ITE CA2 Pharm 3 Flashcards
Ancef with hx penicillin allergy
Higher Risk
If the patient’s penicillin reaction was less than 10 years ago OR they had IgE-mediated symptoms after receiving a penicillin OR they had a severe non-IgE-mediated reaction, do not give cephalosporins. Recommend skin testing to the patient before future surgical procedures. If unsure about the reaction and timing, recommend skin testing prior to the administration of penicillins. Skin testing should not be recommended to patients who had a severe exfoliative past reaction to penicillin, such as toxic epidermal necrolysis.
Low Risk
If patient’s penicillin reaction is more than 10 years ago AND they had no IgE-mediated symptoms AND they had no severe non-IgE-mediated reactions, then they are low risk (< 1%) for having a reaction if they receive cephalosporins. The risk of anaphylaxis is very small in these patients.
mechanism of action of echinocandins and name some
caspofungin, micafungin and anidulafungin
Echinocandins are the preferred first line treatment of candidemia. They act by inhibiting 1,3-beta-D-glucan synthase and cell wall synthesis.
-azoles
name some
MoA
other considerations
The azole class of antifungals includes voriconazole, fluconazole, and itraconazole. These act by inhibiting the P-450 dependent enzyme 14-alpha-demethylase which converts lanosterol to ergosterol for the cell membrane. Both fluconazole and voriconazole have been used to treat candidemia. Itraconazole is not used for systemic infections. The azoles will inhibit cytochrome P-450 enzymes including CYP2C19, CYP3A4, and CYP2C9. Care must be taken when giving azole antifungals with other cytochrome metabolized medications.
Amphotericin B
MoA
side effects
Amphotericin B was the drug of choice for decades. It acts by binding ergosterol in fungal cell membranes causing cellular leaking and cell death. However several randomized clinical trials have shown non-inferiority with azole and echinocandin antifungals. Therefore these classes are now the preferred first line treatment of candidemia as amphotericin can be nephrotoxic, cardiotoxic, and associated with hypokalemia and anaphylaxis
Candida glabrata is intrinsically resistant to .
Candida glabrata is intrinsically resistant to fluconazole.
obesity and butyrylcholinesterase activity
increased
what drugs cause direct cerebral vasodilation
Calcium channel blockers, nitroglycerin, hydralazine, nitroprusside, and adenosine cause direct cerebral vasodilation.
Midaz in uremia
Uremia will result in a higher concentration of free-fraction, unbound midazolam. The dosage should, therefore, be decreased especially when used as premedication
where is angiotensinogen made
liver
what clotting factors are made outside the liver
3, 4, von willebrand (von w is made in liver and also in endothelial cells)
where are platelets made
megakaryocytes in the plasma
most common complication of retrobulbar block
retrobulbar hemorrhage
Clevidipine
class
metabolism
how are other drugs in its classed metabolized
Clevidipine is an intravenous, ultra-short acting, dihydropyridine calcium channel antagonist with selectivity for arteriolar vasodilation that is rapidly metabolized by plasma and red cell esterases providing its short duration of action. The other calcium channel blockers are metabolized by the cytochrome P450 system in the liver.
Muscarinic effects of cholinergic drugs include
Nicotinic effects of cholinergic drugs include
Muscarinic effects of cholinergic drugs include bradycardia, bronchospasm, miosis, salivation, lacrimation, defecation, urination, and sweating.
Nicotinic effects of cholinergic drugs include muscle fasciculations, weakness, paralysis, and tachycardia.
Muscarinic effects with mnemonic
Mnemonic devices for muscarinic effects:
SLUDGE-Mi “Sludge Me”: Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis, Miosis
DUMBELS: Defecation/Diaphoresis, Urination, Miosis, Bradycardia/Bronchospasm, Emesis, Lacrimation, Salivation
how do dex and clonidine work
Alpha-2 receptors are found presynaptically and inhibit norepinephrine release. Clonidine and dexmedetomidine are alpha-2 agonists. They cause a decrease in sympathetic outflow from the central nervous system, leading to sedation and bradycardia. Clonidine has a 200:1 selectivity for alpha-2 compared to alpha-1. Dexmedetomidine preferentially binds alpha-2 with a ratio of 1600:1.
The mechanism of beta-agonist induced bronchodilation is
The mechanism of beta-agonist induced bronchodilation is via Gs effects, cAMP generation, activation of protein kinase A, decreased intracellular calcium, and resulting airway muscle relaxation.
Stimulation of central (nicotinic or muscasrininc?) acetylcholine receptors can lead to seizures.
Stimulation of central nicotinic acetylcholine receptors can lead to seizures. Caution should be used in patients who are taking nicotinic acetylcholine receptor agonists such as varenicline when considering the use of physostigmine to reverse central depressant effects of anticholinergic medications.
medications with nicotinic properties
medications with nicotinic properties include varenicline, bupropion, dextromethorphan, hexamethonium, and several nondepolarizing neuromuscular agents.
What is the anti-inflammatory mechanism of dexamethasone
Dexamethasone is a glucocorticoid that agonizes the NR3C1 receptor (also known as glucocorticoid receptor or GCR) to upregulate anti-inflammatory proteins and repress inflammatory mediator production. Steroids also inhibit prostaglandin synthesis at the beginning of the arachidonic acid pathway.
CYP 450 inducers
Rifampin Phenytoin Carbamazepine Glucocorticoids St. John's Wort Tamoxifen Phenobarbital, Primidone
CYP 450 inhibitors
Grapefruit juice
Protease inhibitors (ritonavir, indinavir)
Azole antifungals (ketoconazole, itraconazole)
Select SSRIs (above)
Cimetidine
Quinidine
Macrolide antibiotics (erythromycin, clarithromycin)
SSRIs and inhibition of CYP enzymes Fluoxetine (Norfluoxetine) Fluvoxamine Paroxetine Sertraline Escitalopram Citalopram
Fluoxetine (Norfluoxetine) 3A4, 2D6 Fluvoxamine 3A4, 2D6, 2C9, 2C19 Paroxetine 2D6 Sertraline 2D6 Escitalopram None Citalopram None
Cimetidine vs ranitidine
Of the two H2-receptor antagonists commonly used in the perioperative setting (cimetidine and ranitidine), ranitidine offers a longer duration of action and fewer side effects.
epi effect on blood vessels
The effect of epinephrine on blood vessels depends on the receptor. Alpha receptors cause vasoconstriction but beta receptors cause vasodilation.
Buprenorphine
Buprenorphine, a partial μ-receptor agonist, is a very effective agent at mitigating opioid withdrawal given its action at the μ-receptor itself. As a partial agonist, it has a ceiling effect for its analgesic and euphoric properties, as well for its respiratory depressive effects. It is often administered in combination with naloxone in an oral formulation to discourage its abuse.
Naloxone vs naltrexone
Naltrexone is an orally bioavailable opioid antagonist. It may be utilized during medication-assisted opioid withdrawal as the withdrawal period nears the end in order to antagonize the effects of opioids. This diminishes any benefit that a patient with an opioid-use disorder may experience should they attempt to further abuse opioids while on this therapy. Acute ingestion of naltrexone in a patient on chronic opioid therapy would precipitate or worsen withdrawal symptoms.
Because naloxone is not orally bioavailable, it has no clinical effect when taken orally in combination with buprenorphine. Should this formulation be abused, however, and either be injected or snorted, the naloxone bypasses first-pass hepatic metabolism and exerts its antagonistic effect, precipitating an acute withdrawal. In this way, this formulation encourages the proper and safe use of the buprenorphine.
Omalizumab
Omalizumab is a monoclonal anti-IgE antibody. It is used as an antihistamine anti-inflammatory for patients with severe asthma.
Budesonide
Budesonide is an inhaled corticosteroid that blocks late-phase reactions to allergens, reduces airway hyperresponsiveness, and inhibits inflammatory cell migration and activation.
Mepolizumab
Mepolizumab prevents eosinophil action by blocking interleukin-5.
Montelukast
Montelukast is a leukotriene modifier used as an alternative to long-acting beta agonist in treating mild intermittent asthma
Immunoglobulin E (IgE)
Immunoglobulin E (IgE) is an antibody synthesized by plasma cells essential in type I hypersensitivity as well as in anti-parasitic immunity. Type I hypersensitivity involves an immunologic reaction to a repeat allergen exposure. This reaction may manifest in a variety of ways including mild allergic rhinitis as well as anaphylactic shock.
Tramadol receptors
It is a μ-opioid receptor agonist, NMDA antagonist, and norepinephrine and serotonin reuptake inhibitor
gabapentin mechanism
The mechanism is decreased transmission of pain resulting from inhibition of voltage-gated calcium channels via binding of the α2-δ subunit.
that results in decreased release of glutamate
which results in decreased production of pain mediator substance P
examples of direct muscarinic acetylcholine agonists.
Bethanechol, carbachol, and pilocarpine are examples of direct muscarinic acetylcholine agonists. These drugs are resistant to breakdown by acetylcholinesterase.
hydrophilic vs lipophilic opioids in spinal
Hydrophilic opioids, which tend to remain within the CSF, have the potential to produce a delayed but longer duration of analgesia. They also cause a generally higher incidence of side effects because of cephalic or supraspinal spread of these compounds. Lipophilic opioids, such as fentanyl and sufentanil, tend to provide a rapid onset of analgesia and their rapid clearance from CSF may limit cephalic spread and the development of certain side effects such as delayed respiratory depression.
Dexamethasone site of action
Dexamethasone’s antiemetic activity is likely mediated via central inhibition of the nucleus tractus solitarii.
Muscle weakness from high magnesium concentrations results from
Muscle weakness from high magnesium concentrations results from inhibition of calcium influx, leading to reduced acetylcholine release.
lidocaine and seizures
Lidocaine decreases seizure duration and should be avoided during ECT.
Terbutaline moa
Terbutaline can be used to slow or halt premature labor via its selective ß2-agonism, which results in uterine relaxation. Like all catecholaminergic agents, it exhibits dose-dependent interaction with other catecholaminergic receptors. Further, this interaction varies from patient to patient.
Glucose intolerance as a consequence of oral terbutaline treatment.
