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nu600 last exam
| Question | Answer |
|---|---|
| what is the most common cardiovascular disease in USA | HTN |
| what values consist of HTN | BP of 140/90 or greater, 95% of cases, secondary at rest such as renal failure |
| 95% of all HT are what type of HTN | Primary |
| what does primary HTN mean | renin angiotenson aldosterone system are implicated. |
| what conditions and activation of what system is resulting the sodium excretion being implicated | low renal perfusion, decreased sodium delivery to distal nephrons and sympathetic stimulation. |
| secondary HTN is as a result of what | renovascular disease, renal artery stenosis, hyper aldosternoism, pheochromocytoma, coarctation of aorta, |
| which cause of secondary HTN can be fixed with surgery | coarctation or aorta, renal artery stenosis, pheochromocytoma |
| sympatholytics do what | depress the SNS |
| 5 subtype of sympatholytics | central acting, adrenergic neuron blocker, alpha adrenergic atag, beta antag, mixed adrenergic antag |
| describe impulse transmission from spinal cord to SNS | pre and post gangtionic, Pre-ganglionic neurons originate at thoraco lumbar of spine, short preganglionic with paravetebral ganglio (fast with ACh), long post ganglionic communicate with target organ. (norepi is neurotransmitter) |
| pre ganglionic neurons originate where | thoraco lumbar T1-L2 |
| length of pre ganlionic are what | short |
| short pre ganglionic fiber and what other ganglion has ACh as neurotransmiter | paravetebral ganglion |
| long post ganglionic’s neurotransmitter is what | norepi this process is slower than the ACh |
| at pre ganglionic site there is a release of ACh which activate what receptor and where | nicotonic acetlycholine on the post ganglion neuron |
| when the nicotinic receptor is stimulated there is release of what which does what | norepi, which activated adrenergic on peripheral tissue |
| ACh activate what on the post ganglionic neuron | nicotinic acetylcholine |
| centrally acting antihypertensive agents act how | prevent the brain from sending signal |
| central acting antihypertensive ie alpha 2 agonist are | clonidine, methyldopa, dexmedetomidine aka Precedex, guanfacine, guanabenz |
| sympatholytic dual action inhibits what | dopa decarboxylase which prevent Ldopa to Dopamine reducing methylation of norepi to epi |
| central alpha adrenergic receptor create a false neurotransmitter called | methyl-norepinephrine and functions on the locus ceruleus to inhibit adrenergic outflow |
| alpha 2 sympatholytic are used in what types of HTN | essential and gestational |
| does methyldopa cross the placenta | yes and it appears to be safe in pregnancy |
| methyldopa does what to SNS | decreases the SNS both centrally and peripherally |
| side effects of methyldopa | sedation, head ache, dizziness, low HR and low BP low SVR, depression and anxiety and parkinsonism |
| other side effects of methyldopa | positive coombs test, hemolytic anemia, bone marrow supression, increased LFTS and renal parameters. dry mouth, NV diarrhea no more for gestational |
| clonidine aka catapres | prototypical central anti adrenergic, |
| ratio of catapres alpha 2 to alpha 1 | 220:1 |
| catapres aka clonidine uses | additiction, anxiety, regional block, chronic pain lowers MAC by 35% |
| Dexmedetomidine aka | precedex |
| precedex ratio of alpha 2 to alpha 1 | 1620:1 |
| precedex and accumulation of narcotics | inhibition of enzymes can potentiate this |
| adverse effect of precedex | hypotension, HTN, brady, NV, tachy, hypoxia, |
| name other central acting alpha 2 | reserpine aka serpalin, metirosine aka demser |
| reserpine aka | serpalin |
| metirosine aka | demser |
| adequate hydration is essential to avoid what intraoperatively | hypotension |
| metyrosine may predispose patients to | arrhythmia with use of VA |
| metrosine is useful for treatment of | pheochromocytoma and cateholamine depletion and depression |
| phenoxybenzamine aka dibenzaline | alpha 1 and alpha 2 long acting |
| dibenzaline metabolizes to an intermediate product that reacts with alpha receptors covalently which causes what | irreversible receptor blockade |
| what does one use phenooxybezamine to treat | pheochromocytoma HTN, ischemic effects of pressors, and treat of BPH to imrove urine flow |
| phenoxybenzamine in contraindicated when | pts cant handle precipitous fall in BP, blunts respnse to phenyephrine, may cause epi reversal, then give norepi instead |
| dibenzaline to treat pheochromocytoma pretreatment how long before surgery | |
| side effects of dibenzaline | head ache, NV crosses BBB sedation |
| what was the prototypical Alpha 1 blocker | Dibenzaline aka pheoxybenzamine |
| selective postsynaptic alhpa 1 drug | phentolamine aka regitine |
| regitine aka phentolamine causes what | vasodialation, decrease SVR and PA pressure, may cause reflex tachy and activates plasma renin |
| phentolamine used in catecholamine infiltration dose | 5-10mg in 10ml of NS within 12 hours of extravasation |
| phentolamine block what two receptors | alpha 1 and alpha 2 |
| block in alpha 1 results in what | vasodilation by blocking alpha1 noepi release |
| phentolamine may cause what | reflex tachycardia |
| dose of phentolamine and uses | 1-5mg slow push, infiltration of pressor, mgmt of HTN from clonidine withdraw, ED |
| Oraverse is what | its pretty much phentolamine used as a reversal by dentists |
| prazosin aka minipres | selective alpha 1 inhibitor, arterial and venous dialation, encourges sodium and water. used with beta blocker and diuretic. |
| adverse effect of minipres aka prazosin | hypotension, syncope, edema, marked hypotension with GA |
| Terazosin aka hytrin causes what | nasal congestion so avoid nasal intubation |
| doxazosin aka cardura compared to minipres | its 50% as potent as minipres, cardura may cause hypotension under anesthesia |
| Beta blockers inhibit what | interaction of epi and norepi and sympathetic drugs, may be selective and non selective |
| beta 1 antag decrease what | spontatneous rate of depolarization, slows AV conduction, increases refractory period of AV node |
| B2 antag may cause what | life threatening bronchospasm |
| when using Beta blocker, even B1 selective antag can cause what | depending on dose may also become a B2 antag |
| non selective beta blockers blunt what | glycogenolysis may also block signs of hypoglycemia, nervousness, tremor and tachycardia |
| contraindication of beta blocker | existing bradycardia, heart blocks, cardiogeneic shock, heart failure |
| beta blocker and diabetic | may cause hypoglycemia, beta 1 agents are preferred in diabetics |
| Inderal is the protypical what | nonselective beta blocker, competes with epi and norepi for beta sites |
| classification of inderal | class 2 antiarrhythmic depress automaticity at SA node and AV conduction velocity. |
| inderal can be used to treat what | HTN and HTN due to pheochomocytoma |
| Inderal and pheochromocytoma | beta blocker should NOT be started until the alpha blocker has be started. without alpha blockers, can cause HTN crisis |
| inderal dose | 2mg every 5 min duration less than 10 min max dose of 12mg a day. |
| what patients are not good candidates for Inderal | pts with constrictive/reactive pulmonary disease |
| inderal and neostigmine and VA | may cause HYPOtension |
| abrupt stopage of inderal | severe HTN followd by MI |
| Nadalol aka corgard | non selective beta blocker. |
| timolol aka blocardren aka timoptic | non selective beta blocker used for aqueous humor increase outflow in glaucoma patients |
| Metoprolol aka lopressor | beta 1 selective kinda, 1-5mg every 3 min max of 3 doses. lasts upto 4 hours. caution with neostigmine or amiodarone, large margin of safety |
| Atenolol | selective Beta1 blocker Dose 5mg q5min x2 dose total dose of 10mg duration 24 hours. excreted by kidney and no hepatic metabolism. pee and pooped unchanged |
| Intraoperative drug of choice for Beta1 blocker for cardiac patients due to ints long duration | Atenolol |
| Esmolol | most Beta1 blocker, low beta2 effects. intraoperative HTN, SVT, Afib or flutter ventricle control |
| esmolol reducsed release of what | renin, making it a titratble agent. |
| dose of esmolol | 1mg blous, infusion 150-300mcg/kg.min |
| how is esmolol metabolized | red blood cell esterase |
| what patients are good candidates for esmolol | its non organ dependent metabolism hepatic and renal patients |
| common situation where esmalol is used | intraoperative HTN SVT afib flutter |
| esmolol supplied in 250mg/ml if you inject 10amps in 250cc give you a concentraion of | 2.5gm/250cc |
| non selective adrenergic antagonist such as | labetalol |
| labetalol aka | trandate |
| labetalol aka trandate is non selective what and selective what | non selective beta and selective alpha 1 antagonist |
| ratio of alpha to beta blockade is | 1:7 strongly favoring beta. non titratable give slow and start low |
| dose of trandate aka labetalol | 5-20mg over 2min total dose of 300mg infusion rate of 2mg/min ratio of 7:1 beta to alpha |
| carvedilol aka coreg | non selective beta and selective alpha1, 3-5 times more potent than labetolol. PO only, preop hydration reduces hypotension and |
| calcium channel blocking does what | slows voltage of sensitive Ca channels, L type or slow channels. controls entry into smooth muscle, cardiac muscle, and cardiac conduction. |
| what stages does Ca go into the cell which the blockers act on | stage 2 where Ca is going in and K out, “plateau” of conduction curve |
| what are the Ca blocker chemical structure groups | phenyl-alkylamines, dihydro-pyridines, benzo-thiazepines, diphenyl-piperazines, diaryl-amino-propylamine |
| the different chemical structures of Ca blockers differ how | depending on the structure the differ in pharmacologic characteristics, interaction and toxicity |
| nifedipine aka procardia aka aldalat chemical structure | dihydro-pyridine, no effect on cardiac conduction |
| how does procardia work | decrease peripheral vascular resistance and increases cardiac output. dilate coronary more so than other agents. |
| procardia is used for what other conditions | esophageal spasm, vascular headache, cardiomyopathy, asthma, primary pulm HTN |
| nifedipine is no longer used as what | intranasal or sub lingual due to cardiac and neurological effect, dizziness, loss of consciousness, Heart block, MI sinus arrest |
| nicardipine aka cardine a dihydro-pyridine, results and used in | decrease SVR, essential and chronic HTN, first dihydro-pyridine for IV use |
| IV dose of nicardipine | 0.625-2.5mg this is half of what is normally used. hepatic-renal clearance , prolong QT segment prolongation |
| nicardipine uses | perioprative HTN, pheochromocytoma, control of cerebral vasospasm, myocardial preservation during bypass, does not cause coronary steal, promotes myocardial oxygen supply and demand balance |
| amlodipine aka norvasc another dihydro-pyridine works where | in periphery decreasing SVR and increasing cardiac output |
| Clevidipine aka clevelox is a unique calcium channel blocker | treat intraoperative HTN |
| Clevidipine is metabolized where | blood and tissue non specific esterase |
| dose of clevidipine is | 0.3-3mcg/kg/min max of 16mcg/kg/min |
| pts with what condition will have prolong recovery and where clearance is reduced | when a patient has pseudocholinesterase deficiency, ie Atypical chonlinestease |
| verapamil aka calan what chemical structure | phenyl-alkamine |
| verapamil aka calan a phenyl-alkamine slows Ca influx via slow channel into where | myocardial and arterial smooth muscle |
| what does verapamil aka calan do | dialate coronary arteries, inhibits coronary artery spasm, and slows SA and AV node without altering intraventricular conduction. |
| verapamil is used to treat | HTN, angina, SVT, arrhythmia and mirgraines |
| dose of verapamil aka calan | 5-10mg bolus, repeast 15-30min PO has significant hepatic metabolism, less bioavailable |
| Diltiazem aka cardizem is what chemical structure | benzo-thiazepine |
| cardizem aka diltiazem is a slow Ca channel blocker similar to verapamil, useful in off pump CABG as is verapamil and esmolol. | |
| what meds can be used in off pump CABG | verapamil, esmolol and cardizem |
| cardizem slows conduction of what | SA and AV node does not affect intraventricular conduction. |
| dose of cardizem | 0.25mg/kg followed by 15mg/hour infusion |
| how does the renin angiotensin work | renin stored in nephron released under low renal perfusion or beta 1 stimulation, renin combines with angiotensinogen to make angiotensin 1, angio1 with ACE is converted to angio2 in lungs. |
| angiotensin2 encourages vasoconstriction and release of what from where which causes increased blood pressure | aldosterone release from the zona glomerulosa |
| release of aldosterone does what | encourage Na absorption in distal convoluted tubule and collecting duct. to absorb Na the nephron has to eliminate K+ or H+ |
| when ACE inhibitors are used what happens | PVR is lowered without reflex tachycardia or changes in cardiac output. reduction of aldosterone reduce sodium reabsorption thus saving K. |
| captopril aka capoten adverse effect | dizziness, fainting and cough |
| Lisinopril aka zestril adverse effect | dizzy heache hypoten NV and cough |
| enapril aka vasotec adverse effect | headache, fatigue, nervousness, chest pain cough |
| ramapril aka altase adverse effect | dizziness headache angioedema, NV cough |
| where are angiotensin2 receptors located | vascular and myocardial tissue, brain, kidney, adrenal cells where aldosterone is produced |
| ACE 2 inhibitor use and GA | refractory hypotension have been reported. |
| ACE 2 inhibitor has much less incidence of what | cough |
| Cozaar aka Losartan blocks angiotensin II at what receptor and lowers what | at the T1 receptor and lowers aldosterone from adrenal cortex |
| Cozaar aka losartan used to treat | chronic HTN |
| consideration for ACE inhibitors and angiotensin II blockers and anesthesia | hypotension with GA, treat with IV fluid first, may require vasopressin agonist, 0.04mg ephedine releases norepi. my cause hyper K with K solutions, hypotensive compounded, Increasea effect of curare and NMB |
| ACE II agents associated with what emergency | Angioedema |
| arterial vasodialtors reduce BP by direct effect of vascular smooth muscle of arterial resistance with little effect on | capacitance vessels |
| what is the prototypical arterial vasodialator | Hydralazine |
| Hydralazine a very effective arterial dilator causes what | reflex tachycardia by stimulating the baroreceptor reflex |
| reflex tachcardia does what to the heart | increase its myocardial oxygen demand |
| hydralazine dose | 10-20mg q6h, in OR 2mg q15min observe for effect. supplied 20mg/ml dilute to 2mg/ml in 10ml syringe. |
| Hydralazine is administered with caution particularly in | sitting position |
| Fenoldopam aka corlopam | rapid vasodilator Dopa 1 receptor agonist. No dopa 2, alpha or beta or CNS effects. |
| fenoldopam aka corlopam works how | decreases peripheral vascular tone while increasing renal blood flow and diuresis. |
| fenoldopam aka corlopam dose | 0.025-2.3mcg/kg/min by continuous infusion NEVER Blous |
| corlopam aka fenoldopam contains bisulfite ie can cause | severe allergic reaction |
| what other agents contain bisulfites | additive in propofol and epinephrine |
| other arterial vasodilators of note | minoxidil, diazoxide these have marked reflex tachycardia and increase cardiac output |
| arterial and venous vasodilators name one | Nitroglycerin, first venous then arterial blood vessels, a nitric oxide compound. |
| dose of nitro | paste is 1-2inches to chest wall, IV 20-4-mcg bolus to effect, infusion 0.5 to 10mcg/min titrate to effect duration is 5 min |
| Sodium Nitroprusside aka nipride | potent arterial and venous smooth muscle dilating effects. decreases preload and after load while lowering BP |
| nipride is used for what and dose | HTN emergencies, CHF or controlled hypotension for surgery. Dose 0.5 to 10mcg/kg/min. average dose is 3mcg/kg/min |
| SNP aka nipride precautions | protect from sunlight, arterial monitoring is required when used, reflex tachycardia and rebound hypertension upon discontinuation, inhibits hypoxic pulmonary vasoconstriction, reduce renal flow |
| SNP aka nipride hazzards | RBC convert to cyanogen which are metabolized in liver, excess of 4mcg/kg/min for over 3 hours may lead to cyanide toxicity. |
| hemolysis and cyanide | hemolysis increases free cyanide, stimulate the release of nitric oxide generating hydroxyl radicals. |
| cynaide toxicity due to SNP aka nipride | may alter mental status, seizures and coma. cardiovascular instability, hypertension due to tachyphylaxis, arrhythmia and ST segement changes. |
| SNP aka nipride toxicity aka cyanide toxicity generally revealed with what physiological state | metabolic acidosis |
| treatment of cynaide toxicity due to nipride | Na nitrate, it converts hemoglobin to methhemoglobin, which competes with cytochrome oxidase for cyanide radicals. |
| treatment of cyanide after Na nitrate admin | sodium thiosulfate provides sulfur donor and prevent accumulation of cyanide radicals. |
| vitamin B12 and cynide | B12 binds to cyanide, trans porting it to the kidneys to be excreted in urine |
| cyanide tox treatment | stop infusion, admin 100% oxygen, treat metabolic acidosis, give 3% Na Nitrate, 4-6mg slow, give sodium thiosulfate 200mg per kg over 15min, consider B12 at 25mg per hour |
| pages 294-99 Ouellette perioperative HTN mangement | |
| autokoids do not circulate to site of action | |
| autokoids are not excreted in glands | |
| autos | self |
| akos | remedy |
| autocoids | array of biological active substances, specialized function to initiate the response to tissue injury. |
| Name different autocoids | histamine, bradykinin, sertotonin 5-HT=5hydroxytyptamine, prostaglandin, |
| seratonin is also known as | 5-HT or % hydroxytyptamine |
| histamine is what | low molecular weight vasoactive amine autocoid |
| histamine structure | B amino ethyl imidazole. |
| where is histamine synthesized | in tissue by decarboxylation of histidine |
| where is histamine stored and with what | composite with heparin and in mast cells |
| why is histamine released | response to stimulation by mast cells, basophils and neurons |
| metabolism of histamine | via methylation by histamine-N-methyl transferase and MAO |
| histamine subtypes | 1, 2, 3, 4, Hic |
| sources of histamine | mast cells, basophils, cardiac smooth muscle. Enterochromaffin |
| what plays a central role in hypersensitivity allergic responses | histamine, H1 receptors |
| H1 cardiac receptors when agonized does what | decrease AV nodal conduction |
| H1 and coronary vessel | vasoconstriction, reduced atrial naturetic peptide |
| H1 and bronchial | bronchospasm |
| difference between H1 and H2 antagonist | H1 has antiemetic and H2 does not. acid blocking |
| H2 stimulation causes | bronchial dilatory, gastric acid stimulation from parietal, dysrhythmia from cateholamine release GERD PEPTIC ULCER |
| H2 vs H1 when it comes to vasodilatation | H2 is less of a vasodilator |
| First-genertation H1 antagonist | not H1 specific, generate dopaminergic, serontenergic in cholinergic response |
| H1 antagonist cause what side effect | somnolence, cognitive dysfunction, cross BBB |
| overdose of H1 anatagonist | psychoses hallucination like schizophrenic breaks |
| histamine release from stomach | ECL enterochormofain like |
| H1 antag Promethazine aka | phnergan |
| H1 antag Hydroxyzine aka | vistaril |
| H1 antag Demenhydronate aka | dramamine |
| H1 antag are effective antiemetics T or F | T |
| H2 blockers like loratadine have no _____ effect. | no ANTIEMETIC |
| H1 antag Diphenhydramine aka | benadryl |
| benadryl can treat what | antiemetic, parkinson like symp, histamine mediated effects, adjunct of anesthesia, SLEEPY, |
| anti-histamine for vertigo and motion sickness | cyclizine and Meclizine |
| Vistaril AKA hydroxyzine can potentiate what and how to give or not to give | potentiate narcotic, DO NOT GIVE IV causes Twave abnormalities, dry mouth |
| Second gen H1 antag | do not cross BBB, fewer undesirable side effect, can still cause cardio toxic effect. |
| example of second gen H1 antag | calritin and cetrizine aka zyrtec |
| name some second gen H2 antag | cimedtine, ranitdine, famatodine, |
| second gen antag H2 are used as treatment of what | peptic ulcers and gerd |
| how do second gen H2 antag work | block parietal cells from releasing HCL |
| Bradykinin is an iimportant ____ and ____ | inflammartoy mediator and vasoactive peptide |
| what is the most potent endogenous vasodilator after allergenic reaction and tissue damage | bradykinin |
| bradykinin component is ____and from the ____system | kallikrein from kinin system |
| precursor of bradykinin is | prekallikdrein |
| changes in what and what or _____can stimulate the conversion of prekallikrein to bradykinin. | ph and temp or tissue damage |
| bradykinin stimulates the release of neuropeptide_____ and ______ | substance P and neurokinin |
| what is involved in the mediator of pain cascade | substance p and neurokinin ie bradykinin |
| what is 10 times more of a potent vasodilator than histamine | bradykinin |
| bradykinin may play a role in _____ _____ and _____ ____. | hereditary angioedema and carcinoid syndrome. |
| Serotonin AKA | 5 hydroxytryptamine, or 5HT |
| Serotonin found through out where in body | GI , CNS and platelets. |
| 5HT receptors belong to what regulatory receptors | G protein coupled transmembrane |
| what neurotransmitter plays a important role in pain | 5HT |
| what biogenic monoamine are responsible for states of mood feelings and motivation | dopamine, norepi, serotonin |
| 5HT1A is implicated in what disorders and or cerebral conditions | psychiatric and immunomodulation and ischemic conditions |
| serotonin synthesis from | tryptophan |
| Serotonin metabolism | via MAO by oxidative deamination |
| non MAO metabolism of serotonin may lead to | hallucinogenic metabolites. |
| where is 5HT action terminated | at the synaptic junction and in outer membrane of platelets |
| 5HT 1b/1d are effective class of____ therapeutics. and is contraindicated in coronary artery disease CAD | migraine therapeutics |
| 5HT2 function is unknown, it is attracted to _____ the site of CSF fluid generation | choroid plexus |
| 5HT4 given for_____ example of drug is____ causes cardiac problems | GERD, drug Cispride |
| 5HT3 has a strong relation with what receptor | nicotinic acytylcholine receptor |
| 5HT3 is found in high levels within the complex of what and where else | bainstem and parasympathetic terminals of the GI tract |
| where does the initiation and coordination of vomiting reflex occur | the dorsal vagal complex |
| site of action of nausea and vomiting initiation | nucleus tractus solitarius area postrema and dorsal motor nucleus of the vagus nerve. |
| antagonism of 5HT3 contributes to | anti-emetic action |
| polymorphism of 5HT3 gene suggest a role in what disorders | psychiatric disorders |
| what are prostaglandins | naturally occurring endogenous substances |
| what are prostaglandins derived from | arachidonic acid |
| metabolite of arachidonic acid via what pathway are endogenous mediators of inflammation | cyclo-oxygenase pathway |
| metabolites of arachidonic acid are considered what typr of receptors | 7 transmembrane domain receptors AKA G protein coupled. |
| prostaglandin are similar to 5HT family in what regard | both are G protein coupled receptors. |
| Prostaglandin play a role in what | SVR, airway resistance, platelet aggregation and increase uterine tone |
| cell membrane phospholipid makes arachadonic acid which makes cox1 and cox2 which make prostanoids T or F | True |
| cox 1 has what positive attribute | cyto protective cox 1 |
| cox 1 because it is a cyto protective is produced how | continuously ie constitutive and its physiologic |
| cox 2 is considered ____; shows up at presence of inflammation | inducible |
| what is the primary site for prostaglandin synthesis | the lungs |
| what can be exacerbated by circulating prostaglandins | asthma |
| what may cause pulmonary HTN and bronchospasm by stimulation of thromboxane | protamine |
| PONV is objective or subjective | subjective in how it feels, untill you puke then we can all see it and might join |
| what percent of pts may feel PONV after surgeory | 30 to 70% |
| deleterious effects of PONV | resources, time of discharge, co morbidities ie HTN, pain, aspiration etc... |
| causes of N&V | infection, pregnancy, vestibular dysfunction, peritonitis, post radition etc.. |
| why do we vomit | eliminate noxious or toxic substances, protective, reminded us what is safe to eat and what is not |
| distention or stimulation of the what provides the strongest stimulus for N&V | distention or stimulation of the duodenum |
| the emetic center is where | in the reticular formation of the medulla |
| chemotherapy anesthetics and opoids act where to cause nausea and vomiting | chemoreceptor trigger zone, prostrema 4th ventricle |
| vomiting centre is where | medulla |
| name some sensory inputs that stimulate the emetic center | afferent impulses from pharynx, GI tract, mediastinum, cerebral cortex, sensory organs |
| where is the CTZ | out side the BBB |
| is the CTZ protected by BBB | NO |
| name CTZ pro emetic agonists | serotonin, dopamine, histamine, ACh, neurokinin 1 aka substance P |
| what kind of approach do we need to treat nausea and vomiting | multimodal |
| name a widely distributed endogenous vasoactive autocoid | serotonin |
| serotonin evokes complex changes within what throughout the body | vascular beds |
| what acts as a key neurotransmitter in emesis and pain transmission | Serotonin |
| where is serotonin released from | enterochromafin of the small intestine |
| describe how the vomiting reflex in the medulla is initiated | serotonin stimulated the vagal afferent pathways through 5HT3 receptor which initiates the vomit reflex |
| 5-HT3 is what | serotonin receptor |
| 5-HT3 aka | 5 hydroxytryptamine type 3 |
| name some serotonin antagonists | zofran or ondansetron, granisetron, dolasetron, palonosteron |
| adverse effects of serotonin antag | headache, dizziness, constipation or diarrhea |
| why give serotonin antag | chemotherapy, post radiation, pregnancy, PONV |
| Prototype of drug of SSRA | ondansetron |
| ondansetron | 4 to 8mg IV may repeat 1 or not at all. onset 30min elimination 4 hours |
| dolasetron aka anzemet metabolite that is responsible for its antiemetic effects | hydro-dolasatron |
| hydrodolasetron T1/2 and strength when compared to dolasetron | 8hours and 100 times more potent than dolasetron. |
| dose of dolasetrong aka anzemet | 12.5 mg IV, PO 50-100mg just like zofran |
| granisetron aka kytril | more specific than ondansetron, chemo therapy, coverage for 24hrs, expensive, 1 mg before induction or 20-40mcg/kg |
| polonasetron aka aloxi | newest, not a rescue antiemetic. 40 hours half life, dose 0.25mg IV prior to chemo |
| any difference in efficacy or safety between the different serotonin receptor? and why use them then | no difference except the length of half life in body. |
| corticosteroids have antiemetic properties | TRUE |
| possible mechanism of corticosteroids | intracellular interaction that regulate expression. prolonged onset. not really known why it works. used in multimodal to enhance efficacy of 5HT3 antag |
| phenothiazine aka compazine aka phenergan antipsychotic, used for chemo and radiation NV | |
| phenothiazines, compazine, phenergan mechanism of action | inhibition of dopamine, muscarinic and H1 receptors, Side effect hypoten and extrapyramidal symptoms |
| promethazine aka pheergan other uses | allergy to blood transfusion, anaphylaxis to H1 blocking action. NOT FOR sub q. venous irratent, burns |
| butyrophenones aka droperdol | antipsychotics, inhibition of dopamine |
| dose of dropperidol | 0.625 - 1.25mg one time dose, for chemo and radiation, PONV |
| adverse effect of droperidol | long QT, black box warning, only used for pts with no response to other means |
| dropperidol comes in 2.5mg/ml so how much is the one time dose if using the bigger range | 0.5ml or 1.25mg BUT should give small dose. 0.625 |
| adverse effects of droperidol and OD and QT | 50mg in 24 hours pts die. Torsade de pointes, 12 lead needed prior, QT greater than 440ms for men and 450 in women NO GO. follow up ekg within 3 hours. |
| Droperidol is in the class with which antipsychotic | haldol, D1 and D2 blocker |
| cannabinoids aka WEED, AKA SKUNK, AKA Green monster, AKA CUSH, AKA | hahaha you still reading this....Mary J |
| mechanism of action of week not known | TRUE |
| First pass metabolism of weed | liver, biliary |
| adverse effect of weed | euphoria, dysphoria, sedation hallucination. abrupt withdrawl symptoms, autonomic effects, orthostatic hypotension |
| weed used for | chemo NV apetitie. |
| cholindergic agents | no net propulsive activity. not useful for treating motility. increase contractions |
| prokinetic agents | coordicnated GIT propulsive motility. act on motor neurons, increase ACh but not interfering with normal motility. |
| ACh why is it not used for cholinergic agent | affects both nicotinic and muscarinic receptors. degraded fast by acetylcholineesterase |
| what is a direct cholinergic receptor agonist that resists enzymatic hydrolysis | Bethanechol |
| Indirect chilnergic agents | ACh inhibitors, eg neostigmine for paralytic ileus |
| why does decreased motility of GIT happen | supperession of ACh release from myenteric motor neurons mediated by D2 dopanminergic receptors. |
| mechanism of action of prokinetic agents | antagonize the inhibitory effect of dopamine on myenteric motor neurons, |
| examples of prokinetics are | metocopramide and domperidone |
| drugs in the benzamides family are | metoclopramide and trimethobenzamide |
| mechanism of action of benzamides | dopamine receptor blocker |
| side effect of dospamine receptor blockers | extrapyramidal, restessness, dystonia, parkinsonian |
| metoclopramide | GIT propulsive motility, upper GI, increase esophageal sphincter tone, stiumlate enteral and small instestinal contractions. NOT significant on COLON |
| metoclopramide mechanism of action on GIT | dopamine receptor antagonism, 5HT4 agonist, vagal and central %HT3 antagonist |
| metoclopramide antiemetic action | antag dopamine receptor in CTZ |
| metoclopramide aka | reglan |
| reglan aka metoclopramide | NV with GI dysmotility, reflux not heal, gastroparesis improvement, diag procedures intestinal intubation or contrast radiography, post op ileus, hiccups. |
| why reglan not used for bowel anastamosis | dont want to actively mobilize the bowel |
| H1 antag and anticholinergics are used to prevent what | motion sicknes, vertigo, |
| adverse effects of H1 antag and anticholinergics | sedation, dizziness, confusion, dry mouth, cycloplegia, and urine retention |
| examples of H1 antag and anticholinergics | Diphenhydramine, dimenhydrinate aka dramamine |
| Dimenhydranate aka | dramamine |
| menier’s disease is aka@ vertigo like symptoms, aka hydrops aka endolymphatic hydrops | |
| meclizine | aka antivert a antihistamine anticholinergic |
| serotonin atagonist drugs@ ondansetron, dolasetron, granisetron good for PONV, DO NOT increase Ph or reduce aspiration pneumonitis | |
| Anti histamine H4 blockers | good for inflam conditions involving mast and eosinophils, allergic conditions, asthma, Rheumatoid arthritis being studied. |
| anti-cholinergics like scopolamine treats motion sickness cause by stimulation of what | vestibular apparatus |
| the vestibular apparatus is rich in what recceptor sites | muscaarinic cholinergic type 1, M1 receptors |
| can scopolamine cross BBB why? or why not? | yes, it is a tertiary amine like atropine |
| Is scopolamine a rescue drug and some side effect | no can be given prophylaxix but not for acute vomiting, makes you sleepy and thirsty |
| scopolamine non selevtive M1 antag dose and route | skin patch, 1mg over 72 hours, onset two hours |
| scopolamine contraindication | close angel glaucoma, GI or urin obstruction, metabolic dysfunction |
| neurokinin 1 atag include what drug@ aprepitant aka emend | |
| aprepitant aka | emend |
| emend aka apreitant blocks what, which is a regulartory peptine in GIT and CNS | substance P |
| this is the only FDA approved neurokinin one antagonist | Emend aka aprepitant |
| high risk patient should take emend how much and how long before induction | 40mg PO three hours prior to induction |
| propofol and ponv | subtheraputic dose can be used |
| ephedrine and NV from postural and hypotension | dose 5 to 10mg every 5 to 10min prn |
| stimulation of what accu point decreased of PONV | stimulation of P6 accu point, loacted in palmaris longus and flexicarpi radialus or wrist |
| strategies to prevent PONV | regional, TIVA, high FIO2, hydration, N2O avoidance, min opioids, Minimize Neostigmine |
| other causes of PONV | pain, hypotension, hypoxemia, hypoglycemia, increased ICP, GI bleeding |
| be alert to EKG changes after 5HT3 Blockers, or droperidol why | prolonged QT possible torsade de pointes |
| deglutition aka | swallowing |
| cough has a pressure of | 100torr |
| cranial nerves associated with cough | 9 and 10. glassopharyngeal and vagus |
| swallowing and breathing | parallel pathways, voluntary and involuntary mechanism are at play, |
| pharyngeal reflex or _____blocks the respiratory pathway and forcefully expels foreign matter. | gagging |
| define aspiration pneumonitis | inflow of highly acidic gastric content triggering severe inflammatory reaction |
| with aspiration pneumonitis injury occurs to the | trachea, bronchioles, lung tissue, pulmonary capillary endothelium |
| how long does it take for the inflamatroy reponse to kick in with aspiration pneumonitis | 6-12 hours or so |
| reflux from the latin | refluere, which means to flow back |
| aspirate is drive from latin | spire, means to breath upon, now mean inhilation of solid or liquid into airway. |
| mendelson in 1946 spoke of aspiration of stomach contents into the lungs during | OB anesthesia. |
| aspiration depends on two key parameters which makes it more deleterious | Ph less than 2.5 and volume greater than 25ml. |
| what produces HCL acid | gastrin and the perital cell of stomach |
| mendelson syndrome | Ph of less than 2.5 and volume more than 25ml |
| process of deglutition | peristalic waves 3 to 4 a min, mixing gastric contents, and ideally 3% of gastric volume ie chyme enter the small bowel per min |
| reasons why gastric volume emptying may be delayed | entrogastric inhibitory nervous reflex |
| what can we give for Entrogastric Inhibitory Nervous Reflux | |
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