Term
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Definition
(synthetic PGE1 analog) is the most effective in both preventing and treating NSAID gastropathy
causes a dose related diarrhea in 25 to 40 per cent of patients, it is reserved for high-risk patients |
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Term
| NSAIDs (Non-Steroidal Anti-Inflammatory Drugs ) |
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Definition
most frequently used agents to provide antiinflammatory analgesia for rheumatologic diseases, and other musculoskeletal pain states
cyclooxygenase inhibition (decr prostoglandin synthesis)
Potential damage to the GI tract (prostaglandins have imp role in protecting the stomach lining, so inhibition for long time can damage GI) , kidneys (analgesic nephropathy)
severity and incidence are increased in the elderly |
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Term
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Definition
| The GI tract can be protected from NSAIDS by the addition of the synthetic prostaglandin E1 analogue *** to stimulate the production of mucous bicarbonate |
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Term
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Definition
| may be selective for cox-3 in the CNS. It has minimal anti-inflammatory effects because it is inactivated by peroxides produced by cells in inflamed tissue. Useful as an analgesia/antipyretic. |
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Term
| amide-type local anesthetics |
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Definition
| **require hepatic cytochrome P450 metabolism to yield more polar metabolites that can be readily excreted in urine. If they accumulate they will block sodium channels in non-target excitable tissues such as heart and brain |
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Term
| ester-type local anesthetics |
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Definition
| fairly short-acting because they are metabolized by plasma and tissue esterases to form para-aminobenzoic acid (PABA) derivatives. PABA is potentially antigenic, so some clinicians assume the risk of hypersensitivity is avoided by using amide-type anesthetics |
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Term
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Definition
| weak bases (charged in acidic environment) |
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Term
| infected, ischemic tissue pH |
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Definition
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Term
| cocaine & benzocaine lipid solubility? |
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Definition
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Term
| chain of anesthetic activity on different nerve fibers |
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Definition
c fibers->a fibers->motor fibers
(pain and proprioception before motor) |
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Term
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Definition
| added to local anesthetic to reduce local blood flow which usefully prolongs the duration of local anesthetic action and decreases bleeding into the wound. |
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Term
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Definition
will directly compete with epinephrine for alpha receptors to reverse vasoconstriction
The increased blood flow will also result in more rapid washout of local anesthetic. There will likely be some increased bleeding and the patient is going to experience a resurgence of pain sensation |
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Term
| biogenic amines serotonin and noradrenaline |
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Definition
| The descending inhibitory pathways from the brain stem to the dorsal horn are mediated by the |
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Term
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Definition
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Term
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Definition
| depress respiration by reducing brain stem chemoceptor sensitivity to reduction in CSF pH, and also reduce pontine and medullary control of rhythmicity and depth |
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Term
| nausea & vomiting, Metoclopramide |
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Definition
**relatively uncommon in recumbent patients receiving morphine, but occurs in over 40 per cent of ambulatory patients. This vestibular mechanism responds to motion sickness therapy (scopolamine, dimenhydrinate)
at higher doses there is a dopaminergic component for which dopamine antagonists are more effective. *** is especially useful because it also counteracts gastro-enteric distention |
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Term
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Definition
| inhibit gastric emptying , incr constipation, incr urinary retention |
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Term
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Definition
| euphoria in nucleus accumbens, dysphoria in limbic and cortical sites, tranquility and anxiolytic effects: in the locus ceruleus, sedation: net central inhibitory effect, although depression of inhibitory pathways may predominate in some cases to produce excitation |
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Term
| side effects of morphine (opiods) |
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Definition
| suppression of cough, Improves pulmonary blood flow and vascularization, release of histamine can result in orthostatic hypotension, flushing, urticaria and pruritis |
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Term
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Definition
| depressed cellular immune response, thermoregulation: hypothalamic effect, usually slightly reduced body temperature |
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Term
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Definition
| affected menstrual cycle, pupillary constriction (miosis): efferent effect via the visceral motor branch of the occulomotor cranial nerve |
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Term
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Definition
Most ***are mu agonists,
A few are kappa agonists (pentazazine), and need a lot more drugs to reverse respiratory repression than would if caused by mu agonists,
pain is a powerful physiological antagonist of ** respiratory depression, which can be a problem if the pain suddenly remits |
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Term
| Naloxone (and the longer acting opioid antagonists, nalmefene and naltrexone) |
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Definition
| are more potent antagonists at mu- than kappa- opioid receptors |
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Term
| morphine, heroin, and fentanyl |
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Definition
| relatively selective mu-opioid agonists |
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Term
| nalbuphine, pentazocine, butorphanol, diphenoxylate, propoxyphene, or fentanyl analogs such as sufentanyl |
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Definition
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Term
| opioid antagonists, opioid |
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Definition
| *** can wear off before the respiratory depressive effects of the **, so observe for relapse of respiratory depression!!! |
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Term
| Phenothiazines (e.g. perphenazine) and butyrophenones (e.g. droperidol) |
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Definition
| may be used to treat postoperative nausea. Opioids cause peripheral vasodilatation which the body will counteract via alpha1-adrenergic sympathetic responses. *** block these with the possibility of severe postural hypotension |
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Term
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Definition
| This opioid is 80x as potent as morphine but note that with the skin patch bioavailability is 100% (no first pass effect). |
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Term
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Definition
| The cough reflex, integrated centrally in the medulla, is very sensitive to *** so that useful cough suppression is possible without respiratory depression or addiction. Most commonly used suppressants are dextromethorphan and codeine |
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Term
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Definition
| The opioid drugs widely used in clinical practice belong to two major classes, the chemical relatives of morphine, and synthetic drugs described as *** derivatives |
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Term
| “piperidine” derivatives (class of opiod drugs) |
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Definition
| popular analgesic, meperidine, belongs in this class as do fentanyl and its relatives that are so very potent. So, also, does loperamide which is only available for oral use, is poorly absorbed, probably works locally within the gut wall, and does not cross the blood-brain barrier. These features make the drug safe enough for OTC use and it is effective in increasing transit time. It does this because, like morphine, it is an agonist at mu-receptors |
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Term
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Definition
| an agonist at opioid receptors, but it is taken by mouth, poorly absorbed, and little reaches the CNS. So it acts on the gut as an opioid without unwanted systemic effects |
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Term
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Definition
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Term
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Definition
| Injections of *** are used in the treatment of bradycardia, asystole and pulseless electrical activity (PEA) in cardiac arrest because the main action of the vagus nerve of the Parasympathetic nervous system on the heart is to decrease heart rate. *** blocks this action. Is a competitive antagonist for the muscarinic ACh receptor. |
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Term
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Definition
| Used for short-term muscle relaxation in anesthesia and intensive care, usually for facilitation of endotracheal intubation. Despite its adverse effects, including life threatening malignant hyperthermia, hyperkaliemia and anaphylaxis, it is perennially popular in emergency medicine because it arguably has the fastest onset and shortest duration of action of all muscle relaxants. |
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Term
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Definition
| aminosteroid non-depolarizing (does not cause initial stimulation of muscles before weakening them) NM blocker or muscle relaxant used in modern anaesthesia, to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. |
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Term
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Definition
| Removes vagal inhibition on heart (increased heart rate), Mydriasis (beautiful lady, but her vision is blurred due to cycloplegia [loss of accommodation]), Relaxes bronchial smooth muscle, Antisialagogue (inhibits saliva and bronchial secretions), Anhidrosis (inhibits sweating), Urinary retention and constipation, Mental confusion and hallucinations, Reduce gastric acid secretion |
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Term
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Definition
| Parasympathomimetic and a reversible AChE inhibitor. Cholinergic neurotransmission is still rapid but not brief. Neostigmine binds to the anionic site of cholinesterase. The drug blocks the active site of AChE so the enzyme can no longer break down the ACh molecules before they reach the postsynaptic membrane receptors. This allows for the threshold to be reached so a new impulse can be triggered in the next neuron. In myasthenia gravis there are too few ACh receptors so with the AChE blocked, ACh can bind to the few receptors and trigger a muscular contraction. |
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Term
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Definition
| It is used to improve muscle tone in people with myasthenia gravis and in anesthesia at the end of an operation, to reverse the effects of non-depolarizing muscle relaxants such as rocuronium. |
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Term
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Definition
| Parasympathomimetic and a reversible AChE inhibitor. Cholinergic neurotransmission is still rapid but not brief. To prevent constant stimulation once the ACh is released, an enzyme called AChE is present in the endplate membrane close to the receptors on the post synaptic membrane, and quickly hydrolyzes ACh. |
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Term
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Definition
inhibits AChE in the synaptic cleft, thus slowing down the hydrolysis of ACh.
Used to treat muscle weakness in people with myasthenia gravis. |
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Term
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Definition
| Acts as a depolarizing NM blocker. It imitates the action of ACh at the NM junction, acting non-competitively on muscle type nicotinic receptors. It is degraded not by AChE but by butyrylcholinesterase, a plasma cholinesterase. This hydrolysis by butyrylcholinesterase is much slower than that of ACh by AChE. |
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Term
| Onabotulinium Toxin Type A (BTX-A): aka (Botox) |
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Definition
| a neurotoxin that blocks neuromuscular transmission. Used to treat muscle spasms and Upper Motor Neuron syndrome, inhibits sweating. Injecting overactive muscles with minute quantities of BTX-A results in decreased muscle activity by blocking the release of ACh from the neuron by preventing the vesicle where the ACh is stored from binding to the membrane where the NT can be released. This will effectively weaken the muscle for a period of three to four months. |
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Term
| Onabotulinium Toxin Type A (BTX-A): aka (Botox) |
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Definition
The toxin proteolytically degrades the SNAP-25 protein (a SNARE protein) which is required for vesicle fusion that releases NTs from the axon endings (in particular ACh). Botulinum toxin specifically cleaves these SNAREs, and so prevents neurosecretory vesicles from docking/fusing with the nerve synapse plasma membrane and releasing their NTs.
Though it affects the nervous system, common nerve agent treatments (namely the injection of atropine ) will increase mortality by enhancing botulin toxin's mechanism of toxicity |
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Term
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Definition
| Though it affects the nervous system, common nerve agent treatments (namely the injection of *** ) will increase mortality by enhancing botulin toxin's mechanism of toxicity |
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Term
| Explain why atropine minimizes adverse effects without compromising the therapeutic effects of an AChE inhibitor in treatment of Myasthenia Gravis |
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Definition
| An AChE inhibitor prevents breakdown of ACh at all cholinergic synapses, including ganglionic nicotinic receptors, all post‐ganglionic muscarinic receptors, and NM nicotinic receptors. Myasthenia Gravis affects post-synaptic receptors. The therapeutic effects are due to increased ACh at NM nicotinic receptors, whereas most unwanted effects are autonomic muscarinic and are thus blocked by atropine (prototypical muscarinic antagonist) without interfering with the intended cholinergic effects at motor end‐plate nicotinic receptors. |
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Term
| Explain how depolarizing and non-depolarizing NM agents produce paralysis of skeletal muscles |
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Definition
Neuromuscular (NM) nicotinic antagonists produce non‐depolarizing skeletal muscle paralysis by competitively blocking nicotinic receptors in the NM junction (compete with ACh). Also mentions curare, used by the tribesmen of the Amazon. Since non-depolarizing NM blockers are competitive receptor antagonists, a cholinergic drug (like neostigmine) can be used to reverse the block, but keep an eye on the patient in case the cholinergic drug wears off before the NM blocker!
*Remember: Competitive antagonism can always be overcome by increasing the concentration of agonist!!! |
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Term
| Explain why indirect cholinergic drugs can reverse the effects of non-depolarizing NM blockers, but intensify the skeletal muscle paralyzing effects of succinylcholine |
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Definition
| NM nicotinic antagonists produce non‐depolarizing skeletal muscle paralysis by competitively blocking nicotinic receptors in the NM junction. An AChE inhibitor such as pyridostigmine would enhance ACh competition for those receptors and reverse the paralysis. A NM nicotinic agonist such as succinylcholine will depolarize motor endplates and prevent repolarization. An AChE inhibitor such as pyridostigmine would intensify the paralysis. |
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Term
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Definition
| stimulation of GABAB receptors inhibits glutamate release in the spinal cord (used to treat muscle spasms in MS/ALS) |
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Term
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Definition
| inhibits release of calcium from the sarcoplasmic reticulum (used to treat tetany/malignant hyperthermia). |
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Term
| cyclobenzaprine, hydroxyzine , Lorazepam |
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Definition
| • All sedative drugs reduce tonic somatic alpha and gamma motor neuron tone. Some, such as ***, are marketed for muscle spasms. Sedating antihistamines such as *** and benzodiazepines such as *** have similar efficacy. |
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Term
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Definition
| potent CYP inducer, dose‐related neurotoxicity, rare idiosyncratic agranulocytosis. good for focal seizures |
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Term
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Definition
| only for absence seizures, minimal learning impairment, valproic acid is an option. prevents absence seizures by blocking calcium channels in the thalamus (so does valproic acid) |
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Term
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Definition
| 1st line drug to abort acute generalized tonic‐clonic seizures, status epilepticus |
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Term
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Definition
| broadest spectrum for treatment of epileptic seizures, relatively less impairment of cognitive function, higher risk of fetal malformations, rare idiosyncratic liver failure |
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Term
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Definition
| used for all types of seizures except abcense. elimination pathway saturates within therapeutic dose range, bad side effects- gum overgrowth and hirsuitism, fetal hydantoin syndrome |
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Term
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Definition
| sedating and potent CYP inducer (dangerous for pregnancy!). Used to treat epilepsy |
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Term
| DRESS syndrome: adverse effects associated with aromatic amine (epoxide-forming) antiepileptic drugs (e.g., phenytoin, phenobarbital, carbamazepine). |
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Definition
| Failure to detoxify drug metabolites related to a genetic deficiencyof drug metabolizing enzymes and acquiring herpes virus 6 which causes inhibition of the same enzymes. Accumulation of reactive drug metabolites leads to alteration of cellular proteins. The proteins become immunogenic, and a dramatic immune attack on the modified proteins in multiple target organs ensues. 2/10,000 people. |
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Term
| Stevens – Johnson syndrome. (adverse effects associated with aromatic amine (epoxide-forming) antiepileptic drugs (e.g., phenytoin, phenobarbital, carbamazepine). |
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Definition
- T cell mediated response. Beginning looking like erythema multiforme, with lesions appearing symmetrically on elbows, knees, palms & soles. Later - Nikolsky's sign (toxic epidermal necrolysis) superficial layers of skin slip free from the lower layers with a slight rubbing pressure. Large areas of the skin will blister and peel away leaving wet, red and painful areas. Rare -6 cases per million, but
10%-30% of pt’s health records say they have this (over diagnosed). Han Chinese, Hong Kong Chinese and Thai w/ genetic HLA-B* 1502 should not be given these. If you catch one of these don’t just switch them to another aromatic drug b/c it will happen again. |
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