Exam 6 - Autocoids and Antiemetics
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| T/F: Autocoids are not biologically active. | False-consist of an array of biologically active substances
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| Where are autocoids synthesized? | At the site of action whose specialized function is to initiate the response to tissue injury
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| What are the 4 key autocoids as r/t to drug therapy? | Histamine, bradykinin, serotonin, prostaglandins
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| What is histamine? | Naturally occurring low molecular weight vasoactive amine autocoid
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| Where and how is histamine synthesized? | Synthesized in tissues by decarboxylation of histidine
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| What is histamine released in response to? | Stimulation by mast cells, basophils, and neurons
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| What mediates the initial response to tissue injury? | histamine
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| What are the origins of the word "autocoid"? | "autos"=self, "akos"=remedy
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| Histamine is stored in an intricate composite with ____________. | Heparin
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| Who rec'd the Nobel Prize in Physiology and Medicine for their work on histamine and curare? | Bouvet (1957)
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| What catalyzes the metabolization of histamine and how is histamine metabolized? | Catalyzed by histamine-N-methyl transferase; methylation
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| After methylation, histamine is further degraded by what enzyme? | monoamine oxidase (MAO)
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| What are the 5 receptor subtypes for histamine? | H1, H2, H3, H4, Hic
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| Histamine induced excitation is mediated by _____ receptors and _______. | H1; primary sensory neurons
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| In what body tissues can H1 receptors be found? | Most body tissues, including cardiac smooth muscle, histaminergic nerves of the brain, enterochromaffin-like cells of the antrum
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| Which histamine receptor plays a central role in hypersensitivity allergic responses? | H1
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| What changes occur with H1 cardiac receptor agonism? | Decrease AV nodal conduction, mediate vasoconstriction in coronary vessels, reduced atrial natriuretic peptide
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| What is the function of atrial natriuretic peptide? | Vasodilation
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| How does H1 agonism affect the airway? | Induces bronchospasm
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| H2 agonism (constricts/dilates) the airway. | dilates
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| How does H2 agonism affect the stomach? What conditions can H2 agonism increase instances of? | Stimulates gastric acid secretion; GERD and peptic ulcer disease
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| (H1/H2) stimulation results in sustained generalized vasodilation of slower onset. | H2
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| What are the cardiac effects of H2 agonism? | Positive chronotropic effects, dysrhythmias
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| Why does H2 agonism in cardiac tissue lead to dysrhythmias? | D/t histamine-induced catecholamine release
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| 1st gen H1 antagonists (are/are not) H1 specific. | are not
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| 1st gen H1 antagonists elicit what 3 types of responses? | Dopaminergic, serotonergic, cholinergic
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| H1 receptor antagonists (do/do not) cross the BBB. | do
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| What neuro symptoms can H1 antagonists elicit? | Somnolence, cognitive dysfx
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| An overdose of H1 antagonists can lead to what effects? | Toxic psychoses w/hallucinations resembling schizophrenic breaks
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| Name three H1 receptor blockers. - Generic (Trade) - | Promethazine (Phenergan), hydroxyzine (Vistaril), demenhydronate (Dramamine), diphenhydramine (Benadryl)
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| What are H1 receptor blockers effective at treating? | PONV (effective antiemetic), motion sickness, pruritis
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| H2 blockers (do/do not) exhibit antiemetic effect. | do not -- used in allergic rhinitis
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| Which H1 antagonist can be used to treat drug-induced extrpyramidal rxn and Parkinson-like symptoms? | Diphenhydramine
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| (H1/H2) antagonists can be used as an adjunct in anesthesia d/t the production of sedative effects of long duration. | H1
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| What types of drugs are cyclizine and meclizine and what do they treat? | 1st gen antihistamines used to treat vomiting associated w/motion sickness and vertigo
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| Which antihistamine is used to potentiate narcotics? | Hydroxyzine (Vistaril) - don't give IV
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| Which antihistamine is associated with T-wave abnormalities? | Hydroxyzine (Vistaril)
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| 2nd gen antihistamines (do/do not) cross the BBB. | Do not
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| Which generation antihistamine has a greater specificity at the H1 receptor: First or second? | 2nd gen
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| True/False: Cardiotoxicity of newer 2nd gen antihistamines does not occur. | False--remains if metabolism is inhibited
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| What are two examples of 2nd gen H1 receptor antagonists? | Loratidine (Claritin), cetirizine (Zyrtec)
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| Identify 3 second gen H2 antagonists. | Cimetidine, ranitidine, famotidine
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| What are second gen H2 antagonists used for and how do they achieve this effect? | Tx PUD and GERD by blocking histamine effect on parietal cells (secrete HCl) of the stomach
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| _________ is a potent inflammatory mediator and vasoactive peptide. | Bradykinin
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| What is the most potent endogenous vasodilator released after allergic reactions and tissue damage? | Bradykinin
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| Bradykinin is a product of what biochemical cascade? | Kallikrein-kinin system
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| (Histamine/Bradykinin) modulates the series of events that accompany inflammation (vasodilatation, increased cell permeability, hyperalgesia, pain). | Bradykinin
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| Where is bradykinin stored? | CNS
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| What are circulating kallikreins activated by? | plasma proteases
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| How are pH and temperature involved with bradykinins? | Changes in pH and temperature can activate prekallikrein and lead to the conversion of prekallikrein to bradykinin after tissue damage
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| What does bradykinin stimulate? | Release of neuropeptides: substance P and neurokinin
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| Bradykinin is a potent (algesic/analgesic). | algesic
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| What incites the mediators of the pain cascade and the pain "wind up"? | Bradykinin
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| Bradykinin is (more/less) potent than histamine as a vasodilator. | more (10x more)
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| What substance is thought to play a role in hereditary angioedema, carcinoid syndrome, and septic shock? | Bradykinin
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| What are the two receptors for bradykinin? What type of receptors are they? | B1, B2; G-protein coupled receptors
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| (B1/B2) is the more active bradykinin receptor body, causing ________ and _________. | B2; inflammation, bronchoconstriction
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| Where are serotonin receptors primarily found? Where else are they located? | Primarily cerebral and CNS; also GI tract, platelets
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| What receptor body families do 5-HT receptors belong to? | G-protein coupled
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| What roles are 5-HT receptors integral in? | Pain signaling and inflammation
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| Dopamine, norepi, and serotonin are responsible for what neurologic states? | Mood, feelings, motivation
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| How many different 5-HT subtypes are there? | 14
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| What is the 5-HT(1a) subtype implicated in? | Psychiatric d/o, immunomodulation, cerebral ischemia
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| What is serotonin generated from? | Tryptophan
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| How is serotonin metabolized to its inactive form? | Oxidative deamination by MAO
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| Where is the action of 5-HT terminated? | At the synaptic junction and in the outer membrane of platelets
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| Which 5-HT receptor agonists are effective as migraine therapeutics? Who are they contraindicated in? | 5-HT 1b/1d; contraindicated in patients w/CAD
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| What does the 5-HT2 receptor subtype have a high attraction to? | Choroid plexus (site of CSF production)
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| Identify a 5-HT4 agonist? What have they been used to treat? Why were these removed? | Cispride; GERD, IBS, constipation; cardiac problems
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| Ongoing neuropsychiatric research is ongoing with agonists of which 5-HT subtype? | 5-HT4
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| 5-HT3 has a strong relation with the (nicotinic/muscarinic) ACh receptor. | nicotinic
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| Where are 5-HT3 receptors found? Where are the highest levels located? | CNS; highest levels in the dorsal vagal complex of the brainstem and parasympathetic terminals of the GIT
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| What region of the brain is responsible for the vomiting reflex, and what 5-HT receptor subtype is found in this region? | Dorsal vagal complex; 5-HT3
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| What does the dorsal vagal complex (vomiting reflex) consist of? | Nucleus tractis solitarius, area postrema, dorsal motor nucleus of the vagus
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| What does antagonism of 5-HT3 contribute to? | Anti-emetic action
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| What does polymorphism of the 5-HT3 gene play a role in? | Psychiatric disorders
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| Prostaglandins are metabolites of _______> | arachidonic acid
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| What do the metabolites of arachidonic acid play a role in? | Inflammation
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| Arachidonic acid is broken down through which pathway? | Cyclooxygenase
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| Prostaglandins are members of what family of receptors? | G-protein coupled
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| Prostaglandins play a role in what other parts of the body? | Systemic vascular resistance, airway resistance, platelet aggregation, increased uterine tone
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| Which COX isoform exhibits cytoprotective activity? | COX1
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| Which COX isoform is induced at the site of inflammation with rapid increases in its amount during inflammation? | COX2
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| Which COX isoform is constitutive (always occurring), and which is inducible (only with pain)? | COX1=constitutive; COX2=inducible
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| Inhibition of (COX1/COX2) predisposes to CV insult (e.g. MI, stroke, heart failure). | COX2
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| What is the primary site for prostaglandin synthesis? | Lungs
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| The suppression of what COX1 product triggers cardioprotection? Which medication achieves this effect? | Thromboxane-A2 (TXA2); ASA
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| Name two COX2 inhibitors associated with MI and sroke. | Vioxx, Celebrex
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| What condition does thromboxane exacerbate? | Bronchoconstrictive dz (asthma)
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| Pulmonary vasoconstriction may occur as a result of circulating levels of what two products? | Prostaglandin, thromboxane
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| Protamine (stimulates/depresses) TXA production. What effect does this have? | stimulates; pulmonary HTN and bronchospasm
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| What percentage of surgical patients may experience PONV? | 30-70%
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| Identify states of health/dz that predispose a patient to N/V. | Infx, pregnancy, vestibular dysfx, CNS issues, peritonitis, hepatobiliary d/o, post-radiation, GI d/o, SE from meds
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| There is a (strong/weak) memory association with vomiting. | strong
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| Where does the vomiting stimulus originate in the GIT? What provides the strongest stimulus in the gut? | Anywhere in the GIT; Distention or stimulation of the duodenum
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| The vomiting reflex is controlled in what area of the brain ("emetic center")? | Reticular formation of the medulla oblongata
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| What is the strongest stimulator for emesis? | Duodenal distention
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| Identify the antagonist associated with each of the following emetic agonists: 1)Serotonin 2)Histamine 3)ACh 4)DA 5)Neurokinin (Substance P) 6)Endorphins (opioids) | 1)Zofran 2)Promethazine 3)Scopolamine 4)Droperidol 5)Aprepitant 6)Narcan
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| In what two pathways does N2O stimulate the emetic center? | Vestibular portion of the 8th nerve and vagus nerve
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| Sensory input arises from afferent impulses originating from what 5 areas of the body? | 1)pharynx 2)GIT 3)mediastinum 4)cerebral cortex 5)sensory organ
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| The CTZ (is/is not) protected by the BBB. | is not
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| Which area can specifically be targeted by anesthesia providers in the treatment or prevention of PONV? | Chemoreceptor trigger zone (CTZ)
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| What are the different hormones that stimulate the CTZ, leading to pro-emetic scenarios? | Serotonin, histamine, ACh, dopamine, substance P (neurokinin)
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| Serotonin is a widely distributed hormone that evokes complex changes on what body system? | Cardiovascular system--vascular beds (serotonin is an endogenous vasoactive autocoid)
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| Where is serotonin released from? | Enterochromaffin cells of the small intestine
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| How does serotonin initiate the vomiting reflex? | Stimulates vagal afferent pathways through 5-HT3 receptor stimulation, which initiates the vomiting reflex in the medulla
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| Through what pathways does serotonin initiate the vomiting reflex? | Vagal afferent
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| Serotonin is a key neurotransmitter in the transmission of _______ and _______ | Emesis, pain
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| Identify the 4 serotonin antagonists. | Ondansetron, dolasetron, granisetron, palonosteron
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| What are the most common SE of serotonin antagonists? | HA, dizziness, constipation or diarrhea
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| What are the indications for the use of serotonin antagonists in treating nausea? | 1) chemo induced 2)post-radiation 3)PONV 4)vomiting w/pregnancy
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| Which medication is the standard/prototypical selective serotonin receptor antagonist? | Ondansetron
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| What is the onset and T1/2 of Zofran? | 15min onset; T1/2 4h
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| What is the trade name for dolasetron? | Anzemet
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| Which SSRA is a prodrug? | Anzemet
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| What is the product of metabolism of dolasetron and how much more potent is it than the parent drug? What is the T1/2 of dolasetron? | Rapidly metabolized to hydro-dolasetron; 100x more potent than dolasetron; T1/2 8h
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| What are the IV and PO doses of dolasetron (Anzemet) and when are they given? | 12.5mg IV prior to end of surgery; 50-100mg PO 2hr pre-op (as effective as Zofran for ppx).
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| What are the SE of dolasetron (Anzemet)? | HA, dizziness, increased appetite
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| What is the trade name for granisetron? | Kytril
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| Which has more receptor specificity: granisetron (Kytril) or ondansetron (Zofran)? | Granisetron (Kytril)
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| What is Kytril commonly used in? | Anti-emetic in chemotherapy
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| What is the IV dose of granisetron (Kytril) and when is it given? What is the T1/2? | 1mg or 20-40mcg/kg IV immediately prior to induction; T1/2 9h but coverage for up to 24h
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| What are the SE of granisetron (Kytril). What limits its usage? | HA, diarrhea, sedation; cost
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| What is the newest SSRA? | Polonasetron (Aloxi)
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| Polonasetron (Aloxi) is used as a (prophylactic/rescue) antiemetic. | Prophylactic
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| What is the IV dose of polonasetron (Aloxi) and when is it used? | 0.25mg IV, given prior to chemotherapy
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| What are common SE w/polonasetrong? | HA, constipation, diarrhea, dizziness, less common: bradycardia, hypotension, tachycardia
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| Which SSRA is not recommended for PONV? | Polonasetron (Aloxi)
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| What has been determined among all SSRAs in regards to safety/efficacy? | No difference exists among the SSRAs
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| Corticosteroids are used to enhance the efficacy of what other class of antiemetics? | SSRAs
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| True/False: The mechanism of action of corticosteroids in treating PONV is well defined. | False
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| What is the IV dose of decadron (corticosteroid) given for nausea and when is it given? | 4-10mg IV around induction
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| Identify two phenothiazines. In what other application are phenothiazines used, other than as anti-emetics? | Compazine, phenergan; used as antipsychotics
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| In what scenarios are phenothiazines used as antiemetics? | Chemo- + radiation therapy; PONV; Tx of allergic blood transfusion reactions
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| What is the mechanism of phenothiazines? | Inhibition of central DA, muscarinic, and H1 histamine receptors
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| What are the SE to phenothiazines? | CNS depression, somnolence, hypotension, possible EPS -- *think compazine*
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| What mechanism allows phenothiazines to treat anaphylaxis? | Blocking of H1 histamine receptors
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| Compazine and/or phenergan should not be given (IM/PO/IV/SQ). | SQ
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| True/False: Compazine/Phenergan is non-caustic and can be delivered IV without complications. | False=Compazine/Phenergan are venous irritants and should be liberally diluted
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| Butyrophenones are classified as _________. | antipsychotics
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| Which receptors do butyrophenones inhibit to combat N/V? | Inhibit central DA receptors
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| Identify a butyrophenone used in the treatment of N/V. What is its dose and when is it given? | Droperidol; 0.625-1.25mg x1 prior to induction
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| In what scenarios is droperidol used? | Chemo/Radiation therapy, PONV
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| What are the SE to droperidol? | Prolonged QT interval
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| Which antiemetic has a Black Box warning? | Droperidol
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| Patients receiving droperidol at doses of greater than ______mg over ______h have died. | 50; 24
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| What should be done prior to giving droperidol? | 12-lead ekg
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| What two ekg changes have been reported with droperidol? | QT prolongation and torsades
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| What are the QT measurements for men and women that would serve as a contraindication for droperidol? | 440ms=men, 450ms=women
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| When should an ekg be done with administration of droperidol? | Prior to administration and 3h post
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| What is the usual dose of droperidol and when is it given? | 0.625mg preop
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| Besides droperidol, what other butyrophenone is used as an antiemetic? What receptors does it block? | Haldol; blocks D1 and D2 receptors
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| True/False: The doses for haldol as an antipsychotics are the same as those when used to treat N/V. | False=Antiemetic doses are much lower
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| The mechanism of action of cannibinoids (is/is not) fully known. | is not
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| Describe the pharmacokinetics of cannabinoids. | 1)Readily absorbed orally 2)Extensive 1st pass metabolism 3)Limited systemic BA d/t excretion of metabolites
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| Through what routes are the metabolites of cannabinoids excreted? | Biliary
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| Identify a cannabinoid used in the treatment of N/V. | Dronabinol
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| What are the SE of dronabinol? | Euphora or dysphoria, sedation, hallucinations
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| What can abrupt withdrawal of cannabinoids lead to? | Withdrawal syndrome (restless, insomnia, irritability)
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| What are the autonomic (sympathetic) effects of cannabinoids? | Tachycardia, palpiations, conjunctival injection, orthostatic hypotension
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| What is the indication for cannabinoids (dronabinol)? | Chemo-induced N/V
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| What are two types of agents that increase GI motility? | Cholinergic agents and prokinetic agents
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| True/False: Cholinergic agents are useful in the treatment of motility disorders. | False
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| True/False: Prokinetic agents are useful in the treatment of motility disorders. | True
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| What is the method of action of cholinergic agents? | Stimulate cholinergic receptors which enhance contractions in an uncoordinated manner, producing limited propulsive activity
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| What is the method of action of prokinetic agents? | Enhances coordinated GIT propulsive motility by acting at receptor sites on motor neurons and increasing the release of ACh.
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| Which agent is more effective at producing coordinated propulsive GIT motility: cholinergics or prokinetics? | Prokinetics
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| Identify a prokinetic GIT motility agent. | Reglan
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| Identify a cholinergic GIT motlity agent. | Bethanechol
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| Which receptors does bethanechol work as an agonist on? | Muscarinic
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| What does bethanechol resist? | Enzymatic hydrolysis
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| Bethanechol is a/an (direct/indirect) cholinergic agent. | direct
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| Identify an indirect cholinergic agent and what is its classification? | Neostigmine; anticholinesterase inhibitor
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| What has neostigmine been used to treat? | Paralytic ileus
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| What is the pathology behind decreased motility of the GIT? | Results from suppression of ACh release from myenteric motor neurons mediated by stimulation of D2 DA receptors.
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| What are the two ways that prokinetic agents enhance GIT and treat N/V? | 1)Antagonize inhibitory effects of DA on myenteric motor neurons 2)Relieve N/V by antagonism of DA receptors in CTZ
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| Identify two prokinetic agents. | Metoclopramide, domperidone
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| Identify two benzamides used in the treatment of N/V. | Metoclopramide, trimethobenzamide
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| What is the antiemetic mechanism of action of benzamides? | Central blockade of DA receptors
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| The SE of benzamides are mainly _________. | Extrapyramidal
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| What are the SE of benzamides? | (Mainly EPS)==>Restlessness, dystonias, Parkinsonian sx
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| How does reglan influence specific areas of the GIT? (3) | 1)Enhances coordinated GIT propulsive motility of the upper digestive tract 2)Increases LES tone 3)Stimulates antral and small intestinal contractions
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| Reglan (does/does not) have significant effects on motility in the colon. | does not
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| What are the 3 mechanisms of action of Reglan in the GIT regarding receptor agonism/antagonism? | 1)DA receptor antagonism 2)5-HT4 receptor agonism 3)Vagal and central 5-HT3 receptor antagonism
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| What is the MOA of Reglan as an antiemetic? | Antagonize DA receptors in the CTZ
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| Which antiemetic should not be given to dystonic and dysphoric patients? | Reglan
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| What are 6 therapeutic uses for Reglan? | 1)N/V 2/t GI dysmotility 2)GERD (symptomatic relief) 3)Gastroparesis 4)GIT radiography 5)Post-op ileus 6)Persistent hiccups
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| What two types of medications can be used in the prevention/treatment of motion sickness or vertigo? | H1 receptor antagonists and anticholinergics
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| What is Meniere's disease and what is used to treat it? | Inner ear d/o that causes vertigo, tinnitus, and hearing loss. Treated with either anticholinergic (scopolamine) or H1 receptor antagonists (dimenhydrinate).
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| What are three different 5-HT3 antagonists? | Ondansetron, dolasetron, granisetron
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| 5-HT3 antagonists (do/do not) increase gastric pH and reduce incidences of aspiration pneumonitis. | Do not
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| What promise do H4 antagonists (anti-histamines) show in medicine? | Treatment of inflammatory conditions involving mast cells and eosinophils.
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| What are three different therapeutic applications for H4 antagonists? | Allergic conditions, asthma, rheumatoid arthritis.
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| The vestibular apparatus is rich in what types of receptors? | Muscarinic cholinergic type I (M1)
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| Name two different anticholinergic tertiary amines. | Scopolamine, atropine
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| Which medication is the only anticholinergic that is suitable for PONV? | Scopolamine
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| What is the onset of scopolamine when administered as a transdermal patch? | 2h
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| How much scopolamine is absorbed over 72h? | 1gm
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| In what conditions is scopolamine contraindicated? | Closed angle glaucoma, GI or urinary obstruction, metabolic dysfx
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| When should scopolamine be administered in order to limit exposure of the newborn to medication? | 1h before c-section
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| True/False: TDS patches are MRI compatible. | False
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| What is the elimination half-time of scopolamine? | 5h
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| Identify the only neurokinin 1 receptor antagonist that is FDA approved. | Aprepitant (Emend)
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| What is the MOA of Emend? | Blocks substance P, which is a regulatory peptide in the GIT and CNS thought to be involved w/vomiting reflex
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| What is the T1/2 of Emend? | Up to 12h
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| How much and when should high-risk patients take aprepitant (Emend) in treating N/V? | 40mg PO within 3hrs prior to induction
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| What limits widespread use of aprepitant (Emend)? | Cost
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| When benefit does propofol serve after extubation? | May be useful adjunct for PONV
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| How does ephedrine serve to alleviate PONV? | Alleviates PONV when it is 2/t postural changes or hypotention.
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| What are the doses of ephedrine that are usually given? | 5-10mg q5-10min
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| How long ago was acupuncture and acupressure documented in Chinese medicine? | 2500yrs
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| What is the MOA of acupuncture/acpressure in treating N/V? | Stimulation of the *P6* accupoint decreases PONV by blocking abnormal energy flow to relieve s/s of illness.
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| Where is the P6 accupoint located? | Between the palmaris longus and flexicarpi radialus of the wrist
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| What are approaches to anesthesia that can be used to decrease the incidence of anesthesia? | Regional, TIVA, higher FiO2, hydration, no N20, minimize opioids, minimize neostigmine
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| What are possible causes for PONV? | Pain, hypotension, hypoxemia, hypoglycemia, increased ICP, GIB
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| What are the most common reasons for adults and children to have protracted stays in the PACU or unexpected hospitalization? | N/V
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|
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