Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove Ads
Don't know
remaining cards
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

nu600 last exam

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
Created by: Rooz