Term
| Whats the problems with racemic drugs? |
|
Definition
| They can have different pharmacological effects. They can differ in rates of absorption, metabolism, excretion and affinity for receptor sites. |
|
|
Term
| Why is it important to balance the anesthetic agents we use |
|
Definition
| Using multiple drugs during a case will allow us safely administer drugs without over dosing one particular drug or having too much side effects from one drug over another. |
|
|
Term
| the autonomic nervous system consists of what three things? |
|
Definition
| SNS/PNS/ and Enteric nervous systems. |
|
|
Term
| whats the difference between the visceral motor system and somatic nervous system |
|
Definition
| visceral motor system refers to all effectors of the autonomic nervous system such as SNS/PNS/Enteric nervous system. While the somatic motor system deals only with muscles. |
|
|
Term
| This nervous system controls the involuntary muscles |
|
Definition
|
|
Term
|
Definition
| a cluster of nerve bodies in the PERIPHERAL nervous system. Area filled with large amount of synapses. |
|
|
Term
| the upper airways refer to what parts of the body |
|
Definition
|
|
Term
| what is the difference between 1st order and 2nd order efferent neurons |
|
Definition
| 1st order always begin in brain or spinal cord. They are myelinated while 2nd order neurons are in the peripheral and are unmyelinated. They terminate with effector organ. |
|
|
Term
| difference between sympathetic and parasympathetic 2nd order efferent neurons |
|
Definition
| sympathetic 2nd order neurons release norepi or epi while parasympathetic 2nd order neurons always release acetylcholine. |
|
|
Term
| what type of neurotransmitter is released by 1st order neurons? what receptor does it bind to? Is it the same for PNS and SNS? |
|
Definition
| all first order neurons in PNS and SNS release acetylcholine and this NT binds to nicotinic receptors. |
|
|
Term
| What type of receptor does the NT released by the 2nd order neurons in the parasympathetic bind to? |
|
Definition
| parasympathetic 2nd order effector neurons bind to muscarinic receptors on their target cell. |
|
|
Term
| the exception to 2nd order effector neurons in sympathetic nervous system to releasing the NT Norepi is when sympathetic innervates what part of the body and does so with acetylcholine? |
|
Definition
| Sympathetic normally always releases Norepi from its 2nd order neuron. One exception is when it innervates sweat glands and vessels and releases acetylcholine instead that acts on a muscarinic receptor. |
|
|
Term
| the effector ganglion of the _______ is closest to the spinal cord? |
|
Definition
| sympathetic ganglion lies in "chains" closest to the spinal cord MOST OF THE TIME |
|
|
Term
| The effector ganglion of the _____ nervous system is closest to its target cell most of the time. |
|
Definition
| Parasympathetic most often has its ganglion closest to the effector organ. |
|
|
Term
| muscarinic receptors are also known as ___ Receptors in the peripheral system |
|
Definition
|
|
Term
| which nervous system has long post ganglionic fibers |
|
Definition
|
|
Term
| What nervous system only innervates visceral structures serviced by cranial nerves or lying within the abdominopelvic cavity |
|
Definition
|
|
Term
| ____ nervous system Effects associated with maintenance of function |
|
Definition
|
|
Term
| saliva production by the ___ nervous systme |
|
Definition
| parasympathetic. (para does food, so you need saliva for food digestion.) |
|
|
Term
| urinary retention caused by ___ nervous system |
|
Definition
| sympathetic nervous system. Conserve water for fight or flight!! |
|
|
Term
| The effector ganglion of the _____ nervous system is closest to its target cell most of the time. |
|
Definition
| Parasympathetic most often has its ganglion closest to the effector organ. |
|
|
Term
| ____ nervous system Effects associated with maintenance of function |
|
Definition
|
|
Term
| saliva production by the ___ nervous systme |
|
Definition
| parasympathetic. (para does food, so you need saliva for food digestion.) |
|
|
Term
| post ganglionic cholinergic neurons are from the _____ nervous system |
|
Definition
| parasympathetic nervous system |
|
|
Term
| predominant para tone is found where? |
|
Definition
| iris, salivary glands, SA node, ciliary muscles, bladder, gut, uterus |
|
|
Term
| anti-parasympathetic drug is? |
|
Definition
|
|
Term
| are babies or adults primarily driven by parasympathetic NS? What happens under stress? |
|
Definition
| babies are primarily para despite having high heart rates. what this means is that a little stress like intubation will activate this para response and cause profound bradycardia that is life threatening. The intervention? Atropine!! |
|
|
Term
| what are autonomic nerve plexuses |
|
Definition
| area where sympathetic and parasympathetic nerve fibers intermix. Form nerve bundles. |
|
|
Term
| To treat the reflexes of bronchospasms and laryngeal spasms from intubation we would given ____ for bronchospasms and _______ for laryngeal spasms. |
|
Definition
| Bronchospasms can be treated with opioids to block the sensory/pain pathway. Bronchial muscles are smooth muscle so paralytics will not work. To treat laryngeal spasms you can give paralytics. |
|
|
Term
| the central command for the ANS is found in the? |
|
Definition
|
|
Term
| cardiac and vasomotor centers are found in the? |
|
Definition
|
|
Term
| What is autonomic dysreflexia? Whats another name for it? What are its sx? What causes it? Most common cause? |
|
Definition
| Automic dysreflexia also known as autonomic hyperreflexia is an emergency. It most often occurs in spinal cord injuries at or above T6. Its caused by overstimulation of the autonomic nervous system (involuntary nervous system). It presents with paroxsymal HTN, sweats above the injury, bradycardia, flushing of the skin and headaches. It is caused by stimuli via the afferent pathways from below the spinal cord injury level. Most common afferent signal is from full bladders or constipation. So signals can't get to the brain beacuse they get stopped at the level of injury, that signal gets spread out over the spinal cord and causes a reflexia and propabagates SNS responses to constrict below injury which then makes hte heart beat slower. Above injury body compensates and vasodilates due to the higher SVR on the heart. |
|
|
Term
| are the number of beta receptors and epi reduced in older adults? |
|
Definition
| NOOOOOOO. The only thing that changes is that these receptors get "down-regulated". That means they won't respond as strongly when NE/EPI binds to them because there are so many NT already in circulation they develop a tolerance. |
|
|
Term
| Why do older adults have a diffcult time regulating their temperature as well? |
|
Definition
| Older adults have less muscle mass and less energy stores to sustain efficent muscle contractions (shivering) to generate heat efficently when cold. They also do not vasoconstrict their peripheral vasculature as well to conserve heat when its cold out. |
|
|
Term
| Explain what diabetic neuropathy is and how it effects the body and things such as hemodynamics, pain, thermo regulation and gastroparesis. |
|
Definition
| Diabetic neuropathy occurs with diabetics with poor glucose managmenet over long periods of time. It causes microvascular injury to nerves in the peripheral which service such things as motor neurons, pain fibers and the autonomic nervous system. Therefore it effects nearly the entire body. Sx develop depending on what nerves are effected. Effected nerves mess up adequate microvascular blood supply to the various areas of the body while at the same time other areas blood supply is screwed directly by diabetics which further causes more nerves to be damaged. |
|
|
Term
| A class of drugs that mimic name norepi/epi are called sympatho____ |
|
Definition
|
|
Term
| difference between sympatholytic and sympathomimetic |
|
Definition
| sympatholytic is a drug which antagonizes the receptors for epi or norepi while sympathomimetic is an agonist drug for aderenergic receptors. |
|
|
Term
| drugs for myathenis gravis work by? |
|
Definition
| decreasing the effectiveness of aceytlcholinesterase. Less of that means more acetylcholine in the synapses to activate the receptors on the postsynaptic membrane. |
|
|
Term
| the two types of cholinergic receptors are |
|
Definition
1. nicotinic
2. muscarinic |
|
|
Term
| glutamate receptors are for excitatory or inhibitor |
|
Definition
|
|
Term
| what refers to the relative safety window for a drug where you're between where the dose is therapeutic and toxic |
|
Definition
|
|
Term
| do anesthetic drugs have a large therpeutic index or small therapeutic index |
|
Definition
| Small therapeutic index which means they are very high risk |
|
|
Term
| whats the difference between pharmodynamics and pharmokinetics?> |
|
Definition
| pharmodynamics is biochemical and physiologic effects of drugs. While pharmokinetic is a targeting of drugs to specific applications and focusing on proven therapeutic windows.Pharmacokinetics describes the drug concentration-time courses in body fluids resulting from administration of a certain drug dose, pharmacodynamics the observed effect resulting from a certain drug concentration. |
|
|
Term
| Is drug binding equivalent to drug effect? |
|
Definition
|
|
Term
| the propensity of the drug-receptor complex to elicit a physiological effect is govenrened by a characterisitic constant known as? |
|
Definition
|
|
Term
| Drug potency is comprised of what two factors? What's the percentage it also reflects? |
|
Definition
| Drug potency is derived from drug efficacy and affinity. It is meausred as the effective concentration of a drug to give 50% maximal effect. |
|
|
Term
| If a drug has receptor affinity but no efficacy it is known as? |
|
Definition
| an antagonist. So it can bind (affinity) but it does not elicit a physiological effect (Efficacy) from the binding. |
|
|
Term
| what are the four factors that contribute to pharmokinetics |
|
Definition
1. absorption
2. distribution
3. metabolism
4. excretion |
|
|
Term
|
Definition
|
|
Term
| Describe the conceptual framework for "surfing" and the PK-PD principles. |
|
Definition
| As an anesthesia provider we are tasked with maintaining safe drug concentrations in patients with an intended goal of keeping patients asleep. We keep people asleep but not deeply asleep so that we can safely recover someone in short notice. ITs a delicate balance that can be thought of like surfing a wave. We aim to be on the steep slope of the wave or crest. This way with little changes in concentration we can significantly reduce the effect of anesthesia. The approach of administering anesthesia can be described in three ways. One approach is pharmodynamics (PD) PD focuses on the effect of the drug. We care less about concentration and just want to see that the drug is working. So we give propofol and watch the BIS monitor to see a sleepy EEG. or give a paralytic and see 2/4 on the TOF. Perfect. The next approach is Pharmokinetics. (PK). In PK we apply some science and base our anesthesia administration off of known concentration-effect relationships. We titrate drugs to known therapeutic windows. Example is giving an agent specific vaporizer. A third approach is known as the "pharmaceutic approach". This approach is like winging it while in the OR and knowing that you can do this because all our drugs are short acting so you can always back down if you need to. You're not being accurate here or as much precision because you have some lee-way with the types of drugs your giving. |
|
|
Term
| This drug administration approach focuses on concentration-effect relationships of anesthesia drugs |
|
Definition
|
|
Term
|
Definition
Biophase is also known as the plasma-effect site relationship. Drugs exert their biological effect at the “biophase,” also called the “effect site,” which is the immediate milieu where the drug acts upon the body, including membranes, receptors, and enzymes. The biophase can be thought of like its own compartment. A drug enters the central compartment (blood supply and organs) then takes time to travel to the peripheral (everything else like fat tissue, skin ect) and now the biophase compartment (the peripheral too, but the peripheral part that specifically pertains to what the drug is suppose to work on). Although it is not possible to measure drug concentration in the biophase (think about it how do you measure how much drug is binding to receptors in brain tissue without killing someone) , using rapid measures of drug effect we can characterize the time course of drug effect. PK is drug concentration in blood while pd is drug effect seen in BP, awareness and vitals.
|
|
|
Term
|
Definition
| drug concentration in plasma. |
|
|
Term
| What characteristic of the drug will effect its concentration in the plasma? |
|
Definition
| How much it has a tendency to bind to proteins. More protein bounded drugs will have lower plasma concentrations. |
|
|
Term
| Describe ionization and drugs |
|
Definition
| Drugs are usually in a mixture of 50/50 for ionized and non-ionized. IF they are ionized they are water soluble and usually too big to enter a cell. Non-ionized drugs are lipid soluble and can pass the cell membrane. |
|
|
Term
| When the pH and Pka are similar what is the % of drug that is ionized |
|
Definition
|
|
Term
| a drug is more ionized when the pH is greater or less than the pKa? Why? |
|
Definition
| if the pH is greater than the pKa then it is more ionized. Proton donation |
|
|
Term
| describe the central compartment |
|
Definition
| it contains 75% of the blood volume but only comprises 10% of the total mass. |
|
|
Term
| back end kinetics refers to? |
|
Definition
| The time it takes for a drug to go down in 50% |
|
|
Term
| What is the difference between the alpha and beta phase in drug concentrations |
|
Definition
Multiphasic absorption : Drugs injected intravenously are removed from the plasma through two primary mechanisms: (1) Distribution to body tissues and (2) metabolism + excretion of the drugs. The resulting decrease of the drug's plasma concentration follows a biphasic[disambiguation needed] pattern (see figure).
[image]
Plasma drug concentration vs time after an IV dose
- Alpha phase: An initial phase of rapid decrease in plasma concentration. The decrease is primarily attributed to drug distribution from the central compartment (circulation) into the peripheral compartments (body tissues). This phase ends when a pseudo-equilibrium of drug concentration is established between the central and peripheral compartments.
- Beta phase: A phase of gradual decrease in plasma concentration after the alpha phase. The decrease is primarily attributed to drug metabolism and excretion.[7]
|
|
|
Term
| elimination half time refers to |
|
Definition
| time it takes for drug concentration to be reduced by 50% |
|
|
Term
| What is the elimination half life? What is the equation for it? |
|
Definition
T 1/2B= 0.693 x Vd / Cl (Memorize this constant) elimination Half life of a drug is directly proportional to the volume of the distribution and inversely proportional to the clearance.Half life = 0.693 x Vd/ total body clearance
Alpha half life = plasma / distribution half life
Beta half life = tissue / elimination half life
Most of the drugs have alpha half life and remain in the plasma. Drugs having beta half life have two half lives, one in the plasma and one in the tissues. They are highly distributed drugs. Their total time of elimination is more.
|
|
|
Term
| how many elmination half lives are needed to remove a drug from the body |
|
Definition
|
|
Term
| elimination half time is proportional or inversely proportional to clearance? |
|
Definition
| inversely proportional to clearance. |
|
|
Term
| the elimination rate of drugs by the kidney are proportional to? |
|
Definition
| the drug concentration. More drug then the more the kidneys will work to eliminate it. |
|
|
Term
| temp and pH elmination pathways are known as |
|
Definition
|
|
Term
| reaction catalyzed by enzymes in blood and tissue to elminate a drug are known as |
|
Definition
| ester hydrolysis reactions |
|
|
Term
| In order to maintain a steady plasma concentration the infusion rate must |
|
Definition
| be equal to the rate of drug clearance |
|
|
Term
| describe the difference between the two phases of metabolism. |
|
Definition
| Phase 1 prepares drugs for phase II. During phase I the body uncovers a drugs useful functional group or adds a functional group so that in phase II enzymes will recognize it and start the next step. During phase II body links the exposed functional groups with polar molecules or enzymes to be eliminated. |
|
|
Term
| Which phase of metabolism is known as the functional phase |
|
Definition
|
|
Term
| which phase of metabolism is known as the conjugation phase? |
|
Definition
|
|
Term
| most quantitatively abundant CYP in the liver |
|
Definition
|
|
Term
| Glucuronosyltransferase used in which phase of metabolism |
|
Definition
| phase two. Matches this enzyme with functional groups from phase one. |
|
|
Term
| most common inherited risk factor for thrombus and is found in approximately 5% of the population |
|
Definition
| Factor V Leiden. These patients have a nine-fold increase for a thrombus |
|
|
Term
| The most common inherited bleeding DISEASE is? |
|
Definition
|
|
Term
| Why do we need von willebrand factor |
|
Definition
| VWF is always circulating in the blood and is also released from granulation of platlets. WVF adheres to damaged sub-endothelium collagen. After it binds here it acts as a receptor for platelets to bind to since platelets have a glycoprotein on their surface which fits perfectly with WVF. |
|
|
Term
| What are two treatment modalities for someone with low VWF? |
|
Definition
| Give DDAVP or cryoprecipitate |
|
|
Term
| how does splenomegaly contribute to decreasing platelet count |
|
Definition
| Splenomegaly accelerates platelet clearance. |
|
|
Term
| hemophilia A is deficiency in what factor |
|
Definition
| deficiency in factor VIII (hemoph III a A ) |
|
|
Term
| coagulation factors and plasminogen activators are cleared by what organ? |
|
Definition
| liver. So liver failure patients typically have a abnormal regulation of homeostasis. They can be hypercoagulopathic or at risk for bleeding. |
|
|
Term
| IF the wrong type of blood is given to a patient then what part of the immune system is activated? |
|
Definition
|
|
Term
| platelets are? and made from? |
|
Definition
| platelets are granulated cells (no nucleus) made from bone marrow megakaryocytes. |
|
|
Term
| What are the two types of glycoproteins found on the surface of platelets |
|
Definition
| glycoproteins IIa and IIb/IIIa |
|
|
Term
| Does FFP have to be compatible with the receipts ABO type? |
|
Definition
|
|
Term
| Does Platelets have to be compatible with the receipts ABO Type? |
|
Definition
|
|
Term
| Albumin is made where? What type of activity does it have with hemodynamics? |
|
Definition
| it is made in the liver and exerts an oncotic pressure (colloid osmotic pressure) |
|
|
Term
| anti-coagulants decrease formation of? |
|
Definition
|
|
Term
| what are the four steps to platelet plug formation |
|
Definition
1. adhesion
2. activation
3. Aggregation
4. Fibrin production |
|
|
Term
| The most powerful platelet activator is? |
|
Definition
|
|
Term
| tissue factor is also known as ___ and ____ |
|
Definition
| Factor III and thromboplastin |
|
|
Term
| Tissue factor comes from? What does it do? |
|
Definition
| It is released from damaged sub-endothelial tissue or from leukocytes. It can bind to activate Factor VII. |
|
|
Term
| Is tissue factor and factor VII part of the intrinsic or extrinsic pathway |
|
Definition
| Extrinsic PATHWAY.. Tissue factor + Ca ---> Factor VII ---> Factor X |
|
|
Term
| for platelet aggregation to occur they need two things.... |
|
Definition
|
|
Term
| the average life of a platelet is? |
|
Definition
|
|
Term
| extra platelets are stored in the? What causes them to be released |
|
Definition
| spleen. Sympathetic stimulation and contraction of the spleen releases reserves of platelets |
|
|
Term
| excess and old platelets are destroyed where |
|
Definition
| destroyed by phagocytosis in spleen and liver |
|
|
Term
| what are the two granules located on the platelets that are released after they are activated and change in morphology? What are in each granule. (OR SAC) |
|
Definition
1. Dense Granules (SAC-Serotonin, ADP, Ca)
2. Alpha Granules (VWF, fibrinogen, Factor VIII) |
|
|
Term
| VWF binds to glycoprotein receptors __ and ___ on the platelet. This is important because we make drugs that target these same platelet receptors to prevent them from sticking to VWF. |
|
Definition
|
|
Term
| platelets can bind to each other during primary homeostasis by ____ which acts like a glue. |
|
Definition
| Fibrinogen. NOT FIBRIN!!! Fibrin is secondary homeostasis. The unactivated version of fibrin is fibrinogen. IT is for gluing platelets together. |
|
|
Term
| What glycoprotein receptor on platelets is the site for fibrinogen gluing multiple platelets together |
|
Definition
|
|
Term
| The SOLE initiator of thrombin (original start to all the cascades) is? |
|
Definition
|
|
Term
| NSAIDS and ASA inhibit platelet aggregation by inhibiting what? |
|
Definition
| They inhibit thromboxane A2 which is normally released from platelet granules. Thromboxane A2 is used to activate and attract more platelets to continue aggregation. IT is also needed to expose the glycoprotein receptors so that fibrinogen can glue platelets together |
|
|
Term
| Fibrin stabilizing factor is factor ____ |
|
Definition
|
|
Term
| a deficit in extrinsic factors will result in abnormal PT, PTT or INR? |
|
Definition
| PT is prolonged. PTT is normal. |
|
|
Term
| a deficit in intrinsic factors will result in abnormal PT, PTT, or INR |
|
Definition
|
|
Term
| Coumadin effects to ____ pathway |
|
Definition
| extrinsic pathway. (Coumadin is given orally from external!) |
|
|
Term
| Heparin effects the ___ pathway |
|
Definition
| Intrinsic pathway (Heparin IS DIRECT IV internal!!) |
|
|
Term
| What catalyzes prothrombin into thrombin? |
|
Definition
|
|
Term
| Fibrin is dissolved by plasmin and becomes fibrin split products that are cleared by the ___ and ___ |
|
Definition
| liver and kidney. If liver disease and kidney disease is present then patient at risk for accumulation of split products and that means BLEEDING. |
|
|
Term
| tPa is made by? stimulated by? to bind to? |
|
Definition
| tPa is made by the endothelium and becomes activated from thrombin (yes thrombin not only activates fibrin but also activates its enemy). tPa binds to fibrin to inactivate it thereby break up clots. |
|
|
Term
| streptokinase is made from? |
|
Definition
| made from beta hemolytic streptococci. |
|
|
Term
| List the final common pathway of coagulation |
|
Definition
| Factor Xa + Factor V ---> changes antithrombin II to thrombin IIa ---> Thrombin IIa changes Fibrinogen I to Fibrin Ia ---> Fibrin clot begins and Factor VIII comes in to stabilize. |
|
|
Term
| the drug heparin works by? |
|
Definition
| increasing the affinity of antithrombin by 1000 fold. |
|
|
Term
| Name four natural endogenous anti-coagulation substances |
|
Definition
1. anti-thrombin
2. Protein C
3. Nitric Oxide and Prostacylcin
4. Heparin |
|
|
Term
| anti-thrombin is made in? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| anti-thrombin binds to thrombin and factor? |
|
Definition
|
|
Term
| the half life of heparin is? |
|
Definition
| 1-2 hours. without presence of renal or liver disease |
|
|
Term
| if you have a deficiency of anti-thrombin will helparin work? |
|
Definition
| Heparin does not work independently. It only makes anti-thrombin work more efficently. |
|
|
Term
| Does heparin cross the placenta? |
|
Definition
| NOOOOOOOO. So it can be given to pregnant patients. |
|
|
Term
| low molecular weight heparin inhibits? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| why do anesthesia people not like giving LMWH? |
|
Definition
| B/C its associated with hematomas at neuroaxial blocks. |
|
|
Term
| Heparin works on the ________ pathway |
|
Definition
|
|
Term
| what kind of patients should not given UF Heparin |
|
Definition
| eye, brain or spinal cord surgery patients. |
|
|
Term
| HITT can be caused by ___ and or ____ |
|
Definition
|
|
Term
|
Definition
| Heparin induced thormbocytopenia with thormbosis. So you have a drop in your platelet with a concurring event of thrombosis in your body. This is mediated by an immune response attacking your own platelets via IgG antibodies. This complex of antibody/platelet/heparin propagates more destruction of platelets and loss of clotting factors. |
|
|
Term
|
Definition
| 30-50% reduction in platelet count and plt count <150,000. and in presence of either heparin or LMWH |
|
|
Term
| Describe how protamine works |
|
Definition
| Protamine works by binding to heparin and causing a neutralization reaction. Protamine is a positively charged cation. The result of this is a formation of a salt. |
|
|
Term
| Describe the dosing for protamine |
|
Definition
| 0.5mg for every 100units of heparin in the last 4 hours. Administer over 20 minutes but no more than 50mg/10min. |
|
|
Term
| Side effects and risks of protamine administration |
|
Definition
| The biggest risk is for pulmonary edema and cardiovascular collapse and right ventricle failure caused by IgG/complement immune reaction. Anaphylaxis and histamine may also be triggered by IgE hypersensitive antibodies. Pretreat with benadryl. People at risk are those on NPH insulin, previous protamine exposure, fish allergeies (protamine comes from fish sperm) and vasectomies. |
|
|
Term
| Arixtra is anti____factor. It is an heparin alternative. |
|
Definition
| Anti - Xa factor. Does not inhibit thrombin. Not reversible. Long half life. Renal clearance. No for renal disease. |
|
|
Term
| Rivaroxaban (xarelto) directly inhibits? |
|
Definition
| Xa. It is an alternative to coumadin for Afib. |
|
|
Term
| Describe Dabigatran (Pradaxa) |
|
Definition
| A pro-drug. Directly inhibits thrombin. Very predictable drug. Metabolized by renal. Good alternative for coumadin for afib or stents. |
|
|
Term
| Hirudin comes from? Good for? |
|
Definition
| comes from leech saliva. Directly inhibits thormbin. Good for pt with HIT or HITTs. Not reversible. |
|
|
Term
|
Definition
| Vit K which is needed for multiple clotting factors. It also inhibits protein C and S. |
|
|
Term
| Warfarin is metabolized by? |
|
Definition
|
|
Term
| Warfarin you should stop therapy for surgery how much in advance? |
|
Definition
|
|
Term
| Does warfarin cross the placenta? |
|
Definition
|
|
Term
|
Definition
| inhibiting COX. Which means inhibiting platelet aggregation. |
|
|
Term
| When should you stop ASA before a procedure? |
|
Definition
| 1 week prior to surgery because it lasts the life of the platelet which is around 7-9 days. |
|
|
Term
| Pruinergic receptors do what with platelets |
|
Definition
| They are receptors on platelets that are binding sites for ADP. When stimulated they begin to aggregate and activate. |
|
|
Term
| Plavix is a thienoypyridine which means it works by? |
|
Definition
| Selectively inhibits ADP induced platelet aggregation. Lasts the life of the platelet. So need to stop one week prior to surgery. |
|
|
Term
| Name two glycoprotein IIb/IIIa receptor inhibitors |
|
Definition
| Integrilin, aggrastat and abciximab |
|
|
Term
| Thrombolitic drugs work by? |
|
Definition
| promoting plasmin mediated break down of fibrin and fibrinogen |
|
|
Term
| side effects from thrombolytic drugs |
|
Definition
| reperfusion arrhythmias, hypotension. allergic reaction |
|
|
Term
| what is the drug that is used during cardiac or liver surgeries to prevent breakdown of fibrin |
|
Definition
|
|
Term
| How does desmopressin work in regard to homeostasis and the kidneys. |
|
Definition
| Desmopressin is the synthetic version of vasopressin. It beinds to V2 receptors which are located in the renal collecting duct and peripheral endothelium. When it binds to V2 receptors of the renal collecting ducts it adds more aquaporins to help reabsorb more water. (Anti-diuretic). When it binds to V2 receptors in the endothelial walls of blood vessels it promotes release of von Willibrand Factors. It can help treat mild hemophilia, type 1 vonWillibrand disease, off set side effects of anti-platelet drugs |
|
|
Term
| What is the syndrome for when a person aspirates gastric contents |
|
Definition
|
|
Term
| The highest risk for aspiration is during what times of anesthesia administration |
|
Definition
|
|
Term
| List risk factors for patients who will get N/V |
|
Definition
| Females, non-smokers, menstration, DM, pregnancy 6-8 weeks, anxiety, volatile agents and NO2, |
|
|
Term
| why does anxiety cause N/V |
|
Definition
| stress hormones increases gastric contents and air swallowing. |
|
|
Term
| What age group is more at risk for nausea and vomiting post op |
|
Definition
|
|
Term
| The vomiting center receives input from what four areas |
|
Definition
1. chemoreceptor trigger zone
2. GI tract
3. Vestibular system
4. cerebral cortex |
|
|
Term
| The vomiting center is located in? |
|
Definition
|
|
Term
| The chemotactic trigger zone is located in the? |
|
Definition
| medulla at the floor of the 4th ventricle |
|
|
Term
| What are the 6x agonists that cause N/V |
|
Definition
1. dopamine (d2)
2. serotonin (5HT3)
3. Histamine (H1)
4. Muscarinic
5. Opioid
6. Neurokinin (NK1) |
|
|
Term
| how does the chemotactic trigger zone communicate with the vomiting center? |
|
Definition
| via D2 and 5HT3 receptors |
|
|
Term
| How do enterochromaffin cells in the GI tract communicate to vomiting center |
|
Definition
| They actually communicate via Serotonin which then causes an AP up the vagus nerve to the chemostatic trigger zone which then sends D2 and 5H3 Neuro transmitters to vomitus center. |
|
|
Term
| How does the vestibular center communicate with the vomitus center |
|
Definition
| they communicate via H1 and muscarinic receptors |
|
|
Term
| How does the cerebral cortex communicate with the vomitus center? |
|
Definition
| via direct neuronal links |
|
|
Term
| How does the vestibular center communicate with the vomitus center |
|
Definition
| they communicate via H1 and muscarinic receptors |
|
|
Term
| How does the cerebral cortex communicate with the vomitus center? |
|
Definition
| via direct neuronal links |
|
|
Term
| benzos are metabolized by? |
|
Definition
|
|
Term
| Can versed by used as an induction agent? |
|
Definition
|
|
Term
| What does versed do to cerebral metabolic oxygen and cerebral blood flow?> |
|
Definition
| it decreases cerebral metabolic oxygen and decrease cerebral blood flow |
|
|
Term
| Why do we avoid using benzos with people in 1st trimester? |
|
Definition
| increase risk of cleft lip and palate. |
|
|
Term
| What precautions would you take with any pregnant women and benzos? |
|
Definition
| Benzo's will cross the placenta and can negatively effect the baby. So wait until the very last minute the lady is on the table and drapped. |
|
|
Term
| what drug do you give to reverse benzos? how does it work? |
|
Definition
| Give flumazenil. It competes with the binding sites for benzos. IT is a competitive antagonists. |
|
|
Term
| How do you dose flumazenil? |
|
Definition
| give in increments. Start with 0.2 mg and give in 1-2 minute intervals. Total dose is 1mg. |
|
|
Term
| do elderly patients tolerate versed, ativan or valium better? |
|
Definition
|
|
Term
| activation of gaba receptors causes what to the cell membrane |
|
Definition
|
|
Term
| what ion is related to gaba receptors |
|
Definition
|
|
Term
| what drug acts on NMDA receptors |
|
Definition
|
|
Term
| What Neuro transmitter does ketamine block? |
|
Definition
| blocks glutamate from binding to NMDA receptors. |
|
|
Term
| methohexital can causes what type of side effect? |
|
Definition
| convulsive activity. Can cause myoclonus. Not a real seizure. |
|
|
Term
| the most important characteristic of barbiturates that decide how well they will distribute is? |
|
Definition
|
|
Term
| most protein bounded barbiturate is |
|
Definition
|
|
Term
| if a patient is very acidotic will there be more or less ionized drug of pentothal |
|
Definition
| there will be less ionized drug and therefore more drug available to cross and have a stronger effect. Since pentothal is in aqueus solution it has a pH of 10.0. Therefore when it enter the blood (pH 7.40) it will protonate. |
|
|
Term
| onset of action for pentothal |
|
Definition
|
|
Term
| if a patient who has hypovolumeia how should you administer a barbiturate |
|
Definition
|
|
Term
| Whats the side effect of barbiturates on the liver after 2-7 days |
|
Definition
| the liver becomes stimulated by increase barbiturates and it increases the number of microsomal enzyme activity and induction. This results in increase metabolism of all drugs for a period of 30 days. |
|
|
Term
| what is the best sedation for cerebral injuries? |
|
Definition
| barbiturates because they decrease cerebral oxygen requirements and decrease cerebral blood flow. Has cerebral protective qualities. |
|
|
Term
| barbiturates can trigger porphyria which is? |
|
Definition
| a metabolic disease from defects in enzymes that synthesize hemoglobin. Barbiturates can induce acute symptoms of the disease which is abd pain, mental status changes, dark urine and vomiting. |
|
|
Term
| how do you treat porphyria |
|
Definition
| iv glucose and heme infusion. opioids for pain sx managment. phenothiazine for N/V and small dose benzo for insomnia |
|
|
Term
| KETAMINE causes a dissociative anestehsia which is a disconnect from? |
|
Definition
| disconnect from thalamocortical and limbic systems |
|
|
Term
| to avoid emergence delirium given? |
|
Definition
|
|
Term
| Do inhaled anesthetics have more effect on AP or NT at the synapses? |
|
Definition
| NT at the synapses. Either pre or post. |
|
|
Term
| Inhaled anethetics increase NT's ___ and ___ |
|
Definition
| increase glycine and gaba |
|
|
Term
| when you inhibit nmda it causes |
|
Definition
|
|
Term
| when you inhibit nicotinic receptors in the brain what happens |
|
Definition
|
|
Term
| what receptors will inhibit noxious stimuli |
|
Definition
|
|
Term
| What two things can effect NMDA receptors |
|
Definition
| Nitric oxide and ketamine |
|
|
Term
| during stage II of general anesthesia what do you worry most about? |
|
Definition
| pt is in their delerium or excitation stage. It is a dangerous part of anesthesia. Pt's autonomic system is in an uncontrolled flux. Any stimulation will causes tachy/HTN/rigidity and crazy eyes. The biggest worry is larygneal spasms if you try and intubate!! |
|
|
Term
| when would you see stage II for general anesthesia? during propofol administration or gas? |
|
Definition
| GAS!!! propofol pushes you straight to level III. |
|
|
Term
| How would you know you are in stage III of general anesthesia? |
|
Definition
| pupils will be constricted. No abnormal autonomic responses and respirations are regular. |
|
|
Term
| What stage of anesthesia do we want? |
|
Definition
| Stage III is general anesthesia |
|
|
Term
| The most commond type of receptor in the body that reacts with drugs are? |
|
Definition
|
|
Term
| Describe a typical inotropic receptor |
|
Definition
| An inotropic receptor is made up of 5 subunits which are sites of binding for anesthetic drugs. They involve fast synaptic trasnmission between cells. |
|
|
Term
| What is signal transduction? |
|
Definition
| Describes how a receptor translates input from outside a cell to inside a cell. Its seen with transmembrane receptors like g-proteins. The message is carried to second messangers which are actually in the cell cytosol. |
|
|
Term
| what is the difference between upregulation and down regulation with receptors in relation to how they react |
|
Definition
IF you have long term use of a certain drug like a beta blocker then you have a desensitization of the receptor and that results in up-regulation which is the body adding more receptors to the cell membrane to compensate for extra drugs in the body because the body does not want to be BLOCKED it wants to perform its job and produce beta responses. So now if you reverse this with a drug that is an agonist and have long term use of agonist in the body then the body wants to down regulate or otherwise decrease the number of receptors so that those chronic high levels of agonist drug will not be as effective.
Down Regulate = decrease # of receptors
Up Regulate = Increase # of receptors. |
|
|
Term
| Whats the difference between a drug binding at orthosteric and allosteric sites |
|
Definition
| IF a drug binds to same site as the intended neurotransmitter then its binding to the orthosteric site. (ortho = right, correct). While if the drug binds to a site on a receptor other than the normal site for the NT then its binding to the allosteric site. |
|
|
Term
| What is the difference between efficacy and affinity of a drug |
|
Definition
| Affinity refers to a drugs liklihood to bind to a receptor while efficacy is what refers to as the degree of reaction/response a drug will have after it binds. |
|
|
Term
|
Definition
| Is a substance which is a mirror image of itself but not superimposable. Each drug will rotate in different directions. When you have a 50/50 equal concentration of both enantiomers then you have a racemic mixture. This cancels out the optical activity. |
|
|
Term
| What is the difference between efficacy and potency? |
|
Definition
| Efficacy is the ability of a drug to illicit an effect. If it illicit's a strong response it has a strong efficacy and therefore the drug is a "full agonist". If it illicit's a response but its not the receptors full potential then that drug is called a "partial agonist" |
|
|
Term
| Why is our goal as clinicians to strive for balanced anesthesia? |
|
Definition
| We want balance anesthesia because we understand that different drugs have different modes of actions and side effects. By taking the best and worse qualities of each during specific cases we can minimize the toxicity and adverse reactions and therefore improve patient outcomes. |
|
|
Term
| What's the different between using two drugs as additives or two other drugs that are used in a synergistic way? |
|
Definition
| If two drugs are used as "additives" it just means that you need half the dose of each drug to get the intended result. While synergistic drug therapy uses less than half of the expected dose of each drug to get the desired effect. The reason why synergistic drugs work so much more effectively is because they complement each other therefore making it easier to get your desired outcome with less of a drug. |
|
|
Term
|
Definition
| Leiden disease is the most commonly inherited risk factor for thrombus. Individuals are 9x more likely to have hypercoagulopathic states. |
|
|
Term
| The most common site for production of coagulation factors is? |
|
Definition
|
|
Term
| Describe the common pathway |
|
Definition
| Common pathway when activated starts with Factor X. Factor X activates Prothrombinase which catalzyes the change of prothrombin to thrombin. Thrombin then activates fibrinogen to change to fibrin. |
|
|
Term
| What will Jehova's witnesses accept for products during surgery |
|
Definition
| They will not accept primary components. However they will accept albumin, Factor VII and IX. |
|
|
Term
| whats the difference between drugs that are anti-coagulant and fibrinolytic agents |
|
Definition
| Anti-coagulant drugs work early in the cascade by preventing the formation of a fibrin layer (Prevent secondary homeostasis) while fibrinolytic agents are late to the game and work to break down fibrin that's already there. |
|
|
Term
| What is the difference between efficacy and potency? |
|
Definition
| Efficacy is the ability of a drug to illicit an effect. If it illicit's a strong response it has a strong efficacy and therefore the drug is a "full agonist". If it illicit's a response but its not the receptors full potential then that drug is called a "partial agonist" |
|
|
Term
| Why is our goal as clinicians to strive for balanced anesthesia? |
|
Definition
| We want balance anesthesia because we understand that different drugs have different modes of actions and side effects. By taking the best and worse qualities of each during specific cases we can minimize the toxicity and adverse reactions and therefore improve patient outcomes. |
|
|
Term
| What's the different between using two drugs as additives or two other drugs that are used in a synergistic way? |
|
Definition
| If two drugs are used as "additives" it just means that you need half the dose of each drug to get the intended result. While synergistic drug therapy uses less than half of the expected dose of each drug to get the desired effect. The reason why synergistic drugs work so much more effectively is because they complement each other therefore making it easier to get your desired outcome with less of a drug. |
|
|
Term
|
Definition
| Leiden disease is the most commonly inherited risk factor for thrombus. Individuals are 9x more likely to have hypercoagulopathic states. |
|
|
Term
| The most common site for production of coagulation factors is? |
|
Definition
|
|
Term
| Describe the common pathway |
|
Definition
| Common pathway when activated starts with Factor X. Factor X activates Prothrombinase which catalzyes the change of prothrombin to thrombin. Thrombin then activates fibrinogen to change to fibrin. |
|
|
Term
| What will Jehova's witnesses accept for products during surgery |
|
Definition
| They will not accept primary components. However they will accept albumin, Factor VII and IX. |
|
|
Term
| whats the difference between drugs that are anti-coagulant and fibrinolytic agents |
|
Definition
| Anti-coagulant drugs work early in the cascade by preventing the formation of a fibrin layer (Prevent secondary homeostasis) while fibrinolytic agents are late to the game and work to break down fibrin that's already there. |
|
|
Term
| how does uPA and tPA work? |
|
Definition
| The goal of uPA and tPA is to turn plasminogen into plasmin. Plasmin is the active form and natural defense the body has to break down fibrin clots. In order for plasminogen to be converted to plasmin we need a trigger. The normal trigger in the body is called a plasminogen activator. So two types of natural activators are called urokinase type plasminogen activator and tissue type plasminogen activator. |
|
|
Term
| What is antithrombin? Where is it made. What pathways does it inhibit. What is its relationship to heparin? |
|
Definition
| it is a naturally occurring plasma protein made in the liver which inhibits the intrinsic and common pathways. Since antithrombin is a natural defense against uncessary clotting the body also has another natural substance "heparin" which can also be released which augments the effectivness of antithrombin by 1000x. |
|
|
Term
| What is HITT? How is it diagnosed? |
|
Definition
| Known as heparin (LMWH too) induced thrombocytopenia with thormbosis. If a patient has had either UFH or LMWH in 3-15 days after first exposure or 12-24 hours after repeated dosing then they are at risk. Diagnosis is drop in platelet count by 30-50% and plt count <150K. |
|
|
Term
| what is protamine? How does it work? How do you dose it? What should you watch out for? What are risk factors for complications from protamine. |
|
Definition
| Protamine is a heparin antagonist. It is a cationic protein which binds to heparin and forms a salt. Its dosed by 0.5 mg /100units of heparin in the last four hours. You need to give it slowly because it can cause a hypersensitivity reaction due to IgE mediated immune response or have hemodynamic and pulmonary failure. Patients at risk are those on NPH insulin |
|
|
Term
| what is amicar used to treat? |
|
Definition
| its anti-fibrinolytic. It will inactivate fibrin. |
|
|
Term
| Explain how desmopressin works? Its used to treat what platelet disfunction? Prior to the OR when would you gave intra nasal compared to when you would give IV? Side effects? |
|
Definition
| Desmopressin, also known as DDAVP, is used to treat vonwillebrands disease, uremic induced platelet dysfunction. Give 30 min prior to surgery IV or 2hours prior intra nasal. Hyponatremia, fast administration can cause hypotension, |
|
|
Term
| Explain how anticholinesterase drugs cause nausea |
|
Definition
| Anticholinesterase drugs are those that decrease the enzyme which gets rid of acetylcholine in the synaptic cleft. With less acetylcholinesterase then that means more acetyl choline. More acH means more activated Muscarinic receptors. Which means nausea. |
|
|
Term
| what drug would you give if you wanted to prevent post op ilieus related to opioid administration? How does it act? |
|
Definition
| entereg. It is selective to peripheral opioid receptors but not central because it does not easily cross the blood borne barrier. |
|
|
Term
| A person with a stomach pH < than ___ is at the greatest risk for mendelson syndrome |
|
Definition
|
|
Term
| why are patients who receive anti H1 drugs at risk for bronchospasms |
|
Definition
| because histamine is blocked at H1 sites it then overloads H2 sites in the stomach and lungs causing increase gastric acid and increase bronchospasm. |
|
|
Term
| Name a drug that acts on NK1 receptors |
|
Definition
|
|
Term
| midazolom increases the risk of _____ in 1st trimester of pregnancy |
|
Definition
| cleft lip and palate. So don't give them to pregnant moms |
|
|
Term
| whats the difference between small doses and large doses of barbiturates on brain activity |
|
Definition
| small dose has increase low voltage, fast beta waves which means there's cloudiness in brain activity. High doses exhibit high voltage slow delta waves which resembles sleep. |
|
|
Term
| what are some other meds you may consider giving with ketamine to off set its side effects |
|
Definition
| Blunted hemodynamics because of stimulating SNS. Give verapamil to blunt increase in HR/BP. Pts will drool so give glycopyrolate. Pts also have an increase chance for focal seizures. Give aminophylline to decrease seizure threshold. |
|
|
Term
| How does cryprecipate work? |
|
Definition
| Rich in Factor VIII (Stabilizing factor) and von willibrand factor and fibrinogen |
|
|
Term
| What makes low molecular weight heparins different? |
|
Definition
| Partially purified. Longer T1/2 (4 hours). More effect on factor 10 than on thrombin (lower efficacy -> give more). Causes less thrombocytopenia and osteoporosis than heparin. More predictable dose-response |
|
|
Term
|
Definition
| Stored (-) charge, strongest organic acid in the body |
|
|
Term
| Describe the medical uses for Leeches |
|
Definition
| Have anesthetic and anticoagulant in saliva. Anticoagulant = hirudin |
|
|
Term
| Coumadin (warfarin) mechanism of action.... |
|
Definition
| Oral Anticoagulant. Vitamin K analog. Blocks effect of vitamin K (causes in vivo vitamin k deficiency). Inhibits synthesis of 7, 9, 10, prothrombin, and protein C. NO EFFECT on existing clots |
|
|
Term
|
Definition
| Heparin-induced thombocytopenia: heparin + platelets = antigen -> body mades antibody against platelets |
|
|
Term
|
Definition
| Protease inhibitor that binds to and inhibits thrombin *in leeches* |
|
|
Term
|
Definition
| Prodrugs. Irreversibly inhibit binding of ADP to platelet receptors |
|
|
Term
|
Definition
| a biologically inactive compound that becomes active after it enters the body |
|
|
Term
| How is Estrogen used in homeostasis |
|
Definition
| Hemostatic agent (enhances clotting). Increases production of some factors and plasminogen production. Decreases anti-thrombin activity |
|
|
Term
| What is hofmans elimination? |
|
Definition
| Elimination of a drug solely in the plasma with no assistance from organs. Great drug for renal and hepatic failure patients. As pH and temperature decrease, Hofmann Elimination also decreases. As pH and temperature increase, Hofmann Elimination increases. |
|
|
Term
| What does large first pass drug pharmokinetics mean? |
|
Definition
| Just means that PO meds which when absorb from the GI tract enter the blood it enters through the hepatic circulation and in the case of large first pass hepatic effects, will be cleared to a large degree from the liver. Therefore those drugs need a larger amount of PO strength to overcome this. |
|
|
Term
| Anesthesia to the stellate ganglion would result in what Sx |
|
Definition
| ipsilateral head and neck, resulting in Horner syndrome, characterized by ptosis, miosis, enophthalmos, and anhydrosis on the affected side. |
|
|
Term
| SNS exits the central nervous system from what levels |
|
Definition
|
|
Term
| What are the different types of sympathetic ganglia? |
|
Definition
1. Paravertebral ganglia: Most common. There are 22 pairs of ganglia
2. Prevertebral: Ganglia in spine and innervate stomach
3. Collateral ganglia: Ganglia are located near the effector organ. (Adrenal gland) |
|
|
Term
| whats the difference between white rami and grey rami? |
|
Definition
| White rami receive mylienated axons from spinal cord. They then cross through the grey rami before exit as unmylinated nerves. |
|
|
Term
| What do alpha 2 receptors do? |
|
Definition
| inhibit NE release from the presynaptic membrane |
|
|
Term
| what are the only two presynaptic adrenergic receptors? |
|
Definition
|
|
Term
| Activation of alpha 1 results in what after signal transduction |
|
Definition
| phospholipase C (NOT ADENYL CYCLASE) Kinase and IP3 = Increase Ca and constriction of smooth muscle. |
|
|
Term
| Stimulation of beta 1 and 2 results in what after signal transduction |
|
Definition
| increase CaMP, stimulation of adenyl cyclase. |
|
|
Term
| Stimulation of alpha 2 results in what signal transduction |
|
Definition
|
|
Term
| when would sympathetic post ganglion fibers release no2? |
|
Definition
| at blood vessels there is an exception where post ganglion SNS fibers will release NO2 instead of NE |
|
|
Term
| For a postganglion fiber to respond to AcH, the NT has to bind to what two areas on the nicotinic recpetor? |
|
Definition
|
|
Term
| what part of the adrenal medulla acts like a post ganglion and is the site for synapse with the preganglion fiber? |
|
Definition
|
|
Term
| Explain what the adrenal medulla does |
|
Definition
| it is stimulated only by the SNS via a preganglionic fiber that synapses with the chromaffin cells. NT AcH is released to chromaffin cells and causes AP. Adrenal medulla then secretes NE 20% and Epi 80% into the blood as HORMONES (NOT NEURO TRANS). Aids in the stress response. |
|
|
Term
| What are the two exception in the SNS where there is a post ganglion fiber that does not secrete NE? Where is this and what NT is released? What drug would you give to block this area's function |
|
Definition
Sweat glands receive input via post ganglionic fibers from the SNS that secrete AcH!! To stop sweating give an anticholinergic
In the kidneys the SNS innervates the smooth muscles of the vascular beds of the kidneys. The post ganglionic fibers here release dopamine. |
|
|
Term
|
Definition
|
|
Term
| 75% of PNS is carried via what nerve |
|
Definition
|
|
Term
| acetylcholinesterase does what to AcH |
|
Definition
| hydrolyzes AcH to choline and acetate. Whereby choline is reabsorbed back into the presynaptic membrane for recycling. |
|
|
Term
| cholinergic (Muscarinic) receptors will do one of two things in the PNS |
|
Definition
| Either inhibit adenyl cyclase or activate phospholipase C |
|
|
Term
| Which M receptors are inhibiting? What do their G proteins produce and what ion doe they let in? |
|
Definition
| M 2 and four inhibit adenyl cyclase and let in K ions to hyperpolarize cell membrane and decrease cAMP. |
|
|
Term
|
Definition
| Made in the presynaptic terminal by Acetyl COA combining with choline with the help of the enzyme choline acetyltransferase (ChAT) |
|
|
Term
| Beta 2 stimulation in the kidneys results in? |
|
Definition
|
|
Term
|
Definition
| prevent release of NE at postganglia |
|
|
