Neuro Exam 2 Flashcards
bacterial meningitis treatment age 0-4 wks
ampicillin + cefoxatime or aminoglycoside (gentamicin/tobramycin)
bacterial meningitis treatment 1 mo-50yo
vancomycin + cefoxatime or ceftriaxone
+ampicillin if Listeria
bacterial meningitis treatment >50yo
vancomycin + ampicillin +cefoxatime
vancomycin +ceftriaxone (+ampicillin if Listeria_
bacterial meningitis treatment w/ impaired cellular immunity
vancomycin + ampicillin + cefepime or meropenem
bacterial meningitis treatment if recurrent
vancomycin + cefoxatime or ceftriaxone
bacterial meningitis treatment if basilar skull fracture
vancomycin + cefoxatime or ceftriaxone
bacterial meningitis treatment w/ head trauma, neurosurgery, or CSF shunt
Vancomycin + ceftazadime, cefepime, or meropenem
gentamycin and tobramycin MAO
aminoglycoside
binds 30s ribosome subunit
bactericidal
gentamycin and tobramycin AE
nephrotoxicity
ototoxicity
Teratogenic
Dose adjust in renal impairment
ampicillin MAO
inhibit PBPs of bacterial cell wall synthesis
bactericidal
cefoxatime MAO
3rd gen cephalosporin
inhibit PBPs of bacterial cell wall synthesis
bactericidal
ceftriaxone MAO
3rd gen cephalosporin
inhibit PBPs of bacterial cell wall synthesis
bactericidal
ampicillin AE
pseudomembranous colitis
Dose adjust in renal impairment
Cefoxatime AE
Rose adjust in renal impairment
Injection site pain/phlebitis
Rash, diarrhea, vomiting
(Same as meropenem)
Ceftriaxone AE
Rose adjust in renal impairment
eosinophilia, thrombocytosis
Meropenem MAO
inhibit PBPs of bacterial cell wall synthesis
bactericidal
Meropenem AE
Rose adjust in renal impairment
Injection site pain/phlebitis
Rash, diarrhea, vomiting
(same as cefoxatime)
Vancomycin MAO
inhibition of transpeptidation and transglycosylation
bactericidal
Vancomycin AE
nephrotoxicity
Ototoxicity
Dose adjust in renal impairment
Dexamethasone adjunct for bacterial meningitis
Lower host responses that cause hearing loss
Reduce CSF TNFa, IL-1, inflammation, and edema
Aspergillus tx
1) voriconazole 2) ampho b
mild blasto tx
1) itraconazole 2) fluconazole
severe blasto tx
ampho b then itraconazole
candidiasis tx
fluconazole
Coccidiomycosis tx
1) fluconazole or itra 2) ampho b
cryptococcus tx
ampho b + flucytosine then fluconazole
histoplasmosis tx
1) ampho b + itraconazole 2) fluconazole
mucormycosis tx
1) ampho b 2) posaconazole
sporotrichosis tx
ampho b or itra
Amphotericin B MOA
forms pores in fungal cell membrane
fungicidal
Amophotericin B AE
nephrotoxic- reduced w/ liposomal form
Given IV due to poor CNS entry
Infusion rxn- pretreat with NSAIDs, steroids, antihistamines
“Azoles” MOA
block 14a-sterol demethylase, disrupting fungal cell membrane phospholipids
Fungistatic, possible -cidal at high doses
“Azoles” that can penetrate BBB
Fluconazole and voriconazole
“Azoles” AE
Cyp inhibitors
Drug-drug reactions
GI upset, nausea
Flucytosine MOA
converted by fungal cytosine deaminase to 5-FU, which blocks thymidylate synthase and disrupts DNA synthesis
Flucytosine AE
Orally active, enters CSF
Not used alone- rapid resistance
Bone marrow toxicity: anemia, leukopenia, thrombocytopenia
abnormal LFTs
Adverse effects result from metabolism to 5-FU, possibly by intestinal flora
analgesia
relief of pain without intentional production of AMS
anxiolysis
decreased apprehension with no change in level of awareness
sedation
Conscious: dose dependent
protective reflexes intact
independent maintenance of airway
Response to physical or verbal stimulation
Unconscious: loss of 1+ of above components
general anesthesia
concurrent loss of all protective reflexes
preferred route of general anesthesia
inhalational and IV
more immediate control over dose/duration
minimum alveolar concentration
concentration in the inspired gas required to render half of a group of patients unconscious (unresponsive to painful stimuli)
Measure of potency
Meyer-Overton hypothesis
anesthetic activity is directly linked to lipid solubility Greater potency (smaller MAC) with more lipophilic drugs
MOA inhaled anesthetics
potentiation of inhibitory neural pathways: GABA(A) and glycine signaling, reinforcement of 2 pore K channels
Inhibition of glutamatergic signaling
transfer entropy
measure of directional interactions around brain areas
During anesthesia, feedback TE is reduced
Reduced cortical interactions (reduced integration)
Guedel stage/plane 1
delirium, breath holding, increased BP, increased muscle tone, pupil dilation
structure of volatile agents
contain halogens to remove risk of sparking
isoflurane, desflurane, sevoflurane
blood/gas partition
absolute mass of anesthetic is determined by the amount needed to be accumulated in the blood in order to reach equilibrium with the alveolar gas
Dependent upon lipophilicity
Less lipophilic=smaller compartment in the blood that needs to be saturated
speed of induction
insoluble anesthetics (ex N2O) reach equilibrium in the blood very rapidly in comparison to anesthetics that are more lipophilic and tightly bind plasma proteins (ex halothane)
factors affecting anesthetic equilibration
concentration of inspired gas (only variable that can be modified by anesthetist), respiratory rate, solubility (partition coefficient), rate of blood flow to lungs, cardiac output, tissue distribution
reflex response to PaCO2
PaCO2 rises in response to inhaled anesthetics
reflex response is lost in all agents except N2O
N2O + opiod CV effects
opiod blocks the reflexive sympathomimetic effect and unmasks the direct depressive action of N2O
mechanisms of CV depression by anesthetics
decreased sympathetic outflow peripheral ganglion blockade decreased adrenal catecholamine release baroreceptor attenuation decreased Ca influx vagal stimulation
inhaled anesthetics with an irritating odor
enflurane, isoflurane, desflurane
inhaled anesthetics with analgesia
N2O
inhaled anesthetics that cause muscle relaxation
enflurane, isoflurane
inhaled anesthetics that cause arrythmias
halothane, sensitizes the myocardium to circulating catecholamines
inhaled anesthetics that cause hepatic toxicity
halothane
inhaled anesthetics that cause seizures
enflurane
N2O adverse effects
N/V
increased rates of spontaneous abortions, inhibitor of vitamin B12 synthetase, myelin sheath degeneration, second gas effect, diffusional hypoxia, air space perforation
N2O benefits
additive anesthetic effects with volatile component (vapor sparing effect)
reduced inspired volatile concentration
mild analgesic
MOA IV anesthetics
reinforce inhibitory actions of GABA/glycine
Ketamine also inhibits NMDA receptor system for glutamate (bind at different sites)
Anasthetics that reinforce GABA inhibitory actions
Benzodiazepines- shift the dose response curve for GABA to the left, increasing potency not efficacy
Barbituates- prolong binding of GABA to its receptor (increased efficacy), at high concentrations can open Cl- channel in absence of GABA)
Etomidate
Propofol- can function like GABA itself in high concentrations
CNS depression w/ anesthetics
Barbituates- dose increases depression, can lead to coma and death
Benzodiazepines- reach a ceiling effect, unless added with other depressants
rate limiting step of IV anesthetic elimination
release of drug from adipose tissue
accumulation in fat is due to relatively poor blood supply
Lipophilic- half life increases over time with continued administration
anesthetic drugs with high half lives
diazepam and thiopental
anesthetic drugs with short half lives
etomidate and propofol
etomidate- less significant changes in half life over time
IV anesthetics that increase cerebral blood flow
Ketamine
IV anesthetics that decrease cerebral blood flow oxygen requirements and decrease RR
thiopental, etomidate, propofol
IV anesthetics that increase ICP
Ketamine
IV anesthetics that stimulate HR and inhibit CO/MAP
thiopental and propofol
IV anesthetics that have no effect on CV system
Etomidate
IV anesthetics that increase HR and CO/MAP
Ketamine
Thiopental AE
porphyria (via CYP induction)
IV anesthetics that are anti-emetic
propofol
Propofol AE
infusion syndrome: metabolic acidosis, rhabdomyolysis, arrhythmias, renal failure
usually minimally responsive to inotropes or cardiac pacing
Etomidate AE
inhibits steriodogenesis
Lowers cortisol
Not used in ICU
Ketamine effects
analgesic intact pharyngeal/laryngeal reflexes bronchodilator hallucinations dissociative anesthetic- little effect on the cortex/neuronal activity
most rapid acting inhaled anesthetic
desflurane
Mechanism of emergence from unconsciousness
distribution of drug to non-neuronal tissue
Succinylcholine AE
acts on ryanodine receptor in SR releases Ca Causes muscular contraction, stimulated metabolism (increased temperature) Myoglobinuria? Antidote- dantrolene
Lidocaine MAO
needs both hydrophilic and lipophilic characteristics in order to dissolve into nerve to block sodium channel activity from the inside
preferentially binds to receptors in the activated or inactivated state
pH>pKa by 1.0 unit
90% of dose will be uncharged (unionized)
% solution
x % solution = x grams/ 100 mL
x : y solution
x grams/ y mL
drugs that cause pupillary dilation (mydriasis)
sympathomimetics
drugs that cause pupillary constriction (mitosis)
parasympathomimetics
drugs that cause pinpoint pupils
opiods inhibit the inhibitory neurons that act on the Edinger-Westphal nucleus
Gardner’s eye
unilateral, fixed mydriasis and photophobia
eye is unresponsive to pupillary light and accommodation reflex
Caused by contact with plants containing alkaloids scopolamine and atropine (Datura, Angel’s trumpets)
Absorption of topical conjunctival drugs
1) spillage onto cheeks- vasoconstriction
2) systemic via lacrimal drainage+absorption through GI mucosa or direct absorption into ocular vessels
3) cornea- absorbs small, lipophilic drugs for transfer to AH
4) Conjunctiva/sclera- absorb large, hydrophilic drugs
Dipivefrin
prodrug for epinephrine (sympathomimetic)
activated by esterases for better corneal penetration
used to treat glaucoma
effects of muscarinic antagonists
cycloplegia- loss of accommodation
mydriasis- pupils dilate, loss of adaptation
increased IOP
systemic effects- xerostomia, tachycardia, HA, somnolence
indications for use of muscarinic antagonists
iris/uveal tract inflammatory conditions
eye examination
muscarinic antagonist contraindications
glaucoma- by interrupting flow of AH, retina and optic nerve are compressed
sulfite preservative allergy
muscarinic antagonists for ocular therapy
atropine cyclopentolate homotropine scopolamine tropicamide
open angle glaucoma treatment
decrease AH production and increase AH outflow by sympathomimetics
closed angle glaucoma treatment
surgical iridectomy
decrease IOP pre-op by muscarinic agonists
Contraindications for direct acting miotics
phakic lens- promotes cataracts
Previous history of retinal detachment/tears
iritis, uveitis, inflammatory conditions of anterior chamber
Cholinergic-mediated medical conditions (CV failure, asthma, peptic ulcer, GI spasm)
Glaucoma first line tx
prostaglandin analogs
Prostaglandin analog AE
brown pigmentation of iris, eyelid, and eyelashes
Increased eyelash length/thickness
prostaglandin PGFa2 analogs
latanoprost
travoprost
bimatoprost (Latisse)
prodrugs activated by esterases for better corneal penetration
Glaucoma tx alternatives
B-receptor antagonists Carbonic anhydrase (II) inhibitors
B-receptor antagonists
Timolol
Levobunolol
Metipranolol
Carteolol
Carbonic anhydrase II inhibitors
Dorzolamide
Brinzolamide
B2 blockers MOA
Reduce IOP by inhibiting production of AH by decreasing caMP/PKA stimulation
CA2 inhibitors MOA
reduce IOP by reducing HCO3 secretion and fluid transport
CA2 inhibitors AE
taste disturbances (dysgeusia= bitter taste) Sulfonamides: allergic rxn, agranulocytosis, aplastic anemia, fulminant hepatic necrosis, SJS, toxic epidermal necrolysis, other blood dyscrasias
direct acting miotics drug classes
muscarinic agonists
cholinesterase inhibitors
Contraindications for Echothiophate
closed angle glaucoma (due to increase in IOP)
additive toxicity with organophosphates and carbamate
phenylephrine MOA
sympathomimetic
a agonist
decrease IOP by increased outflow of AH from the eye
apraclonidine MOA
sympathomimetic
a2 agonist
decrease IOP by increased outflow of AH from the eye
Brimonidine MOA
sympathomimetic
a2 agonist
decrease IOP by increased outflow of AH from the eye
Naphazoline MAO
sympathomimetic
a agonist
decrease IOP by increased outflow of AH from the eye
Tetrahydrozoline MOA
sympathomimetic
a agonist
decrease IOP by increased outflow of AH from the eye