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Pharm Exam 2
| Question | Answer |
|---|---|
| What are some SE of VAAs? | apnea, bradycardia, hypotension from vasodilation and increased ICP. |
| what are SE of propofol | apnea, hypotension |
| what are SE of succs | increased ICP, intraocular pressure (contraindicated in glaucoma), intragastric pressure (aspiration). |
| what are SE of ketamine | increased ICP, and a vagolitic response with increased HR and BP |
| what is ethnopharmacology? what is another name for it? | ethnic pharmacology; cultural and environmental factors that influence Rx response; takes into account a culture's traditional use of plants for medicinal purposes. |
| What is skunk cabbage used for? Who used it? | Winnebago and Dakota tribes use this to stimulate the removal of phlegm in asthma. used in respiratory and nervous disorders and in rheumatism and dropsy (inflammatory condition of the abdomen) |
| what was creosote bush used for? | bronchitis; A tea of the leaves was used for bronchial and other respiratory problems |
| what was pleurisy root used for? who used it? | The Natchez drank a tea of the boiled roots as a remedy for PNA and was later used to promote the expulsion of phlegm |
| waht was wormwood used for? who used it? | The Yokia Indians of Mendocino County used a tea of the boiled leaves of local species of wormwood to cure bronchitis. |
| what was partridgeberry used for? who used it? | The Cherokee used a tea of the boiled leaves. Frequent doses of the tea were taken in a few weeks preceding the expected date of deliver to speed childbirth. |
| what was blue cohosh used for? | To promote a rapid delivery, an infusion of the root in warm water was drunk as a tea for several weeks prior to the expected delivery date. |
| what is pharmacogenomics? | How a person’s genome or genetic coding affects their response to pharmacologic agents. |
| what is xenobiotics? | term applied to all chemical substances that a person is exposed that has some effect on the body (geographic environment, food/drink, other habits and behaviors); |
| When the body is exposed to xenobiotics, or the drugs that are administered to it, the drugs undergo ________ reactions that is mediated by the _______ system. | phase I & II ; CYP450 system |
| what enzyme is responsible for the breakdown of caffeine, Zofran, and theophylline | CYP1A2 |
| What enzyme is reponsible for the breakdown of decadron, fentanyl, oxycodone | CYP3A4 |
| vitamin K is found in what vegetables? what rx does it alter? | in leafy green such as kale and spinach alter effectiveness of Coumadin |
| what are the 4 Gs? what do they affect? | The 4 Gs are garlic, ginger, ginseng, ginkoba effect on bleeding |
| what do phytochemicals do? | antioxidant and antiinflammatory effects; can induce CYP1A2 which increase phase 1 processes |
| what foods are phytochemicals found in? | leafy greens, carrots, pumpkins, tomatoes, and cruciferous vegetables such as broccoli, brussel sprouts and cauliflower |
| what affects does grapefruit have on drugs? name some examples | interferes with first pass metabolism and transportation of many Rx: felodipine, versed, erythromycin. |
| what does grapefruit do to CYP enzyme activity and subsequently drug levels | inhibit CYP enzymes; increases plasma level of Rx |
| what are solanaceous glycoalkaloids | a chemical in potatoes, tomatoes and eggplant that inhibits plasma cholinesterase enzymes (acetylcholinesterase, butyrylcholinesterase |
| 1 serving of potatoes can do what to what drugs? | interferes with metabolism of esmolol, ester-type local anesthetics, NMB agents, cocaine |
| who are the heaviest ETOH consumers? | males 18-44 |
| additive depressant effects of ETOH does what to other drugs? | additive depressant effects of alcohol, it is known to increase the sensitivity to other drugs. |
| what does acute ETOH consumption result in? | changes in sensorium that may result in psychomotor impairments that may lead to injury, vomiting, delayed gastric emptying, and the inability to make rational decisions. |
| how does chronic alcohol consumption affect the body? | . It causes profound effects upon the nervous, CV, GI and renal systems. Also affects the immune system (altered immune response), leading to impaired healing and infection. Results in increased length of stay in ICU and hospital. |
| how does alcohol affect drug distribution and metabolism? | affects our physiological processes, hypoalbuminemia and impaired blood flow through the liver affects drug distribution and metabolism. Eg. Duration of NMB may be prolonged. |
| what enzyme does ETOH induce? | CYP2E1 |
| because of ETOH enzyme induction, what drugs would you have to administer more of? | administer more than the usual amounts of drugs for propofol, barbiturates, opioids and the MAC of inhalational agents |
| what compounds are found in cigarette smoke? | Cigarettes contain benzene, polyphenols, arsenic, carbon monoxide, and polycyclic aromatic hydrocarbons (PAHs). |
| PAHs induce what enzymes? | CYP1A1, CYP1A2, CYP2E1 |
| what is PAH? | polycylic aromatic hydrocarbons |
| PAHs have been found to cause genetic mutations contributing to what? | development of cancer |
| what % of the pop is on 1 med, and what % is on 3 or more prescription meds? | 46%, 20% |
| how many genes does each human contain? | 30,000 |
| what is a gene? | basic unit of inheritance that is responsible for a trait or characteristic) |
| what is a genome | all genes, complete instruction manual |
| what are the 4 nitrogenous bases and how do they pair? | Adenine always pairs with thymine Cytosine always pairs with guanine |
| the human genome contains how many DNA base pairs? | 3 billion; this combo of base pairs give the DNA sequence (serve as directives for cell to synthesize proteins) |
| what are DNA package units called? | chromosomes |
| how many chromosome pairs do we have? | 23 pairs |
| how many autosomal chromosomes do we have? | 44 |
| what is a polymorphism | variation/mutation existing in > 1% of population. |
| what is a single nucleotide polymorphism? | when one nucleotide replaces another |
| what does a single nucleotide polymorphism do to drug response? | results in individual differences in drug responses (differences in enzyme activity) |
| ultra-rapid metabolizers have variant in which CYP enzyme? | CYP2C19*17 |
| which enzyme variant appears in swedes, ethiopians and chinese and in what percentage? | CYP2C19*17; 18%, 18%, 4% |
| What ethnic groups have a variant in CYP enzymes known as CYP2C19*17? | swedes, ethiopians, chinese |
| what enzyme has been identified to be involved with approx. 25% of all Rx metabolism including B-blockers, amide Las, antiemetics and opioids | CYP2D6 |
| The enzyme CYP2D6 has been identified to be involved with approx. 25% of all Rx metabolism including _____ | B-blockers, amide LAs, antiemetics and opioids |
| individuals with Red hair have mutation in what gene and how does this change their MAC requirements? | have mutation of melanocortin-1 receptor gene, and they statistically require higher MAC concentration as compared to dark haired individuals. |
| who has longer recovery time after G/A with propofol (males or females?) | males...losers. |
| who synthesized sulfuric ether and when? | • 1540 – Valerius Cordis |
| who synthesized N2O and when? | • 1774 – Joseph Priestly |
| who synthesized chloroform and when? | • 1831 – Samuel Guthrie |
| Morton successfully demonstrates what drug on ether day (what did he call it)? | letheon (ether + orange oil) |
| who synthesized all halogenated hydrocarbons used today? when did he do this? | • 1950s – Ross C. Terrell and his team (Baxter labs) |
| how did TERRELL synthesize VAAs used today? What type of chemistry and what were they originally working on? | Significant advancements in fluorine chemistry during the development of the atomic bomb led to the discovery of the halongenated agents |
| what were the first VAAs created by terrell | fluroxene, methoxyflurane, halothane |
| for an ideal inhalation agent, you would want a (high/low) solubility in blood and tissue? | low solubility in blood and tissue |
| ideally, how would you want VAAs to affect CBF and CMR? | 5. Minimal effect on cerebral blood flow (CBF) and cerebral metabolic requirements of O2 (CMR) |
| describe N2O | N2O is an inorganic gas and is not halogenated. |
| all modern anesthetics are what? | hydrocarbons |
| why was cyclopropane removed from market? | popular in 1960s was removed from the market as it was explosive and highly flammable |
| Agent development was based on ______ of ether molecule. | structure activity relationship |
| Halogenation means that hydrogen molecules on the hydrocarbon structure have been replaced with halogen molecules such as _______ | chlorine, bromine, fluorine. |
| what measurement may inform us that equilibrium has been reached (does in alveolar = dose in brain)? | Measuring the inspired and expired anesthetic gas concentration (Fi/Fe) |
| What is FI and what factors affect FI? | fraction of inspired gas or inspired gas concentration; affected by (1) FGF rate (2) breathing circuit volume - 6L (3) circuit absorption. |
| what is Fa and what can affect it | arterial gas concentration; may be affected by ventilation/perfusion mismatch |
| what is FA and factors can affect it | fraction of alveolar gas or alveolar gas concentration; may be affected by (1) uptake, (2) ventilation (3) concentration effect (4) 2nd gas effect |
| after uptake into the blood, concentration of the agent is now referred to as _______ | partial pressure (mmHg) or tension - partial pressure exerted by gas form of agent |
| how are concentration of the agent and partial pressure of the agent related? | they are directly proportional to one another, but do not necessarily EQUAL one another. |
| development of ____ is necessary for uptake into the blood and development of concentration at site of action | FA |
| the ultimate objective during induction is to have FA = FD. What limitations may prevent this? | Vapor/gas delivered is increasingly diluted by volume of the circuit (6L) and then by the volume of the lung in establishing the FA. |
| name the descending series of concentrations? | FD > FI > FA > Partial pressure arterial > partial pressure in brain |
| 1% of an agent equals how much pressure? | 1% of 760 mmHg, or 7.6 mmHg. |
| 2% of an agent equals how much pressure? | 15.2 mmHg |
| what is the FA/FI ratio? | rate of rise; or the rate of equilibrium from FA toward initial FI; the key to understanding uptake and distribution of VAAs |
| solubility of gaseous agents is desirable or not desirable? | not desireable (stays in blood and brain longer); solubility encourages agent to remain in blood and not enter alveoli; adds time to induction and emergence |
| what is development of alveolar concentration (FA) necessary? | needed for bulk uptake into blood in order to develop concentration gradient at site of action (brain) |
| describe the 3 components of the uptake equation | (1)cardiac output (alveolar blood flow), (2) concentration gradient (difference in partial pressure btwn alveoli gas and venous blood), and (3) blood/gas solubility of agent |
| describe scenarios where any of the uptake variables equal zero and, thus, no uptake of agent can occur | patient cant be in cardiac arrest (No alveolar blood flow/CO), agent has not fully equilibrated (no concentration gradient), agent can't be insoluble in blood. |
| what does increased uptake during induction do to rate of rise? is this good or bad? | reduces rate of rise (FA/FI ratio) which is bad during induction |
| what are situations that increase uptake and decrease rate or rise | increased CO (high output sepsis, incr. HR, a fib with RVR); increased agent solublity |
| patients with low HR and CO may have what kind of inductions? | sudden and deep inductions |
| patients with high cardiac output may have what kind of inductions? | slower inductions |
| name 4 techniques that can offset an increased uptake in order to speed induction | (1) increase FD (overpressuring/concentration effect) (2) increase FGF to offset dilution from breath circuit (3) increase alveolar ventilation (4) 2nd gas effect |
| what are the components of the distribution equation? what does distribution begin with? | distribution begins with UPTAKE. (1) tissue group perfusion (tissue blood flow) (2) a-v concentration gradient (difference in partial pressure btwn arterial blood and tissue) (3) tissue to blood partition coefficient (tissue solubility of the agent) |
| what organs receive the greatest perfusion/distribution? what are they called? | “vessel rich groups” (“central compartment”): brain, heart, liver, lungs, kidneys (receive anesthetic sooner than muscle and fat) |
| equilibrium betwen 2 phases is expressed as what? | partition coefficients |
| equilibrium implies that the same ____ exists in 2 phases | partial pressure; but does not imply equality of concentration within 2 phases. |
| The PA and ultimately the PBr (partial pressure in brain) of inhaled anesthetics are determined by 2 factors: | (1) input (delivery) into alveoli and (2) loss of the drug from the alveoli into the arterial blood. |
| Input of anesthetics into the alveoli depends on 4 kinetic principles: | 1. Inspired partial concentration of the anesthetic gas 2. Alveolar ventilation 3. Characteristics of the anesthetic breathing system 4. Functional residual capacity (FRC) of the patients lungs (about 20-25 cc/kg |
| 3 factors that determine inspired partial pressure gradients necessary to establish anesthesia: | anesthetic input (machine to alveoli), anesthetic loss (alveoli to blood), arterial blood to brain (PBr) |
| Induction objective: a high _____ is required during the initial administration of the anesthetic | inspired partial pressure (PI) |
| outcome of high initial input (PI) | offsets the impact of uptake (loss); accelerates the induction of anesthesia as reflected in the rate of rise of the PA, and thus the PBr |
| overtime, the uptake in blood ____, and the delivered % must also _____ | decreases, be decreased to match decreased uptake and maintain a constant steady state and optimal PBr |
| what is the concentration effect? | impact of FI on rate of rise of PA; states that the higher the FI, the faster the PA approaches the FI |
| what is the PI | inspired partial pressure |
| define the blood/gas partition coefficient | Reflects the portion of the anesthetic that will be soluble in blood, binding to blood components, and not wanting to enter the brain to participate in anesthesia (not readily enter the tissues).the rate of equilibrium between blood and gas phase. |
| what is the Meyer Overton rule | anesthetic potency of inhalation agent correlates directly with lipid solubility |
| if the Rx is more soluble in blood, what does it do to how fast the person is anesthetized | slower brain and spinal cord uptake and slower the patient is anesthetized; soluble Rx stays in blood in greater proportions |
| BG solubility coefficient of 2 = what concentration in blood to equal what concentration in lung? | the concentration in blood must equal 2% to achieve a concentration in the lung of 1% |
| what does a low BG coefficient mean to speed of equilibrium? | equilibrium is reached more rapidly |
| what is the BG coefficient of des? | 0.42 |
| what is the BG coefficient of N2O | 0.46 |
| what is the BG coefficient of sevo | 0.65 |
| what is the BG coefficient of iso | 1.46 |
| what is the BG coefficient of halo | 2.54 |
| what is the BG coefficient of ether | 12 |
| define the Oil/gas partition coefficient | solubility in fat/brain; indicator of anesthetic potency - how efficiently it can access and affect the brain; the higher the coefficient, the more potent the agent |
| what is the OG coefficient of N2O? | 1.4 |
| what is the OG coefficient of des | 19 |
| what is the OG coefficient of sevo | 47 |
| what is the OG coefficient of iso | 91 |
| what is the OG coefficient of halo | 224 |
| what is another theory besides the meyer overton to describe how VAAs may work? | Another theory is specific protein theories (receptors): GABA agonist theory and receptor-based alcohol site |
| VAAs do not participate in _____ | structure activity relationships |
| what are main factors of agent potency | compound size and compd hydrogen bond activity (shape plays minimal role) |
| define MAC | Defined as a minimum alveolar concentration at equilibrium in which 50% of subjects do not respond to painful stimulus (gross purposeful movement of head or extremities). |
| neonates require ____ MAC concentrations | higher |
| MAC is the primary clinical measurement of what | potency |
| The physio-chemical property used to describe potency is the _______ | Oil/gas partition coefficient |
| how is OG coefficient related to MAC values? | inversely related; OG = 1/MAC |
| what is the MAC of halo | 0.75 |
| what is the MAC of iso | 1.17 |
| what is the MAC of des | 6.6 |
| what is the MAC of sevo | 1.8 |
| what is the MAC of N2O | 105 |
| can full anesthetic doses be achieved witn N2O? | nope |
| what is MAC awake? how do we calculate it? | The MAC at which 50% of subjects will respond to the command “open your eyes”; 1/3 of MAC value |
| how do you determine MAC ratio? | MAC awake / MAC |
| when would you use MAC awake? | when approaching emergence |
| VAAs with a MAC ratio of ______ are considered potent anesthetics; what are examples | 0.3-0.4; des, sevo, iso |
| MAC ratio of _____ is considered a weak anesthetic; what is an example | 0.6; N2O |
| what is MAC BAR | MAC BAR (Block autonomic/adrenergic response): MAC necessary to block the adrenergic response (changes in plasma Norepi, HR and MAP) to skin incision |
| how do you calculate MAC bar? | 1/3 higher than MAC |
| when would you use MAC bar? | prior to skin incision or intubation |
| what are factors that decrease MAC? | incr. age; hypothermia; depressant Rx (benzos, opioids); a-agonists; acute ETOH; metabolic acidosis, hypoxemia, anemia, hypotension, hyponatremia, pregnancy, certain rx |
| what drugs can decrease MAC | opioids, benzos, barbiturates, chlorpromazine, hydroxyzine, N2O, ketamine, verapamil, lidocaine, clonidine, a-methyldopa, reserpine, chronic amphetamines, lithium, levodopa |
| what are factors that increase MAC? | decreased age, hyperthermia, hyperthyroidism (incr. HR), hypernatremia, chronic ETOH; acute ampetamines, MAOIs, cocaine, levodopa, polycythemia |
| when the is concentration effect more effective? | when the agent is more soluble (such as iso) |
| what are 2 compoenents of the concentration effect? | (1) increasing inspired concentration (PI) to increase alveolar concentration (PA) (2) augmentation of tracheal inflow - inflow of VAAs into lungs to fill void space produced by uptake of gas (helps to suck in more gas) |
| define the second gas effect | The ability of a high-volume uptake of one gas (the first gas) to accelerate the rate of increase of the PA of a concurrently administered “companion gas”. |
| is the second gas effect helpful for agents that are already fast, such as des and sevo? | nope |
| which agent benefits from second gas effect | isoflurane |
| why is N2O a good adjunct gas for the 2nd gas effect | high volume of N2O (very insoluble) moves quickly OUT of the lung leaving the "companion gas" behind in the alveoli |
| how is venturi effect related to VAAs | second gas effect: incr uptake of second gas reflects increased tracheal inflow and concentration of second gas |
| define alveolar ventilation | the portion of the tidal volume that actually crosses the alveolar membrane and enters the blood (tidal volume - anatomic dead space x RR) |
| what percentage is dead space of the tidal volume (or minute ventilation) | 30% |
| what does increasing alveolar ventilation do to uptake | promotes input of anesthetic agent to OFFSET uptake |
| alveolar ventilation is what percentage of minute ventilation? | about 60 - 70% |
| how do you increase alveolar ventilation? | increase RR and Vt on ventilator; recruit alveoli by adding PEEP or valsalva maneuver |
| what is the net effect of increasing a persons minute ventilation? | Faster rate of rise of the PA towards the PI, thereby increasing the speed of induction. |
| how can the rate of rise of PA be offset by decreased delivery of VAA to the brain when manipulating minute ventilation? | hyperventilation can cause decrease in PaCO2 and thus decrease cerebral blood flow (vasoconstrict) |
| how can increasing minute ventilation affect the heart, and what does this do to uptake? | increased positive pressure decreases venous return and thus decreases uptake of agent (d/t decreased blood flow) |
| how is physiologic dead space calculated? | anatomic dead space + alveolar dead space |
| what is the significance of the Bohr equation | quantitave estimate of dead space; expresses ratio of dead space ventilation (Vd) relative to tidal ventilation (Vt) |
| what is the bohr equation | Vd/Vt = PaCO2 - PECO2 / PaCO2 PECO2 is mixed expired CO2 |
| Branched chains longer than ___ carbon atoms demonstrate diminished effect | 5 |
| Halothane containing 5 halogens are more prone to produce _____than ethers with 5 halogens | arrythmias |
| Ethers also contain ____that reduces arrhythmias. | Oxygen |
| what cellular effects do VAAs have (what electrolyte does it affect)? | reduce intracellular calcium concentrations in heart and vascular smooth muscle; Ca influx to sarcolemma is reduced and Ca release from sarcoplasmic reticulum is depressed --> diminished contractility of myocardium and vasodilation |
| in the presence of normocapnea, what do VAAs do to the vessel | potent vasodilator |
| what do VAAs increase neuro-wise | ICP and CBV/CBF |
| what do VAAs decrease neuro-wise | CMRO2 and CPP |
| the uncoupling of normal relationship of CBF and CMRO2 is seen most with what drug | 1 MAC of iso |
| how does N2O affect CMRO2 and CBF | increases both |
| what do VAAs do to EEGs | dose-related suppression; at high concentration produce electrical quiescence; burst suppression; skew evoked potentials |
| why aren't VAAs used during neuromonitoring | can increase latency (time to response) and decrease amplitude of evoked potential |
| what VAA is linked to epileptiform activity in peds? | sevo |
| what do VAAs decrease cardiac-wise | MAP (by reducing SVR), CO, CI; halothane reduced MAP by direct myocardial depression |
| what does N2O do to BP | increases SVR and MAP |
| what VAAs affect HR? | iso and des increase HR 5-10% from baseline |
| what can you give to counter increased HR from des or iso | fentanyl during steady state; esmolol or lidocaine during induction or emergence |
| why does des increasing HR during anesthesia annoy people? | dimishes the reliability of HR as a guide to anesthetic depth |
| what VAAs produce coronoary steal | iso and des |
| when is coronary steal the most dramatic | in presence of hypotension |
| how do VAAs initiate anesthetic preconditioning (APC) | Activating pro-cardiac pathways such as RISK, reperfusion injury salvage kinase pathway |
| what is ischemic preconditioning (IPC) | VAAs also may be beneficial during ischemic preconditioning (IPC) where brief ischemia is induced, which leads to long-term cardio protection;heart ischemia initiates complex cell signaling mechanisms that attempt to reduce ischemia and last for 3 hours |
| what do VAAs do to responsiveness to CO2 and O2 | VAAs reduced responsiveness to CO2, and Vt reduces as agent concentration increase The brainstem responds by increasing RR to a point; hypercarbia ensues; the brainstem’s reponse to hypoxia is diminished |
| neuromuscular-wise, what do VAAs predominately affect | post-junctional membrane |
| what do VAAs do to skeletal muscles | dose-dependent relaxation of skeletal muscles; potentiate the effects of NMBs |
| what does TIVA do to NMB dosages? | requires higher NMB dosages |
| how much dantroline is given to MH crisis | 2.5 mg per kg repeat every 5 minutes up to 10 mg per kg |
| what agents can trigger MH | VAAs, N2O, succs |
| what are sevo delivery recommendations to reduce incidence of cmpd A formation | do not exceed 2 MAC hours at flow rates of < 2L/min; now recommended for low flow anesthesia |
| what do VAAs do to hepatic blood flow | decreases total hepatic blood flow (halothane), however iso, des and sevo have beenshown to increase or maintain hepatic artery blood flow |
| what is mechanism of injury of VAAs on liver | hepatocyte hypoxia; limiting attenuation in portal vein blood flow |
| describe the mechanisms involved in halothane hepatitis | diminished portal blood flow; increased reductive metabolism |
| what are the 2 forms of halothane hepatitis | mild halothane hepatitis, fulminant hepatic failure |
| Increase in MAC coefficient = | decr in potency and OG partition coefficient |
| Reversal of anesthetic effect can be achieved with the _____ | application of pressure restoring membrane shape. |
| how do blood/gas coefficients affect emergence | insoluble agents facilitate emergence while soluble agents slow it |
| how do oil/gas coefficients affect emergence | anesthetic agents with a high oil/gas partition will slow the emergence from anesthesia, especially in tissues with a poor blood supply (muscle/fat) |
| for time constants, and ___ change toward equilibrium is utilized for calculations as opposed to 50% in T1/2 used in IV pharmacokinetics | 63% |
| how many time constants are required to achieve a 98% change of volume | 4 63, (63 + 23) = 86, (86 + 9) = 95, (95 + 3) = 98 |
| Each subsequent increment of ____minutes represents a 63% change of the remaining volume towards equilibrium | 1-2 |
| time constant for brain = | 100 - 200 / 100 = 1-2 mins |
Created by:
rwilson
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