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378 Cards in this Set
- Front
- Back
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Name the 5 major analgesics
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Acetaminophen
NSAIDS Opiates Anesthetics Tramadol (Take AN OAT for pain) |
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Name 3 drug types that can be analgesics but are not major ones.
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Anti-depressants
Anti-convulsants alpha-2 adrenergic agonists |
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WHat are the 4 major types of pain?
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Physiologic
Neuropathic Inflammatory Dysfunctional |
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what causes dysfunctional pain?
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not sure, there is no noxious stimulus present
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2 examples of inflammatory pain?
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Arthritis and gout
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What is neuropathic pain due to?
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Nerve damage (ie during surgery)
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What are some examples of physiologic pain?
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Burn, poke, scratch
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what type of receptor senses pain?
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Nociceptors!
(free nerve endings) |
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What type of afferent fibers carry pain?
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A delta and C
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what type of channel is the pain TRP channel?
what type of stimuli does it sense? |
Cation Channel (I TRiPped over the cat)
Senses hot cold, wasabi, pH, menthol, capsaicin, some mechano |
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What type of channel is the ENaC channel?
What type of stimuli does it sense? |
Cation channel (Na is positive)
Senses mechano stimuli |
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What type of channel is the ASIC channel?
What type of stimuli does it sense? |
Cation channel (member of the ENaC superfamily)
Senses pH (ASIC person throws up ACIDIC vomit) |
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What nociceptor channel is a part of the ENaC superfamily?
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ASIC (bc ASICS are SUPER shoes)
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What type of channel is P2X? P2Y?
Which works faster? What does each sense? |
P2X is ligand gated
P2Y is G-protein P2X works faster than P2Y bc it is ligand gated vs. G-protein (X is before Y in alphabet) P2X and P2Y sense ATP (from cell rupture) |
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What type of receptor is a Bradykinin?
what does it do to the affected cell? What does it sense? |
G-protein
Increases Intracellular calcium Senses Kinins (bradyKININ) |
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what are the 3 major classes of sensory afferent fibers?
WHich convey pain? |
A beta
A delta C A delta and C convey pain |
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What type of info does A delta fibers carry?
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cold and heat
high-intensity mechano pain |
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what type of info does C fiber carry?
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heat
intense mechanical chemical (it's multimodal!) |
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For A beta, A delta, and C fibers...
what is each's speed of conductance? |
A beta = fast
A delta = intermediate C = slow |
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What NT and receptors carry ascending pain in spinal cord and up?
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Glutamate!
AMPArs NMDArs |
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what can long/strong pain stimuli activate to cause release of neuromodulatory neurons such as Substance P and BDNF?
why would you want this? |
mGLUrs
if you use enough GLUe, you can modulate anything into what you want! It helps make these stimuli feel much more painful so we respond and cause less damage to ourselves. |
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Are there local inhibitory circuits WITHIN the spinal cord or is pain regulated all in the brain?
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There are local inhibitory circuits in spinal cord
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What are the 5 main inhibitory NTs?
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Glycine
Opioid peptides NE GABA Serotonin (5-HT) GONGS make pain go away bc all you can focus on is the noise! |
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What is allodynia?
What is hyperalgesia? |
Allodynia is when you get pain from normally unpainful stimuli (even "aloe" can hurt)
Hyperalgesia is when you get increased pain from normally noxious stimuli (ie you get more (hyper) pain (algesia) from painful stimuli. a pinch hurts a lot! |
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Which way does hyperalgesia shift the pain intensity(y) v. stimulus intensity (X) curve?
Allodynia? |
Hyperalgesia shifts it up
Allodynia shifts it to the left |
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What are the 3 analgesics used to treat acute and musculoskeletal pain?
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Tramadol
Opioids NSAIDS My muscles hurt a TON |
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What are the 2 analgesics used to treat neuropathic pain?
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Amitriptylene
Gabapentin My nerves Are Gay |
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what analgesic is used for migraines?
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Triptans
Migraines make you Trip |
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what is an example of an analgesic that acts at site of injury?
what type of pain do these decrease |
NSAIDS
Decrease pain associated with inflammatory reaction |
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what is an example of an analgesic that alters nerve conduction?
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Local anesthetics
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name 2 analgesics that modify transmission in dorsal horn?
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Opioids
Some antidepressants |
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what 2 analgesics affect the central component and the emotional aspects of pain?
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Opioids
antidepressants (same as those that work in dorsal horn) |
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What is the main goal of an analgesic? what do we want without causing impairment of...
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we want pain relief
without impairment of : cognitive function memory motor coordination consciousness |
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How good is acetaminophen at reducing inflammation?
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TERRIBLE
it has absolutely NO antiinflammatory properties |
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how good is analgesia from acetaminophen?
What limits it? |
Superior
Patient perception limits it (people think since it's OTC that it can't be that good) |
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If you give acetaminophen with an opioid, how long should you give the opioid, and what do you do after?
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use opioid with it for 2-3 days, then continue use of just acetaminophen
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what is mechanism of action of acetaminophen?
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Not clear
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what are the three major NSAIDs?
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Aspirin
Ibuprophen Naproxen Tylenol AIN't an NSAID |
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what type of pain are NSAIDS especially good at relieving?
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Inflammatory Pain (duh)
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what are the 2 major disadvantages of NSAIDS?
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GI problems
Kidney effects |
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how fast is Aspirin absorbed and distributed?
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Rapidly
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What can chronic use of aspirin lead to?
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Gastric irritation, erosion, hemorrhage, and renal tubular necrosis (GI and kidney just like all NSAIDS)
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Does aspirin or Ibuprofen have more adverse side effects?
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Aspirin has more
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Does Naproxen or Ibuprofen have a longer half life?
Which is more potent? |
Naproxen
Naproxen (All day strong, all day long!) |
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what is the mechanism of action of NSAIDs?
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COX blockers
They block cyclooxygenase pathway which normally breaks down AA into prostaglandins which mediate pain |
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3 drug types of opioids?
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opiates
opiopeptins synthetic drugs that mimic actions of opiates |
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what type of opioids are endogenous?
which are from alkaloids of opium poppy? |
opiopeptins are endogenous (peptin is inside us)
Opiates are from alkaloids of opium poppy |
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what plant do the opiates come from?
which do they NOT come from? |
papaver somniferum
eschscholzia californica (california poppies cannot be used for fun!) |
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what type of receptor are the opioid receptors?
What are the three types? Which is responsible for the most pain relief? |
G-protein coupled
Mu, Kappa, Delta Mu for More pain relief |
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what three effects do opioid receptors produce inside a cell?
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Decrease presynaptic Ca influx
Increase postsynaptic K efflux Decrease adenylyl cyclase activity |
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Where are Mu opioid receptors located?
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Supraspinal, spinal, peripheral
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Where are delta opioid receptors located?
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Just spinal (the Dummies of the opioids)
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Where are kappa opioid receptors located?
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Periphery and some spinal!
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What endogenous ligands bind to:
Mu opioid receptors? Delta? Kappa? |
Endorphins/endomorphins
Enkephalins Dynorphins |
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What are the three full agonists of opioids?
2 partial agonists? |
Codeine Morphine Oxycodone (.COM companies are FULL of shit)
Nalorphine, Pentazocine (NiP is to bite PARTIALLY) |
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Do opioid antagonists alter analgesia produced by NSAIDS and general anesthetics?
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NO
different mechanisms of action |
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What are the three opioid antagonists?
Which is/are reversible Which is/are irreversible |
Naloxone, Naltrexone, beta-chloro-naltrexamine
Naloxone and Naltrexone are reversible beta-chloro-naltrexamine is irreversible NX stops opioids from working in NX! beta-chloro-naltrexamine has an I in it so it's Irreversible |
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what are the 4 different sites of opioid action?
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Brain stem
Emotional Dorsal horn Nociceptors (opioids BEND your sense of pain) |
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what are the 3 NTs involved in descending inhibitory control?
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5-HT, Opioids, NE
The SON stops descending! |
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Are opioids best at relieving sharp inermittant pain and neuropathic pain, OR dull, constant pain?
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Dull constant pain!
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what is an example of a fast opioid used for intraoperative use?
What is an example of slow for peri and post operative analgesia? |
remifentanil
Morphine |
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what is the major side effect of opioids?
what other thing do they do? |
Respiratory depression (antitussive effect)
they also Elevate Mood |
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is the dose of opioids needed to suppress cough reflex higher or lower than that needed for analgesia?
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LOWER, which is why we need to be careful when using them
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what are 7 adverse effects of mu opioid receptors?
Do Kappa have more or less analgesia and adverse effects? |
Respiratory depression
Nausea Vomiting Constipation Dependence Tolerance Muscle rigidity Kappa has less than Mu |
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is a single opioid or a combo of opioids a better drug?
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COMBO!
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which analgesic can cause itching and bronchoconstriction?
why? |
Opioids, bc activation of opioid receptors in the periphery causes histamine release!
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do opiates cause pupils to dilate or constrict?
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Constrict!
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what is definition of tolerance?
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adaptation of the system in response to chronic drug exposure
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patients with tolerance to opioid require ________ than normal doses to achieve same pain relief?
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HIGHER
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True or false:
Tolerance occurs for all effects of a drug equally? |
FALSE
(ie - tolerance to opioids can still give respiratory depression but not relieve pain! BAD!) |
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what is physical dependence?
how long must an opioid be used to develop tolerance? |
adaptation of the system in response to exposure of the drug
about 5 days! |
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Can you develop dependence from one or 2 uses of a drug?
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NO, must be used for at least 5 days
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what does removal of a drug or rapid dose reduction result in for someone with a drug dependence?
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Withdrawal syndrome
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how common is addiction to opioids?
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RARE, most are actually dependence!
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which is physiological and which is psychological?
Addiction and dependence? |
Addiction is psychological
Dependence is physiological |
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what is a pseudoaddiction?
how can it be differentiated from addiction? |
seen in patients with severe UNRELIEVED pain, where main goal is to RELIEVE pain
In pseudoaddiction, the drug seeking is resolved when the pain is adequately resolved |
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what 2 things is clinical use of opioid analgesics limited by?
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Tolerance to analgesic effects
Failure of tolerance to respiratory depression |
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what is clinial use of opioids NOT limited by?
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ability to cause Dependence or addiction
especially for SHORT TERM (<5 days) relief of pain |
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how many schedules of drugs are there?
Which is most restricted? |
3 schedules
Schedule I is most restricted |
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what is abuse potential of Schedule I drug?
How do you prescribe it? |
Very high
CANNOT Prescribe it! clinically unavilable for use in US |
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What is abuse potential of Schedule II drugs?
How do you prescribe it? can prescription be refilled? |
high abuse potential
written prescription always required No refills! need new prescription |
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What is abuse potential of Schedule III drugs?
How do you prescribe it? can it be refilled? |
lower abuse potential
can phone in prescription can refill it |
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which schudule drugs need a DEA number and are monitored?
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ALL 3 schedules need it!
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examples of:
Schedule I drugs Schedule II Schedule III |
I = heroin
II = morphine, oxycodone III = hydrocodone and codeine mixtures, meperdine, methadone |
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which word has NO pharmacological meaning?
What does it have a meaning in? |
Narcotic
It's a legal term |
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what is the only common factor of narcotics?
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abuse potential, usually causing addiction
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what opioid cannot be used orally?? why?
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Morphine, because of first pass metabolism in liver.
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what are two oral opioids that can be used for mild to moderate pain?
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Codeine, Propoxyphene
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what is the other name for propoxyphene?
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Darvon or darvocet
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what are three oral opioids used for moderate to severe pain? their schedules?
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Hydrocodone III
Oxycodone II Meperdine III say OHM for analgesia from moderate to severe pain! |
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what are the three other uses of codeine other than analgesia?
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Antitussive (resp. depression)
Sedative (sleepiness) Antidiarrheal (constipation) |
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what is the level of analgesia of codeine similar to?
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NSAIDS (mild to moderate pain)
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what dose of codeine can cause respiratory depression?
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60-100 mg
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what 2 drugs is codeine usually used in combo with?
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Aspirin and Acetaminophen
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How much analgesia does codeine itself provide?
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Absolutely NONE, it must be converted by P450s in liver to Morphine
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why do some people not get pain relief from codeine?
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because there are differences in P450s from person to person and the codeine could not be metabolized at all or just very slowly
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is it clinically possible to get adequate doses of each drug using the available mixtures of codeine and acetaminophen? WHy?
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NO, there is not an adequate dose of acetaminophen
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what are the 4 combinations of tylenol with codeine?
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1 = 8 mg codeine
2 = 15 mg codeine 3 = 30 mg codeine 4 = 60 mg codeine All have 300 mg tylenol |
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what is the recommended dose of acetaminophen every 4 hrs?
how much do you get taking 2 tablets of tylenol #3? |
1000 mg
600 mg (not enough!!) |
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what is structure of hydrocodone?
Which is more effective? |
it's a semi-synthetic analogue of codeine (hydroCODEINE)
hydrocodone is more effective! |
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what are the 2 positives to using hydrocodone over codeine?
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less GI and euphoria
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what is analgesic dose of hydrocodone?
how long does it last? |
5-10 mg (much less than codeine)
4-8 hours |
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what is in vicodin and vicodin ES?
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vicodin = 5 mg hydrocodone and 500 mg acetaminophen
vicodin ES = 7.5 mg hydrocodone and 750 mg acetaminophen BOTH have less than adequate acetaminophen |
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what is structure of oxycodone?
does it have more or less side effects than codeine? |
semisynthetic analogue of codeine (oxyCODEINE)
has more side effects than codeine (whereas hydrocodone had less!) |
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3 different formulations of oxycodone?
which has adequate dose of aspirin/acetaminophen? |
Percodan = 5 mg with 325 ASPIRIN
Percocet = 5 mg with 325 Acetaminophen Tylox = 5 mg with 500 Acetaminophen NONE have adequate dose of aspirin/acetaminophen |
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what is meperdine (demerol)?
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synthetic Mu-receptor agonist
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what is efficacy of meperdine close to?
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morphine
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what is its main adverse effect?
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causes dysphoria
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what is the primary use for meperdine? what shouldn't you use it for?
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primary for PERI operative anesthesia NOT postoperative
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what is unique about the metabolite of meperdine?
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its half life is 3x longer
and it promotes seizures |
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what is propoxyphene analgesia equivalent to?
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650 mg aspirin
1 gram acetaminophen |
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what do you have to worry about when giving propoxyphene?
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combo with aspirin/acetaminophen is additive
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what is the major disadvantage of propoxyphene?
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mildly toxic doses can give convulsions
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which opioid is now off the market for higher risk of suicide, less pain relief than others, and higher risk of abuse?
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Propoxyphene
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what three NT properties does tramadol have?
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Opioid
Serotonin adrenergic |
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is tramadol or morphine better in severe pain?
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Morphine
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What are 2 major disadvantages of Tramadol?
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Relatively weak opioid activity in CNS
Only works well combined with somethign else. |
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what schedule is tramadol?
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Not scheduled anywhere
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what are three main advantages of tramadol in terms of what it doesn't cause?
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Tolerance
Dependence Addiction Also, less constipation and respiratory depression than other opioids |
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when can tramadol cause respiratory depression?
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with impaired renal function.
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what is probably responsible for lack of abuse potential of tramadol?
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The mixed mode of action through Serotonin, Opioid, and adrenergic.
also, at higher doses, the serotonin and adrenergic effects produce Dysphoria rather than euphoria Therefore, you get good analgesia at a lesser "opioid" dose |
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what is Tramadol contraindicated with?
what should it be used with caution with? why? |
contraindicated with MAOIs
Caution with SSRIs, bc serotonin syndrome due to serotonin effects |
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what is the major side effect of tramadol?
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dizziness
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what patient should tramadol be avoided with?
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Epileptics, bc it could cause seizures
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what is tramadol overdose Neurotoxicity? CV toxicity?
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significant
Small |
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what 3 opioids are used parenterally?
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Morphine
Fentanyl Meperdine |
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What is the most popular parenteral analgesic and why?
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Fentanyl, bc it's fast and quick recovery
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what analgesic is safer in patients with impaired kidney fxn?
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fentanyl
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which opioid analgesic shows the most muscle rigidity?
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Fentanyl
(Fentanyl makes you firm) |
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parenterally, does meperdine or fentanyl take longer to peak analgesia and is longer lasting?
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Meperdine
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does meperdine or fentanyl show more respiratory suppression?
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meperdine
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whose fault is it that most patients receive inadequate pain relief?
Why? is it founded? |
the practitioners!
for fear of addiction/dependence NOT founded because these are not issues in ACUTE pain relief (<5 days) |
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How does cannabis work?
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not sure,
but agonists at CB1 receptors |
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what shoudl you use for perioperative analgesia?
with what? |
Fentanyl or meperdine
along with induction agent like midazolam |
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what should you use for pre/post op analgesia?
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tramadol and acetaminophen or
codeine and acetaminophen |
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what do COX 2 inhibitors do?
Why are they good? why ar ethey bad? |
block inflammation promoting substance COX 2
good because work as well as NSAIDS but with fewer stomach problems Bad bc of heart attacks and stroke |
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Why are segmented filamentous bacteria important in our gut?
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THey are required for expression of Th17 lymphocytes in the gut
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what 4 things do Th17 Lymphocytes do?
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Produce IL 17 and 22
Suppress excessive immune response suppress mucosal infections mediate inflammatory autoimmune disease |
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when we use antibiotics, what usually ends up taking care of the infection?
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It is our immune system.
The antibiotics just make it easier for our immune system to combat the bacteria |
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what are 2 ways bacterial pathogens introduce themselves to the host?
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Adherence
Toxin secretion |
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3 ways bacteria leave cells?
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invasion, apoptosis, necrosis
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how do pathogens adhere to host cells?
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PILI that carry ADHESINS on their tips
(P and CF pili) |
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What do P pili bind?
CF pili? |
P pili = digalactoside
CF = intestinal binding |
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2 ways bacteria disseminate themselves?
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1. direct its own invasion of epithelial cells, causing apoptosis and mild inflammation
2. Allow M Cells in Peyer's patches to take it up, be taken up by macrophages, and disseminated |
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How many types of secretion systems are there for bacteria?
What is Type III secretion |
6 different types
Type III involves injecting bacterial proteins through 3 membranes (3=3) from bacteria into host cell: Bacterial inner membrane Bacterial outer membrane Host cell membrane |
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what is the difference bw mode of infection bw e. coli and salmonella?
|
e. coli adheres with pedastals
Salmonella invades |
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what does legionella cause?
|
Coiling phagocytosis
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what does yersinia cause?
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Macrophage apoptosis
(YER a SINner macrophage, so kill yourself) |
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WHat do we know about how salmonella invades?
Spreads? |
A good amount
Very little about how it spreads once it gets in |
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Are there adequate nutrients inside phagosomes or vacuoles for bacteria?
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NO
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What are 2 main ways bacteria compete with host cells for nutrients?
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1. Highly competetive transport systems
2. Lyse the phagosome to gain access to cytosol |
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What are the 2 main ways bacteria get out of cells?
Which causes apoptosis? Necrosis? |
1. Bacteria replicates in cell and causes apoptosis allowing escape (APOPTOSIS)
2. Bacterium rapidly lyses the vacuole and replicates within the cell (NECROSIS) |
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What type of reaction does apoptosis bring about? What does this allow the bacteria to do?
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MILD inflammatory reaction
Makes membranes leaky, making it easier for bacteria to invade neighboring cells |
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How are bacteria that lyse the cell and then replicate able to overcome the large inflammatory reaction?
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They release tons of bacteria, overloading the inflammatory rxn!
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What bacteria gets out of cells by recruiting actin, propelling itself by constantly adding actin to the leading edge to perforate the membrane?
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Listeria monocytogenes
Rickettsia coronii |
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What is a main defense mechanism used by macrophages and other cells to attack invaders?
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Reactive Oxygen and Nitrogen species
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What are the 4 reactive oxygen and nitrogens used by cells and macrophages to ward off invaders?
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Peroxide
Superoxide Hydroxyl radical Peroxynitrate |
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What do bacteria produce to counteract the reactive oxygens and nitrogens that macrophages and cells use to try and kill them?
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Catalase
Peroxidase Superoxide dismutase |
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How does the host cell detect a bacterial invader?
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Toll Receptors and TLRs!
these cell surface receptors detect bacteria and their products |
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What do TLR-2 sense?
TLR-3? TLR-4? TLR-9? |
Gram + bacteria
Double stranded RNA Gram - bacteria Unmethylated CpG dinucleotides |
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In humans, is CpG dinucleotide methylated? what about bateria? What is significance of this and what detects it?
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Humans it's methylated
Bacteria is UNmethylated TLR-9 receptors sense UNmethylated CpG dinucleotides, meaning there is bacteria present |
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4 major defenses host cells have against bacteria?
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1. Prevent adherence (Ig, opsonization)
2. Phagocytosis 3. Deptrive of essential nutrients 4. Reactive oxygen and nitrogen |
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What is the Murray collection?
|
Collection of 433 enterobacteria bw 1914 and 1954,
ONLY 2 were resistant to penicillin |
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What is responsible for virtually all drug resistance?
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PLASMIDS transferred bw species
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2 major things happening that make it hard for antibiotic usage?
|
1. New sophisticated diseases occur all the time (HIV,Syphilis)
2. RESISTANCE |
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Is resistance increasing or decreasing in e. coli? due to what?
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INCREASING
Plasmids |
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what is the major killer in wars?
|
DISEASE due to so many people being brought together that can contain bugs people have never been exposed to before
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why are bugs initially drug resistant?
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because they make their own antibiotics to compete with other bacteria, so they need to continually evolve to survive
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What is difference in cell wall bw gram + and -?
|
gram + has 90% peptidoglycan
gram - has low peptidoglycan, but high LIPID content |
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What color do gram - and + bacteria stain and why?
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gram - = pink, because they do not incorporate the primary stain, only the counterstain
gram + = crystal violet, bc they incorporate the primary gram stain |
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If an antibiotic compromises the integrity of the cell wall, is it bacteriostatic or bactericidal?
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bactericidal, bc osmotic stress will destroy the cell and rupture it.
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Is a bacteriostatic drug always bacteriostatic, and same thing for bactericidal?
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NO, it can be one for one bacteria and the other for another
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Are cell wall inhibitors bactericidal or bacteriostatic?
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CIDAL, bc the wall is weak and will lyse due to osmotic pressure
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What are the limitation of beta-lactams?
|
1. cell must be rapidly growing
2. cell must have lots of peptidoglycan (GRAM +!) |
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How do beta lactams work?
|
inhibit transpeptidase
which is responsible for crosslinking bw strands in the wall |
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what are the 4 main categories of B-lactam antibiotics?
|
1. Penicillin
2. Cephalosporins 3. Carbapenems/Monobactams 4. Combination therapy (Cell WALL = your PCC puts a WALL around you by giving you a cubicle) |
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Is penicillin G or V more acid resistant?
what is significance of this? |
V
Penicillin V is used to treat oral infections since there is usually a lot of acid involved |
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|
what are the "anti-staphylococcal penicillins", why aren't they used anymore for staph infections?
Are they acid resistant? stable to penicillinases? |
Methacillin
Nafcillin Oxacillin Cloxacillin Dicloxacillin not used bc MSRA developed they are NOT acid resistant, but they are stable to penicillinases. |
|
|
what are the 2 extended spectrum penicillins? which causes diarrhea?
|
Ampicillin
Amoxicillin Ampicillin causes diarrhea (bc it AMPS up your colon!) |
|
|
what is f oral of Extended spectrum penicillins (amox and amp)?
how many gram - pathogens are resistant to them? |
100% (good orally)
40% are resistant |
|
|
what are the 2 anti-pseudomonal penicillins?
what are and aren't they effective against? |
carbenacillin
piperacillin effective against P. aeruginusa and other gram - bacilli EXCEPT Klebsiella |
|
|
Do most oral penicillins have high or low bioavailabilty? What is the exception?
|
LOW
exception is AMOXICILLIN |
|
|
what does food do to the absorption of penicillins?
|
DECREASES it, so can stay in gut longer and kill commensal bacteria
|
|
|
how are penicillins metabolized by humans?
|
THey AREN"T, excreted through kidney
|
|
|
what 2 penicillins cause platelet dysfunction?
|
Penicillin G
Carbenicillin |
|
|
how much of population is allergic to penicillins?
|
2%
|
|
|
3 mechanisms of resistance to Penicillins?
|
1. Beta-lactamases
2. Altered penicillin binding proteins 3. decreased permeability to drug |
|
|
how many amoxicillin resistant bacterai are resistant to combo drugs that include b-lactamase inhibitors?
|
10%
|
|
|
what are the three b-lactamase inhibitors?
|
Sublactam
Tazobactam Clavulonic Acid (Stop The Cleavage of b-lactams!) |
|
|
what is augmentin?
Piptaz? |
Amoxicillin + clavulonic acid
tazobactam + piperacillin |
|
|
how do cephalosporins differ structually from penicillins?
|
modified b-lactam ring with 2 different r groups
|
|
|
what are cephalosporins especially good against?
|
oral cavity anaerobes!
|
|
|
2 1st generation cephalosporins?
|
Cephalexin
Cefazolin |
|
|
3 2nd generation cephalosporins?
|
Cefoxitin
Cefuroxime Cefaclor |
|
|
4 3rd generation cephalosporins?
|
Cefixime
Ceftriaxone Ceftazidime Cefotaxime |
|
|
1 4th generation cephalosporin?
|
Cefepime
|
|
|
what are 2 "other" b-lactam antibiotics?
which is BROADEST SPECTRUM b-lactam? which is narrow? |
Carbapenems
Monobactams Carbapenem is broadest spectrum (bc there are a lot of carbs) Monobactam is narrow spectrum |
|
|
are carbapenems and monobactams resistant to b-lactamases?
|
YES HIGHLY
|
|
|
What does vancomycin do?
Is it a b-lactam? |
Inhibits incorporation of MURAMIC ACID into peptidoglycan
NOT a b-lactam , but a tricyclic glycopeptide |
|
|
How has resistance emerged to Vancomycin?
|
virginiamycin used in animal feed, and is related
|
|
|
2 adverse effects of impure vancomycin (mud)
|
1. nephrotoxicity
2. ototoxicity |
|
|
What two classes of antibiotics work by inhibiting the 30s ribosomal subunit?
|
Aminoglycosides
Tetracyclins |
|
|
What 2 classes of antibiotics work by inhibiting the 50s ribosomal subunit?
|
Macrolides
Clindamycin |
|
|
Which antibiotic inhibits peptidyl transfer on large ribosomal subunit?
|
Chloramphenicol
|
|
|
are tetracyclins more active against gram + or -?
|
gram + bc a t looks like a +
|
|
|
why do doxycyclin and minocyclin have better f orals than tetracyclin?
|
bc they are more lipophilic
|
|
|
what are the major side efffects of tetracyclins?
|
Discolored teeth
photosensitivity hepatic and renal toxicity less bone growth GI upset |
|
|
is tetracyclin bacteriocidal or static?
aminoglycosides? |
tetra is static
aminoglycosides are cidal |
|
|
Name 3 aminoglycosides.
|
Streptomycin
Tobramycin Neomycin B |
|
|
How are aminoglycosides used?
what are they effective against and why? |
usually used with other antibiotics
only effective against aerobic organisms, bc the transport of the drug is oxygen dependent |
|
|
what is f oral of aminoglycosides? why?
|
POOR, because lots of positive side chains
|
|
|
where are the two places aminoglycosides usually accumulate?
|
inner ear
renal cortex |
|
|
what are the three main side effects of aminoglycosides?
|
Ototoxicity (with deafness and vertigo)
Nephrotoxicity Paralysis (rare) |
|
|
are aminoglycosides first line drugs? why?
|
NO
resistance and ototoxicity |
|
|
Are macrolides bacteriostatic or cidal?
|
Static at low concentrations
Cidal at high |
|
|
how do macrolides work?
|
irreversibly bind 50s subunit and block TRANSLOCATION of ribosome along mRNA
|
|
|
3 main macrolides. name them.
|
Erythromycin
Azithromycin Clarithromycin |
|
|
what is the spectrum of macrolides (erythromycin)? what does this mean?
|
SAME as penicillins
MAIN SUBSTITUTE for those with penicillin allergy |
|
|
how do you give macrolides? any special cases?
|
orally
ERYTHROMYCIN is acid sensitive so the tablet must be coated |
|
|
3 major side effects of macrolides?
|
GI problems
ototoxicity (not as much as aminoglycosides) cholestatic jaundice |
|
|
what is the major concern with using macrolides?
|
They inhibit CYP3A4 (big MACs are 3.84)
so lots of drug interactions |
|
|
4 contraindications for prescribing macrolides?
|
1. patient has liver function (bc metabolized there)
2. Carbamazapene 3. Cyclosporin 4. Warfarin |
|
|
what is main mode of resistance to macrolides? why?
|
Plasmid associated ESTERASE
bc esterase breaks ester bond of macrolides |
|
|
How often do we use Chloramphenicol? why?
|
RARELY, bc LOW therapeutic index, because it blocks peptidyl transferase in humans too which is bad!
|
|
|
what is spectrum of chloamphenicol?
|
BROAD against ALL BACTERIA and MICROORGANISMS
(CHLORine in the pool kills everything!) |
|
|
why does chloramphenicol have interactions? with what drugs specifically?
|
because it inhibits some P450s
Phenytoin Warfarin Tolbutamide |
|
|
what is main mode of resistance to chloramphenicol?
|
Plasmid encoded ACETYL-COA TRANSFERASE that inhibits chloramphenicol
Plasmids ACT on chloramphenicol |
|
|
what is spectrum of clindamycin?
|
IDENTICAL to erythromycin (which is same as penicillins)
|
|
|
what type of bacteria is clindamycin used to treat?
|
ANAEROBIC bacteria (whereas aminoglycosides is aerobic)
|
|
|
what are the three major side effects of clindamycin?
|
Diarrhea (2-20%)
Skin rash (10%) pseudomembranous colitis (.01-1%) |
|
|
what bacteria is responsible for Pseudomembranous colitis?
What potentiates this along with clindamycin? |
C. difficile
Opioids bc they inhibit gut motility (constipation!) |
|
|
how do you treat pseudomembranous colitis?
|
stop clindamycin
give Vancomycin + Metronidazole + Cholestyramine |
|
|
how do quinolones work?
|
Inihibit Gyrase/Topoisomerase IV
|
|
|
How do anti-metabolites work?
|
folate antagonists
|
|
|
what are the three main antibiotics that inhibit metabolism?
|
Quinolones
Anti-metabolites Anti-myobacterial agents |
|
|
what is the main use of Quinolones (Nalidixic acid)?
how good are they against systemic infections? |
UTIs\
BAD |
|
|
what do gyrases/topoisomerases do during replication?
|
get the kinks out when the strand is winding/unwinding
|
|
|
what is the prototypical quinolone?
|
Ciprofloxacin
|
|
|
What do most quinolones contain?
|
F atom
|
|
|
what is the treatment of choice for acute UTI?
|
Ciprofloxacin (fluroquinolone that inhibits DNA gyrase/topoisomerase)
|
|
|
what is the common ending for the fluoroquinolones?
|
oxacin
(except nalidixic acid) |
|
|
what is the main side effect with fluoroquinolones?
|
Arthropathy (especially with kids with CF)
|
|
|
overall, are fluoroquinolones well or poorly tolerated?
|
Generally well tolerated
|
|
|
how does methenamine treat UTIs?
|
low pH of urine allows it to break down into formaldehyde.
Formaldehyde kills bacteria |
|
|
how is nitrofurantoin used to treat UTIs?
WHat is major side effect? |
Prodrug that BACTERIA enzymatically reduce
can induce DNA damage |
|
|
What do anti-metabolites work on?
|
FOLATE biosynthesis of bacterai
|
|
|
what three things do bacteria use to synthesize folate?
|
PABA
pteridine glutamate |
|
|
why don't anti-metabolites hurt humans?
|
bc they inhibit folate synthesis, and humans do not make folate, they must ingest it
|
|
|
what do sulfonamides do?
|
an anti-metabolite that is a COMPETITIVE inhibitor of enzymes that act on PABA, therefore inhibiting folate synthesis
|
|
|
Are sulfonamides potent?
|
NO
|
|
|
what is trimethoprim?
|
An anti-metabolite that inhibits
DI HYDROFOLATE REDUCTASE (DHFR) the last step in converting dihydrofolate to tetrahydrofolate (folate) |
|
|
why can we safely use trimethoprim?
|
bc it is selective against BACTERIAL DHFR, and 100,000 fold lesspotent on human DHFR
|
|
|
How common is resistance to Trimethoprim and Sulfonamide combo therapy? why?
|
RARE due to combo therapy
|
|
|
What are the three forms of TB and how are they different?
|
TB - readily curable, kills in 1-20 yrs if untreated
MDR TB - resistant to first line drugs, kils in 1-10 years if untreated XDR TB - resistant to first and second line drugs, can kill in 15 days |
|
|
what is cure rate of XDR TB?
|
30% (not good, bc it is resistant to first and second line drugs)
|
|
|
what protects mycobacteria and minimizes drug access to them?
|
Mycolic Acids (WAXY)
|
|
|
How long is treatment for TB?
What is preferred treatment for it? what is considered cured? |
at least 6 months
Treatment by Direct Observation Treatment (DOT) is preferred. cured when successive sputum samples show no m. TB |
|
|
what are the 4 first line drugs for TB?
|
Isoniazid (Niazid)
Rifampin Ethambutol Pyrazinamide |
|
|
how does Isoniazid work on TB?
|
Inhibits Fatty acid synthase I, which makes mycolic acid
|
|
|
Why is isoniazid NEVER used alone?
|
development of resistance
|
|
|
how does Isoniazid become active?
|
it is a prodrug that bacterial enzyme katG oxidizes to acitve form
|
|
|
4 adverse effects of isoniazid?
|
peripheral neuritis
Liver damage Neurotoxicity with phenytoin B6 deficiency |
|
|
how does rifampin work to stop TB?
|
inhibits bacterial RNA polymerase
|
|
|
what is one weird side effect of Rifampin?
|
DISCOLORS urine, sweat, contact lenses
|
|
|
what is a drug contraindicated for rifampin use? why?
|
Oral contraceptives
bc rifampin induces many P450s |
|
|
how does ethambutol work to stop TB?
|
inhibits cell wall synthesis
|
|
|
what is due to toxicity from ethambutol?
|
Inability to see red and green
vision changes rash and itching (like you're on ETHer) |
|
|
how does pyrazinamide work to stop TB?
|
stops mycolic acid synthesis
|
|
|
what major problem can ethambutol cause?
|
Jaundice and dark urine
|
|
|
what are the 2 combo drugs used for TB? which is used first and after how long do you switch to the other?
|
Rifater and Rifamate
Use rifater first 3 months, then switch to rifamate (riFATer is fatter than rifamate bc it contains 3 drugs instead of just 2) |
|
|
what is in rifater and what is it?
|
Isoniazid + rifampin + pyrazinamide
it is first line drug for TB used for first three months (Rifamate is used after that |
|
|
what is in rifamate and what is it?
|
Isoniazid + rifampin
it is a first line drug for TB used after 3 months on rifater |
|
|
what are the three main antifungals and how do they work?
|
Nystatin
Azoles Amphotericin B work by altering fungal membrane permeability by messing with ergesterol synthesis |
|
|
What two drugs do you supplement Nystatin with?
|
rifampin or flucytosine
|
|
|
which azole is teratogenic?
|
Voriconazole
(voriconazole is VERy bad) |
|
|
which antifungal agent is given by IV only?
|
Amphotericin B
|
|
|
which antifungal agent is toxic and should only be used for systemic infections?
|
Amphotericin B
|
|
|
how do you take Nystatin? why?
|
Oral troche bc its not absorbed from gut
|
|
|
what is mycolog and what does it do?
|
topical cream for fungal skin infections
Nystatin + triamcinolone |
|
|
what type of infection is Clotrimazole useful for? why?
|
vaginal infections, thrush, athletes foot
bc it isn't absorbed past where it is applied |
|
|
which azole do you need to decrease oral dose by 50% in Chronic Kidney Disease? Why?
|
Fluconazole
bc it is given orally, NOT metabolized so only cleared by kidney |
|
|
which azole is NOT used vaginally and instead used for toenail and skin infections?
|
Ketoconazole (KEep KEtoconazole away from my vagina!)
|
|
|
which azole works on CYP2C19?
what 2 things does this cause for the drug? |
Voriconazole
1. polymorphisms cause 4x differences in blood concentrations 2. it is saturable, meaning that a linear dose increase can give exponential blood increase |
|
|
what drug is especially good against aspergillus and ESOPHAGEAL candidiasis?
what is its f oral? |
voriconazole
.95 f oral = good! |
|
|
what type of azole (pill, cream, troche) is best for vaginal infections?
thrush? |
Vaginal = creams
Thrush = troches |
|
|
what is major problem with systemic azoles?
|
interaction with many drugs (esp. voriconazole which inhibits CYP2C19
|
|
|
what drug is used for Azole resistant fungi?
|
Caspofungin
|
|
|
what two major patient populations is Ab prophylaxis recommended for?
|
1. Certain cardiac problems
2. Joint replacements |
|
|
what type of nerves do local anesthetics block?
|
BOTH affferent AND efferent
NOT just the ones that have noxious stimuli |
|
|
what are the three layers of a nerve from inside out?
|
Endoneurium
Perineurium Epineurium |
|
|
List in order the differential functional blockade of local anesthetics.
|
1. 1st pain (sharp localized)
2. 2nd pain (dull long lasting slow arrival) 3. Temperature 4. Touch 5. Proprioception 6. skeletal muscle tone |
|
|
what are the 5 general types of local anesthesia?
|
Surface/Topical
Infliltration Regional Intraarticular Intravenous Regional (Bier Block) |
|
|
what is the downside of surface/topical local anesthesia?
|
it is only effective in areas covered by mucous membrane
|
|
|
With which general type of local anesthesia is there a potential for overdose and interference with wound healing?
|
Infiltration
|
|
|
What general type of local anesthesia is used to desensitize areas distal to a tourniquet?
|
Intravenous regional (Bier Block)
|
|
|
Generally, how do local anesthetics work?
|
By blocking Na channels
|
|
|
At rest, are there more closed or inactivated sodium channels?
|
Closed (bc inactivation is right after they are stimulated, but these are at rest)
|
|
|
what 2 states of sodium channels do Local Anesthetics bind with higher affinity?
which do they not really bind to? |
Open and inactivated
don't bind to Closed |
|
|
what does a local anesthetic binding to the inactive state of Na channel do?
|
delays return to resting state and therefore increases the refractory period
|
|
|
what is the difference bw tonic and phasic inhibition with LA?
with which is there more of an effect of LA? |
Tonic occurs with INFREQUENT depolarizations
Phasic is use dependent where the degree of inhibition depends on the frequency of impulses |
|
|
How is more inhibition caused by phasic inhibition (use dependent)?
|
stronger stimulus = higher frequency of activation = more open and inactivated Na Channels = higher inhibition and anesthesia!
|
|
|
what does a higher lipid solubility of a local anesthetic do for:
potency? length of onset of anesthesia? length of duration of action? tendency for CV toxicity? |
increases it
longer length of onset longer duration of action higher tendency for CV toxicity |
|
|
what are 2 low potency, short duration LAs?
|
procaine
2-chloroprocaine |
|
|
what 3 LAs have moderate potency and intermediate duration?
|
Lidocaine
Prilocaine Mepivicaine |
|
|
what 5 LAs have high potency and long duration?
|
Tetracaine
Dibucaine Bupivicaine Etidocaine Ropivacaine |
|
|
what are the two different structures of LAs? What 3 common structures do they share
|
Amides and Esters
all have aromatic ring, tertiary amine, alkyl chain |
|
|
are amide or ester LAs more stable in solution?
Which has a higher risk of allergy? How is each metabolized? |
Amides are more stable in solution
Esters have higher allergy risk Amides are broken down by mixed fxn oxidases (CYP450) Esters are broken down by pseudocholinesterases |
|
|
what is the only NATURALLY occurring LA?
what are its two main properties? |
COCAINE
topical anesthetic and VasoCONSTRICTOR |
|
|
what was the first synthetic LA?
|
Procaine (Novacaine)
|
|
|
what are the 5 ESTER local anesthetics?
which has Rapid sensitization? |
Cocaine
Procaine (Novocaine) 2-chloroprocaine Tetrocaine Benzocaine Benzocaine is rapid sensitization |
|
|
what are the 7 AMIDE local anesthetics?
|
Lidocaine
Prilocaine Etidocaine EMLA (lido + prilo) Mepivacaine Ropivicaine Bupivicaine |
|
|
which bupivicaine is used for all types of blocks?
which is less toxic? |
+- is used for all blocks
- is less toxic |
|
|
what does each of the following do to LA activity?
Vasoconstrictors Site of injection alkalinization pregnancy |
increase duration by decreasing blood flow
influences dose, onset, duration and success rate decreases latency of onset and increases potency increases dermatomal spread and potency |
|
|
Why do you rarely use LA in extremities?
|
Due to possible hypoxia and tissue damage
|
|
|
As pH increases, what what happens to the fraction of LA in free base (uncharged) form?
what does this mean? Is it faster or slower onset when bicarbonate is added? |
it Increases, meaning greater membrane permeability, better accesss to nerve
FASTER onset bc it increases pH |
|
|
is charged or uncharged LA more potent at Na channels?
|
Charged, but uncharged still works better bc it gets there faster and thats what determines
|
|
|
what 2 types of toxicities can develop if LA is absorbed and distributed systemically?
|
CNS and CV
|
|
|
What does protein binding do to LA duration of action?
|
NOTHING, protein binding is NOT important with current LAs!!
|
|
|
are amide or ester LAs metabolites active?
|
Amide are Active!
|
|
|
What does renal failure do to Vd of each type of LA (amide and ester)
|
increases Vd of both
(both bc 2 kidneys!) |
|
|
What does hepatic failure do to Vd or each type of LA (amide and ester)
Why? |
it increases amide but NOT ester Vd, bc ONLY amides are metabolized by liver CYP450) (esters by pseudocholinesterases!)
|
|
|
what do b-adrenergic and histamine h2 antagonists due to LA amide and ester clearance?
what about cardiac failure? |
both decrease AMIDE but NOT ester clearance
|
|
|
what does Pregnancy do to LA amide and ester clearance?
Cholinesterase deficiency or inhibition? |
Pregnancy INCREASES amide clearance but not ester (only thing to increase clearance of amides)
Decreases clearance of Esters, NOT amides |
|
|
which type of LA has active metabolites?
|
Amides are Active (not esters)
|
|
|
what two LAs can have allergic rxns?
why? |
Procaine or benzocaine
Metabolite of procaine is PABA, which is an allergen (ie PABA free sunscreen!) |
|
|
what is the half life of Amide LAs?
Ester LAs? |
amides = hours
esters = seconds to minutes amides longer bc they are broken down by LIVER! |
|
|
What is the progression of signs and symptoms of LA CNS toxicity?
(Old test question) |
1. Vertigo and tinnitus
2. ominous feelings and circumoral numbness 3. Garrulousness 4. Tremors, myoclonic jerks, convulsions |
|
|
which 2 LAs can have neurotoxic effects?
|
2-Chloroprocaine
(fixed with new formulation, but generics can still use old formulation) Spinal lidocaine (5% lidocaine has PERMANENT nerve block) |
|
|
does CV or CNS toxicity occur at higher dose for Local anesthetics?
Which clinical effects are seen first? |
CV toxicity occurs at higher dose (bc the heart has more muscle than CNS, so it takes more to get through)
However, you see CV effects clinically first |
|
|
do LAs vasoconstrict or dilate at low doses?
high doses? |
constrict at low doses
Dilate at high doses (we inject high doses, so we get dilation) |
|
|
when can a topical allergy to Benzocaine or solarcaine occur?
|
after 1-2 applications only!
|
|
|
What are most "allergies" to LAs usually actually?
|
a TOXIC reaction to the LA or Epi
|
|
|
what are the 5 goals of anesthesia?
|
Amnesia
Sleep induction Loss of pain responses Skeletal muscle relaxation Loss of reflexes |
|
|
what are the 4 stages of anesthesia?
|
Stage I = Analgesia/amnesia
Stage II = Disinhibition/delerium Stage III = Surgical anesthesia (unconsciousness) Stage IV = Medullary depression |
|
|
For general anesthetics, does pain relief always occur at doses required for surgical anesthesia?
|
NO, sometimes need multiple drugs
|
|
|
what are 5 indications for using general anesthesia?
|
extreme anxiety or fear
mentally or physically disabled poor patient cooperation age traumatic procedures |
|
|
what are the two different types of general anesthetics?
|
Volatile/inhalation
Intravenous |
|
|
what are 5 volatile anesthetics?
|
Sevoflurane
Halothane Isoflurane Nitrous Oxide Ether volatile anesthetics SHINE |
|
|
what goal of anesthetics do volatile anesthetics not fulfill?
|
NONE, they do it all!
(amnesia, Loss of consciousness, loss of reflexes, sleep induction, skeletal muscle relaxation) |
|
|
Is the Therapeutic index of Volatile Anesthetics low or high?
what does this mean? |
LOW
they are dangerous if used incorrectly |
|
|
how do you counteract too high of levels of general anesthetic?
|
CAN"T
There aren't any pharmacological antagonists out there |
|
|
for volatile anesthetics, what is the relationship bw:
1. inspired anesthetic concentraion and rate of induction 2. ventilation rate and induction rate 3. blood flow to lungs and rate of onset |
1. direct
2. direct 3. INDIRECT (means that the amount of drug in the blood is more diluted since more blood is reaching lungs) |
|
|
What is the MAC analagous to for volatile anesthetics?
|
Ec 50
the concentration at which 50% of patients don't move when you hurt them |
|
|
What is relationship of Potency to MAC for volatile anesthetics?
|
MAC = 1/P
(bc the higher the potency of the drug, the less you need to have 50% of patients not move |
|
|
What is the Meyer Overton Rule for volatile anesthetics?
|
Potency is correlated with its solubility in oil (Oil/gas coefficient)
MAC = 1.3 / (oil/gas coefficient (delta)) Therefore, the higher the oil/gas coefficient (solubility in oil), the less it's going to take to get 50% of people to not move |
|
|
How is a high oil/gas coefficient related to induction time for volatile anesthetics?
what about for the MAC? |
high oil gas coefficient
causes longer induction time causes smaller MAC (so there is a tradeoff bw fast induction and high potency) |
|
|
What is the distribution of concentration of volatile anesthetics over time?
|
early = high brain
later = medium muscle latest = low fat |
|
|
are anesthetics that are relatively insoluble in the blood and brain eliminated faster or slower than those that are soluble?
|
Faster bc all they need to do is be filtered
|
|
|
Why is nitrous oxide good?
why is it bad? |
Good bc:
Fast acting, Great analgesic, safe, cheap, can be used with other stuff Bad bc: it can expand closed cavities (pneumothorax, closed cavities in lung (CF, Emphysema, Asthma) Diffusion hypoxia |
|
|
what are three negatives of ether?
|
1. spontaneously explosive
2. Respiratory irritant 3. high incidence of nausea and vomiting (during induction and wearing off) |
|
|
what are the negatives of halothane?
|
volatile, narrow margin of safety
LESS analgesia and muscle relaxation Hepatotoxic Decreased BP Increased sensitization of myocardium to catecholamines |
|
|
what is the most common General Anesthetic used today?
What are its two main disadvantages? |
Isofluorane
Volatile Decreases BP due to decreased resistance |
|
|
what are the 5 main side effects of inhalation/volatile general anesthetics?
|
Lower metabolic rate of brain
Increase in intracranial pressure Respiratory depression Cardiac depression Vasodilation 2 brain, 1 heart, 1 lung, 1 vasodilation |
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which Volatile GA produces the least cardiac depression?
which causes the most arrhythmias? |
Isofluorane (which is why it's the most used)
Halothane = arrhythmias |
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Which volatile GA produces the least increase in intracrainial pressure?
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Isofluorane!
Which is why it's the most used along with little cardiac depression |
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rank four volatile anesthetics in airway irritation from worst to best.
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Nitrous
Sevofluorane Halothane Isofluorane (best for airway, IC pressure, AND cardiac depression) |
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Which Volatile anesthetic can cause Fulminant hepatic necrosis?
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Halothane
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What condition can ALL volatile anesthetics cause?
how do you treat it? |
Malignant hyperthermia
Dantrolene, and restore electrolytes |
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what is odd about the name "IV anesthetics"?
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bc they are NOT true anesthetics!
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If "IV anesthetics" aren't true anesthetics, then what 2 categories do they fall under?
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sedative/hypnotics
amnestics |
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what are the 5 IV anesthetics?
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Barbiturates
Etomidate Propofol Ketamine Midazolam |
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What is midazolam used to treat?
What type of drug is midazolam? how is it different than the others in its class? |
for IV GA
benzodiazapene different bc it has way more good properties than the other benzos |
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what is a major disadvantage of IV GAs that is not usually encountered in volatile anesthetics?
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All are cleared by liver, not case for volatiles
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which IV GA does not have respiratory depression at clinical doses?
which doesn't have direct myocardial depression? |
Versed
Etomidate |
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What type of drug is Ketamine?
What does it work on? what type effect does it have? |
An IV General anesthetic
Blocks glutamate receptors Causes Dissociative anesthesia (no loss of consciousness, but you disassociate with your body) |
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what are the post op emergence phenomena of ketamine?
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disorietnation
sensory and perceptual illusions vivid dreams |
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what type of drug is etomidate?
what is good about etomidate? what is bad about it? |
a IV GA
minimal cardiac and respiratory toxicities high incidence of nausea and vomiting (Etomidate is an Emetic) |
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Which IV GA has antiemetic properties?
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Propofol
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what are the three benefits of Midazolam (Versed) when used as an IV GA?
what is the bad thing? |
Great anxiolytic
Amnestic NO respiratory depression Bad bc it's not analgesic |
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What is the only IV GA that has analgesic properties?
Which IV GA has the shortest half life? |
Ketamine
Propofol has shortest half life |
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how quickly do IV GAs wear off after first dose?
what about after repeated doses? WHy? |
Very fast (patients could wake up in surgery)
Can be very long acting due to being stored in muscle and fat |
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which adjuvant is used with IV GAs for:
1. anxiolytic and anterograde amnesia? 2. analgesia? |
1. Benzodiazepines
2. Opioids (Fentanyl, morphine) |
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what are the two safest parenteral anesthetics for pregnant women?
Are volatile GAs safe? What two drugs are associated with altered development in first (second) trimester? |
Propofol and Midazolam
(bc no PMs!) All are except Nitrous! Benzodiazepines and Barbiturates are Bad for BaBies! |
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what is the unitary hypothesis?
is it true? |
that all Volatile Anesthetics work the same way (bc U is by V in alphabet)
Probably not true |
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what is the most likely mechanism for most Anesthetics?
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modulating synaptic transmission at low levels
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what receptor can ALL General anesthetics act on?
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GABA
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For general anesthetics...
do Inhibitory targets change Ec50? what about excitatory targets? |
Inhibitory lowers Ec50
Excitatory doesn't change Ec50 |
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what is probably the safest/best IV GA drug?
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Propofol!
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