Notes in Year 2::MSN::Exam 5

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Published 09/27/2024 {{c1::Hyperalgesia}} is {{c2::in}}-creased sensitivity to painful stimulus
Published 09/27/2024 {{c1::Analgesia}} is {{c2::absence}} of sensitivity to painful stimulus
Published 09/27/2024 {{c1::Allodynia}} is pain produced by a {{c2::non-noxious}} stimulus
Published 09/27/2024 {{c1::Hypoesthesia}} is {{c2::de}}-creased sensation
Published 09/27/2024 {{c1::Parasthesia}} is {{c2::abnormal}} sensation, i.e. prickling
Published 09/27/2024 {{c1::Dysethesia}} is {{c2::impaired}}, disagreeable sensation
Published 09/27/2024 {{c1::Pain}} is the subjective awareness of tissue injury that begins with activation from {{c2::nociceptive}} stimuli
Published 09/27/2024 Pain pathway consists of {{c1::transduction}}, {{c2::transmission}}, {{c3::modulation}}, and {{c4::perception}}
Published 09/27/2024 {{c1::Nociception}} is the {{c2::unconscious}} detection of tissue injury and a function of first and second order neurons
Published 09/27/2024 {{c1::Aβ}} sensory neurons are {{c2::large::size}}, {{c3::myelinated::non-myelinated/myelinated}} fibers that transmit info about touch and pressure
Published 09/27/2024 {{c1::Aδ}} sensory neurons are {{c2::small::size}}, {{c3::myelinated::non-myelinated/myelinated}} fibers that carry info about touch and pressure
Published 09/27/2024 {{c1::C}} sensory neurons are {{c2::small}}, {{c3::non-myelinated::non-myelinated/myelinated}} fibers that carry info about touch and pressure
Published 09/27/2024 {{c1::Nociception}} is the unconscious detection of {{c2::tissue injury}} and a function of first and second order neurons
Published 09/27/2024 {{c1::Free nerve endings::pain receptor types}} are found in skin, muscle, joints, bone, and viscera
Published 09/27/2024 {{c1::Untreated}} pain sensitizes/activates normally {{c2::latent}} pain receptors, leading to {{c3::increased}} pain and inflammation
Published 09/27/2024 {{c1::Aδ}} pain fibers carry {{c2::fast}}, {{c3::sharp/prickly}} pain that is {{c4::well}} localized
Published 09/27/2024 {{c1::C}} pain fibers carry {{c2::slow}}, {{c3::dull/burning}} pain that is {{c4::poorly}} localized
Published 09/27/2024 {{c1::Aδ}} pain fibers are alternatively called type {{c2::III}} fibers
Published 09/27/2024 {{c1::C}} pain fibers are alternatively called type {{c2::IV}} fibers
Published 09/27/2024 {{c1::Afferent}} neurons in the dorsal horn receive nociceptive stimuli from {{c2::sensory nerve fibers}} that can be modulated via {{c3::inhibitory}}…
Published 09/27/2024 {{c1::Efferent}} neurons in the dorsal horn carry input from the {{c2::CNS}} that modulate nociceptive inputs
Published 09/27/2024 {{c1::Primary afferent}} neurons enter the spinal cord and can synapse on {{c2::second order}} neurons or {{c3::interneurons}}
Published 09/27/2024 Prolonged primary afferent neuron pain stimulus can result in {{c1::central sensitization}} in which pain transmission continues for minutes after the…
Published 09/27/2024 The {{c1::spinothalamic}} tract carries {{c2::pain}}, {{c3::temperature}}, and {{c4::pressure}}
Published 09/27/2024 The {{c1::spinoreticular}} tract is involved in {{c2::arousal}}
Published 09/27/2024 The {{c1::spinomesencephalic}} tract is involved in {{c2::affect}} and {{c3::emotions}} related to pain
Published 09/27/2024 The {{c1::spinohypothalamic}} tract is involved in {{c2::reflexes}} from pain
Published 09/27/2024 {{c1::Modulation}} phase of the pain pathway is where {{c2::processing}} of signals occurs
Published 09/27/2024 Pain {{c1::tolerance}} occurs in the {{c2::modulation}} phase of the pain pathway
Published 09/27/2024 {{c1::Calcitonin gene related peptide (CGRP)}} is a neuropeptide in the {{c2::ascending}} nociceptive pathway that is implicated in {{c3::migraines::p…
Published 09/27/2024 {{c1::Glutamate}}, {{c2::neurokinin-1}}, {{c3::substance P}}, and {{c4::CGRP}} are neuropeptides involved in {{c5::propagation}} of pain signals
Published 09/27/2024 {{c1::GABA}}, {{c2::opioids}}, {{c3::norepinephrine}}, and {{c4::serotonin}} are neuropeptides involved in {{c5::cessation}} of pain signals
Published 09/27/2024 {{c1::Peripheral sensitization}} occurs when nociceptors in the PNS become more sensitive to stimuli following an injury
Published 09/27/2024 Peripheral sensitization is occurs due to {{c1::inflammatory}} mediators and recruitment of {{c2::Aδ}} and {{c2::C}} fibers
Published 09/27/2024 {{c1::Central sensitization}} occurs when the CNS becomes hypersensitive to pain signal, resulting in {{c2::allo}}-dynia and {{c2::hyper}}-dynia
Published 09/27/2024 Central sensitization is due to {{c1::increased}} activity in the {{c2::dorsal horn}}
Published 09/27/2024 {{c1::Nociceptive-induced}} inflammation is due to overactivation of primary afferents that stimulate release of {{c2::substance P}}, {{c3::histamine}…
Published 09/27/2024 {{c1::Viscerosomatic}} reflex occurs when pain/dysfunction in an {{c2::organ}} causes pain in {{c2::somatic tissues}} due to shared neural pathways
Published 09/27/2024 Viscerosomatic Reflex Spinal Facilitation1. {{c1::Peripheral irritation}}2. {{c2::CNS sensitization}}3. {{c3::Neighboring neuron sensitization}}4. {{c…
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Published 09/27/2024 {{c1::Sensory-discriminative}} system in the pain matrix encodes the {{c2::location}} and {{c2::intensity}} of pain
Published 09/27/2024 {{c1::Affective-motivational}} system in the pain matrix encodes the {{c2::suffering}} associated with feelings of pain
Published 09/27/2024 {{c1::Cognitive-behavioral}} system in the pain matrix encodes the {{c2::conscious behavior}} towards a painful stimulus or ongoing painful experience
Published 09/27/2024 {{c1::Insular}} cortex is involved in {{c2::emotional}}, {{c3::cognitive}}, and {{c4::memory-related}} aspects of pain
Published 09/27/2024 {{c1::Posterior}} portion of the {{c2::insular}} cortex is involved in {{c3::sensory}} aspects of pain
Published 09/27/2024 {{c1::Hippocampus}} encodes {{c2::memory}} to painful stimuli
Published 09/27/2024 {{c1::Amygdala::brain structure}} is involved in {{c2::fear/anxiety}} related to pain and encodes emotional {{c3::salience}} to it
Published 09/27/2024 {{c1::Prefrontal}} cortex is involved in {{c2::cognitive}} aspects of pain, i.e. attention, interpretation, modulation, and coping strategies
Published 09/27/2024 The {{c1::prefrontal}} cortex and the {{c2::limbic}} system interact to modulate emotional response
Published 09/27/2024 {{c1::Anterior cingulate}} cortex is involved in the {{c2::unpleasantness}} and {{c3::anticipatory}} emotional aspects of pain
Published 09/27/2024 A lesion in the insular cortex results in {{c1::asymbolia}} in which a person can localize pain, but has no affective component
Published 09/27/2024 {{c1::Enkephalin}}, {{c2::endorphin}}, and {{c3::dynorphin}} are endogenous opioid peptides released in response to pain and stress
Published 09/27/2024 Endogenous opioid peptides are found in the {{c1::brain}}, {{c2::spinal cord}}, {{c3::adrenal medulla}}, and {{c4::gut neural plexuses}}
Published 09/27/2024 {{c1::Met-enkephalin}} and {{c1::Leu-enkephalin}} are endogenous opioids that differ only in the terminal amino acid
Published 09/27/2024 Which opioid receptor do endorphins have the strongest binding to?{{c1::μ (mu)}}
Published 09/27/2024 Which opioid receptor do enkephalins have the strongest binding to?{{c1::δ (delta)}}
Published 09/27/2024 Which opioid receptor do dynorphins have the strongest binding to?{{c1::κ (kappa)}}
Published 09/27/2024 {{c1::Mu}}-opioid receptors are involved in {{c2::respiratory}} inhibition, slowed {{c3::GI}} transit, and modulation of {{c4::hormone/NT}} release
Published 09/27/2024 {{c1::kappa}}-opioid receptors are involved in {{c2::psychotomimetic}} effects and slowed {{c3::GI}} transit
Published 09/27/2024 Opioids reduce nociception by {{c2::inhibiting}} {{c1::afferent}} stimulation to the brain and {{c2::modulating}} {{c1::efferent}} stimulation from th…
Published 09/27/2024 Interneurons place an inhibitory tone on {{c1::primary afferent}} or {{c1::secondary}} (glutaminergic) neurons to inhibit ascension of nociceptive sig…
Published 09/27/2024 Which G-protein are opioid receptors linked to?{{c1::Gi (inhibitory)}}
Published 09/27/2024 On {{c1::pre}}-synaptic neurons, opioid receptors {{c2::decrease}} {{c3::Ca2+}} influx to {{c2::decrease}} {{c4::neurotransmitter}} release
Published 09/27/2024 On {{c1::post}}-synaptic neurons, opioid receptors {{c2::increase}} {{c3::K+}} efflux to cause {{c4::hyperpolarization}} of the neuron
Published 09/27/2024 Opioids directly {{c2::inhibit}} {{c1::GABA}}-ergic interneurons, thereby releasing the inhibitory break on "pain-inhibitory" neurons
Published 09/27/2024 {{c1::Morphine}} is purified from opium and is the standard of comparison for analgesics
Published 09/27/2024 Opioid-mediate respiratory depression is {{c1::dose}}-dependent and may initially present as {{c3::in}}-creased {{c2::PaCO2}}
Published 09/27/2024 Opioid-induced {{c1::hyperalgesia}} can occur with chronic use
Published 09/27/2024 {{c1::Truncal rigidity}} is a side effect of opioid use that is apparent with large, rapid IV doses of highly {{c2::lipid}}-soluble opioids, i.e. {{c3…
Published 09/27/2024 Administration of a {{c1::partial}} mu-opioid agonist with a {{c1::full}} mu-opioid agonist can precipitate {{c2::withdrawal}} symptoms
Published 09/27/2024 {{c1::Loperamide}} and {{c2::Diphenoxylate}} are mu-opioid {{c3::agonists}} that act as anti-{{c4::diarrheals}}
Published 09/27/2024 Opioids {{c1::decrease}} uterine tone and may cause {{c2::prolonged}} labor
Published 09/27/2024 {{c1::Naloxone}} is a mu-opioid {{c2::antagonist}} that exerts effects within {{c3::1-3}} minutes
Published 09/27/2024 {{c1::Naltrexone}} is a mu-opioid {{c2::antagonist}} that blocks virtually all effects of {{c3::heroin}} if administered every few days
Published 09/27/2024 Strong mu-opioid agonists include {{c1::Meperidine}}, {{c2::Methadone}}, {{c3::Morphine}}, {{c4::Hydropmorphone}}, and {{c5::Oxymorphone}}
Published 09/27/2024 Pentazocine is a mu {{c1::partial agonist}} and kappa {{c1::agonist}}
Published 09/27/2024 Nalbuphine is a mu {{c1::antagonist}} and kappa {{c1::full agonist}}
Published 09/27/2024 Buprenorphine is a mu {{c1::partial agonist}} and kappa {{c1::antagonist}}
Published 09/27/2024 Butorphanol is a mu {{c1::partial agonist}} and kappa {{c1::full agonist}}
Published 09/27/2024 Butorphanol is administered {{c1::parenterally}} and has a duration of {{c2::3-4}} hours
Published 09/27/2024 Buprenorophine is administered {{c1::parenterally}} or {{c1::sublingually}}, has a duration of {{c2::>8}} hours, and a half-life of {{c3::20-70}} h…
Published 09/27/2024 Nalbuphine is administered {{c1::parenterally}} and has a duration of {{c2::4-8}} hours
Published 09/27/2024 {{c1::kappa}}-opioid receptor agonists have {{c2::less}} potential for abuse
Published 09/27/2024 Naloxone has {{c1::poor}} oral absorption and a duration of {{c2::1-2}} hours
Published 09/27/2024 Naltrexone has {{c1::good}} oral absorption and a duration of {{c2::~48}} hours
Published 09/27/2024 Nalmefene is a mu {{c1::antagonist}} that is administered via IV and has a half-life of {{c1::8-10}} hours
Published 09/27/2024 Aliimopan and Methylnaltrexone are mu {{c1::antagonists}} that have poor {{c2::CNS}} penetration, thereby reversing {{c3::constipation}} without preci…
Published 09/27/2024 Opioids are distributed first in highly {{c1::perfused}} tissues and over time, reservoirs may develop in {{c2::muscle}} and {{c2::fat}}
Published 09/27/2024 Metabolism of opioids occurs via {{c1::glucoronidation}}, {{c2::N-methylation}}, {{c3::CYP3A4}}, and {{c4::CYP2D6}}
Published 09/27/2024 CYP{{c1::2D6}} metabolizes {{c2::codeine}} into {{c3::morphine}}
Published 09/27/2024 CYP{{c1::3A4}} oxidizes {{c2::phenylpiperidines}} in the {{c3::liver}} and {{c3::gut}}
Published 09/27/2024 {{c1::Nociceptive}} and {{c1::inflammatory}} pain represents a(n) {{c2::intact}} nervous system
Published 09/27/2024 {{c1::Neuropathic}} pain represents a(n) {{c2::damaged}} nervous system
Published 09/27/2024 {{c1::Acute}} pain serves a(n) {{c2::adaptive}} function whereas {{c1::chronic}} pain does not
Published 09/27/2024 Features of dysfunctional pain include1. {{c1::alterations in neurotransmission}}2. {{c2::decreased inhibition}}3. {{c3::structural reorganization}}4.…
Published 09/27/2024 {{c1::Glial}} cells are activated by {{c2::substance P}} to secrete {{c3::cytokines}}, {{c4::nitrous oxide}}, and {{c5::prostaglandins}}
Published 09/27/2024 {{c1::Primary}} hyperalgesia occurs at the site of {{c2::injury}}
Published 09/27/2024 {{c1::Secondary}} hyperalgesia occurs at the tissue surrounding the {{c2::injury}}
Published 09/27/2024 {{c1::Peripheral}} sensitization can become {{c1::central}} sensitization if left untreated, resulting in pain levels that don't correlate to the init…
Published 09/27/2024 {{c1::Peripheral}} sensitization is {{c2::heat}}-sensitive whereas {{c1::central}} sensitization is not
Published 09/27/2024 {{c1::Central}} sensitization responds well to {{c2::anti-epileptic}} and {{c2::anti-depressant}} drug classes
Published 09/27/2024 {{c1::Peripheral}} sensitization responds well to {{c2::NSAID}} drug class
Published 09/27/2024 Which drug class targets the brain, peripheral sensitization, and central sensitization? {{c1::TCAs}}
Published 09/27/2024 Drugs that target {{c2::peripheral}} sensitization block {{c1::Na+}} channels
Published 09/27/2024 Drugs that target {{c2::central}} sensitization block {{c1::Ca2+}} channels and {{c1::NMDA}} receptors
Published 09/27/2024 Can't-miss-diagnoses for pain include {{c1::cancer}}, {{c2::infection}}, {{c3::fracture}}, and {{c4::ongoing tissue damage (nerve compression)}}
Published 09/27/2024 Complex Regional Pain Syndrome presents with {{c1::neuropathic pain}}, {{c2::autonomic features}}, {{c3::trophic changes to skin/hair/nails}}, and {{c…
Published 09/27/2024 {{c1::Primary}} headaches are due to intrinsic dysfunction of the nervous system
Published 09/27/2024 {{c1::Secondary}} headaches are signs of underlying medical conditions or injuries
Published 09/27/2024 {{c1::Trigeminal autonomic cephalgia}} has features of {{c2::unilateral}} headache and prominent cranial {{c3::parasympathetic}} autonomic features
Published 09/27/2024 {{c1::Cluster}} headaches are an example of {{c2::trigeminal autonomic cephalgia}}
Published 09/27/2024 {{c1::Status migrainosus}} is a debilitating migraine lasting {{c2::> 72}} hours
Published 09/27/2024 {{c1::Chronic}} migraines are intermittent attacks typically occuring {{c2::15+}} days per month
Published 09/27/2024 Migraine {{c1::without::with/without}} aura is common and characterized by throbbing, periodic attacks that last {{c2::4-72}} hours
Published 09/27/2024 Migraine {{c1::with::with/without}} aura is classic and is characterized by a warning sign that precedes the migraine
Published 09/27/2024 Typical aura include {{c1::flashes of light}}, {{c2::zigzag lines}}, {{c3::scintillating scotoma}}, and {{c4::unilateral numbness}}
Published 09/27/2024 Migraine auras are thought to be caused by {{c1::hyperexcitability}} of neurons
Published 09/27/2024 Migraine {{c1::with::with/without}} aura carries an increased risk of {{c2::stroke}}
Published 09/27/2024 Pathophysiology of {{c1::tension}} headaches is thought to be {{c2::activation}} of {{c3::pericranial myofascial}} nociceptors
Published 09/27/2024 Preventive pharmacology for tension headaches includes {{c1::TCA}}, {{c2::beta blockers}}, and {{c3::anti-convulsants}}
Published 09/27/2024 Trigeminal autonomic cephalgias are characterized by pain and autonomic features in the distribution of CN {{c1::V1 (ophthalmic)}} 
Published 09/27/2024 {{c1::Cluster}} headaches are often associated with history of {{c2::smoking}} and {{c2::alcohol}} use
Published 09/27/2024 Preventive pharmacology for cluster headaches includes {{c1::Ca2+ channel blockers}}, {{c2::anticonvulsants}}, {{c3::lithium carbonate}}, {{c4::TCA}},…
Published 09/27/2024 Red flag signs/sxs for headaches can be remembered by the mnemonic SNOOPS: {{c1::systemic symptoms}}, {{c2::secondary risk factors}}N: {{c3::neurologi…
Published 09/27/2024 Can't-miss-diagnoses for headaches include {{c1::meningitis}}, {{c2::intracranial hemorrhage}}, {{c3::brain tumor}}, {{c4::giant cell (tempo…
Published 09/27/2024 {{c1::Medication overuse}} headaches are persistent, recurring headaches due to regular use of {{c2::analgesics}}, {{c3::ergotamines}}, and/or {{c4::t…
Published 09/27/2024 Treatment for medication-overuse headaches includes {{c1::discontinuation}} of all analgesics for {{c2::10-12}} weeks after washout period (2 weeks)
Published 09/27/2024 Differential diagnoses for abrupt, sudden onset thunderclap headache include {{c1::subarachnoid hemorrhage}} and {{c2::intracerebral hemorrhage}}
Published 09/27/2024 Workup for thunderclap headache includes {{c1::noncontrast head CT}} and {{c2::lumbar puncture}} if former is negative
Published 09/27/2024 Subarachnoid hemorrhages are caused by rupture of {{c1::intracranial aneurysm}} in 80% of cases and occur during {{c2::non-strenuous}} activity in ~50…
Published 09/27/2024 Brain tumors in the {{c1::posterior}} fossa are {{c2::faster}} growing and {{c2::more}} likely to produce headaches
Published 09/27/2024 First line treatment for trigeminal neuralgia is {{c1::Carbemazepine}}, {{c2::Gabapentin}}, {{c3::Lamotrigine}}, or {{c4::Baclofen}}
Published 09/27/2024 The {{c1::trigeminovascular}} system relays nociceptive signals to produce the perception of {{c2::migraine}} pain
Published 09/27/2024 CN {{c1::V}} releases {{c2::calcitonin gene-related peptide (CGRP)}} on a vascular bed, causing vaso-{{c3::dilation}} and resultant smooth muscle {{c4…
Published 09/27/2024 {{c1::Cortical spreading depression}} starts with {{c2::hypoxia}} in the {{c3::posterior}} portion of the head that spreads forward, activates CN {{c4…
Published 09/27/2024 {{c1::Alcohol}}, {{c2::aspirin}}, and {{c3::phenytoin}} follow {{c4::0}}-order kinetics
Published 09/27/2024 Alcohol has a molecular structure similar to {{c1::water}} allowing it to distribute to all aqeuous spaces
Published 09/27/2024 {{c1::90}}% of alcohol is oxidized by the {{c2::liver}} and {{c1::10}}% is excreted via the {{c2::lungs}} and {{c2::urine}}
Published 09/27/2024 In {{c1::first}}-order kinetics, {{c3::metabolism}} of a drug {{c2::increases}} with {{c3::concentration}}
Published 09/27/2024 In {{c1::zero}}-order kinetics, a {{c2::constant}} amount of drug is metabolized per unit time
Published 09/27/2024 {{c1::Ethanol}} is converted to {{c2::acetaldehyde}} via {{c3::alcohol dehydrogenase}}, using {{c4::NAD+}} as a cofactor
Published 09/27/2024 {{c1::Acetaldehyde}} is converted to {{c2::acetate}} via {{c3::aldehyde dehydrogenase}}, using {{c4::NAD+}} as a cofactor
Published 09/27/2024 {{c1::Disulfiram}} is a drug that inhibits {{c2::aldehyde dehydrogenase}}, resulting in accumulation of {{c3::acetaldehyde}} and shitty hangover sympt…
Published 09/27/2024 Excess {{c1::NADH}} in the liver results in {{c3::increased}} {{c2::de novo lipogenesis}} and {{c3::decreased}} {{c2::gluconeogenesis}}
Published 09/27/2024 {{c1::Fomepizole}} is a drug that inhibits {{c2::alcohol dehydrogenase::enzyme}} to prevent conversion of {{c3::methanol}} to {{c3::formaldehyde}}
Published 09/27/2024 Drugs that cause Disulfiram-like reactions1. {{c1::Sulfonylureas}}2. {{c2::Procarbazine}}3. {{c3::Cephalosporin}}4. {{c4::Griseofulvin}}5. {{c5::Metro…
Published 09/27/2024 Acetaminophen at less than {{c2::4}}g/day is primarily metabolized via {{c1::conjugation}} or {{c1::glucoronidation}} 
Published 09/27/2024 Acetominophen beyond {{c1::4}} g/day is metabolized by {{c2::cytochrome P450 2E1}} into a toxic metabolite
Published 09/27/2024 Ethanol is an {{c1::inducer}} of CYP450 2E1 and will {{c1::induce}} metabolism of acetominophen into the {{c2::toxic metabolite}}
Published 09/27/2024 {{c1::Acetylcysteine}} restores {{c2::glutathione}} in order to continue reducing ROS
Published 09/27/2024 Alcohol {{c1::increases}} {{c2::inhibitory}} pathways and {{c1::decreases}} {{c2::excitatory}} pathways
Published 09/27/2024 Alcohol allosterically {{c1::potentiates}} the function of {{c2::GABA (inhibitory)}} pathways and has additive effects with {{c3::benzodiazepines}} an…
Published 09/27/2024 Alcohol {{c1::inhibits}} {{c2::NMDA (excitatory)}} pathways, which are {{c3::highly}} sensitive to its effects
Published 09/27/2024 Alcohol causes {{c1::depression}} of myocardial contractility and {{c2::remodeling}} of cardiomyocytes
Published 09/27/2024 Alcohol causes {{c1::vasodilation}} of smooth muscle and {{c2::depression}} of the {{c3::vasomotor}} center
Published 09/27/2024 Alcohol-induced {{c1::vasodilation}} results in {{c2::hypo}}-thermia in cold environments
Published 09/27/2024 Treatment of acute alcohol intoxication includes {{c1::dextrose}}, {{c2::electrolyte solutions}}, {{c3::magnesium}}, and vitamins {{c4::B1 and B9}}
Published 09/27/2024 Possible mechanisms of EtOH-induced hepatotoxicity include production of {{c1::acetaldehyde}}-protein adducts that induce {{c2::collagen}} production …
Published 09/27/2024 Possible mechanisms of EtOH-induced hepatotoxicity includes {{c1::increased}} ratio of {{c2::NADH to NAD+}}, resulting in {{c3::TG synthesis}}, {{c4::…
Published 09/27/2024 Chronic alcohol use results in {{c1::neuro}}-toxicity via {{c2::atrophy}}, {{c3::demyelination}}, and {{c4::nutritional deficiency}}
Published 09/27/2024 {{c1::Fetal alcohol}} syndrome is the leading cause of {{c2::intellectual disability}} in Western societies
Published 09/27/2024 Permanent effects of Fetal Alcohol Syndrome include underdevelopment of {{c1::midfacial}} region, {{c3::microcephaly}}, {{c2::intellectual disability}…
Published 09/27/2024 {{c1::Physical dependence}} is the need for continued drug exposure to avoid {{c2::withdrawal}} symptoms
Published 09/27/2024 {{c1::Tolerance}} is a {{c2::reduced}} effect upon repeated exposure to a constant drug effect, or the need for an {{c2::increased}} dose to maintain …
Published 09/27/2024 {{c1::Psychological}} dependence is the compulsive desire to use a drug despite adverse consequences
Published 09/27/2024 Can psychological dependence on a drug exist without physical dependence and tolerance?{{c1::YES}}
Published 09/27/2024 Long-term ethanol exposure results in increases in {{c1::number}} and {{c1::activity}} of enzymes that metabolize it
Published 09/27/2024 {{c1::Opposing neuroadaptation}} is the concept that wherever alcohol causes {{c2::acute}} changes, there are {{c2::chronic}} neurological adaptations…
Published 09/27/2024 EtOH acutely {{c1::increases}} GABA-mediated Cl- influx and chronically {{c2::decreases}} GABA binding/affinity
Published 09/27/2024 EtOH acutely {{c1::increases}} {{c2::intra}}-cellular Ca2+ concentration and {{c1::decreases}} Ca2+ influx
Published 09/27/2024 EtOH chronically {{c1::decreases}} Ca2+ uptake and {{c2::increases}} dihydropyridine binding
Published 09/27/2024 EtOH acutely {{c1::decreases}} NMDA channel activity and chronically {{c1::increases}} number of the NMDA receptors
Published 09/27/2024 EtOH acutely {{c1::increases}} and chronically {{c1::decreases}} concentration of cAMP
Published 09/27/2024 EtOH acutely {{c1::decreases}} concentration of IP3 and DAG
Published 09/27/2024 {{c1::Acamprosate::drug}} is an NMDA {{c2::antagonist (or modulator)}} used to reduce alcohol cravings
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