Term
| Mechanism of hyper-reflexia in UMN disease |
|
Definition
inhibitory regulation of the muscle spindle (gamma) motor neurons is lost, the sensitivity of the muscle spindles consequently increases, and
hyperactivity of the myotactic reflexes (hyper-reflexia / spasticity) results |
|
|
Term
|
Definition
| Antispasmatic- Increases GABA-A receptor mediated inhibition. Acts in spinal cord on alpha motor neurons. Relieves spasms caused by local pathology, UMN disease (cerebral palsy, paraplegia) also used to manage tetanus |
|
|
Term
|
Definition
| Antispasmatic - GABA-B Agonist which are located on nerve terminals in the CNS. Decreases NT release. Use in cord injury, MS and ALS. Side effects: sedation, dizziness, muscle weakness and seizures/hallucinations on sudden withdrawel |
|
|
Term
|
Definition
| Antispasmatic - Centrally acting Alpha 2 agonist. Short acting. Decreases muscle tone and spasms, good for MS. Side effects: Hypotension, Bradycardia, Sedation, Asthenia, dry mouth. Don't use w CYP1A2 inhibitors esp. fluvoxamine and ciproflaxin. |
|
|
Term
|
Definition
1. Centrally acting muscle relaxant related to tricyclic antidepressants.
2. Doesn’t directly relax muscle or decrease neuronal conduction.
3. Use: As for carisoprodol (Soma). Not clear whether efficacy is due to
muscle relaxation, sedation, or placebo effect.
4. Not useful in treating spasticity associated with neurological disorders.
5. Has same side effects as tricyclics. Also has anti-muscarinic properties |
|
|
Term
|
Definition
1. Centrally acting skeletal muscle relaxant.
2. CNS depressant with both muscle relaxing and sedative properties.
-- Metabolite = meprobamate, a common sedative-hypnotic drug.
3. Muscle relaxing properties are minimal; Does not directly relax skeletal
muscle.
5. Use: As adjunct to rest, analgesics, PT, and other measures for relief of
discomfort due to musculoskeletal disorders. Clinical studies
have not established that relief is due to skeletal muscle
relaxation or sedation, but most experts feel that the relief is
secondary to the sedative effects.
6. Ineffective as therapy for muscle spasticity of chronic neurological
disorders, such as MS, cerebral palsy, stroke, and spinal cord injury |
|
|
Term
|
Definition
decreases excitationcontraction
coupling in the muscle fibers themselves by interfering with the release of Ca2+ from the sarcoplasmic
reticulum. 3. Adverse effects
a. muscle weakness
b. sedation / fatigue
c. diarrhea
c. symptomatic hepatitis (with chronic treatment).
4. Therapeutic Uses:
a. The treatment of spasticity associated with upper motor neuron
disorders.
b. Malignant hyperthermia |
|
|
Term
|
Definition
for treatment of spasticity associated with cervical
dystonia (A and B), blepharospasm (A), and strabismus (A).(A cleaves SNAP-25, B cleaves Synaptobrevin). |
|
|
Term
| When would you use a Serotonin (5-HT3) Receptor Antagonists? What is it not good for? |
|
Definition
for nausea and vomiting
associated with chemotherapy, radiation therapy, and surgery and anesthesia; they are not
particularly useful in the treatment of motion sickness |
|
|
Term
| Side effects of the Serotonin (5-HT3) Receptor Antagonists |
|
Definition
| headache and prolonged cardiac QTC interval |
|
|
Term
| Side Effects of Dopamine (DA2) Receptor Antagonists |
|
Definition
hypotension, anxiety, drowsiness, dysphoria, and extrapyramidal symptoms.
Droperidol is associated with prolongation of the cardiac QTc interval |
|
|
Term
| Which drugs are particularly useful for motion sickness and vertigo, and also helpful for PONV |
|
Definition
Histamine (H1)/Acetylcholine Receptor Antagonists
Promethazine, dimenhydrinate, diphenhydramine, and hydroxyzine |
|
|
Term
| Side effects of Histamine (H1)/Acetylcholine Receptor Antagonists |
|
Definition
Sedation and Dry mouth. Promethazine is also
associated with extrapyramidal symptoms. |
|
|
Term
| What is the Neurokinin 1 (NK1) Substance P Receptor Antagonist and what is it used for? |
|
Definition
Aprepitant: delayed nausea and vomiting particularly associated with cisplatin chemotherapy;
it is also useful for treating postoperative nausea and vomiting |
|
|
Term
| What are the uses and side effects of the cannibinoids? |
|
Definition
treatment of cancer
chemotherapy related nausea and vomiting. SE include activation of Central sympathetic system and marijuana like "Highs" |
|
|
Term
| When would you use a benzodiazepine as an antiemetic |
|
Definition
| For anticipatory nausea and vomiting |
|
|
Term
| Mechanism of action of local anesthetics? |
|
Definition
| Cross nerve cell membrane and block sodium gated channels. Does not affect membrane potential. |
|
|
Term
| What determines the speed of onset of local anesthetics? |
|
Definition
| PKa, most are basic but the closer the PKa to physiological pH the faster it will act. The active form is usually charged but the uncharged form is what is needed to cross the membrane. If an area is infected/ischemic it is likely to be acidic and the it there will be less drug in the uncharged form that is able to cross the nerve cell membrane and act on the sodium channel. |
|
|
Term
| What affects the potency and duration of the local anesthetics? |
|
Definition
| Lipid solubility increases both. Duration is also increased by increased protein binding. |
|
|
Term
| What factors affect the susceptibility of nerve fibers to local anesthetic blockade |
|
Definition
Size, myelination, and activity. They bind more avidly to inactivated and activated sodium channels then to resting sodium channels. In general autonomic fibers, small unmyelinated fibers mediating pain sensation,
and small myelinated mediating pain and temperature sensations are blocked
before larger myelinated fibers mediating postural, touch, pressure, and motor information |
|
|
Term
| How are the ester and amide anesthetics metabolized respectively |
|
Definition
Esters: Psuedocholinesterases=fast,
Amides: Cytochrome P450 |
|
|
Term
| Which type of anesthetics have a metabolite that commonly causes allergic responses |
|
Definition
| Esters, PABA is the metabolite |
|
|
Term
| Which type of anesthetics have a longer duration of action and a larger volume of distribution? |
|
Definition
|
|
Term
| How do you prevent and treat the central CNS effects from the local anesthetics |
|
Definition
Prevention: Benzodiazepines
Treatment: Benzodiazepines, O2 and barbituates |
|
|
Term
|
Definition
| Topical anesthetic, associated w methemoglobinemia |
|
|
Term
|
Definition
| Long-lasting amide associated with cardiovascular toxicity. |
|
|
Term
|
Definition
| An intermediate acting amide that is also used intravenously to suppress cardiac dysrhythmias |
|
|
Term
|
Definition
| A short duration ester with negligible surface activity [2]. Rarely used clinically |
|
|
Term
|
Definition
An amide with an o-toluidine metabolite that may cause methemoglobinemia. The
topical anesthetic Emla cream is a combination of lidocaine and prilocaine |
|
|
Term
|
Definition
A pure S-enantiomer amide with similar onset, potency and duration to
bupivacaine; however, it has a higher therapeutic index due to low affinity for cardiac cell sodium channels |
|
|
Term
| Which drugs are possible inducers of malignant hyperthermia |
|
Definition
| Organic inhalents: Desflurane, Isoflurane and Sevoflurane |
|
|
Term
|
Definition
| Inorganic gas. Can NOT be used as sole agent because MAC = 105% |
|
|
Term
|
Definition
| Inhalation agent, low solubility = rapid onset/emergence. High volatility. Risk of malignant hyperthermia. |
|
|
Term
|
Definition
| Inhalation agent, moderate solubilty, pungent odor. Risk for Malignant hyperthermia |
|
|
Term
|
Definition
| A non-pungent inhalational agent suitable for inhalational inductions; associated with a higher incidence of emergence delirium in some pediatric populations. Risk of malignant hyperthermia |
|
|
Term
| What are the two barbituates used in IV induction of general anesthesia? What are some of their characteristics? |
|
Definition
| Sodium Thiopental, Methohexital. Used a lot for induction. Rapid distribution after one dose. Accumulation after repeated doses. |
|
|
Term
|
Definition
| Central Alpha 2 agonist. Sedation and analgesia but poor amnesia |
|
|
Term
|
Definition
| IV for gen anesthetic. Cardiac stability but not used for maintenance due to adrenocortical suppression. |
|
|
Term
|
Definition
| IV for general anesthesia. Complete Anesthetic, NMDA Antagonist like PCP. Produces Dissociative Anesthesia, bronchodilation, sympathomimetic effects and causes an increase in intracranial pressure. |
|
|
Term
|
Definition
| Most commonly used general anesthetic in US. Flat CSHT, avoid if they have an egg allergy |
|
|
Term
| What general effects do the inhaled general anesthetics have on the Cerebral system. Which is the exception? |
|
Definition
| Increased CBF, but decreased Cerebral O2 consumption. They all increase intracranial pressure. Nitrous oxide increases O2 consumption. |
|
|
Term
| What effects do inhaled general anesthetics have on the cardiovascular system? |
|
Definition
| All decrease blood pressure except N2O which has no effect on the cardiovascular system. |
|
|
Term
| What effects do the inhaled general anesthetics have on respiratory rate |
|
Definition
| They all increase RR but decrease tidal volume and overall decrease VO2. |
|
|
Term
| What effects do the inhaled general anesthetics have on respiratory rate |
|
Definition
| They all increase RR but decrease tidal volume and overall decrease VO2. |
|
|
Term
| What effects do the IV general anesthetics have on the cerebral system |
|
Definition
| Decrease CBF, CMRO2 and ICP. Except Ketamine which increases CBF and ICP and has no effect on CMRO2 |
|
|
Term
| What effects do the IV general Anestheitcs have on the Cardiovascular system. |
|
Definition
| Etomidine has no effect. Barbituates and propofol decrease MAP, Ketamine increases MAP. |
|
|
Term
| Effects of IV general Anesthetics on respiratory system |
|
Definition
| Decrease RR and VO2 except ketamine which has no effect. |
|
|
Term
| Name the inhaled general anesthetics |
|
Definition
| Nitrous oxide, Desflurane, Isoflurane, and Sevoflurane |
|
|
Term
| Name the IV general Anesthetics |
|
Definition
| Barbituates (Sodium thiopental, and methohexital), Profonol, Etomidate, Ketamine, dexmedetomidine |
|
|
Term
|
Definition
- diazepam (Valium®)
- alprazolam (Xanax®)
- larazepam
- temazepam (Restoril)
- zolpidem (Ambien®)
- zaleplon (Sonata ® )
- escopiclone (Lunesta ®) |
|
|
Term
| List the Barbituates in the sedative hypnotic section? |
|
Definition
- phenobarbital (Luminal®)
- pentobarbital (Nembutal®)
- thiopental (Pentothal®) |
|
|
Term
|
Definition
Listed under other sleep agent. a. an agonist at a receptor subtype for melatonin
b. major indication is for insomnia characterized by difficulty in sleep
onset; major effect appears to be reducing latency to sleep,; not much
effect on sleep maitneance
c. adverse effects: sedation, dizziness, nausea
d. not associated with rebound insomnia or withdrawal; not a controled
drug |
|
|
Term
|
Definition
diazepam, baclofen, tizanidine, clyclobenzaprine HCl,
Carisoprodol, dantrolene, botulinum toxin A, botulinum toxin B |
|
|
Term
| What are some of the central effects of the opioids |
|
Definition
2. depression of respiration
3. suppression of cough (antitussive effect)
4. mioisis of pupil (in intoxicating doses; except meperidine [Demerol])
5. nausea and vomiting
6. euphoria or dysphoria
7. sedation and drowsiness, light sleep, mental confusion
8. myoclonus, seizures (high doses) |
|
|
Term
| What are some of the peripheral effects of the opioids |
|
Definition
1. gastrointestinal: constipation, due to:
a. decreased gastric motility and secretion
b. decreased intestinal secretion
c. increased tone of intestinal smooth muscle
d. decreased peristaltic contractions of intestines
2. cardiovascular: vasodilation, orthostatic hypotension
(histamine release)
3. skin: urticaria (histamine release)
4. urinary tract: increased contraction of bladder
increased contraction of sphincter
5. uterus: decreased uterine contractions |
|
|
Term
| What are the most common effects of opioids seen in clinical settings |
|
Definition
1. *sedation and drowsiness
2. * nausea and vomiting (esp. ambulatory patients)
3. * constipation
4. urinary retention
5. urticaria |
|
|
Term
| What should you never give someone that is on a MOA inhibitor |
|
Definition
| meperidine (Demerol ®), it could cause coma or even death |
|
|
Term
| List the Strong opioid agonists |
|
Definition
| 1.Morphine 2.Hydromorphine 3.Fentanyl 4.Methadone 5.oxycodone 6.meperidine(demerol) |
|
|
Term
| List the intermediate opioid agonists |
|
Definition
| 1.Codeine 2.Hydrocodone 3.Tramadol |
|
|
Term
| List the weak opioid agonists |
|
Definition
|
|
Term
| What is (Percocet®, Roxicet ® ) |
|
Definition
| Oxycodone + Acetaminophen |
|
|
Term
| loperamide (Imodium ®) and diphenoxylate (with atropine in Lomotil ®) |
|
Definition
| Opioid. weak CNS actions but very strong GI actions; used for diarrhea |
|
|
Term
|
Definition
| weak opioid; common in OTC cold preparations for antitussive effects |
|
|
Term
|
Definition
a. diacetylmorphine; metabolized to morphine in brain (i.e., a prodrug)
b. not approved for use in U.S.; known as diamorphine in Europe |
|
|
Term
| List the opioid antagonists |
|
Definition
| 1.Naloxone 2.Naltrexone 3.Alvimopan |
|
|
Term
|
Definition
1. pure antagonist at multiple opioid receptors for Rx of overdose
2. short duration of action
3. parenteral administration only |
|
|
Term
|
Definition
1. pure antagonist for treatment of opioid and alcohol abuse, blocks euphoric
effect of parenteral opioid
2. reduces craving for alcohol and other drugs of abuse
3. oral administration only
4. as Vivitrol ®, sustained release, injectable form, one month duration |
|
|
Term
|
Definition
1. A mu-specific opioid antagonist effective in the GI tract
2. used in-hospital only to help restore GI motility in patients having bowel resections |
|
|
Term
|
Definition
mixed partial agonist/ antagonist:
A. agonist at mu receptors but with low intrinsic activity; very weak antagonist
activity
B. As Buprenex ®), used as post-op analgesic; advantage over morphine is
questionable |
|
|
Term
|
Definition
Mixed Opioid Agonist-Antagonists. formulation includes naloxone to prevent abuse via
iv injection but retain oral effectiveness |
|
|
Term
| What different classes of drugs have been used to treat neuropathic pain |
|
Definition
| Specific antiepileptic drugs (gabapentin), antidepressants (amitriptyline), Na+ and Ca2+ channel blockers, opioids, corticosteroids have shown some efficacy. |
|
|
Term
| Competitive antagonist of benzodiazepines |
|
Definition
|
|
Term
| Which benzo would be used for preop sedation |
|
Definition
|
|
Term
| What class of drugs are the 5HT1 D agonists |
|
Definition
|
|
