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176 Cards in this Set
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what are micrometastases?
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small metastases that are too small to detect, derived from tumor stem cells
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what is the tumor growth fraction
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the fraction of tumor cells NOT in G0 phase
index of how well they will respond to treatment |
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the nitrosureas are useful for what kind of tumor?
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brain tumors (bc they cross the BBB)
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what is the regimen used for Hodking's disease?
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MOPP (or MVPP)
Mechlorethamine Vincristine (oncovin) Procarbazine Prednisone |
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what is the mechanism of methotrexate? It is specific to cell in which stage?
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folic acid analog
inhibits DHFR S phase specific (can't synthesize DNA) |
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what are the issues with using methotrexate and how can you overcome that?
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cells can become resistant
to solve that: give methotrexate, then give folinic acid (a rescue drug) to facilitate recovery between doses |
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what is the mechanism of resistance to 6-mercaptopurine and 6-thioguanine?
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down regulation of HGPRT, the enzyme that activates the agents to be incorporated into DNA
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what is a common adjuvant agent to 6-mercaptopurine?
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allopurinol (inhibits xanthine oxidase which breaks down 6-mercaptopurine)
also lower Uric acid production from dying cells |
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what is the mechanism of capecitabine?
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it is an oral prodrug of 5-FU
it prevents thymidinylate synthetase |
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how do the anthracyclines work?
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they intercalate between DNA molecules
cell cycle nonspecific actinomycin, doxorubicin, and daunorubicin |
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what is the mechanism and main side effect of bleomycin?
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DNA scission
pulmonary fibrosis at high doses very little myelosuppression |
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what is the difference between vincristine and vinblastine?
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vinecristine: mild, non-dose-dependent myelosuppression
vinblastine: graded, dose-dependent myelosuppression |
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how does the mechanism of paclitaxel differ from the vinca alkaloids?
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vinca alkaloids: prevent microtubules polymerization
paclitaxel: prevent microtubule DISassembly (enhances phosphorylation) |
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how does cisplatin work?
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cross-links DNA
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what is the mechanism of tamoxifen?
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it is a partial agonist of the estrogen receptor...you still get a response but the response is just smaller
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what is the mechanism of letrozole, anastrozole, and exemestane?
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they inhibit aromatase, so you don't get enzymatic production of estrogen from androgens
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what is the mechanism of leuprolide?
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it is a GnRH-agonist...in pulsatile delivery it gives you GREATER androgen production (bad for prostate cancer!)
in continuous dosing you get desensitization so you get a decrease in androgens (GOOD!) |
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why is prednisone useful as a cancer trx?
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it suppresses proliferation of lymphocytes in leukemias, lymphomas, and myelomas
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what is the mechanism of brentuximab-vedotin?
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anti-CD30 (targets CD30+ tumor cells) conjugated to a mitotic spindle poison (vedotin)
great for hodgkin lymphoma! |
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what agents most strongly cause allopecia?
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alkylating agents
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what agents most strongly cause heart toxicity?
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anthracyclines
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what agents cause rental tubule toxicity and organ of cotti toxicity?
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cisplatin
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what are the principal signs of opioid intoxication?
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1. respiratory suppression
2. miosis 3. comatose state |
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what receptors are responsible for the pain reduction and the SEs of opioids?
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Mu receptors are responsible for both
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where are opioid receptors NOT located?
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large myelinated fibers
cerebellum so opioids don't effect motor control systems |
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how do opioids function at a cellular level?
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prevent Ca influx
increase K efflux prevents NT release at pain fiber junctions |
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what are the cardiovascular side effects of opioids?
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bradycardia, orthostatic hypotension, peripheral vasidilation (due to histamine release)
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what are the GI side effects of opioids?
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constipation
decreased mucous secretion slowed motility |
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opioid tolerance:
occurs when? what effects do NOT develop tolerance? |
6 weeks
miosis and constipation DO NOT become tolerant respiratory depression DOES become tolerant so you can increase dose in terminal patients even when tolerant |
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what are the opioid withdrawal symptoms?
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all the signs of sympathetic stimulation
except for GI hypermotility |
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how is physical dependence on opioids defined?
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presence of withdrawal symptoms
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do opioids influence the sensory/disciminatory or the motivation/affective component of pain?
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motivational/affective
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what is morphine's onset and duration of action and why?
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at neutral pH only 20% is uncharged and able to cross BBB. therefore it has a slow onset and long duration of action
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what is the process of morphine metabolism?
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glucuronidated in the liver, the M-6-Glucuronidate metabolite is VERY active (10% of metabolite products)
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which is a bigger concern for morphine, Liver or Kidney disease?
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Kidney (liver nabd)
in kidney failure, M-6 Glucuronidate is NOT excreted and accumulates...you get opioid toxicity! |
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variability in opioid pharmacodynamics is due to
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a huge number of multifactorial influences
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variability in opioid pharmacokinetics is due to
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variability in renal function
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what is the 2nd choice to morphine, and how is it different?
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hydromorphone
more lipid soluble more potent faster onset metabolites are less active (so less concern for pt w/ renal failure) |
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what is the mechanism of the codeines (specific)?
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they are metabolized to the morphines by the liver enzyme CYP2D6
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why is heroin so fast-acting?
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even though it is a pro-drug it crosses the BBB very quickly and is then de-acetylated to a morphine-derivative
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what is the main side effect of meperidine
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its metabolite (nor-meperidine) is a CNS stimulant that can cause serotonin syndrome
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what are the main symptoms and cause of serotonin syndrome
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meperidone OD
1. neuromuscular hyperactivity 2. autonomic hyperactivity 3. altered mental status |
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what is the use for buprenorphine?
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it is a partial mu receptor agonist
useful for people who abuse opioids |
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what is a MAC?
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Minimum Alveolar Concentraiton
the alveolar concentration at which 50% of people have no response to a noxious stimulus |
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what is the blood gas partition coefficient and what is the implication?
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high blood gas coefficient=>high solubility =>Poor delivery to brain because much of it is dissolved rather than staying in gas form.
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what is the MAC of Nitrous Oxide
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110%, so it is only good when combined with other volatile anesthetics
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a patient takes longer to wake up when they are under a volatile anesthetics with HIGH or LOW solubility?
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takes longer with a highly soluble anesthetic because there is a reservoir of anesthetic in the blood.
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which volatile anesthetic is NOT irritating to the airways?
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sevoflurane (isoflurane and desflurane ARE irritating)
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how do volatile anesthetics work?
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Increase: GABA and Glycine transmission (decreased CNS activity)
Decrease Glutamate activity |
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what is the major side effect of volatile anesthetics
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cardiopulmonary suppression
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what agents cause malignant hyperthermia and how do you treat it?
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the volatile anesthetics and succinylcholine can cause malignant hyperthermia
treatment: dantrolene (muscle relaxant) |
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what is the mechanism of ketamine?
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NMDA antagonist
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what is the main problem with using Ketamine?
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emergence delirium
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how is midazolam used?
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as an anti-anxiety pre-medication agent
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how does fentanyl compare to morphine?
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more lipid soluble
faster onset higher potency shorter acting |
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how does fentanyl effect other anesthetic agents?
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it slightly reduces the MAC of volatile anesthetics
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what is the process of anesthesia for a patient without asthma/smoking hx?
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midazolam (pre-med anxiolytic)
fentanyl given intermittently(opioid analgesic) inducted with propofol (CardioPulm depressant, could also use Etomidate or Ketamine) maintained with desflurane (and possible NOS) |
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what volatile anesthetic would you use for a patient with asthma or a history of smoking?
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sevoflurane...non-irritant
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how is the use of Remifentanil different than the other -fentanils?
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remifentanil is a VERY STRONG respiratory depressant so you can only use it after intubated
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how is metabolism of the amide anesthetics different than the esthers?
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amides are metabolized in the liver
esthers are metabolized by plasma estherases |
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both amides and esthers have ______ amines and are active as ________
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tertiary amines that are active in the ionized, protonated form. (but they must be in non-ionized to cross membranes!)
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why would you add a base to a local anesthetic?
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increasing the pH increases the portion of anesthetic in the non-ionized form so more gets into cells (where it becomes ionized!)
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what are the symptoms of local anesthetic toxicity? (in increasing concentrations)
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lightheadedness
tinnitus unconscious seizures coma respiratory arrest cardiac toxicity |
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why are amide local anesthetics preferred over esthers?
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esthers are more likely to cause an allergic reaction
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how are ropivicane and bupivacaine different/
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ropivacaine is an enantiomer of the racemic Bupivicaine
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what are the subtypes of depression?
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Major depression types:
1. atypical (hypersomnia or hyperphagia) 2. seasonal 3. reactive (to loss or major life event dysthymia: less severe than major depression |
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what are the main 2 theories of depression pathogenesis?
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decreases serotonin and NE
neuronal death (and neurogenesis in treatment supported by 2 week dosing for an effect) |
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what is the on-target and off-target mechanisms of TCAs?
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on target: blocks reuptake of Monamines
off-target: blocks Histamine, Muscarine, and Adrenergic receptors. (mediate SEs!) |
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what are the side effects of TCAs?
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Antimuscarinic: blurred vision, xerostomia, urinary retention, constipation
CV: slowed conductance, orthostatic hypotension (adrenergic blockade) Antihistamine: sleepiness |
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how are the side effects of SSRIs different than TCAs?
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SSRIs have fewer off-target SEs
SSRIs cause anorexia, TCAs cause weight gain |
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how do SSRIs interact with other drugs
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SSRIs inhibit multiple CYPs
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how do SNRIs work?
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they inhibit reuptake of both Serotonin (5-HT) and NE with NO off target effects
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how do MAOIs work?
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they IRREVERSIBLY inhibit PRESYNAPTIC degradation of monamines => more release of monoamine NTs
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what are the concerns with MAOI side effects?
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when taken with SSRIs: serotonin syndrome (agitation, diarrhea, fever, hyperreflexia, mania)
when tyramine is ingested: tyramine toxicity: HTN, arrhythmias, stroke, HA |
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Lithium side effects:
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tremors, confusion, convulsions
cardiac arrhytmias |
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how do the amphetamines work?
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they increase dopamine and NE release by multiple mechanisms
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what is the one CNS stimulant that has no abuse potential?
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Atomexidate: prevents NE reuptake
used only for ADHD, not for narcolepsy |
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how is a sedative different than a hypnotic
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sedatives: exert calm
hypnotics: produce drowsiness, sleep |
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why arent benzodiazepines considered general anesthetics?
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although they produce sedation and hypnosis they do NOT produce loss of sensation
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how do Benzos work?
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they bind GABA(a) receptors in the limbic system (amygdala, hippocampus) causing hyperpolarization of post-synaptic membrane
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what is the action and use of flumazenil?
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it blocks GABA receptors: prevents action of benzodiazepines (used to recover from BZ OD)
it can't be used to recover from Barbiturate poisoning because it acts at a different site on the GABAergic-R |
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how are BZs metabolized?
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exclusively by cyt P450s
mainly CYP3A4 and CYP2C19 |
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how are anti-depressant drugs metabolized?
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all by renal excretion
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what is the order of half life of the major Benzodiazepines from longest to shortest?
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Longest: diazepam (anxiolytic)
lorazepam (insomnia) Alprazolam (insomnia) Midazolam (pre-anesthetic) |
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what are the SE concerns for the Benzos?
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Cardiopulmonary toxicity
but...this is rare because BZs have a high TI |
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why are BZs preferred over Barbs?
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Barbs have a lower TI
produce cardio-respiratory suppression |
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at a cellular level, how do BZs fx different than Barbs?
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BZs increase frequency of GABAergic Cl- channel opening
Barbs increase duration of GABAergic Cl channel opening and at high doses can open the channel themselves (agonists) |
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what should patients taking benzodiazepines or barbiturates avoid?
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EtOH
they are heavily metabolized by CYP enzymes |
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what is the anxiolytic use for propanolol?
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debilitating stage fright types situations
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what is the use for buspirone?
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chronic anxiety (takes a couple weeks for onset, has few side effects)
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what is the concern for dosing with phenytoin?
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you can saturate the CYP system at high doses, so small increases in dosing lead to huge plasma concentration increases
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what is the concern with using valproic acid
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it is very effective but is 2nd line use because of hepatotoxicity
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what are the causes (biochemical and anatomical) of schizophrenia?
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increased D2 receptors
increased ventricle size cortical atrophy basal ganglia atrophy |
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what determines whether a drug is good treatment for schizophrenia?
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it blocks D2>>>D1
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what two circuits have increased activity in schizophrenia?
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mesolimbic and ventral mesostrial dopamine pathways
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how is signalling of D1 receptors different than D2 receptors? (3 ways)
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D1 receptors: inc. cAMP
D2 receptors: dec. cAMP D1: usually presynaptic D2: usually post-synaptic D1: increases presynaptic DA reuptake D2: decreases Glutamine transmission |
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which antipsychotics cause anti-muscarinic side effects?
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chlopromazine and thioridazine
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which antipsychotic drug causes alpha-adrenergic blocking side effects?
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chlopromazine (orthostatic hypotension)
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which antipsychotic drug causes pituitary DA blockade side effects?
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halperidol: prolactin release => infertility and impotence
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which antipsychotic drugs cause H1 antihistamine side effects?
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chlorpromazine and clozapine
sedation, weight gain |
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what is neuroleptic malignant syndrome?
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collapse of the autonomic nervous system
sweating, salivation, uncontrolled BP happens to patients on antipsychotics or on parkinsons patients who d/c dopaminergics suddenly |
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what are the long term central side effects of antipsychotics?
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parkinson's like symptoms (rigidity and tremor)
tardive dyskinesia (due to DA-r upregulation) facial movements |
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parkinsons's disease is due to death of which population of neurons?
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substantia nigra
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huntington's disease is due to death of which population of neurons?
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striatum
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Amyotrophic Lateral Sclerosis is due to death of which population of neurons?
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motor neurons in the spinal cord and cerebral cortex
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what is the genetic/biochemical cause of huntington's disease?
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triplet repeat that leads to mitochondrial dysfunction
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activation of the D1 receptors in the nigrostriatal pathway eventually leads to ____ of the thalamus
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disinhibition (=> movement)
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why do anti-cholinergics work as therapy for parkinson's?
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the D2 indirect nigrostriatal pathway is activated by muscarinic receptors
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what is the best agent for parkinson's treatment and when does it wear off?
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L-DOPA, wears off in 3-5 years
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what are the peripheral side effects of L-DOPA?
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precursor for DA made to NE
causes nausea, orthostatic hypertension, arrhythmias, vomiting |
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what is action of carbidopa and entacapone?
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it inhibits peripheral metabolism of L-DOPA to NE, so you get no peripheral side effects and more L-DOPA delivered to brain.
Only good in COMBO therapy |
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what is the difference between selegiline and rasagiline?
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they both inhibit MAOb (increased dopamine)
selegiline is metabolized to amphetamines, so it has the side effect of INSOMNIA |
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Dopamine agonists are contraindicated in...
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people with heart or mental problems
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how is apomorphine administered/dosed?
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in people with advanced disease
given subQ between doses of other drugs |
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what are the three mechanisms of amantadine?
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Increased DA synthesis
Muscarinic antagonists NMDA antagonist |
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how does memantine work?
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it is a low affinity NMDA receptor trx for alzheimers. prevents Ca overload excitotoxicity
you need glutamate for normal brain function...so a low affinity drug is best |
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which diuretics act from the blood side of the nephron/
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spironolactone and eplerenone
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which diuretics act by INDIRECT inhibition of target transporters?
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carbonic anhydrase inhibitors
spironolactone |
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single nephron GFR = ?
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K(constant) x (Pdiff - Pi (Osmotic pressure in capillary))
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what is the normal fractional reabsorption of Na at the proximal tubule, loop of henle, DCT, and CD?
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65%, 25%, 7%, 3%
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how (step by step) do diuretics get into the lumenal space?
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Na/K ATPase (Na out)
Na symported with alpha-KG alpha KG exchanged for organic base (diuretic IN) |
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how is a natriuretic different than a saluretic?
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saluretic causes increased excretion of both Na AND Cl
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what is the net result in the urine and blood of a person on a carbonic anhydrase inhibitors?
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urine: alkalinized (more NaHCO3 in urine)
blood: acidified (less HCO3 in blood) |
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why do many natriuretics cause kaliuresis?
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if you increase Na in the lumen BEFORE the DCT, then you set up a high luminal [Na], which drives exchange of Na for K, more K in urine!
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why is the natriuretic benefit of CA inhibitors limited?
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they act before the macula densa, so the GFR is toned down
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what are the indications for CA inhibitors?
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Glaucoma, epilepsy, altitude sickness, counteracting diuretic induced metabolic alkalosis
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how do mannitol and glycerin work as diuretics?
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they are freely filtered and never reabsorbed
wash away the osmotic gradient |
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what are the indications for the osmotic agents?
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glaucoma
acute renal failure post-dialysis disequilibrium |
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what are the adverse reactions of the osmotic diuretics?
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hyponatremia with dehydration (unique)
pulmonary edema (due to suddenly increased BV) mannitol bad with intracranial hemorrhage glycern can cause hyperglycemia |
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what is the mechanism of loop diurectics?
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inhibition of Na-K-2Cl symporter
K immediately goes back into lumen, so this sets up a negative interstiail gradient This gradient draws divalents (Ca and Mg) into interstitium to make medullary concentration loss of concentration in descending loop loss of dilution in ascending loop |
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how is furosemide metabolized?
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it is the only one that is glucuronidated in the kidney
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how is furosemide's activity differerent than the other loop diuretics?
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it is also a weak CA inhibitor, and it increases systemic venous capacitance
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thiazide diuretics act on what transporter?
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Na-Cl symporter in the DCT
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how do thiazides effect Uric acid and Ca urinary excretion?
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decreased Ca excretion: Ca transport is more active with less Na present)
Uric Acid excretion increased: increased urine flow |
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why can you get dehydration with loop diuretics but not with thiazides?
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loop diurectics wash away medullary gradient, make ADH ineffective
thiazides do not effect medullary salt concentraiton |
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which has more potential to increase diuresis, thiazides or loop diuretics?
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loop diuretics (act at ascending loop)
90% of salt has been reabsorbed by the time it reaches DCT for thiazides) |
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which group has a longer t1/2, thiazides or loop diuretics?
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thiazides
don't need to be dosed as often |
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what are the indications for thiazides?
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hypertension
CHF edema nephrolithiasis and osteoporosis (Ca reabsorption inc) diabetes insipidus (paradoxically DECREASES urine output) |
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what are the interactions of thiazides with other drugs?
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inc. effect of anesthetics
NSAIDs decr. thiazide effectiveness Amphotericin B and corticosteroids increase risk of cardiac arrhythmias |
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how do K-sparing diuretics work?
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block Electrogenic Na Channel (ENaC)
prevents intracellular Na gradient driving K and H into lumen) |
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what are the indications for Amiloride and Triamterene?
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used with loop diuretics and thiazides to prevent K wasting
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what are the effects of aldosterone on the nephron? (what are the mineralcorticoid antagonists?)
|
increased ENaC activity
increased Na/K ATPase on BL membrane net: Na reabsorption K and H excretion antagonists: spironolactone, Eplerenone |
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what are the off-site effects of vasopressin-drugs?
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AVP and Lypressin act on V1 receptors to vasoconstrict
synthetic Desmopressin does not have V1 activity! |
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what 3 effects does AVP have on the nephron?
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1) aquaporin insertion
2) increased Na-K-2Cl activity at TAL 3) increased urea reabsorption in CD |
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what is the cause of diabetes insipidus?
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loss of production of vasopressin (ADH)
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what are the adverse effects of AVP?
|
nasal mucosal drying and coronary artery constriction
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how does probenecid work?
|
it inhibits the organic anion transporter at both the PCT and DCT. Main, long term effect at DCT where it decreases Uric acid reabsorption
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what must you consider for diuretic dosing in nephrotic syndrome?
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many diuretics are protein bound and with significant loss of albumin the drugs diffuse out into interstitial space, so you need a HIGHER DOSE to get the same effect
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what are the most common causes of diuretic "resistance"
|
noncompliance (with drug or Na intake)
NSAID antagonism low GFR (due CHF) misdiagnosis |
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what are the side effects of spirinolactone?
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hyperkalemia, gynecomastia, agranulocytosis
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which diuretic can you use to treat hypercalcemia?
|
furosemide
|
|
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which cytochrome is responsible for metabolizing opioids to morphine?
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CYP2D6
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what is unique about methadone?
|
it has an ultra long t1/2 compared to the other opioids
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what is the use for mu opioid mixed agonist/antagonists?
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mild, ACUTE pain relief with fewer side effects
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how are TCAs metabolized?
|
by liver microsomal enzymes
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what is the theory for how anti-depressants (particularly SSRIs) produce therapeutic benefits only after 2 weeks administration?
|
cause hippocampal neurogenesis (by increased BDGF
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which SSRI has high 1st pass metabolism?
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Sertraline
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which antidepressants cause significant drug interactions?
|
SSRIs
they inhibit multiple CYPs |
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what is the difference in pharmacokinetics between duloxetine and venlafaxine?
|
duloxetine is more highly protein bound and heavily requires liver metabolism (contraindicated in liver failure)
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what are the main side effects of SSRIs and SNRIs?
|
no off-target effects like TCAs
Anorexia nausea insomnia sexual dysfx |
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what are the proposed mechanisms of lithium?
|
prevent intracellular signalling (IP3, GSK-3beta kinase, 5-HT receptors)
also enhances glutamate reuptake |
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how do amphetamines work?
|
increase NE and DA release by multiple mechanisms:
MAO inhibition increased vesicular and non-vesicular release |
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what is ADHD drug that has no abuse potential? how does it work?
|
Atomexidate
NE reuptake inhibitor |
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what are the drug interactions are concerning with BZs?
|
additive interactions with EtOH or Barbs
no concerning CYP induction |
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what are the contraindications to barbiturates?
|
pain (can increase pain sensitivity!)
pulmonary insufficiency (cardiorespiratory depression) |
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what anticonvulsant can increase phenytoin metabolism?
|
carbamazepine when given in combo increases metabolism of phenytoin
carbamazepine also increases its own metabolism |
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how does valproic acid work?
|
it inhibits Na channels, Ca channels, AND facilitates GABA transmission
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how does primidone work?
|
it is metabolized to phenobarbital (same uses)
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how does lamotrigine work?
|
it inhibits Na channels
also inhibits glutamate release |
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how does Gabapentin work and how is it used?
|
it binds V-gated Ca channels facilitating GABA transmission?
used in combo therapy |
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which antiepileptics cause megaloblastic anemia?
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phenytoin, primidone
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which antiepileptics cause thrombocytopenia?
|
valproic acid and pregabalin
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what are the neuroleptic drugs that work by blocking 5-HT2 receptors?
|
Clozapine and Risperidone
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the anti-muscarinic drugs benztropine and trihexyphenidyl produce what therapeutic effects?
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help with tremor and rigidity
do NOT help with bradykinesia |
|
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which alzheimer treatment (AChE inhibitors) has the longest halflife?
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Donepezil
|
|
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which alzheimer's treatment (AChE inhibitors) has the most dangerous side effect?
|
Tacrine: hepatotoxicity
|
