Term
| What is pain? Is it subjective or objective? |
|
Definition
| What the patinet says it is. It is ALWAYS subjective |
|
|
Term
| Is pain understood greatly? Do we undertreat or overtreat pain? |
|
Definition
| Processes are poorly understood, and it is actually undertreated |
|
|
Term
| What are the different types of pain? |
|
Definition
| Nociceptive, visceral, and neuropathic pain |
|
|
Term
| What are the types of nociceptive pain? |
|
Definition
Somatic and visceral
Somatic: Noxius stimulation of periphery (nerve fibers)
Visceral: noxius stimulation of visceral nerve fibers (internal organs)
=referred pain |
|
|
Term
| What is another name for visceral pain? |
|
Definition
|
|
Term
| What is neuropathic pain? Where does it occur (periphery or cns)? |
|
Definition
Pain caused by abnormal processing of sensory information
Either in periphery or CNS |
|
|
Term
| Types of neuropathic pain: |
|
Definition
Lower back pain
Neuropathy
Guillian-Barre Syndrome
Heavy metal toxicity
HIV/AIDS neuropathies
Multiple sclerosis
cancer pain (often)
Trigenimal neuroalgia
Post herpetic neuralgia
Post stroke central pain
Trauma
-Carpal tunnel syndrome
-Cervical or lumbar radiculopathy
-Spinal cord injury
-Stump pain (phantom limb) |
|
|
Term
| What is the role of the pharmacist in pain management? |
|
Definition
Drug-drug interactions
Adverse drug reactions |
|
|
Term
| What is the main step in acute pain managment? |
|
Definition
|
|
Term
| Which NSAIDS are salicylates? |
|
Definition
Acetyl Salicylic Acid
Diflusinal |
|
|
Term
| Which NSAIDS are arylalknoic acids? |
|
Definition
|
|
Term
| Which NSAIDs are propionic acids? |
|
Definition
Ibuprofen
Naproxen
Ketorlac |
|
|
Term
| Which NSAID is an oxicam? |
|
Definition
|
|
Term
| Which compound discussed in the NSAID lecture is NOT an NSAID? |
|
Definition
|
|
Term
| How are NSAIDs classified? |
|
Definition
|
|
Term
| What are the main actions of NSAIDs? (3) |
|
Definition
Anti-inflammatory
Anti-pyretic
Analgesia |
|
|
Term
|
Definition
| Inflammation is a nonspecific immune response to damaged tissue or infection |
|
|
Term
| What are the hallmark signs of inflammation? |
|
Definition
|
|
Term
| What prosteglandins are associated w/ inflammation? |
|
Definition
|
|
Term
| How do NSAIDS work to stop inflammation? |
|
Definition
They block the production of PGE2 and PCI2, which cannot increase vascular permeability and release cytokines, cgrp, substance P and lead to an AP-->Pain.
All of this is blocked |
|
|
Term
| What part of the brain regulates body temperature? What happens when you get a fever? |
|
Definition
Hypothalamus
The temp set point is elevated when you get a fever |
|
|
Term
|
Definition
| Infection, tissue damage, inflammation |
|
|
Term
|
Definition
| IL1 will induce PGE2 production, which makes the hypothalamus increase the temperature. |
|
|
Term
| How do NSAIDs reduce fever? |
|
Definition
| Block Il1 stimulation of PGE2, so the hypothalamus is not induced, and no fever ensues |
|
|
Term
| What type of pain do NSAIDs treat? |
|
Definition
|
|
Term
| What are the two ways that NSAIDs treat pain? |
|
Definition
1. Reduce inflammation and edema, and decrease pro inflammatory mediators
2. Inhibit PGE2, PGF2, and PGD2, which have been shows to stimulate pain receptors on free nerve endings |
|
|
Term
| What type of pain are NSAIDs good for treating? |
|
Definition
|
|
Term
| What is the mechanism of action of NSAIDS? |
|
Definition
| They ihibit COX (reversibly or irreversibly--ASA) which converts arachidonic acid to PG |
|
|
Term
| How is the MOA of ASA different than other NSAIDs? |
|
Definition
| It irreversibly inhibits COX by acetylating SER530 |
|
|
Term
| How do the physiological and pathological actions of prosteglandins compare? |
|
Definition
Temperature control: Fever
GI Motility: Diarrhea
Gastric secretions: Ulceration
Uterine contraction: Dysmenorrhea
Etc |
|
|
Term
| What NSAID is a good tocylitic agnet. Why? |
|
Definition
Indomethacin
It inhibits synthesis of PG, especially PGF2, which is responsible for uterine contractions.
This drug is a good tocylitic agent |
|
|
Term
| COX1 or COX 2: Uterine contractions? |
|
Definition
|
|
Term
| What NSAID can be used ot close the ductus arteriosus? Why? |
|
Definition
Indomethacin and Ibuprofen
PG play an important role in maintaining the patency of the ductus arteriosus during development |
|
|
Term
| What NSAID can be used to trat Bertters syndome? What is the disease? |
|
Definition
Indomethacin (along w/ K sparing diuretics and K supplement)
COX 2 is induced, so increased PGEs
This disease causes hyperplasia of the kidneys and increased Barttin |
|
|
Term
| What type of cancer prevention is associated w/ NSAIDS? What drugs? |
|
Definition
50% reduction in colon cancer
ASA and NSAIDS |
|
|
Term
| What type of NSAID has a greater reduciton in colon cancer? Why? |
|
Definition
| COX 2. Link beteen inhibition of COX2 and decreased polyp formation has beedn made in the GI |
|
|
Term
| What NSAID is associated w/ cardioprotection? Why? |
|
Definition
Low dose aspirin
Low dose does not cause a significant increase in bleeding, but does inhibit blatelets.
Also associated w/ decreased circulation of C-reactive protein |
|
|
Term
| Where are NSAIDS absorbed? |
|
Definition
| Rapidly from the GI tract |
|
|
Term
|
Definition
Phase 1 cyp
Phase 2 glucoronidaiton |
|
|
Term
| How are NSAIDS eliminated? |
|
Definition
|
|
Term
| What is a large reason for drug-drug interactions with NSAIDS? |
|
Definition
| They are highly bound to plasma proteins. Must watch for D-D interactions |
|
|
Term
| What is the primary SE of NSAIDs? |
|
Definition
|
|
Term
| Hypersensitivity in NSAIDS? |
|
Definition
| Rare but serious that does not appear to be an immune rxn, rather inhibition of COX pathway shunts AA over to teh LT pathway for an asthma like rxn |
|
|
Term
| What is the rationale behind GI SE of NSAIDs? |
|
Definition
NSAIDs inhibit COX1, so there is a decrease in PGE2 and PCI2 which produce cytoprotective cells.
Acidic molecules cna irriate gastric mucosa |
|
|
Term
| Which NSAIDs have higher risk of gastric SE? Which have a lower risk? |
|
Definition
Higher: Indomethacin, Meloxicam, Salicylates
Lower: Ibuprofen, diclofenac, COX 2 selective agents |
|
|
Term
| How can you decrease GI SE with NSAIDs? |
|
Definition
1. Decrease the dose
2. Use PPI or PG analog (misoprolol)
3. Use enteric coated formulations |
|
|
Term
| Renal Side effects of NSAIDs? |
|
Definition
| Individuals with pre existing Heart problems, loop diuretics, or hypovolemia may suffer compromised renal function in the form of reduced renal blood flow and reduced GFR. These can lead to renal failure |
|
|
Term
| What are some other SE of NSAIDs? |
|
Definition
-Hypersensitivity/Bronchospasm
-Gouty symptoms
-Reye's syndrome
-Increased hemorrhage |
|
|
Term
|
Definition
| Hepatic injury and encephanopathy in children with viural infection (ie chicken pox). Link to ASA although association is not clear |
|
|
Term
| What population are NSAIDs CI'd in? Why? What should you use instaed? |
|
Definition
Asthmatics
Shift AA metabolism to form LT, which can constrict the airways
Use APAP |
|
|
Term
| What happens durin a salicate toxicity? What are the SE? |
|
Definition
Uncoupling of Oxidative Phosphorylation (which leads to a metabolic shutdown)
-Respiratory alkalosis, metabolic acidosis, hyperpyrexia, vomiting, hearing loss |
|
|
Term
| What are two common drug NSAIDs? |
|
Definition
Warfarin and ASA: Bleeding
Methodrexate and NSAIDs: Decrease renal blood flow/uric acid buildup/gout |
|
|
Term
| What is the gold standard NSAID? |
|
Definition
|
|
Term
| What is the driving force for the anti-thrombotic effect of ASA? |
|
Definition
| Platelet effect on TXA2, which inhibits platelet aggregation and vasodilates |
|
|
Term
| What two things are inhibited by ASA? How do they contradict each other? |
|
Definition
TXA2 is an inhibitor of platelet aggregation and a vasoconstrictor
PCI2 (prostacyclin) is an inhibitor of PGI2, whcih causes vasodilation.
TXA2 works primarily on platelets, while PGI2 works on the endothelium. Plts are irreversibly inhibited so the effect lasts longer there |
|
|
Term
| What is the most potent NSAID? |
|
Definition
|
|
Term
COX 1 vs COX 2
-Inducers?
-Location
-Produces
-Repressed by? |
|
Definition
COX 1:
-Found throughout the body (mostly GI, Kidney, and plts)
-Constituitavely expressed
-Produces PGE2 and PCI2
COX2
-Derived from prostaglandins
-Inducable
-Found @ site of inury
-Induced by IL 1beta, TNF alpha, growth factors
-Repressed by anti-inflammatory agents (IL4, IL10, IL13, glucocorticoids) |
|
|
Term
| What is APAP effective at treating? |
|
Definition
| Antipyretic and analgesic |
|
|
Term
|
Definition
| Not clear, most likely acting centrally (but fewer GI effects) |
|
|
Term
| How does hypatotoxicity occur w/ APAP? |
|
Definition
Primary metabolism is glucoronidaiton.
However, secondary is via cyp and then scavenged by glutathione.
W/ OD, depletion of glutathione. Buildup of the ROS/RNS that cause hepatotoxicity |
|
|
Term
| How much glutathione must be depleted in order to have APAP OD? |
|
Definition
|
|
Term
| What does glutathione depletion lead to a buildup of? |
|
Definition
| N-acetyl p-benzoquinonequine |
|
|
Term
| How does one treat an APAP OD? |
|
Definition
-Induce vomiting
-Administer N-acetylcystenine (an antioxidant and a glutathione prescursor) |
|
|
Term
| Why do you not give glutathione for an APAP OD? |
|
Definition
| Bc it can't get into the cells. |
|
|
Term
| What must opioids do in order to be an effective pain reliever? |
|
Definition
|
|
Term
| Do opioids act centrally or peripherally? |
|
Definition
|
|
Term
| What are the three classes of analgesic agents? What type of pain does each treat? |
|
Definition
Non opioid: mild
Opioids: severe
Analgesic adjuvants: little analgesic effect alone (ex. muscle relaxants, antidepressants, anti anxiety) |
|
|
Term
| What are the three classes of analgesic agents? What type of pain does each treat |
|
Definition
Non opioid: mild
Opioids: severe
Analgesic adjuvants: little analgesic effect alone (ex. muscle relaxants, antidepressants, anti anxiety) |
|
|
Term
| What are the 3 opioid receptor subtypes? |
|
Definition
|
|
Term
| What are some examples of strong opioid agonists? What about weak? Antagnist? Mixed agonist/antagonist? |
|
Definition
Strong=morphine/fentanyl
Weak=codeine
Antagonist=naloxone/natrexone
Mixed=nalbuphine/butorphanol |
|
|
Term
| What receptor are most opioids agonists at? |
|
Definition
|
|
Term
| What is the SE of opioids that bind @ kappa recceptor? |
|
Definition
|
|
Term
| What do delta receptors do? |
|
Definition
|
|
Term
| What are enkephalins? What are they naturally slective for? Where are they located? |
|
Definition
derived from pro-enkaphalin
Throughout CNS
Bind to delta selective
Located in catecholamines and in synthetic terminals in adrenal glands |
|
|
Term
| What are endorphins? What do they naturally bind to? Where are they located? |
|
Definition
Deriphed from proopiomelanocortin
Beta endorphin has analgesic activity
Bind to the mu receptor
Pituiatary and hypothalamus |
|
|
Term
| What do endorphins cause? |
|
Definition
|
|
Term
| What are dynorphins? What do they bind to? Where are they located? |
|
Definition
Derived from prodynorphin
Potent analgesic
Binds selectively to the Kappa receptor
Receptors are localized in the pituitary and hypothalamus |
|
|
Term
What do opioid receptors in the brainstem mediate?
Medial thalamus?
Spinal Cord?
Hypothalamus?
Non-CNS? |
|
Definition
Brainstem: respiration, cough, anusea, vomiting,pupillary diameter
Medial thalamus: Deep pain
Spinal cord: Integrate of incoming sensory information
Hypothalamus: neuroendocrine
Non CNS: GI tract |
|
|
Term
| What happens to the pharmacolgic actions of opioids when you are on them for prolonged periods? Which are exeptions to this? |
|
Definition
| Tolerance develops to most effects, except constipation, miosis, and pruritis |
|
|
Term
| What conditions are opioids contraindicated? |
|
Definition
Head injury
Bronchial asthma
Convulsive disorders
Drug-drug interactions
(also pancreatitis, alcohol intoxication, hypovolemic shock-use IV, hypothyroidism, hepatic failure |
|
|
Term
| What type of pain should opioids NOT be used in? |
|
Definition
| Chronic, non-malignant pain |
|
|
Term
| What are some therapeutic uses for opioids? |
|
Definition
Acute pain
Cancer pain
Dyspnea and pulmonary edema
Open heart surgery
Decrease fear in dying
Control withdrawal symptoms (methadone) |
|
|
Term
| What is the main concern with chronic opioid use? |
|
Definition
| Prevention of substance abuse |
|
|
Term
| Where does pain processing occur in the body? |
|
Definition
|
|
Term
| Describe the MOA of opioids at the spinal cord level? |
|
Definition
Afferent pain inhibited at presynaptic and postsynaptic terminals
Presynapticlaly: Decrease CAMP, whihc decreases intracellular Ca, so this decreases the release of NT release (mu, kappa, and delta are here)
-Postsynaptica: bind to receptor, causing an influx of K ions into the neuron leading to hyperpolarization of the neuron and evoking an inhibitory pos synaptic potential (mu receptors only) |
|
|
Term
| What is the supraspinal MOA of opiates? |
|
Definition
| Via mu receptors to inhibit the inhibitory action of GABA ant hus stimulate the actiivty of adrenergic and serotenergic pahtways |
|
|
Term
| Do opioids put you to sleep? |
|
Definition
| No they are sedating, but are NOT hypnotics |
|
|
Term
| What type of pain are opioids better at treating? What type of pain is resistant? |
|
Definition
Better at treating prolonged burning pain than sharp shooting pain
Neuropathic pain is often resistant |
|
|
Term
| Why do rewarding effects of opioids occur? |
|
Definition
| Due to an interaction between opioids and DA in the nucleas accumbens |
|
|
Term
| Which agonists are rewarding? Which are aversive? |
|
Definition
Mu and delta are rewarding
Kapa and my antags are aversive |
|
|
Term
Respiratory Depression:
-What part of brain
-Therapeutic doses
-Combination
-Death? |
|
Definition
-Driect effect on respiratory centers in medulla
-Thx doses depress all phases of respiration (rate, minute volume, tidal exchange)
-Effects compounded (GA, tranquilizers, alcohol, sedative-hypnotics
-Opioid death almost always from respiratory depressions |
|
|
Term
| Effect of opioids on cough? |
|
Definition
| Depress cough centers in the medulla |
|
|
Term
| What are opioids effect on pupils? What receptors do this? |
|
Definition
Pinpoint pupils
Mu and kappa receptors |
|
|
Term
| What drugs will antagonize pupulliary constriciton? |
|
Definition
Naloxone
Atropine
Ganglionic blockers |
|
|
Term
|
Definition
| Directly stimulate the chemoreceptor trigger zone (CTZ) in the area postrema activating the vomiting center |
|
|
Term
| What opiods is muscle rigidity commonly observed with? |
|
Definition
|
|
Term
| What can muscle rigidity in opioids also lead to? |
|
Definition
| Decreased respiratory function,m because muscles become stiff and can't brethe |
|
|
Term
| which drugs can dysphoria and agitations occur infrequently with? |
|
Definition
Meperidine
Codeine
Hydrocodone |
|
|
Term
| Can opiates be used when someone has had a head injury or has an elevated ICP? |
|
Definition
No.
Decreased ventillation can increase PaCO2 and even raises ICP further
Pupil effect (meiosis) may mask changing neurological signs |
|
|
Term
| What do opioids do to CV funciton? |
|
Definition
Vasodilation and HOTN (decrease in symp tone)
Bradycardia (stiulating vagal nerve)
Little/no effect on myocardium |
|
|
Term
| If someone has hives/itching near injection site for an opioid what has happened? |
|
Definition
Not a true allergy, which are very rare
Histamine has been released non-immunologically |
|
|
Term
| Why are facial itching and warmth a common efect following administration of opioids? |
|
Definition
| NOT histamine release, because of the change in blood flow |
|
|
Term
| What is the primary effect of opioid action on the SM in the intestine and stomach |
|
Definition
|
|
Term
| What drugs can be used to treat diarrhea? |
|
Definition
Poorly absorbed opioid agonists
Diphenoxylate (rx)
Loperamide (OTC) |
|
|
Term
| Since opioids cause constipation, do they have an effect on the urinary system? |
|
Definition
| Yes, can cause urinary retention |
|
|
Term
| What happens with opioids and the biliary system? |
|
Definition
| They cause contraction of the sphinctor of ODDI, increased pressure, which can ppt or exacerbate biliary colic |
|
|
Term
| Preggerz chicks and opiates? |
|
Definition
Cross the placenta, not teratogens
May go through withdrawal
But if given during labor, can cause respiratory depression in the baby |
|
|
Term
| What are the two long term effects of opioid use? |
|
Definition
Tolerance
Physcial dependence |
|
|
Term
| What are the withdrawall symptoms of opioids? |
|
Definition
Vomiting
Diarrhea
Cooseflesh
Mydriasis
Drug seeking |
|
|
Term
| What effects does opiate tolerance develop more rapidly to? |
|
Definition
| Analgesia, Respiratory depression, Euphoria |
|
|
Term
| What are some symptoms of acute respiratory failure with Opioids? |
|
Definition
| TRIAD: Coma, miosis, cyanosis Asyphyxia (pinpoint pupils) Biliary spasms Pulmonary edema Muscle twitches, peripheral vasodilation-->HOTN, shock Respiratory failure |
|
|
Term
| Overdose of opiois symptoms? |
|
Definition
Coma
Miosis
Respiratory depression
HOTN
Shock
Hypothermia
Pulmonary edema |
|
|
Term
| What happens if you OD on meperidine? |
|
Definition
May cause mydriasis (antimuscarinic effects)
Seizures |
|
|
Term
| What happens if you OD on a high potench opiate such as fentanyl? |
|
Definition
| You may get acute muscular rigidity, that may impair chest movement and exacerbate hypoventilation |
|
|
Term
| What should you do to treat an opiate OD? |
|
Definition
1. ABC's
2. Naloxone/Naltrexone
3. Monitor |
|
|
Term
| How is naloxone administered, what is is DOA? |
|
Definition
| Administered IV, short DOA (1-4 hours) |
|
|
Term
| What happens when you use opioid antagonist in someonone who is physically dependent? |
|
Definition
|
|
Term
| Drug drug interaction of opiates: Which ones increase CNS depressant effects? |
|
Definition
MAOI's
Tricyclics
Phenothiazines |
|
|
Term
| When you use opioids with CNS depressants, what shoudl you do? |
|
Definition
|
|
Term
| Drug-Drug interactions of opioids: Which ones increase effects of morphine? |
|
Definition
Amphetamines
Anti-histamines
Hydroxyzine |
|
|
Term
| What happens when you combine miperidine and an MAOI? |
|
Definition
Excitation*
Delerium*
Hyperhyrexia
Convusions*
Severe resp depresion |
|
|
Term
|
Definition
Rapid absorption, wide distribiution, and rapid clearance
High first pass effect |
|
|
Term
| Can morphine cross BBB? Why/Why not? |
|
Definition
| Only 0.02% crosses BBB because of hydrophliic |
|
|
Term
|
Definition
| Secondary metabolite 6- glucoronide morphine is active |
|
|
Term
| How is morphine eliminated? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Can heroin cross the BBB? Why/why not? |
|
Definition
| Lipid soluble and crosses BBB faster than morphine |
|
|
Term
| What happens when heroin is administered IV? |
|
Definition
|
|
Term
|
Definition
| Metabolized to morphine in the brain |
|
|
Term
|
Definition
| Readily absorbed orally. 60-87% reaches the plasma |
|
|
Term
|
Definition
|
|
Term
| Receptor affinity of oxycodone? |
|
Definition
|
|
Term
| What is oxycodone often combined with? |
|
Definition
|
|
Term
|
Definition
| Pure oxycodone inside a polymer/acrylic matrix that allows for CR |
|
|
Term
| Why do abusers like oxycontin better than oxycodone? |
|
Definition
You can crush it and get more.
There are no non-narcotics (pure oxy) |
|
|
Term
| What happens if you try and crush the new improved tamper rsistant oxy formulation? |
|
Definition
| If crushed, naloxone is acutely released to counteract the effects of the oxycodone, resuling in withdrawal symptoms in the abuser |
|
|
Term
|
Definition
| A ge;l capsule that utulizes controlled release, but is crush resistant |
|
|
Term
|
Definition
| Synthetic narcotic w/ actions similar to morphine (w/ few exceptions) |
|
|
Term
| What differs between morphine and meperidine? |
|
Definition
| Meperidine: no anti-tussive and may dilate pupils |
|
|
Term
| What is the metabolite of meperidine, what does this do? |
|
Definition
| Normeperidine: strong stimulant and convulsant |
|
|
Term
| Which receptor does meperidine act on? agonist or antagonsit? What does this mean? |
|
Definition
Agonist @ kappa receptors (dysphoria)
Large dose can cause msucle twitches, tremors, and rarely convulsions |
|
|
Term
|
Definition
|
|
Term
| When can fentanyl be used? |
|
Definition
|
|
Term
| What is oralet? Why was it removed from the market? |
|
Definition
Fentanyl pops for kids
Kids bit the sucker, and OD |
|
|
Term
| What is actiq? What is it used for? |
|
Definition
| Fentanyl pop for cancer patinets, for breakthrough pain |
|
|
Term
Transdermal fentnyl
-Primary use
-DOA
-Absorption |
|
Definition
Chronic malignant pain
DOA: 72 hours
Absorption can be variable and lead to increased SE and OD otptential (fever, wound) |
|
|
Term
| Why shouldn't fentanyl patches be used in someone that have not been on opioids before? |
|
Definition
| They are a high dose, you can get a lower dose patch, though |
|
|
Term
| How does methadone differ from morphine? |
|
Definition
| Less sedation, euphoria, emesis |
|
|
Term
| What is methadone used for? |
|
Definition
| Treat heroin withdrawal and pain of terminal cancer |
|
|
Term
| Where does methadone act? |
|
Definition
|
|
Term
| DOA of morphine compared to methadone? |
|
Definition
| Methadone is longer (T1/2 is 15-55 hours) |
|
|
Term
DOA/Peak effect of the following:
Methadone
Fentanyl
Morphone
Merperidine |
|
Definition
Morphine/Meperidine: Middle
Methadone: Long
Fentanyl: Fast |
|
|
Term
| What % and where is codene converted to morphine? |
|
Definition
10%
After it crosses the BBB |
|
|
Term
| What is the main use of codeine? |
|
Definition
| Anti-tussive. Moderate pain |
|
|
Term
| Max analgesia of codeine compared to morphine? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What is the single most highest prescribed drug in the US? |
|
Definition
|
|
Term
| What happens with high doses of D-propoxyphene? |
|
Definition
| CNS stiulation: convulsions, respiratory depression, hallucinations, confusion, coma |
|
|
Term
| What is D-propoxyphene related to structurally? |
|
Definition
|
|
Term
| Analgesis of D-Dorpoxyphene comparatively? |
|
Definition
| 1/2 analgesic potency of codeine (weak) |
|
|
Term
What is pentazocine?
Potency?
recepotr activity? |
|
Definition
Opioid mixed agonist antagonist
1/3 as potent as morphine
Agonst: Kappa
Antagonist: Delta, Mu |
|
|
Term
What is beprenorphine?
Receptor activity? |
|
Definition
Potent, long activing phentherene deriviative
Mu and kappa partial agonist
delta antagonist |
|
|
Term
What is naloxone?
Receptors?
Purity?
Uses?
DOA? |
|
Definition
Antagonizes most opioid receptor agonist (barbitruates @ high doses)
Almost a pur antagonist
Used to reverse coma/resp depression in OD
DOA is short |
|
|
Term
What is naltrexone?
Purity?
DOA? |
|
Definition
Opioid antagonist--pure
Longer DOA than naloxone |
|
|
Term
| What have recent studies show about combinations of opioid antag's w/ agonists? |
|
Definition
| Don't antagonize it, but actually enhance opioid |
|
|
Term
|
Definition
| An emetic thjat acts @ CTZ and in a dopaminergic agonist |
|
|
Term
| What does dextraomethorphan relieve? |
|
Definition
|
|
Term
|
Definition
Act centrally
May bind to receptors and inhibit reuptake of NE/5HT |
|
|
Term
| What is the basic structure of a local anesthetic? |
|
Definition
-Hydrophobic ring
-Linker=ester/amide
-Tertiary amine group |
|
|
Term
| What is the purpose of the aromatic ring in LA? |
|
Definition
|
|
Term
| What is the importance of the ester and amide linkers in LA? Where is each metabolized? |
|
Definition
They are the primary spot for metabolism
Esters: in the plasma by pseudocholinesterases
Amides: in the liver by CYP450 |
|
|
Term
| What role to thet tertiary amines play in LA? |
|
Definition
Lipophilict
Cationized to quat amine, hydrophylic and soluble |
|
|
Term
|
Definition
| Intervere w/ the increase in Na permeability that subserves thedepolarizing phase of an AP, therefore blocking generation of nerve impulses |
|
|
Term
| What do we need to take away from the MOA of LA? |
|
Definition
| It bascially makes it more difficult for AP to be propogated and fired. Block axonal conduction |
|
|
Term
| What happens to the AP when an LA is used? |
|
Definition
| It is squished, less Na enters, so less depolarized, and takes more time |
|
|
Term
|
Definition
|
|
Term
| What do LA do to the threashold potential of AP? |
|
Definition
|
|
Term
| What form of an LA will block Na channels? |
|
Definition
The cationized form
Neutral form has weak effiacy at blocking: Benzocaine |
|
|
Term
| What form of LA can cross where within the body, how does this effect the MOA? |
|
Definition
-Neutral has to be able to cross CM
-Cationized has to block Na channels
Must be in neutral form first, and then convert to the cationic form |
|
|
Term
| What type of channels do LA block? (primiary) |
|
Definition
Voltage gated, use dependent channels
(NOT resting channels or closed ones) |
|
|
Term
| Besides Na, what other things do LA's block? Which can related to ADR? |
|
Definition
| K, Ca, nicotinic receptor mediated conductance, and substance P (which can releate to ADR's) |
|
|
Term
| What is the effect of pH on LA? |
|
Definition
As pH increases, LA shifts to neutral form (which is more readily absorbed, but can't block Na channels)
As pH decreases, shifts to cationized form (which cannot cross the membrane, and therefore cannot block Na channels) |
|
|
Term
| What effect does increased blood flow have on LA activity? What about SE? |
|
Definition
Increased blood flow can move LA away from injection site, which can lead to less activity in the are
-More systemic absorption-->SE |
|
|
Term
| What role does decreased blood flow have on LA? |
|
Definition
| Keeps the LA at the site of injection, so less systemic SE.. and increased efficacy of the drug |
|
|
Term
| Which nerve fibers are effected by LA first? Which are effected last? |
|
Definition
Unmylenated (C fibers) are first
Alpha motor neurons are least effected (large mylenated)
Based on size/mylenation |
|
|
Term
| Order of sensory block/return? |
|
Definition
1. Pain
2. Cold
3. Warmth
4. Touch
5. Deep pressure
6. Motor fxn |
|
|
Term
|
Definition
| Topically to treat dermatitis and itching |
|
|
Term
|
Definition
| Reduce bleeding in oral surgery (constrictive properties) |
|
|
Term
| CNS SE of LA? Too high/too low of a dose? |
|
Definition
low doses: CNS stimulation (restlessness/tremor/convulsion)
high doses: CNS depression (sedation, respiratory depression, loss of consciousness) |
|
|
Term
|
Definition
Act on the myocardium to decrease excitability, conduction, and contraction
Vasodilate (all but coke)
Toxicity=HOTN/Arrythmias |
|
|
Term
|
Definition
Ventricular tachydardia
Ventricular fibrillation |
|
|
Term
|
Definition
| Excitatory conditions from catecholamines |
|
|
Term
|
Definition
| anti-arrythmic properties |
|
|
Term
|
Definition
| Stimulatory effects on the heart |
|
|
Term
| What are some SE from severe LA toxicity? |
|
Definition
Circum-oral tongue numbeness
Lighheadedness
Tinnitis
Visual disturbances
Respiratory arrest
Mucular twitching
Convulsions
Unconsciousness
Coma
CV Collapse |
|
|
Term
|
Definition
Rare, but not unheard of
Allergic to easter derived metabolite PABA
They may also be allergic to stabalizers/adjuvants |
|
|
Term
| What is the therapeutic use of cocaine? |
|
Definition
| Provides vasoconstriction and anesthesia in oral surgeries |
|
|
Term
|
Definition
|
|
Term
| Which LA are esters and can cause allergic rxn? |
|
Definition
Procaine
Tetracaine
Articaine |
|
|
Term
|
Definition
|
|
Term
| Why isn't procaine as common amymore? |
|
Definition
Low potency
Slow onset
Short DOA |
|
|
Term
| Administration of procaine? |
|
Definition
| Confined to infiltration anesthesia |
|
|
Term
Lidocaine:
-DOA
-Administration
-Other fun facts |
|
Definition
-Intermediate DOA
-Patches, SC, IM, iV (wide range clinically)
-Class 1C anti-arrythmic
-Drug and metabolite are a primary source of severe toxic effects |
|
|
Term
|
Definition
|
|
Term
| What LA can produce prolonged anesthesia for procedures such as the post OP period? |
|
Definition
|
|
Term
|
Definition
| More cardiotoxic than equi-effective lidocaine |
|
|
Term
|
Definition
| As potent as bupivacaine w/ less cardiotoxic effects |
|
|
Term
| What drug was developed as an alternative to bupivacaine? |
|
Definition
|
|
Term
| DOA/Type of Link of Ropivacaine? |
|
Definition
|
|
Term
| Potency/CV of ropvacaine? |
|
Definition
| Slightly less potent than bupccacaine w/ less CV effects |
|
|
Term
| What is bupvacaine used for? |
|
Definition
| Continuous influsion (epidural) lasts for days |
|
|
Term
| What type of anesthesia is Ropivacaine used for? |
|
Definition
| Both regional and epidural |
|
|
Term
| What type of anesthesia is tetracaine used for? |
|
Definition
| Topical preps and spinal anesthesia |
|
|
Term
| Which LA should not be usd obsterically due to neonate toxicity? |
|
Definition
|
|
Term
| Mepivacaine: DOA/Type of link |
|
Definition
Amide
Intermediate DOA (simialr to lidocaine w/ 20%>>>potency |
|
|
Term
| Prilocaine: Link type and DOA? |
|
Definition
| Amide w/ intermediate DOA |
|
|
Term
| What is the drug of choice of IV regional blocks (LA)? |
|
Definition
|
|
Term
| Which LA has a SE of methemoglobinemia? |
|
Definition
|
|
Term
| What LA has both an amide and an ester group? |
|
Definition
|
|
Term
|
Definition
| Dental surgeries, rapid onset (1-6 minutes_ |
|
|
Term
| Which LA is poorly soluble so it can be used topically? |
|
Definition
|
|
Term
| Which LA is in many OTC meds? |
|
Definition
|
|
Term
| Which LA is not a benzoate, ester, or amide? |
|
Definition
|
|
Term
| Goals of general anesthesia? |
|
Definition
-Analgesia
-Amnesia
-Hypnosis
-Muscle relaxation
-Inhibition of autonomic reflexes |
|
|
Term
| What pharmacokinetic property is most important to look at when using general anesthetics? (ADME) |
|
Definition
|
|
Term
| DO you want a general anesthetic to have a fast or slow induction rate? Is it better to keep the patient on anesthesia for a long period or short period? |
|
Definition
Fast
Short period-->Better recovery |
|
|
Term
| Are IV GA given all at once or over a period of time? |
|
Definition
|
|
Term
| Describe distribution of the drug after adimistration of a GA? |
|
Definition
| It first distributes to areas of high blood flow and low volume (like the brain), and then it goes to areas of lower blood flow and higher volume (ex. adipose/muscle) |
|
|
Term
| General anesthetic flow in body: (frst-->last) |
|
Definition
| Blood-->Brain/viscera-->Lean muscle-->adipose |
|
|
Term
| GA relationship of T1/2 and DOA? |
|
Definition
| May have a long T1/2 but they all have a fairly short DOA comparitavely |
|
|
Term
| How does one prolong the effect of a GA? |
|
Definition
| Redosing, duration is dose dependent |
|
|
Term
| Who may need less of a GA dose? Why? |
|
Definition
| The elederly, because they have a smaller Vd. |
|
|
Term
| What is the most frequently used IV inducing GA? |
|
Definition
|
|
Term
| DOA of thiopental? What is it usually used for? |
|
Definition
Ultrashort acting (5 minutes)
Inducing agent, then start another gas agent |
|
|
Term
| What is the gold standard GA inducing agent? |
|
Definition
|
|
Term
Thiopental:
-Induction
-Unconscious rate
-Amnesia quality
-Analgesia quality
-Muscle relaxation qty |
|
Definition
Pleasant induction
Rapid unconsciousness
Good amnesia
Poor analgesia, Poor muscle relaxation |
|
|
Term
| What is the MOA of thiopental? |
|
Definition
Binds to GABAa recepor, increases Cl influx into cell.
This stimulates inhibitory neuronal systems |
|
|
Term
| What CNS effects does thiopental have? |
|
Definition
It decreases cerebral metabolism and O2 utilization
It decreases cerebral blood flow and ICP
Therefore it protects the brain against hypoxic/ischemic injury |
|
|
Term
| Direct cardiovascular effects of thiopental? |
|
Definition
Peripheral vasculature: decrease BP, vascular resistance, CO, venodilation (HOTN,Schock), venodilation occurs due to increased venous capitance
Myocardium: direct depressant. Lowers contractility |
|
|
Term
| Indirect CV effects of thiopental? |
|
Definition
| HR is increased via barostatic reflex |
|
|
Term
| How does the anesthesiologist know that thiopental is working well? |
|
Definition
| HR is increased via barostatic reflex |
|
|
Term
| What happens to people who have a high sympathetic tone when placed on thiopental? What can be done to comabet this? What causes this? |
|
Definition
They experience a profound drop in BP (hypovolemia, HF, CAD, BB block)
Often take an anti-anxiety prior to reduce the tone.
This is caused by a redistribution of CO |
|
|
Term
| Respiratory effects of thiopental? |
|
Definition
| Respiratory depression occurs in a dose-dependent fashio |
|
|
Term
| Do you need muscle relaxants alng w/ thiopental? |
|
Definition
| Yes, because you still have trachael/laryngeal reflexes |
|
|
Term
| If you have asthma, can you use thiopental? |
|
Definition
|
|
Term
| Renal/GI/Liver effects of thiopental? |
|
Definition
| No significant effects upon short term use: should continue to monitor RBF |
|
|
Term
|
Definition
Some action at GABAa
Enhances Cl conductance @ glycine
But the MOA is not fully known |
|
|
Term
|
Definition
| Decreases cerebral blood flow and metabolism |
|
|
Term
|
Definition
Decreased BP, vascular resistance, HR, CO, Central venous pressure is unchanged
Greater degree of Bp reduction than thiopental |
|
|
Term
| Propofol vs Thiopental: Which has more CV depression? |
|
Definition
|
|
Term
| Which GA burns on injection? What makes it do that? |
|
Definition
| Propofol: Phenol component |
|
|
Term
| Time to take effect of propofol: |
|
Definition
|
|
Term
| Which GA is the one where the patinets can resume conversation in recovery w/o pause? |
|
Definition
|
|
Term
| Can propofol be used for maintenence, or is it only a good inducing agent? |
|
Definition
|
|
Term
| Euphoria or dysphoria of propofol? |
|
Definition
|
|
Term
|
Definition
| Activates GABAa receptors |
|
|
Term
| What is the primary indication for etomidate? |
|
Definition
| Used in patients @ risk of HOTN |
|
|
Term
| CNS effects of etomidate: |
|
Definition
Decrease cerebral blood flow/ICP
Decrease O2 metabolic rate |
|
|
Term
|
Definition
Minimal ventilatory depression
Lower incidence of apnea |
|
|
Term
|
Definition
Minimal changes in all parameters
Well suited for pts w/ CV risk factor |
|
|
Term
| What is the GA drug of choice for pts w/ heart problems? |
|
Definition
|
|
Term
| Etomidate: Muscluloskeletal system? How do you fix this? |
|
Definition
Myoclonus
Controlled though adjuct txy: midrazolem |
|
|
Term
| What is the MOA of Ketamine? What is special about this? |
|
Definition
| Antagonist of NMDA: non competative |
|
|
Term
| What GA is the only one that acts by inhibition of stimualtory neuronal systems? |
|
Definition
|
|
Term
| Which GA causes a "dissociative" feeling where you are out of body? |
|
Definition
|
|
Term
| What population is ketamine used in? |
|
Definition
| Patients at risk for HOTN and bronchospasm |
|
|
Term
| What muct you be sure to give along with ketamine? |
|
Definition
| Something that causes amnesia, they are not asleep, just dissociated from their body |
|
|
Term
| What are CNS SE of ketamine? |
|
Definition
| -Unpleasant dreams: reduced by benzo's barbs and N2O -Increase in cerebral blood flow and ICP |
|
|
Term
| CV effects of Ketamine? What patinets are these good in, CI? |
|
Definition
Increased HR, BP, CO due to sympathetic stimulation.
Good in pts who get HOTN during anesthesia
Bad for pts who are at risk for MI |
|
|
Term
| What GA is the most effective bronchodilator? |
|
Definition
|
|
Term
|
Definition
Small dsoes=minimal ventilatory depression
Profound analgesia reduces airway reflexes (intubation) |
|
|
Term
| Other random SE of ketamine? |
|
Definition
-Salivary tracheobronchal secretions increased
Non purposeful tonic/clonic/ athenoid movements
Nystigmuc/phonation occur |
|
|
Term
| What opioid medication is used as an GA? |
|
Definition
|
|
Term
| WHy are opioids used as GA NOT reliable for? What are they used for? |
|
Definition
Amnesia
Used for pre-op/induction/maintenence/post-op pain |
|
|
Term
| What is the shortest acting opioid? |
|
Definition
|
|
Term
| What GA is the one exception to the rule of distribution? |
|
Definition
|
|
Term
| How is remifentanil metabolised? |
|
Definition
|
|
Term
| What GA stops actions after 8 minutes of turning it off? |
|
Definition
|
|
Term
| What are 2 things to consider when choosing an inhaled general anesthetic? |
|
Definition
|
|
Term
What is the most potent inhaled GA?
What is the weakest inhaled GA (maybe not considered GA) |
|
Definition
|
|
Term
| WHy is solubility important when choosing an inhaled GA? |
|
Definition
Because drug must get to the brain
Directly coorelated w/ the blood:gas ratio.
But if it gets absorbed from the lung-> blood (high ratio stays there) so it takes longer to get to the brain. Delays induction |
|
|
Term
| What are the physiochemical properties of inhaled general anesthetics? |
|
Definition
Highly lipid soluble
Ethers: except halothane
-low metabolism |
|
|
Term
| Which inhaled general anesthetic is not an ether? Why is this important? |
|
Definition
Halothane
Important bc of toxicities (breaks down faster) |
|
|
Term
IGA that smell good (names)
How do you administer them? |
|
Definition
-Halothane
-Sevoflurane
-Can give from beginning to end: pleasant induction |
|
|
Term
IGA that smell bad (names)
How do you give them? |
|
Definition
Desflurane
Isoflurane
Give IV and transfer |
|
|
Term
| What population will you be most concerned with the smell of IGA? |
|
Definition
|
|
Term
Halothane:
Blood gas portion, induction rate, recovery |
|
Definition
| High rate: Slow induction, slower recovery |
|
|
Term
|
Definition
60-80% by lungs
Remaining to liver: froms TFA (necrosis ensues) |
|
|
Term
|
Definition
Can depress SA Node and sensitize the heart to catechol induced arrythmias
-So after surg. HR is already high and symp is activated. Ectopic areas by cathechols. SA not workin-->Arrythmias.
Can help treat this by giving a BB |
|
|
Term
| What is the perferred IGA for neurocsurg procedures? |
|
Definition
| Isoflurane: Less decrease in ICP and cerebral blood flow |
|
|
Term
| What IGA is used in patinets w/ compromised myocardial fxn? |
|
Definition
| Isoflurane: Potent coronary vasodilator and CO is maintained |
|
|
Term
| Isoflurane: Blood gas partition, induction, recovery |
|
Definition
Moderate Blood gas partition
Faster induction and recovery than halothane |
|
|
Term
| Desflurane: Blood gas partition, induction, recovery, metabolism, maintenece or induction? |
|
Definition
Low blood gas partition
Fast induction and recovery
99% metbaolized in the lungs
Widely used for maintenance NOT induction |
|
|
Term
| Sevoflurane: Blood/Gas partition, induction, recovery, maintenence or induction? |
|
Definition
Low blood gas parition
Fast induction and recovery
Widely used for surgical maintenance, and induction (mostly throughout in kiddos) |
|
|
Term
| Nitrous oxide: Potency, what is it good for, % concentrations rationale |
|
Definition
Not potent as an anesthetic
Good for analgesia and sedation
50% in dental surg
80% upper limit (bc must have 20% O2)
70% is common |
|
|
Term
| WHat is the #1 to remember about nitrous oxide? |
|
Definition
It makes everything work better
Use less of the drug |
|
|
Term
| What drug class are good adjuvants to general anesthesia, why? Which 2 drugs from this class? |
|
Definition
Benzo's. Good amnesic agnents
Lorazapam, Midazolam |
|
|
Term
| Therapeutic uses of Skeletal muscle relaxants: What does this do to the amount of drug needed for anesthesia? |
|
Definition
Adjuvant to surgical anesthesia
Less anesthetic drug needed |
|
|
Term
| What other procedures are skeletal muscle relaxants good for besides adjuvants? |
|
Definition
| Orthapedic procedures, ie dislocations |
|
|
Term
| Where do most skeletal muscle relaxants act? |
|
Definition
| Ach and nicotinic receptors |
|
|
Term
| What are the two classes of skeletal muscle relaxants? |
|
Definition
Deopolarizing
Non-depolarizing |
|
|
Term
Depolarizing Skeletal muscle relaxant:
-Drug name |
|
Definition
|
|
Term
Succinyl choline:
Onset/ Duration
MOA |
|
Definition
Fast onset: 1 minute
Ultrashort duration: 5-8 minutes
Act as a reversible but persistent agonist of ACH @ nicothinc receptors ant NMJ of skeletal muscles (binds initally, contracts, doesn't release, then relaxes, but molecule still bound. Irreversible. No antidote) |
|
|
Term
| What is the drug of choice for trachael intubation (skeletal muscle relaxant) |
|
Definition
|
|
Term
| What is the MOA of nondepolarising skeletal muscle relaxants? |
|
Definition
Act as ach antagonist @ nicotinic receptors.
Bulky quat amine structure |
|
|
Term
| What reverses action of non-depolarizing skeletal muscle relaxants? |
|
Definition
| Duraction of action is decreased by cholinesterase inhibitors: But not reversible. |
|
|
Term
| How are skeletal muscle relaxants administered? |
|
Definition
|
|
Term
| Succinyl choline metabolism? |
|
Definition
| Plasma esterases, NOT acetyl cholinesterase. |
|
|
Term
| What can happens if a person has a pseudocholinesterase deficiency and is placed in succinylcholine? |
|
Definition
| Can't break it down as quickly.. Short acting drug can last hours, this is a medical emergency. |
|
|
Term
| How are most non-depolarizing agents metbaolized? Which 2 drugs are exeptions, and where are they metabolized? |
|
Definition
Liver.
Atracronium. Mivacronium: Hofmann degredation and are hydrolyzed by plasma esterases |
|
|
Term
| When are the agensts atracurium and mivacurium preferred? |
|
Definition
| Cases of hepatic and renal insuficciency |
|
|
Term
| How would one reverse the blockade from a non-depolarizing agent? |
|
Definition
-Increase the concentration of the noraml NT at the nicotinic receptor
-Cholinesterase inhibitors 9neostigmine/pyridostigmine)
-Muscarinic antagonist (glycopyrrolate) is given to offset the adverse effect of increase in cholinergic activity |
|
|
Term
| What is the main SE of succinyl choline? (when is CI). What is another SE? |
|
Definition
Hyperkalemia
CI in pts w/ burn or spinal cord injury
Autonomic ganglia/adrenal medulla are stimulated leading to bradycardia and HOTN |
|
|
Term
| Which skeletal relaxant elicits histamine release the most as a SE? |
|
Definition
|
|
Term
| Which skeletal muslce relaxant is a sympathomimetic which elicits tachycardia and htn? |
|
Definition
|
|
Term
| When you you ventilate when person is on a skeletal muscle relaxant? |
|
Definition
| ALWAYS. Respiratory parapysis. |
|
|
Term
| Which skeletal muscle relaxant can cause neuromalignant fever? |
|
Definition
|
|
Term
| What age of people is epilepsy most likely to occur? Why? |
|
Definition
<<18: rapid evvelopment
>>60: neurodegenerative |
|
|
Term
| What is the most common cause of seuzires? |
|
Definition
|
|
Term
| What are sources of seizure incidents that are secondary to a primary factor? |
|
Definition
Changes in blood flow or supply to a brian region
Tumor growing in a region of the brain
Traumatic injury
Neurodegeneration
Immune response to an infection |
|
|
Term
| Difference between generalized an partial seizures? |
|
Definition
Partial: often get an aura before
Generalized: no aura, full hemisphere |
|
|
Term
| What type of the brain is affected in absence seizures? |
|
Definition
|
|
Term
| What age group do absence seizures occur most in? |
|
Definition
|
|
Term
| Describe what happens during an absence seizure? |
|
Definition
Altered conscioiusness: stare/gaze during activities
Occur during many times during the day, but only last a few seconds |
|
|
Term
| Who is more likely to get myoclonic seizures? Children or adults? |
|
Definition
|
|
Term
| What is a myoclonic seizure? |
|
Definition
| Characterized by short, jerking contractions |
|
|
Term
|
Definition
Rigidity (tonic) with intermittent periods of jerking movements (clonic)
Usually last for a few minutes |
|
|
Term
| What is status epilepticus? |
|
Definition
Medical emergency
Tonic/clonic seizure that last for a longer period of time w/ no cesssation in contraction activity |
|
|
Term
| Which anti-convulsants are highly protein bound? |
|
Definition
Phenytoin
Fosphenytoin
Carbamazepines
Benzodiazepines
Tiagabine
Valproic Acid |
|
|
Term
| For Na channel blocking drugs: What state of the channel do they promote? |
|
Definition
|
|
Term
| What type of Ca channels does ethosuximide and valproic acid block? |
|
Definition
|
|
Term
| Which anti-convulant drug increases the duration of the GABA channel opening? |
|
Definition
|
|
Term
| Which anti-convulsant drug increases the frequency of GABA channel opening? |
|
Definition
|
|
Term
| What is the MOA of tiagabine |
|
Definition
| Increases GABA in the synapse by inhibiting GAT-1 |
|
|
Term
| If SE occur w/ an anti-convulsant drug, is it better to switch to a new drug or use an adjuvantagent? |
|
Definition
| Due to complinace, it is preferred to switch to a different monothx before adding adjuvants |
|
|
Term
| How do you apporach treatment of seizures? |
|
Definition
| Therapy is symptomatic, often initial treatment is not effective, trial and error, must be adjusted or changed, only 50% achieve complete control |
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Term
| Which anticonvulsants are prodrugs? |
|
Definition
Fosphenytoin
Oxcarbezpeine
Some barbs |
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Term
| Know which anticonvulsants have no metabolic interactions w/ other anticonvulsant drugs? |
|
Definition
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|
Term
| Which anti convulsant drugs cause hepatotoxicity |
|
Definition
Lamotrigine
Valproic Acid
Felbamate |
|
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Term
| Which anti-convulsants cause CNS depression? |
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Definition
|
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Term
| Which anti-convulsants cause renal stones? |
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Definition
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Term
| Which anti-convulsants cause teratogenicity? |
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Definition
|
|
Term
| Which anti-convulsants cause stevens johnsons syndrome? |
|
Definition
Lamotrigine
Phenytoin
Fosphenytoin
Carbamazepine
Barbitruates
Benzo's |
|
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Term
| Which anti-convulsants cause aplastic anemia? |
|
Definition
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