Drugs Flashcards
1
Q
Tramadol
- Mechanism of Action
- Side effects
mnemeonic: “Tram it all”
A
- Partial Mu Opioid receptor agonist; affinity for the mu receptor is 6000 times less than morphine.
- A second, non-opioid mechanism is theorized because there is a lack of reversibility of the analgesia and little withdrawal symptoms following naloxone administration. This other mechanism of action involves tramadol’s ability to inhibit neuronal uptake of norepinephrine and serotonin. Both of these neurotransmitters are involves in the antinociceptive effects of descending inhibitory pathways of the central nervous system.
- The main advantage of tramadol over other opioids analgesics is its lower risk of respiratory depression, constipation, and potential for abuse. Because tramadol binds to the mu receptor, there is a potential for respiratory depression however it is unlikely to be clinically relevant. Additionally, it has only a minor effect on gastrointestinal transit time, leading to a lower risk of ileus. The incidence of nausea and vomiting varies based on a study, while some reported no increased risk others reported an increased risk – the results depended on the dose and circumstances surrounding administration. Tramadol has no clinically relevant hemodynamic effects.
- increased risk of serotonin syndrome and seizures in patients taking SSRIs, SNRIs, TCAs and MAOI.
2
Q
Meperidine
- Mechanism of Action
- Side Effect
A
- Same mechanism of action as morphine, which is acting as an agonist to the mu-opioid receptor. The anti-shivering effect may involve the stimulation of k-opioid receptors. Meperidine also has some local anesthetic effects because of interactions with sodium ion channels. Also, meperidine has stimulant effects by inhibition of the dopamine transporter (DAT) and norepinephrine transporter (NET)
- Shock, seizure, syncope, hallucination (especially among the geriatric population), potential opioid dependency, withdrawal symptoms if discontinued without tapering down, opioid-induced androgen deficiency (chronic use), bradycardia, cardiac arrest, severe hypotension, apnea, respiratory failure.
- Parallel use with cytochrome P450 3A4 inhibitors or discontinuation of P450 inducers causes the increase of the meperidine concentration that can result in a fatal overdose.
- Concomitant use of meperidine and monoamine oxidase inhibitors (MAOI) can cause coma, severe respiratory failure, cyanosis, and hypotension.
3
Q
Butorphanol
- Mechanism of action?
- Side effect profile
A
- Mixed agonist-antagonist used in labor and delivery (partial Mu agonist, Kappa antagonist)
- Can precipitate withdrawal in opioid tolerant patient
- CNS stimulation, mild analgesia
4
Q
Norepinephrine
Epinephrine
Isoproterenol
A
- Norepinephrine:
- Rx: 0.01-0.2 mcg/kg/min
- Sympathomimetic drug: its effects when given by intravenous injection of increasing heart rate and force and constricting blood vessels make it very useful for treating medical emergencies that involve critically low blood pressure.[30] Surviving Sepsis Campaign recommended norepinephrine as first line agent in treating septic shock which is unresponsive to fluid resuscitation, supplemented by vasopressin and epinephrine. Dopamine usage is restricted only to highly selected patients
- Epinephrine:
- Rx: 0.01 - 0.2 mcg/kg/min
- Isoproterenol
- Rx: 2 - 10 mcg/kg/min
5
Q
Drugs associated with MYOCLONUS
mnemonic: “KEPaMine”
A
- Ketamine
- Etomidate
- Propofol
- Methohexital
6
Q
Digoxin
- Mechanism of Action
- Side Effects
- Coniditons that increase risk of Digoxin toxicity
- Rx for Digoxin Toxicity
A
- SERCA, or sarcoplasmic reticulum Ca2+ ATPase, is a calcium pump that acts to replenish the sarcoplasmic calcium stores in the cardiac myocyte during the repolarization phase. This is important because free cytoplasmic calcium in diastole leads to after depolarizations (i.e. arrhythmias) and because the more calcium stores are replenished, the stronger the contraction in the following depolarization cycle (i.e. inotropism).
- However, SERCA is not the only mechanism clearing calcium during the repolarization phase, the other main one is the Na/Ca exchanger. The Na/Ca exchanger extrudes Ca out of the cell in exchange for Na moving into the cell, and thus its activity is influenced by the electrochemical gradient of Na. Digoxin inhibits the membrane Na+/K+ ATPase, leading to increased intracellular Na, which in turn decreases the extrusion of Ca through the Na/Ca exchanger, and allows for more Ca to be sequestered into the sarcoplasmic reticulum by SERCA.
- Yellow vision, HYPOKALEMIA, Nausea vomiting, Dysrhythmia
- Hypokalemia; Hypoxemia; Hypothyroid; Hypoglycemia; Hypomagnesemia; Hypercalcemia
- MgSO4 2 g IV bolus; Digibind - DO NOT Rx with CALCIUM
7
Q
Cephalosporins
- Mechanizm of Action
- State some 1st, 2nd, 3rd, and 4th generation generations
A
- inhibit cell wall biosynthesis by binding Penicillin binding proteins which stops peptidoglycan synthesis. Penicillin binding proteins are bacterial proteins that help to catalyze the last stages of peptidoglycan synthesis, which is needed to maintain the cell wall.
- Generations
- 1st Generation - Cefazolin, Cefalexin
- Activity against MSSA and Strep; Proteus mirabilis, some Escherichia coli, and Klebsiella pneumoniae (“PEcK”)
- 2nd Generation - Cefoxitin, Cefaclor
- Activity against “HEN” Haemophilus influenzae, Enterobacter aerogenes and some Neisseria + the PEcK described above
- 3rd Generation - Ceftriaxone, Cefpodoxime
- Third-generation cephalosporins have a broad spectrum of activity and further increased activity against gram-negative organisms. They may be particularly useful in treating hospital-acquired infections, although increasing levels of extended-spectrum beta-lactamases are reducing the clinical utility of this class of antibiotics. They are also able to penetrate the central nervous system, making them useful against meningitis caused by pneumococci, meningococci, H. influenzae, and susceptible E. coli, Klebsiella, and penicillin-resistant N. gonorrhoeae.
- 4th Generation - Cefepime
- Fourth-generation cephalosporins are zwitterions that can penetrate the outer membrane of Gram-negative bacteria.[25] They also have a greater resistance to β-lactamases than the third-generation cephalosporins. Many can cross the blood–brain barrier and are effective in meningitis. They are also used against Pseudomonas aeruginosa
- 1st Generation - Cefazolin, Cefalexin
8
Q
What are the target receptors of metoclopramide?
A
D2 antagonist
5HT3 antagonist
5HT4 agonist
9
Q
What are the indicated treatments for digoxin toxicity?
A
Digibind
treatment of hyperkalemia (EXCEPT CALCIUM)
magnesium (EXCEPT WITH AV BLOCK)
lidocaine to treat ventricular arrhythmias
10
Q
How are midazolam and diazepam metabolized?
How is lorazepam metabolized?
mnemonic: “LOTs of Glucuronidation”
A
- cytochrome P450 oxidation in the liver
- glucuronidation in the liver (also oxazepam and temazepam) * no active metabolites*
11
Q
Which opioid side effects are associated with Mu 1 receptors? Mu 2 receptors? Kappa receptors? Delta and sigma receptors?
A
Mu 1: urinary retention and euphoria
Mu 2: constipation, physical dependence, and hypoventilation
Kappa: dysphoria and hallucinations
Delta and sigma: dysphoria
12
Q
Which narcotic has local anesthetic activity?
A
meperidine
13
Q
Acute Amphetamine vs Chronic Amphetamine use and its affecto on MAC
A
Acute Amphetamine: Increases MAC
Chronic Amphemine: Lowers MAC
14
Q
What are the OSHA guideline for exposure limits to inhaled anesthetics?
A
N2O: 25 ppm/hour
all others: 2 ppm/hour
15
Q
What are the clinical uses of glucagon?
A
hypoglycemia
reducing biliary spasm
beta-blocker overdose
17
Q
Linezolid Mechanism of Action
A
Linezolid disrupts bacterial growth by inhibiting the initiation process of protein synthesis—a mechanism of action that is unique to this class of drugs.
