Exam 3 Flashcards
(398 cards)
1
Q
What is metronidazole
A
Prodrug that is active against anaerobic bacteria and anaerobic Protozoa
2
Q
What is the “drug class” of metronidazole
A
5-nitroimidazoles; includes tinidazole, behave similarly in mechanism, resistance and spectrum; tinidazole is better tolerated
3
Q
What is the MOA of metronidazole
A
Relies on activation by susceptible organisms; donates electrons to metronidazole which forms a highly reactive nitro radical anion -> radical mediated DNA damage of organisms; can be recycled by losing electron; O2 can compete with metronidazole (when O2 rises, less likely to be active)
4
Q
What organisms have developed resistance to metronidazole via increasing levels of O2
A
T. Vaginalis, G. Lamblia
5
Q
What are the adverse effects of metronidazole
A
- metallic taste
- dry mouth
- Nausea
- HA
- disulfiram-like effect (anti-alch medication designed to induce vomiting)
6
Q
What are the dopamine receptor agonists
A
Apomorphine, bromocriptine, pramipexole, ropinirole
7
Q
What are the monoamine oxidase inhibitors
A
Rasagiline and selegiline
8
Q
What are the catechism-o-methyltransferase inhibitors
A
Entacapone and tolcapone
9
Q
What are the anti-cholinergic drugs
A
Benztropine, biperiden, orphenadrine, procyclidine, trihexyphenidyl
10
Q
What do the dopamanergic neurons from the substantia nigra usually do
A
Inhibit GABAergic output from the striatum (caudate and putamen) (cholinergic has opposite effect)
11
Q
What can be used to treat PD
A
Dopamine agonists or anticholinergic drugs
12
Q
What is levodopa
A
Immediate metabolic precursor to dopamine
13
Q
How does levodopa enter the CNS
A
L-amino acid transporter (LAT); *dopamine cannot cross BBB
14
Q
What is the MOA of levodopa
A
Agonist at dopamine receptors
15
Q
How do you increase the amount of levodopa available to enter the brain
A
Coadministration with a DOPA decarboxylase inhibitor (carbidopa); does NOT cross BBB
16
Q
What are the adverse effects of levodopa
A
- GI: in the absence of carbidopa, causes anorexia, N/V due to activation of chemoreceptor trigger zone
- CV: postural hypotension; when taking large doses or in combo w/ nonselective MAOI/sympathomimetic, can cause HTN
- dyskinesia; choreoathetosis
- behavioral: depression, anxiety, agitation, insomnia, hallucinations, euphoria
- “on-off phenomenon”: give apomorphine to relieve this
17
Q
What is levodopa contraindicated in
A
Psychotic patients, angle closure glaucoma, history of melanoma or suspicious skin lesions, active peptic ulcer
18
Q
What is bromocriptine
A
D2 agonist, also approved for rx of endocrine disorders; extensive first pass metabolism
19
Q
What is pramipexole
A
D3 agonist; approved for treatment of restless leg syndrome; most excreted unchanged in urine; renal insufficiency may require dose adjustment
20
Q
What is ropinirole
A
D2 agonist; approved for treatment of RLS
21
Q
What are the adverse affects of dopamine agonists
A
- GI: anorexia, N/V; constipation, dyspepsia, reflux
- CV: postural hypotension
- dyskinesia
- mental disturbances
22
Q
What are contraindications of dopamine agonists
A
Patients with psych history, recent MI, active peptic ulcer; PVD
23
Q
What are the two forms of monoamine oxidase
A
- MAO-A: metabolizes NE and serotonin
- MAO-B: metabolizes phenylethylamine and benzylamine
- dopamine and tryptamine metabolized equally by both
24
Q
What is selegiline
A
Aka deprenyl; selective irreversible MAO-B inhibitor (inhibits A at high doses); prolongs affects of l-dopa; contraindicated in patients taking meperidine, tricyclic antidepressants, or serotonin reputable inhibitors
25
What is rasagiline
Irreversible MAO-B inhibitor; more potent than selegiline; used as neuroprotective agent for early symptomatic treatment of PD
26
What are catechism-o-methyltransferase inhibitors
COMT metabolizes l-dopa to 3-o-methyldopa, which competes w/l-dopa for transports across BBB; *tolcapone and entacapone prolong activity of l-dopa; entacapone is peripherally acting only; tolcapone may cause increase in liver enzyme levels and causes acute hepatic failure; *side effects -> orange urine, diarrhea, ab pain, sleep disturbances
27
What is apomorphine
Dopamine agonist at D2 receptors; injected for quick relief of off-periods of akinesia w/ dopaminergic therapy; adverse affects: nausea (treat with trimethobenzamide), drowsiness, sweating, hypotension and injection site bruising
28
What is amantadine
Antiviral that has a MOA in PD; can cause livedo reticularis (purplish discoloration of skin); use with caution in ppl w/ history of seizures or heart failure
29
Which anticholinergic drugs are used to treat PD
MAChR antagonists; improve tremor and rigidity but have no effect on bradykinesia; *benztropine, biperiden, orphenadrine, procyclidine, trihexyphenidyl
30
What can be used to treat tremors
B1 antagonists -> metoprolol, propranolol; symptomatic tremor -> primidone (anti-epileptic); topirimate (SSR agonist), alprazolam (benzodiazepine) and botulinum toxin A
31
What can be used to treat the movement aspect of Huntington’s
Reserpine, tetrabenazine
32
What can be used to treat tics
Antipsychotics (tetrabenzaine, haloperidol, pimozide) but these cause weight gain, sedation, irritability ad phobias; alpha agonists are effective with less side effects
33
What is used to treat ALS
Riluzole -> inhibits glutamate release and blocks post synaptic NMDA and kainate type glutamate receptors and inhibits Na+ channels
34
What can be used to treat Wilson dz
Reduce serum copper; penicillamine (cheating agent that forms complex w/copper and excreted by kidney; adverse effects: nephritic syndrome, myasthenia, optic neuropathy, and blood disorders); potassium disulfide: reduces absorption of copper; Trientine:
35
What are the drug classes used to treat glaucoma
Beta blockers, alpha 2 agonists, prostaglandin analogs, carbonic anhydrase inhibitors, muscarinic agonists, and inhibitors of cholinesterase
36
What are the beta blockers used to treat glaucoma
Betaxolol, timolol, metipranolol, levobunolol, carteolol
37
What are the alpha 2 agonists used to treat glaucoma
Apraclonidine and brimonidine
38
What are the prostaglandin analogs used to treat glaucoma
Latanoprost, bimatoprost, travoprost
39
What are the carbonic anhydrase inhibitors used to treat glaucoma
- topical: brinzolamide and dorzolamide
| - systemic: acetazolamide and methazolamide
40
What are the muscarinic agonists used to treat glaucoma
Carbachol and pilocarpine
41
What are the inhibitors of cholinesterase used to treat glaucoma
Demecarium and echothiophate
42
What does the iris circular m do
Constricts pupil to cause miosis; contains M3 receptors
43
What does the iris radial muscle do
Dilates pupil to cause mydriasis; alpha 1 receptors
44
What does the ciliary m do
Accommodation and opens trabecular meshwork to improve outflow of aqueous humor; M3 receptors
45
What receptor is found on ciliary epithelium
Beta; causes increase in aqueous humor productions
46
Activation of what receptor decreases production of aqueous humor
Alpha 2
47
What does activation of the prostaglandin F2 receptor do
Improves uveoscleral or unconventional outflow
48
Does activation of the sympathetic or parasympathetic system increase aqueous outflow
Parasympathetic
49
What is a Scotoma
Area of vision loss or decreased visual acuity surrounded by field of normal vision; *every normal eye has a scotoma (bind spot)
50
What is the goal of treating glaucoma
Decrease IOP by 30% (want it less than 21 mm Hg)
51
What should you do if you want to use 2 agents to treat glaucoma
Administer them 10 min apart
52
What are the first line agents to use in open angle glaucoma
Prostaglandin analogues, beta blockers (timolol favored) and brimonidine
53
What is the second line therapy for open angle glaucoma
Pilocarpine, apraclonidine, topical carbonic anhydrase inhibitors
54
What is the last line therapy for open angle glaucoma
Carbachol, inhibitors of cholinesterase and oral carbonic anhydrase inhibitors
55
Why are beta blockers commonly used for open angle glaucoma
Convenience of dosing and lack of adverse effects
56
Why is timolol favored when treating open angle glaucoma
Lacks local anesthetic effects; available as generic; full antagonist, as effective as pilocarpine, MOA: reducing production of aqueous humor
57
What are the local adverse effects of beta blockers
Stinging, dry eyes, blurred vision, blepharitis, keratitis, conjunctivitis
58
What are the systemic effects of beta blockers
Bradycardia, bronchospasm, hyperlipidemmia, hypoglycemia (in patients on insulin), can interact with orally given verapamil (increased risk of cardiac depression and heart block)
59
What prostaglandin analog is the most effective in lowering IOP
Bimatoprost
60
Do prostaglandin analogs more effectively reduce IOP than beta blockers
Yes
61
When do you give prostaglandin analogs
Once daily at night
62
What are the local side effects of prostaglandin analogs
Corneal erosions, conjunctival hyperemia, iris hyperpigmentation *irreversible, and hypertrichosis (hyperpigmentation around eye lashes and eyelids *reversible)
63
Why is brimonidine the first line alpha 2 agonist used to treat glaucoma
Apraclonidine has frequent allergic reactions
64
What is the effect of alpha 2 agonists
Decreases rate of aqueous humor production
65
What are the adverse reactions to alpha 2 agonists
Dizziness, fatigue, dry mouth, bradycardia, reduced BP
66
What is the algorithm for pharmacotherapy of open angle glaucoma
Start w/ beta blocker, if intolerant, use class alternative, if contraindicated switch to alternative first line agent, if intolerant to prostaglandin use class alternative; if contraindications to all first class agents, use topical carbonic anhydrase inhibitors; if monotherapy fails, use combined therapy; if intolerant use surgical procedure
67
What are the goals of treatment of closed angle glaucoma
Rapid reduction of IOP *pilocarpine -> drug of choice before surgery
68
What is surgical or laser iridectomy
Produce a hole in iris which facilitates the humor outflow; used to treat closed angle glaucoma
69
What drugs are contraindicated in people with open angle glaucoma
Glucocorticoids, fenoldopam, topical anti muscarinic
70
What drugs are contraindicated in people with closed angle glaucoma
Anti muscarinic, drugs with alpha-adrenomimetic activity, tricyclic antidepressants and serotonin/NE reuptake inhibitors (because anti muscarinic actions)
71
What is the suffix for local anesthetics
-Caine
72
What local anesthetics are in the amide chemical class
All the ones with an “i” (not including the i in Caine)
73
What local anesthetic has a very short duration of action
Procaine
74
What local anesthetic is for surface use only
Benzocaine
75
What local anesthetics have a long duration of action
Tetracaine, ropivacaine and bupivacaine
76
Which types of local anesthetics generally have a longer duration of action
Amide; those with ester linkages are more prone to hydrolysis
77
What an reduce the systemic absorption of agents
Use of vasoconstrictors; useful for drugs with intermediate or short durations of actions
78
What is the difference between how ester type local anesthetics versus amide type local anesthetics are metabolized
Ester in the plasma via butyrylcholinesterase enzymes and amide in the liver and excrete in urine
79
What is the MOA of local anesthetics
Block voltage gated Na+ channels
80
What makes a local anesthetic more potent
If it is more lipophilic (tetracaine, bupivacaine, and ropivacaine)
81
What kind of nerve fibers to local anesthetics preferentially block
Smaller fibers; myelinated become blocked before unmyelinated; motor before sensory
82
What is infiltration anesthesia
Injection directly into the tissue; superficial enough to only effect skin or abdominal organs
83
What is block anesthesia
Injection in major nerve trunks; anesthetize region distal to block
84
What is spinal anesthesia
Injection into the CSF in the lumbar space; produces anesthesia over large part of body with a dose that produces negligible plasma levels
85
What is epidural anesthesia
Injection into epidural space; allows for continuous infusion
86
What is intravenous regional anesthesia (bier block)
Used for short surgical procedures on limbs; injection into vein while circulation of limb is isolated with tourniquet; large doses are used
87
what can you inject with a local anesthetic to increase its duration of action
Vasoconstrictor (epi) *use caution when injecting into skeletal mm can cause vasodilation and increase systemic toxicity
88
What adverse effects do local anesthetics have on the CNS
Sleepiness, metallic taste, nystagmus and convulsions, *giving benzodiazepine with the local anesthetic can raise seizure threshold and be preventative against systemic toxicity
89
What side effects can local anesthetics have on the CV system
Block cardiac sodium channels and decrease contractility and cause arteriolar dilation leading to hypotension
90
What is the most cardiotoxic local anesthetic
Bupivacaine b/c long duration of action
91
What is the effect of lidocaine on the heart
Antiarrhthmic; its side effects are mainly CNS
92
What kind of local anesthetics tend to produce allergic reactions
Ester type
93
What are the features of benzocaine
Poor solubility in water, ONLY topical, used for derm, hemorrhoids, premature ejaculation, and anesthetic lubricant (NG tube insertion)
94
What are the features of bupivacaine
Long duration of action; more sensory than motor block
95
What are the features of cocaine
Block nerve impulses and vasoconstriction; used as topical anesthetic or of UE airways
96
What are the features of dibucaine
Toxicity asssociated with injections so now only used topically
97
What are the features of lidocaine
Amide local anesthetic; alternative choice for those allergic to ester type; faster more intense longer lasting and more extensive anesthesia than same dose as procaine; used as antiarrhythmic
98
What are the features of procaine
Lower potency, slower onset, shorter duration of action, used for infiltration anesthesia; metabolized to para-aminobenzoic acid which inhibits action of sulfa abx
99
What are the inhaled general anesthetics
Desflurane, enflurane, halothane, isoflurane, nitrous oxide, sevoflurane
100
What are the IV anesthetics
Dexmedotomidine, diazepam, etomidate, fetanyl, fospropofol, ketamine, lorazepam, methohexital, midazolam, proposal, thiopental
101
What is monitored anesthesia care
Sedation-based anesthetic technique used for minor therapeutic surgical procedures; typically uses midazolam as premedication and propofol
102
What is conscious sedation
Used by nonanesthesiologists; can maintain patent airway and respond to verbal commands, benzodiazepines and opioids (fentanyll) are used because are reversible by receptor antagonists (flumazenil and nalaxone)
103
What is usually used for deep sedation
Propofol and midazolam
104
What is the MOA for general anesthetics
Most use GABA-a and glycine receptors to activate chloride channels;
105
What are the volatile anesthetics
Halothane, enflurane, isoflurane, desflurane, and sevoflurane - liquids at room temp
106
What does the rate that an inhaled anesthetic is absorbed depend on
Concentration of anesthetic in inspired air, ventilation rate, and solubility in air, blood, and CNS
107
What are the features of agents with low blood solubility
Ex: nitrous oxide and desflurane; fast onset of action
108
What drug is an example of an anesthetic with a high blood solubility
Halothane
109
How are inhaled anesthetics eliminated
In lung usually; insoluble in blood elminated more quickly
110
What is the minimal alveolar concentration
The dose that prevents movement in response to a surgical incision in 50% of subjects; measures potency
111
What do MAC values greater than 100% indicate
You must use another agent in conjunction with the one being used
112
What is the effect of inhaled anesthetics on heart rate
Can be mixed; halothane induces bradycardia while desflurane and isoflurane increase HR
113
Which inhaled anesthetic can cause hepatitis
Halothane
114
Which inhaled anesthetics are renal toxic
Enflurane and sevoflurane
115
How do you treat malignant hyperthermia
Dantrolene
116
What are the features of etomidate
IV anesthetic; rapid onset and fast recovery; CV stability
117
What are the features of ketamine
CV stimulation; increased cerebral blood flow
118
What are the features of methohexital
IV anesthetic that is preferred over thiopental for ambulatory procedures
119
What are the features of midazolam
Used in balanced anesthesia and conscious sedation; CV stability and marked amnesia; slow onset and recovery -> flumazenil reversal available
120
What are the features of propofol
Used for induction; can cause hypotension; useful antiemetic properties
121
What are the features of thoipental
Slow recovery; standard induction agent; CV depression; avoid in porphyrias
122
What are the features of fentanyl
IV anesthetic that has a slow onset and recovery -> naloxone reversal available; opioid used in balanced anesthesia and conscious sedation; analgesia
123
What is the MOA of propofol
Targets GABAa receptors; metabolized in the liver; allergic reactions in ppl allergic to eggs
124
Which IV anesthetics increase their half lives dramatically with prolonged infusions
Diazepam and thiopental
125
What are the CNS effects of propofol
Decreases cerebral blood flow which decreases ICP and IOP
126
What is fospropofol
Water soluble prodrug of propofol that is metabolized by alkaline phosphates to propofol and formaldehyde; onset and recovery are prolonged in comparison to propofol; itching and paresthesias are side effects
127
What is the MOA of etomidate
Enhances action of GABA on GABAa receptors; hypnotic but no analgesic effect; minimal CV and resp depression; less rapid recovery rate; metabolized by liver
128
What are the effects of etomidate on the CNS
Potent cerebral vasoconstrictor; decreases cerebral blood flow
129
What are the endocrine effects of etomidate
Adrenocortical suppression; cant make cortisol; limits its use as a continuous infusion
130
What is the MOA of ketamine
NMDA antagonist; eyes can remain open with nystagmus; lacrimation and salivation increased (premeditate with anticholinergic)
131
What are the CNS effects of ketamine
Increases cerebral blood flow -> not recommended for pts with intracranial pathology (increased ICP); causes hallucinations
132
What are the CV effects of ketamine
Increases systemic BP, HR, and CO
133
What is the only IV anesthetic that produces analgesia
Ketamine; also the only one to cause bronchodilation
134
What is the MOA of dexmedetomidine
Alpha-2 agonist; resembles physiological sleep state; decreases HR; used for short term sedation of intubated patients
135
What opioid analgesics are used in combo with IV anesthetics
Fentanyl, sufentanil, remifentanil, and morphine; agonist on opiate receptors
136
What barbiturates are used in combo with anesthetics
Thiopental and methohexital; highly lipophilic, CNS and resp depression; acts on GABAa receptors
137
What is the MOA of benzodiazepines
acts on GABAa receptors; used in perioperative period; antagonized by flumazenil; midazolam is the only water soluble one and is drug of choice for parenteral admin; have anticonvulsant properties
138
What agents can be given to prevent a migraine
Triptans and ergot alkaloids, beta blockers, tricyclic antidepressants, anticonvulsants, and calcium channel blockers
139
Which beta blockers can be used to treat migraines
Propranolol and timolol
140
Which tricyclic antidepressants can be used to treat migraines
Amitrityline and imipramine
141
Which anticonvulsants can be used to treat migraines
Topirimate and valproate
142
Which calcium channel blocker can be used to treat migraines
Verapamil
143
What does BOTOX act on
Motor neurons to decrease their activity; it cleaves SNAP-25 which inhibits Ach release
144
What is the definition of chronic migraine
Fifteen or more days each month w/ HA lasting 4 or more hours in ppl 18 or older
145
What is the physiology behind migraines
Calcitonin gene related peptide released from trigeminal A delta fibers which increases dural vessel vasodilation; substance P and neurokinin A are released from trigem C fibers which increases dural vessel permeability
146
What serotonin receptors do cranial vessels have
5HT-1B
147
What is the target of triptans
Serotonin 5HT1B/D agonists; causes vasoconstriction of cranial vessels and binds to 5HT1D receptors on presynaptic neurons to inhibit release of CGRP; also binds to 5HT1D receptors on trigeminal nucleus in brainstem which modulates ascending painful information
148
What is the prototype for triptans
Sumatriptan; can be given PO, nasal spray, or SC; SC is quickest action
149
What is sumatriptan metabolized by
Monoamine oxidase A
150
Which triptans have shown to be better tolerated and more efficient
Rizatriptan and eletriptan
151
Which triptan has the longest half life
Frovatriptan
152
Which triptans have the most delivery options
Sumatriptan and zolmitriptan
153
What triptans are contraindicated in someone taking MAOIs
Sumatriptan, rizatriptan, and zolmitriptan
154
What are people on SSRIs at risk for when taking triptans
Serotonin syndrome
155
When are triptans contraindicated
In people who have history of ischemic heart disease or other CV disorders and in patients with uncontrolled HTN
156
What are all triptans vasoconstrictors of
Coronary and renal vessels
157
What is the MOA of dihydroergotamine
Nonselectively binds to serotonin receptors as well as adrenergic and dopamine receptors
158
What side effects can dihydroergotamine have
Binding to alpha 1 receptors causes worse vasoconstriction than triptans which can lead to ischemia, vascular dz, acute coronary syndrome or vasospasm
159
What treatment for migraines is safe in all trimesters of pregnancy
Acetaminophen and codeine
160
When can aspirin and ibuprofen be given during pregnancy
First and second trimester only
161
Can you give triptans to someone who is pregnant
No
162
Can you give DHE and other ergot alkaloids to someone who is pregnant
No; abortion risk
163
What drug combinations are useful treatments for migraines
Triptan plus analgesic (sumatriptan and naproxen = treximet)
164
When is valproate given to someone with migraines
When triptans fail as a treatment; works by increasing GABA levels; *contraindicated in pregnant women (decreases IQ scores in offspring)
165
What are the features of verapamil in terms of migraine treatment
First choice for migraine prevention; good side effect profile; normalizes vessel tone
166
What is propranolol or timolol contraindicated in
Patients with asthma
167
Where is the binding site for sodium channel blocker AED’s
Interior side of the channel; can only bind if the activation gate is open (open state or fast inactivated state) *state and use dependent
168
Which sodium blocker AED’s prolong fast inactivation state of Na channel
Carbamazepine, oxcarbazepine, lamotrigine, phenytoin, rufinamide, topirimate, valproic acid, zonisamide and Lacosamide
169
Which Na channel blocker AED’s enhance the slow inactivation of Na channels
Lacosamide; more efficient when stimulus is prolonged; can act in inactivated closed state
170
What are the AED’s that are AMPA receptor antagonists
Topirimate and perampanel
171
Which AED is an NMDA receptor antagonist
Felbamate
172
What is the MOA of tiagabine
Inhibits GAT-1 (reuptake of GABA)
173
What are the AED’s that inhibit the catabolism of GABA
Vigabatrin and valproic acid (inhibit GABA-T)
174
What is the MOA of benzodiazepines
Binds to allosteric site which causes increased GABA binding which increases the frequency of Cl- channel opening
175
What is the MOA of barbiturates
Binds to allosteric site and increases duration of Cl- channel opening; *GABA independent which makes it more lethal than BZD
176
What are the multiple functions of topiramate
GABAa agonist (increases frequency of GABAa receptor activation), fast inactivation of Nav channels and AMPA antagonist
177
What are T-type calcium channels
Mediate 3 hz spike and wave activity in the thalamus which is a hallmark of petit mal seizures
178
What is ethosuximide
Only used for petit mal seizures; antagonist of t type calcium channels
179
What are the antagonists of t type calcium channels
Ethosuximide, valproic acid, and zonisamide
180
Which AED contains sulfa
Zonisamide *allergy
181
What does levetiracetam target
SV2A - synaptic vesicle protein; doesn’t allow glutamate to be packaged
182
What inhibits the alpha2gamma subunit of the P/Q type calcium channel
Gabapentin and pregabalin
183
Which AED targets potassium channels
Retigabine
184
What drugs would you use to treat partial onset seizures
Lamotrigine, oxcarbazepine, perampanel, primodone, lacosamide
185
What drugs would you use to treat generalized onset absence seizures
Ethosuximide, clonazepam, valproic acid
186
What drug would you use to treat generalized onset myoclonic seizures
Clonazepam
187
What drugs would you use to treat generalized onset tonic/clonic seizures
Primidone or phenytoin
188
What are the broad spectrum AED’s
Carbamazepine, phenobarbital, topiramate, valproic acid
189
What drugs do you use to treat Lennox gastaut
Rufinamide, topiramate, clobazam, clonazepam, lamotrigine, felbamate
190
What do you use to treat status epilepticus
Lorazepam, diazepam, phenobarbital, phenytoin, valproic acid, levetiracetam
191
What is the main side effect to AED medication
Suicidal behavior
192
What are the toxic effects of phenytoin
Zero order drug; gingival hyperplasia, hypothyroidism, CV risk (hypotension and arrhythmia), hypocalcemia, vit d deficiency, osteoporosis
193
What other drugs is osteopenia/osteoporosis associated with as a side effect
Carbamazepine, phenobarbital, valproic acid; induce vitamin D CYP450 which reduces vitamin D levels -> cant absorb calcium -> activates PTH to demineralize bone
194
What are the toxicities associated with carbamazepine
Leukopenia, neutropenia, and thrombocytopenia; hypocalcemia; also induces self metabolism (potential loss of efficacy and recurrence of seizures)
195
What is oxcarbazepine
Analogue of carbamazepine with fewer side effects
196
What are the toxicities of phenobarbital
CNS depressant
197
What are the side effects of vigabatrin
Progressive, permanent, bilateral, concentric vision loss; discontinue after 3 months if no response; prescribable only via REMs program
198
What effect can AED inducers have on anticoagulants
Increases metabolism of warfarin -> increased risk of thrombosis
199
What effect can AED induces have on antiviral
Can increase metabolism of HIV medications -> risk of HIV replication
200
What drug reactions do valproic acid and lamotrigine have
Inhibit conjugation of drugs by glucoronosyltransferases causing accumulation of the parent drug (when used together)
201
What drug reactions do phenytoin, carbamazepine, and phenobarbital have
Induce conjugation of drugs by glucoronosyltranferase; causes reduction of parent drug
202
How do newer AED’s minimized drug interactions
Rental clearance; levetiracetam, topiramate, oxcarbazepine, gabapentin, pregabalin, vigabatrin; ****renal insufficiency requires dose adjustment
203
What is the initial therapy for status epilepticus
- In first IV: lorazepam; alternative: diazepam; wait 1 min for response then give lorazepam PRN
- IF NO IV ACCESS, midazolam
- In second IV: fosphenytoin OR phenytoin OR valproic acid OR levetiracetam
204
What are the legal requirements of things that need to appear on a prescription
- Name/Address of prescriber
- Name/Address of patient
- Date prescription was written
- Name and strength and dosage form of medication
- Directions for use
- Quantity to be dispensed
- number of refills allowed
- Prescribers signature
- Prescribers DEA # (2 letter 7 digit)
205
What is the life span of a prescription for a non controlled legend
12 months or number of refills; no legal limit on refills or quantity dispensed; (in MO, limit new script of opioids to 7 day supply); partial filling possible
206
What is the life span of controlled/scheduled legends
6 months or number of refills; *exception is C-V which has a life span of 12 months
207
What is the limit of refills for controlled/scheduled legends
For C-II: NO REFILLS
For CIII-IV: 5 refills over 6 months
For CV: no limit
208
What is the limit of quantity dispensed for controlled/scheduled legends
90 days for CIII-V; 30 days for C-II (up to 90 days with documentation of medical reason)
209
Is partial filling for scheduled/controlled legends allowed
Only for CIII-V until full quantity and all refills dispensed or expiration; ONLY possible for C-II if pharmacist doesn’t have full quantity or on long term hospice care
210
When can physicians fax/electronically/call in scripts
Original prescription or refills for all legend drugs except C-II (only during emergency); faxed prescriptions musts be manually signed
211
What are the rules on prescription transfers
CII cannot be transferred; CIII-V can only be transferred once; nursing home orders not transferable
212
What cannot be changed on a controlled substance prescription
Patients name, drug name, prescribers name, prescribers signature
213
What is an “emergency” for dispense of controlled substances
-immediate administration necessary, no appropriate alternative available, not reasonably possible for prescriber to have a written prescription to pharmacist (have 72 hours to deliver the script)
214
What are the rules about self prescribing and prescribing drugs to family
In MO, cannot self prescribe controlled substances but can non-controlled; can prescribe all legend drugs to family
215
What are the worrisome signs which may indicate HA of pathological origin (secondary HA)
Worst HA, onset of HA after 50, atypical HA for patient, HA w/ fever, abrupt onset, subacute w/ progressive worsening over time, drowsiness, confusion, memory impairment, weakness, ataxia, loss of coordination, paresthesias, abnormal medical/neuro exam
216
What is recommended if any of the worrisome signs are seen
CT and/or LP
217
What are the primary HA disorders
Common migraine (without aura), classic migraine (with aura), chronic migraine, tension HA, cluster HA
218
What are the features of common migraine
Moderate to severe intensity, inhibits daily activities (aggravated by activity), age of onset peaks btw 35-40 y/o; more common in females; 14 or fewer per month; duration of 4-72 hours, unilateral or bilateral; throbbing, sharp pressure; prodrome: mood changes, food cravings, sluggishness, yawning; post drone: fatigue, fog; retreat to dark quiet room; NO AURA
219
What is analgesia
Relief of pain without loss of consciousness
220
What is the difference between opium and opioid
Opium: natural; opioid: natural plus synthetic morphine
221
What are opioid agonists
- natural opium alkaloids: morphine and codeine
- semisynthetic opiates: hydromorphone and oxymorphone
- synthetic opioids: pethidine, tramadol, methadone, fentanyl, alfentanil, remifentanil
222
What are the opioid agonist antagonists
Pentazocine
223
What opioid is a partial mu receptor agonist
Buprenorphine
224
What opioid is a mu receptor antagonist
Naltrexone and naloxone
225
What are narcotic analgesics used in hospital settings for
MI, sickle cell crisis, post op, trauma, cancer, kidney stones, back pain, general anesthesia, palliative care, epidural, antitussive, antidiarrheal
226
What is the MOA of narcotic analgesics
Bind to presynaptic mu receptor an inhibits calcium influx (decreases NT release); also binds to postsynaptic mu receptor and increases K+ effluent to decrease postsynpatic response to excitatory NT
227
What are the effects of morphine, methadone, and fentanyl
Analgesia, relief of anxiety, sedation, slowed GI transit; used for severe pain or adjunct to anesthesia, pulmonary edema (morphine), resp depression, constipation, addiction, convulsions
228
What is meperidine
Strong mu agonist with anticholinergic effects
229
What are the effects of codeine and hydrocodone
Less effacious than morphine; used for moderate pain
230
What are the effects of buprenorphine
Partial mu agonist; reduces craving for alcohol; used for moderate pain; long duration of action
231
What are the effects of nalbuphine
Mu antagonist and k agonist; similar to buprenorphine; used for moderate pain
232
What are the antitussives
Dextromethorphan, codein, and levopropoxyphene; partial mu agonists; reduces cough reflex; not analgesic (except for codeine)
233
What analgesic can cause serotonin syndrome
Tramadol
234
Which endogenous opioid has the greatest affinity for mu receptors
Endorphins > enkephalins > dynorphins
235
Which endogenous opioids have the greatest affinity for delta receptor
Enkephalins > endorphins and dynorphins
236
What are the adverse effects of opioids
Acute: resp depression, N/V, itching, urticaria, constipation, urinary retention, delirium, sedation, myoclonus, seizures
Chronic: hypogonadism, immunosuppression, increased feeding, increased GH, withdrawal effects, tolerance/dependence, abuse, hyperalgesia, impairment while driving
237
What are the contraindications for morphine
Acute respiratory depression, renal failure, chemical toxicity, raise ICP, biliary colic
238
What population of individuals are commonly mistakenly overdosed on opioids
Obese ppl, elderly, infants, those w/ renal failure (morphine and pethidine toxicity), hepatic failure
239
Input from which systems is required for balance
2 of the 3: visual, labyrinthine (judges acceleration and position), and proprioceptive (judges posture)
240
What is disequilibrium
Can be caused by vertigo but usually nonvertiginous ; dysfunction of cerebellum, dorsal columns, basal ganglia
241
What is presyncope
Lightheaded ness caused by orthostasis, arrhythmia, hyperventilation, and aggravated by increased temp, prolonged standing and large meals
242
What is a sensory cause of disequilibrium
Prioprioreceptive deficit, visual impairments, compensated vestibular disorders; worse in the dark *romberg sign
243
What are the motor causes of disequilibrium
Mechanical (arthritis), peripheral or central (motor function), cerebellar, NO Romberg sign
244
What are the cerebellar causes of disequilibrium
No Romberg sign; cannot stand with feet together with eyes open or closed
245
What are the characteristic of peripheral disorders of equilibrium
Intense vertigo, brief nystagmus that can be fatigued, fixed direction of horizontal nystagmus, intense N/V, possible hearing loss, never neuro symptoms
246
What are the characteristics of central disorders of equilibrium
Mild vertigo, persistent nystagmus that cannot be fatigued, direction of nystagmus is not fixed (can be vertical), no latency of nystagmus, mild N/V, rarely causes hearing loss, usually has neuro symptoms
247
What are the peripheral causes of vertigo
Benign positional vertigo, vestibular neuronitis, Menieres dz, drug induced ototoxicity
248
What is benign positional vertigo
Brief episodes of vertigo triggered by change in head position; spontaneous recovery usually; thought to be due to debris floating in endo lymph (mostly in posterior canal)
249
What does the Dix hallpike maneuver diagnose (specifically)
BPV of posterior or anterior canals; posterior is provoked by affected ear down (reverse for anterior canal)
250
What does the supine roll test diagnose
BPV of horizontal canals
251
What meds can be given for BPV
Vestibular suppressants (meclizine, scopolamine, Valium), antiemetic, anxiolytics
252
What is vestibular neuronitis
Spontaneous attack of vertigo that does not involve hearing loss or tinnitus and resolves spontaneously; vertigo, nausea, and vomiting lasting up to 2 weeks; not positional
253
What is meniere’s dz
More prominent in young females; due to an increase in volume of labyrinthine endolymph b/c of poor absorption (endolymph hydrops); recurrent episodes of spontaneous vertigo lasting more than 20 min (typically hours); *low frequency hearing loss, tinnitus and aural fullness
254
What is mal de debarquement
Illusion of movement as aftereffect of travel; duration less than a day; failure of brain to adapt once motion has stopped; RX: meclizine, scopolamine, benzo
255
What drugs can induce peripheral disorders of equilibrium
Alcohol, salicylates, anti-epileptics, quinine, abx (aminoglycosides), diuretics, chemo
256
What is a vestibular migraine
Central disorder of equilibrium; at least 5 episodes of severe vestibular symptoms lasting 5 min to 72 hours; current or previous history of migraine; one or more migraine features w/ at least half of episodes; unaccounted for by other dx
257
What are the features of vascular causes of central disorder of equilibrium
More common in elderly; abrupt onset; ischemia of labyrinth or brainstem; vertigo assoc with neuro symptoms (diploid, dysarthria, hiccups); repeated episodes of isolated vertigo w/o other neuro sx should always suggest non-neuro cause
258
What metabolic disturbances can cause central disorders of equilibrium
Deficiencies of B1 and 12, E, and Cu; hypothyroid (affects cerebellum), Wilson dz (low serum ceruloplasmin)
259
What toxins can cause central disorders of equilibrium
Heavy metals, CO, glue, organic solvent, NO2; ethanol (cerebellar vermis), meds -> DPH, anticonvulsants, 5-FU
260
What is a neoplastic cause of central disorders of equilibrium
CPA tumor *hearing loss and absent corneal reflex 1st symptom and sign
261
What is a paraneoplastic cause of central disorders of disequilibrium
Paraneoplastic cerebellar degeneration; usually from breast, lung or ovary CA; abs to purkinje cells
262
What is friedrichs ataxia
AR; onset before 20, gait ataxia involving all 4 limbs, dysarthria, impaired proprioception in legs, weakness, absent reflexes in legs
263
What is ataxia telangiectasia
AR (chrom 11); pancerebellar degeneration involving nystagmus, dysarthria and gait ataxia beginning in infancy; loss of proprioception and areflexia; immunodeficiency
264
What does vit B12 deficiency cause
Degeneration of posterior columns and lateral corticospinal tracts; caused by surgery, drugs (PPI and metformin), NO2, fish tapeworm); insidious onset, vague fatigue, babinski sign, Romberg sign, increased homocysteine and methylmalonic acid
265
What can cause copper deficiency
Malabsorption or excessive zinc intake; similar to B12 deficiency; decreased serum ceruloplasmin and urine copper
266
What are the characteristics of classic migraine
Aura that usually lasts 15-30 min; commonly visual symptoms
267
What is the definition of chronic migraine
History of HA 15 or more days per month, lasting 4 hours or longer for at least 3 months
268
What are the characteristics of tension-type HA
Mild to moderate intensity; may inhibit bu doesn’t prohibit daily activity; variable age of onset; more common in females; episodic type: last several hours; chronic: waxes and wanes all day; bifrontal or bioccipital; dull squeezing pressure; *no prodrome or aura; behavior not affected
269
What are the characteristics of cluster HA
Severe pain; prohibits daily activity; age of onset 20-50; more common in MALES; associated with sleep apnea; episodic type: 1 or more attacks a day for 6-8 wks; chronic: several attacks per week w/o remission; last 30 min-2 hours; *always unilateral (usually orbitotemporal); prodrome: mild burning in ispilateral canthus or nares; packing, rocking behavior changes; associated w/ ptosis, miosis, conjunctival injection, lacrimation, stuffed or runny nose
270
What are contraindications to triptan use
Ischemic heart dz, PVD, Raynauds, HTN, renal/hepatic impairment, MAOI’s
271
Which triptan has the longest half life and fewest side effects
Naratriptan; don’t use if hepatic or renal impairment
272
What is the only FDA approved treatment for chronic migraine
Botox injection; repeated every 3 months; minimal side effects
273
What are acute treatments for cluster HA
DHE, lidocaine, narcotics, oxygen by mask, sumatriptan
274
What are preventative treatments for cluster HA
Calcium channel blockers, anticonvulsants, lithium, indomethacin, prednisone, ergotamine tartrate
275
What can be used to treat trigem neuralgia
Carbamazepine or oxcarbamazepine
276
What are trigeminal autonomic cephalgias
Group of HA disorders characterized by unilateral trigem neuralgia in assoc w/ ipsilateral cranial autonomic features (cluster HA, paroxysmal hemicarnia, hemicrania continua, SUNCT and SUNA syndrome)
277
What is SUNCT syndrome
Shortlasting, unilateral HA attacks w/ conjunctival injection and tearing; burning stabbing electrical HA in periorbital area lasting seconds to minutes; onset over 50 in men; **rx w/ lamotrigine
278
What is paroxysmal hemicrania
Similar to cluster HA but shorter duration and increased frequency ***rx: w/ indomethacin
279
What are the different types of MS
- Relapsing remitting
- secondary progressive: begin in relapsing remitting category
- primary progressive
- benign
280
Do women or men have a more favorable course with MS
Women
281
Does early or late onset of MS have a more favorable course
Early
282
What is the geographic risk associated w/ MS
More prevalent in temperate climates; risk determined before age 14
283
What studies are used to diagnose MS
MRI of head, C and T spine, multimodality evoked potentials, lumbar puncture for CSF analysis
284
Which drugs are used for MS maintenance (decrease frequency and severity of exacerabations and slow progression)
-mab’s and IFN; *used for relapsing form, not primary progressive
285
What drug is approved to treat primary progressive MS
Ocrevus
286
What medications are used to treat acute exacerbation of MS
Corticosteroids (methylprednisolone), ACTH
287
What is a clinically isolated syndrome
Either: monofocal (single neurological sign caused by single lesion) or multifocal (acute disseminated encephalomyelitis - more than one sign or symptoms by lesions in more than one place)
288
What type of CIS is associated with a high vs low risk of developing MS
- When CIS patients have multiple lesions on MRI, have 60-80% chance of developing MS *high risk
- When do not have multiple lesions, 20% chance -> low risk
289
What is Devic’s dz
Neuromyelitis optica; aquaphorin abs; tx w/ steroids or plasmapheresis followed by immunosuppression
290
What is epilepsy
2 or more unprovoked seizures
291
What types of seizures are most likely to show positive findings on a single EEG
Petit mal
292
What is the most likely way to get positive results on an EEG for all 3 types of epilepsy
3 sleep deprived EEGS
293
What is the most important information in making a diagnosis of epilepsy
History
294
What are simple partial seizures
Focal motor or sensory activity, no loss of consciousness, lasts seconds, no post-ictal state
295
What are complex partial seizures
Nonresponsive staring, possible preceding aura, automatisms, loss of consciousness, lasts 1-3 min, post-ictal state
296
What are secondary generalized seizures
B/l tonic-clonic activity, LOC, 1-3 min, post-ictal state
297
What are absence seizures
Nonresponsive staring, rapid blinking, chewing, clonic hand motions, LOC, lasts 10-30 sec, no post-ictal state
298
What are tonic clonic seizures
B/l extension followed by symmetrical jerking of extremities, LOC, lasts 1-3 min, post-ictal state
299
What are atonic seizures
Sudden loss of muscle tone, head drops or patient collapses, LOC, variable duration, post-ictal state
300
What are myoclonic seizures
Brief, rapid symmetrical jerking of extremities , LOC, lasts less than a few seconds, minimal post-ictal state
301
Which antiepileptic drugs are used to treat partial seizures
Lamotrigine, topiramate, leviteracetam, zonisamide, perampanel, valproic acid
302
What combination of AED’s has been show to be synergistic in treatment of epilepsy
Valproic acid and lamotrigine
303
What supplement should be given to all women of child bearing age on AED
Folic acid; AED’s are folate depleting
304
What features can decipher btw syncope and seizure
Syncope: pallor, sweating, lightheaded ness, positionally related, slow onset, brief unconsciousness
Seizure: urinary or bowel incontinence, tongue injury, tonic/clonic movement, postictal state
305
What is transient global amnesia
Sudden, temporary, isolated loss of memory; no other neuro signs; usually resolves after few hours; doesn’t recur
306
What does consciousness require
Arousal (level of alter ness; ability to interact w/ environment) and awareness (sum of cognitive mental functions)
307
What is delirium
*hallucinations (usually visual)
308
What is obtundation
Need stimuli to arouse
309
What is stupor
Arouses only to noxious stimuli
310
What is coma
Unarousable, unresponsive, unaware
311
What can cause HTN that would lead to a coma
Pheochromocytoma, drugs, increased ICP, PRES
312
What can cause hypotension that would lead to a coma
Addison’s, sepsis, drugs (beta blockers, ca channel blocker, TCA), progression to brain death
313
What can cause hyperthermia that can lead to coma a
Infection, heat stroke, drugs (amphetamines, salicylates), serotonin syndrome, central pontine hemorrhage
314
What can cause hypothermia that leads to a coma
Hypothyroidism, hypoglycemia, exposure, drugs (opioids, sedatives, barb)
315
What are the essential things you must do in your neuro exam for stupor and coma
Pupillary responses, corneal reflex, extraocular movements, cough/gag reflex, motor responses, respiratory patter *in order
316
What is the sympathetic path of the pupillary response
Hypothalamus -> lower cervical cord -> sympathetic chain -> superior cervical ganglion -> CN V -> long ciliary n to dilator (muellers m)
317
What is the parasympathetic path of the pupillary response
Upper midbrain (Edinger wesetfall) -> CNIII -> ciliary ganglion -> short ciliary n (constrictor)
318
What does absent or unequal pupillary responses indicate
Brainstem lesion
319
What is anisocoria
One abnormal pupil; if the abnormal pupil is the large pupil, it should fail to constrict to light; if the abnormal pupil is the small pupil, it will fail to dilate in the dark
320
What do pinpoint pupils indicate
Pontine lesion, opiates, pilocarpine
321
What is a mid position and unreactive pupil indicative of
Sympathetic and parasympathetic dysfunction (midbrain)
322
What can cause pupils to be dilated fixed and unequal
Glutethimide, hypothermia, anoxia, ischemia
323
What do frontal gaze centers vs pontine gaze centers do
Frontal: deviate eyes to opposite side
Pontine: deviate eyes to same side
324
What do conjugate roving eye movements suggest
Brainstem intact; dysconjugate implies brainstem lesion
325
With a hemispheric lesion, which way do the eyes conjugately move with a destructive vs irritative cause
Destructive: toward lesion
Irritative: away from lesion
326
What kind of conjugate deviation will you see in a brainstem lesion
Always destructive: away from lesion
327
What are the different types of nystagmus and the lesions associated with them
- Ping-pong: bihemispheric, midbrain
- Convergence (slow abduction with rapid jerk back): mesencephalon
- retractory: mesencephalon
- bobbing (rapid down, slow up): pons
- dipping (slow down, rapid up): bihemispheric
328
What is the oculocephalic maneuver
Doll’s eye; tests mid-pons
329
What does the caloric reflex test
Aka oculovestibular; lower pons
330
What lesion would cause flaccid reflex
Pontomedullary or metabolic
331
What lesion would cause Cheynes-stokes
B/l hemispheres or diencephalon
332
What lesion causes central neurogenic hyperventilation
Midbrain
333
What causes apneustic breathing
Long inspiration followed by apnea; lesion to mid/low pons; seen in anoxia hypoglycemia and meningitis
334
What causes ataxic respiratory pattern
Medullary respiratory center
335
What is a central transtentorial herniation
Through the foramen magnum; early coma, small pupils, normal EOM, posturing, resp arrest and death
336
What are the signs of a subtentorial mass
Brainstem dysfunction preceding coma (usually oculovestibular), CN palsy, bizarre respiratory partners
337
What are the signs of diffuse/metabolic causes of coma
Confusion and stupor preceded motor signs; motor signs symmetric; pupillary reactions preserved; myoclonus and seizures; acid-based imbalance usually seen
338
What is psychiatric unresponsiveness
Pupils reactive or dilated (cycloplegics), lids actively close, oculocephalic reflexes unpredictable, oculovestibular reflexes physiologic; motor tone is inconsistent or normal; eupnea or hyperventilation usual, no path reflexes, normal EEG
339
What is brain death
Irreversible (cause of coma must be known; must r/o sedative intox, hypothermia, and neuromuscular blockade), complete cessation of brain function including respirations but not heartbeat(no reflexes), persistent
340
Explain the apnea test
Oxygenate to get oxygen > 200 mm HG, disconnect ventilators, catheter 100% O2, observe chest wall for movement, if no respiratory movements for 8 min and arterial blood gas CO2 >60 mm Hg = brain death
341
What are the rules for “persistence” of brain death
Six hours w/ confirmatory EEG, 12 hours with confirmatory EEG, 24 hours for anoxic brain injury w/o a confirmatory EEG
342
What are the initial steps of managing a comatose patient
Insure patent airways, insure breathing and adequate oxygen, insure adequate circulation; history, EKG, glucose, adjust body temp, control agitation
343
What diagnostic testing should you order for a comatose patient
Non contrast head CT and LP
344
What can you do to reduce elevated intracranial pressure
Elevate head of bed, intubate and hyperventilate to PCO2 of 20 mm Hg
345
What is the classic triad of acute progenitor meningitis
Fever, HA, nuchal rigidity
346
What is the standard empiric treatment for acute pyogenic meningitis
Cefotaxime or ceftriaxone + vancomycin; add ampicillin for adults over 50
347
What do you give to someone who had a beta lactam allergy that has acute pyogenic meningitis
Vancomycin + moxifloxacin; add TMP/SMX if they are over 50
348
What do you give to an immunocompromised patient who has acute pyogenic meningitis
Vancomycin + ampicillin + cefepime or meropenem
349
What class of drugs are cefotaxime, ceftazidime, and ceftriaxone
Cephalosporins 3rd gen
350
What class of abx is vancomycin
Glycopeptide
351
What class of abx is ampicillin
Aminopenicillin
352
What kind of abx is trimethoprim/sulfamethoxazole (TMP/SMX)
Benzylpyrimidine/sulfonamide
353
What kind of abx is cefepime
Cephalosporin 4th gen
354
What kind of abx is meropenem
Carbapenem
355
What kind of abx is moxifloxacin
Fluoroquinolone
356
What is the CSF content of a brain abscess
High WBC, increased protein, normal glucose
357
What is the empiric therapy of brain abscesses with unknown source
Vancomycin + ceftriaxone or cefotaxime + metronidazole
358
What does penicillin G treat
Aerobic and anaerobic streptococci
359
What does ceftriaxone treat
Aerobic streptococci, and many enterobacteriaceae
360
When would you use ceftazidime, cefepime, or meropenem to treat a brain abscess
When they complicate a neurosurgical procedure; also covers cases of Pseudomonas
361
When would you discontinue vancomycin for treatment of a brain abscess
If culture comes back and there is no MRSA; substitute with nafcillin or oxacillin
362
What bacteria are the causes of subdural empyema
Aerobic and anaerobic strep, staph, enterobactereae and anaerobic bacteria
363
What organisms are responsible for subdural empyema after neurosurgical procedures or head trauma
Staph and gram negative bacilli
364
What is the treatment for community acquired subdural empyema
Cefotaxime or ceftriaxone + vancomycin + metronidazole
365
What is the treatment for hospital acquired subdural empyema (pseudomonas or MRSA)
Meropenem + vancomycin
366
What is subacute sclerosing panencephalitis characterized by
Neurofibrillary tangles, inflammation of white and grey matter; cognitive decline, spasticity of limbs, seizures
367
Which kind of vaccines offer protection that is greater and longer lasting
Live
368
What Ig’s are produced as a result of live vaccines
IgA and IgG; killed is only IgG
369
Does measles vaccine have the ability to revert to virulence
No; but polio does in small percentage
370
What kinds of vaccines are available for polio
- inactivated: killed vaccine; only one used in USA
| - live attenuated oral vax; can revert to virulence
371
What is the treatment for fungal meningoencephalitis
Induction phase: amphotericin B and flucytosine
| Consolidation phase: fluconazole
372
What is the only way amphotericin B can be administered
IV or directly into CSF
373
What are the adverse effects of amphotericin B
Renal toxicity, acute febrile reaction, anemia
374
Why must flucytosine be given in combination with another drug
Rapid resistance develops if given alone; MOA: inhibits DNA and RNA synthesis
375
What are the adverse effects of flucytosine
Conversion to 5-FU outside of fungal cell leading to bone marrow depression, N/V/D
376
What is the MOA of fluconazole
Inhibits ergosterol synthesis by inhibiting fungal P450 enzymes; very good CSF penetration; adverse effects: limited *widest therapeutic index
377
What classes of drugs cannot be used to treat neuro infections
1st generation cephalosporins (cefazolin), aminoglycosides, tetracyclines (-cycline), macrolides, clindamycin
378
What abx are part of the aminoglycosides
Streptomycin, gentamicin, tobramycin, amikacin, neomycin, paromomycin, kanamycin, netilmiccin
379
What abx are part of the macrolides
Erythromycin, clarithromycin, azithromycin, fidaxomicin
380
Which abx class is ototoxic
Aminoglycosides
381
What is the DEA number comprised of
2 letters (2nd letter is first letter in last name) and 7 digits
382
What is methysergide
Used to treat cluster HA * causes retroperitoneal fibrosis
383
What does a primary verses secondary hemorrhage in the brain look like
Primary: dark purple
Secondary: lighter pink
384
What worsens a stroke outcome
Glucose, hypotension, fever
385
What can mimic stroke
Post ictal state, hyper/hypoglycemia and hepatic disturbances
386
What drug does neuromyelitis optic not respond to
Rituxumab
387
How do you trigger a seizure in someone who has absence seizures
Make them hyperventilate
388
What does mesotemporal sclerosis cause
Seizures
389
What is zolmitriptan
Prodrug
390
What does carbidopa do
Inhibits decarboxylase that metabolizes dopa
391
What is one side effect that adding carbidopa wont help eliminate
Anxiety
392
What is selegiline
MOA-B inhibitor; decreases breakdown of dopamine
393
What are ropinirole and pramipexole
D2 and D3 (respectively) agonists; treat RLS (side effects are impulse control disorders)
394
What is apomorphine
*injectable
395
When would you give DA agonists versus start therapy on l-dopa
< 65 y/o
396
What drug has a side effect of purple skin
Amantadine *livedo reticularis
397
How do you treat meniere’s dz
Lorazepam, sodium restriction, diuretics, surgery
398
What is PRES
Confusion, vision loss, reversible
