOA: binding to E receptor sites in the brain interferes w/normal (=) feedback of E on GnRH which results in increased secretion of GnRH which causes an increased release of LH and FSH and stimulation of ovulation * SE: vaginal dryness, vaginal bleeding, breast tenderness, anxiety, hot flashes, multiple births

Answer 120

* Indications: hypogonadism, pituitary dwarfism, to tx bone marrow suppression and anemia, severe osteoporosis, HRT for female-to-male transsexuals * MOA: alteration of gene transcription, T and all its metabolites attach to specific nuclear receptors and initiates a cascade of reactions that eventually results in alteration of gene transcription * SE: acne, baldness, gynecomastia, priapism, increased risk of prostatic hyperplasia and prostatic CA, exacerbation of sleep apnea, reduced sperm count, infertility; in females can cause virilization; when used in kids can cause abn rate of sexual maturation and can result in diminished ht dt premature closure of growth plates; abn lipid levels, increased LDL, decreased HDL, increases risk of atherosclerosis and CAD; fluid retention and edema, increased RBC count can cause increased blood viscosity and sludging of blood (increased risk of ischemia)

Answer 121

* Indications: anti-androgen tx for advanced prostatic cancer, precocious puberty, endometriosis, uterine fibroids, some protocols of IVF * MOA: synthetic analog of GnRH, interrupts production of T and E * SE: decreased libido, impotence, N/V, hot flashes, night sweats, arthralgias, myalgias, osteoporosis

Answer 122

* Indications: BPH, in lower doses to treat male-pattern baldness, in higher doses to treat prostate cancer * MOA: limits conversion of T to DHT by inhibiting type II 5-alpha reductase * SE: decreased libido, ED, impotency, depression, breast swelling and tenderness * If using, do not allow PG women to handle broken or crushed tablets b/c risk of birth defects

Answer 123

* Indications: initial tx for men w/BPH * MOA: alpha blockers relax SM in prostate and bladder neck thus decreasing blockage of urine flow * SE: weakness, orthostatic hypotension, nasal congestion

Answer 124

* Indications: ED, can also be used to tx pulmonary HTN b/c PDE5 is present in the arterial SM w/in the lungs as well * MOA: phosphodiesterase type 5 inhibitor which blocks the degradation of phosophodiesterase type 5 on cyclic GMP in SM cells lining the blood vessels supplying the corpus cavernosum of the penis * SE: facial flushing, H/A, nasal congestion, heartburn, photophobia, blurred vision, cyanopsia, increased intraocular P, acute angle closure glaucoma, ventricular arrhythmias, severe hypotension, MI, stroke, priapism * C/I in those on NO donors, nitrites/nitrates, those w/severe renal or hepatic impairment, hereditary retinal d/os and in men for whom sexual intercourse is C/I dt CV risk factors such as recent stroke or MI

Answer 125

* Tylenol #3: 30 mg codeine phosphate and 300 mg acetaminophen * Tylenol #4: 60 mg codeine phosphate and 300 mg acetaminophen * DEA schedule CII to CV depending upon dose of codeine, PG category C

Answer 126

* When taken in dosages over the daily limit (greater than 7 g in 24 hrs) leads to oversaturated detoxification pathways and a buildup of NAPQI → excessive NAPQI formation or reduced glutathione stores allows NAPQI to covalently bind to vital proteins and the lipid bilayer of hepatocyte membranes which leads to hepatocellular death and liver necrosis * Tx overdose by removing any remaining drug in stomach by lavage or induction of emesis via ipecac

Answer 127

* PROPHYLAXIS MEDS: Beta-blockers, Calcium channel blockers, Methysergide, Tricyclic antidepressants, Ergotamine, Anti-seizure medications * PRODROMAL PHASE: Triptans * ACTUAL HEADACHE PHASE: Analgesics, Anti-emetics

Answer 128

tx: NSAIDs, steroids, colchicine | prophylactic tx: colchicine, allopurinol, probenecid

Answer 129

hydrocortisone: 1 prednisolone: 4 dexamethasone: 30 betamethasone: 35

Answer 130

appear in pt who has been taking benzos for a while and stop taking the drug; can develop: suicide, seizures, H/A, increased sensitivity to noise, sweating, difficulty falling asleep, pain, wt loss, shaking, blurred vision, increased sensitivity to light, depression, difficulty staying asleep, nervousness; can cause seizure

Answer 131

catatonia, fluctuating blood pressure, dysarthria and fever; associated with neuroleptic drug use and can be fatal if the antipsychotic drug is not immediately discontinued and pt receives tx w/dopamine agonist such as bromocriptine

Answer 132

most severe potential manifestation of hyperthyroidism; ssxs: high fever, irritability, delirium, vomiting, diarrhea, dehydration, hypotension, vascular collapse, coma and death may also occur; usu occurs in pts whom have become septic o Tx includes beta blockade as well as IV iodine to stun the thyroid gland and IV PTU or IV Methimazole o Can also give anti-pyretics for fever

Answer 133

Flumazenil/Romazicon BUT usu no indication to give as can just observe and give supportive care as necessary with same outcomes and risks associated w/flumazenil can outweigh the benefits; gastric lavage w/activated charcoal is not beneficial to a pure benzo overdose as the risk of adverse effects outweigh the potential benefits from the procedure

Answer 134

anticholinergic such as atropine

Answer 135

l-dopa, bromocriptine, amantadine, anticholinergics

Answer 136

25 mcg of cytomel = 60 mg of armour = 100 mcg of synthroid