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30 Cards in this Set
- Front
- Back
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List the generic names / different classes of
a) neuromuscular blocking agents and their antidotes. |
a.
i. non-depolarization- receptor antagonists (bind to site prevent Ach from binding) Types- 1. Curare- paralytic 2. Aminosteroids ii. depolarization- competitive agonists- 1. succinylcholine |
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Discuss the clinical uses and therapeutic indications for
a) neuromuscular blocking agents b) spasmolytic agents. |
a.
1. intubation 2. mechanical ventilation 3. surgical procedures 4. convulsions |
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Relate their actions in the central nervous system / spinal cord / neuromuscular junction / or muscle to the adverse effects, toxicities, contra-indications and drug interactions of:
a) neuromuscular blocking agents b) spasmolytic agents |
a. adverse affects of Succinylcholine:
i. hyperkalemia problems may occur ii. bradycardia iii. malignant hyperthermia toxicities- hperkalemia Contra indications- burn pts, traumatic tissue injury, crush injury |
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Name the anatomical sites and pharmacological mechanisms of muscle relaxation by:
a. neuromuscular blocking agents b. spasmolytic agents |
a- nicotinic cholinergic receptor antagonists, competively inhibits Ach action
b. GABA (inhibition) binds to neuron to inhibit glutamate release |
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What are two types of Curare drugs? What are key points of the two?
Why are they better than Curare? |
long- cisatracurium- no dose adjustment (broken down in blood)
short- mivacurium- rapid recovery, broken by plasma esterase Curare is typically used by people to hunt and paralyze animals (danger) |
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What are types of aminosteroids?
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long- pancuronium
intermediate- vecuronium, rocuronium |
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Compare and contrast Pancuronium, Vecuronium, and Rocuronium?
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Panc- increased heart rate, renal elimination
Vecron- biliary elimination Rocuronium- rapid onset |
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What is functional effect of succinylcholine?
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1. establishes new resting membrane potential
2. stimulates, then paralyzes, Phase I 3. not degraded by Acetolcholinesterase (Phase II) |
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List the generic names / different classes of
b) spasmolytic agents |
All internueuron CNS except #4
1. Baclofen- Gaba-b agonist (presynaptic K channel) 2. Diazepam- GABA-a agonist (post snaptic Cl channel) 3. Tizanidine- a2 adrenergic agonist 4. Dantrolene- ryanodine- antagonist (peripheral muscle)- anecdote for hyperthermia, takes place on ryanodine receptor so Ca is not released |
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What are general adverse effects of spasticity drugs?
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General Adverse
1. sedation- central agents- diazepam, baclofen, tiazedine, dantrolent 2. muscle weakness- dantrolen, diazepam, baclofen, tiazinidine |
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What are the general four spasm medications and general therapeutic uses of each?
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a. baclofen- MS, oral or intrathecal
b. Diazepam- cerebral palsy, iv c. tizanidine- ms and stroke d. dantrolene- sever spasticity |
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What are more specific adverse effects of spasticity drug:
a.dantrolene b. diazepam c. baclofen |
a. liver toxicity, females, pt >35
b. physical dependance c. seizures, withdrawal |
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For non-specific treatment of muscle spasms what two main drugs are used?
What is the name for class of drugs that non-specifically inhibit muscles? |
1. carisoprodol (soma)
2. cyclobenzaprine (Flexeril) polysynaptic inhibitors |
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What are key points of the drugs...
a. Carisoprodol (Soma) b. Cyclobenzaprine (Flexeril) |
a. high abuse potential, meprobromate metabolite
b. non-sedating abilities, tricyclic anti-depressant (problems) |
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List and describe key features of the prototype non-steroidal anti-inflammatory agents (NSAIDs) and the related analgesic agent, acetaminophen.
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1. analsgesic- reduce pain
2. anti-inflam- reduce heat, redness, swelling 3. anti-pyretic-reduce heat |
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Recognize and describe the inflammatory disorders for which NSAIDs can provide safe and effective symptomatic relief.
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Inhibit formation of prostaglandins...
1. pain 2. inflammation 3. fever 4. thrombosis 5. cancer |
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Explain why NSAIDS are generally indicated for these situations.
a. Osteoarthritis and related arthritides b. Bursitis c. Gout |
relieve pain and inflammation of
all joint muscular disorders |
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Explain why NSAIDS are generally indicated for these situations.
d. Ankylosing Spondylitis e. Dysmenorrhea (painful menstruation) |
has elements of inflammation
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Recognize and describe inflammatory or medical disorders for which NSAIDs are generally contra-indicated or ineffective.
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inflammation of gut problems, liver, pancreas
infectious problems of inflammation (infection from virus, bacteria, dicks) |
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Explain why NSAIDs are contra-indicated for these situations.
a. Gastritis b. Colitis c. Pancreatitis |
gut inflammation not indicated due to: COX-1 physiologically needed to combat ulcers in stomach
Pancreatitis is infection inflammation |
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Explain why NSAIDs are contra-indicated for these situations.
d. Hepatitis e. Meningitis f. Endocarditis |
infectious inflammation not indicated fix fever but not infection
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Explain why NSAIDs are contra-indicated for these situations.
g. Bronchitis h. Sinusitis i. Rhinorrhea j. Sepsis/septicemia |
contra indicated for infections
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Explain the pharmacological rationale for development and use of celecoxib as an anti-inflammatory drug.
Explain why it does not affect gastric areas... Why would it still cause edema and increased BP? |
quest to find an anti-inflammatory agent that lacks GI toxicity (gastric sparing NSAID)
Spares Cox-1 so gastric risks are low Renal system uses COX-2 physiologically so it is still affected by drug --> symptoms of edema and BP from kidney effects |
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Differentiate on the basis of their pharmacological mechanism of action, their distinctive therapeutic uses (analgesic, anti-inflammatory, anti-pyretic and antithrombotic actions) and their adverse effects.
1. acetaminophen 2. aspirin, |
Both are analgesic (pain) and anti-pyretic (fever)
1. acetaminophen does not inhibit COX-1 or 2... its action is anti-pyretic action is slightly mysterious Too much = liver problems 2. inhibit COX-1, anti-inflammation, leads to gi ulcers, as a pro-drug is used for antithrombotic levels (80-160 mg). too much = many problems and death |
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Explain the biochemical basis for the hepatotoxicity of acetaminophen and the use of N-acetylcysteine as an antidote.
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In high doses of acetaminophen over production of NAPQI
Steps- 1. NAPQI – modifies reacts irreversibly with cellular proteins catastrophic cell damage Antidote: N-acetylcysteine antidote- must be given early (72+ hrs = lethal) 1. NAC restores cells’ GSH pool 2. NAC is GSH substitute and spares proteins and salvages cells |
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Describe dose-related changes in the pharmacology and toxicology of aspirin and salicylates.
a. 80-160 mg b. 325-1000 mg c. 325mg- 6 g d. 6-10 g e. 10-20 g f. >20g |
a. anti-thrombus (aspirin)
b. analgesic antipyretic c. anti-inflammatory (tinnitus) d. Respiratory alkalosis e. acidosis f. shock, coma |
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What are reasons not to use Aspirin in peds?
What is indicated for instead? |
risk of Reye's syndrome
- acetaminophen, ibuprofen |
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Name COX's following drugs are involved with...
a. salicylic acids b. propionic acids c. para-aminophenols d. coxibs |
a. (aspirin) COX-1>2- in
b. (ibuprofen, naproxin) COX-1 c. (acetaminophen)- weak CNS COX effects d. (coxibs)- COX-2>1 |
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What are the PG's of the specific parts below...and COX?
a. uterus b. vascular endothelium c. stomach/ kidney d. platelets |
A-D all from COX-1
a. PGF2-a b. PGI2 c. PGE2 d. TxA2 |
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What are the PG's of the specific parts below... and COX?
a. inflamed tissue b. inflamed endothelium |
COX-2
a. PGE2 b. PGI2 |
