Neurology Flashcards
1
Q
What do glaucoma drugs do?
A
↓ IOP via ↓ amount of aqueous humor (inhibit synthesis/secretion or ↑ drainage).
2
Q
Glaucoma drugs (α-agonists) - What is the mechanism of Ephedrine?
A
↓ aqueous humor synthesis via vasoconstriction
3
Q
Glaucoma drugs (α-agonists) - What are the side effects of Ephedrine?
A
Mydriasis; do not use in closed-angle glaucoma
4
Q
Glaucoma drugs (α-agonists) - What is the mechanism of Brimonidine (α2)?
A
↓ aqueous humor synthesis
5
Q
Glaucoma drugs (α-agonists) - What are the side effects of Brimonidine (α2)?
A
Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus
6
Q
Glaucoma drugs (β-blockers) - What is the mechanism of timolol, betaxolol, and carteolol?
A
↓ aqueous humor synthesis
7
Q
Glaucoma drugs (β-blockers) - What are the side effects of timolol, betaxolol, and carteolol?
A
No pupillary or vision changes
8
Q
Glaucoma drugs (diuretics) - What is the mechanism of Acetazolamide?
A
↓ aqueous humor synthesis via inhibition of
carbonic anhydrase
9
Q
Glaucoma drugs (diuretics) - What are the side effects of Acetazolamide?
A
No pupillary or vision changes
10
Q
Glaucoma drugs (Cholinomimetics) - What is the mechanism of Direct Cholinomimetics (pilocarpine, carbachol)?
A
↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
11
Q
Glaucoma drugs (Cholinomimetics) - What are the side effects of Direct Cholinomimetics (pilocarpine, carbachol)?
A
Miosis and cyclospasm (contraction of ciliary muscle)
12
Q
Glaucoma drugs (Cholinomimetics) - What is the mechanism of Indirect Cholinomimetics (physostigmine, echothiophate)?
A
Use pilocarpine in emergencies—very effective at opening meshwork into canal of Schlemm
13
Q
Glaucoma drugs (Prostaglandin) - What is the mechanism of Latanoprost (PGF2α)?
A
↑ outflow of aqueous humor
14
Q
Glaucoma drugs (Prostaglandin) - What are the side effects of Latanoprost (PGF2α)?
A
Darkens color of iris (browning)
15
Q
What are the Opioid Analgesics?
A
Morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan, diphenoxylate
16
Q
What is the mechanism of Opioid Anelgesics?
A
Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission—open K+ channels, close Ca2+ channels → ↓ synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.
17
Q
What is the clinical use of Opioid Anelgesics?
A
Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (methadone).
18
Q
What is the toxicity of Opioid Anelgesics?
A
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).
19
Q
What is the mechanism of Butorphanol?
A
Mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia.
20
Q
What is the clinical use of Butorphanol?
A
Severe pain (migraine, labor, etc.). Causes less respiratory depression than full opioid agonists.
21
Q
What is the toxicity of Butorphanol?
A
Can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors). Overdose not easily reversed with naloxone.
22
Q
What is the mechanism of Tramadol?
A
Very weak opioid agonist; also inhibits serotonin and norepinephrine reuptake (works on multiple neurotransmitters—“tram it all” in with tramadol).
23
Q
What is the clinical use of Tramadol?
A
Chronic pain.
24
Q
What is the toxicity of Tramadol?
A
Similar to opioids. Decreases seizure threshold. Serotonin syndrome.
25
What is Ethosuximide used for?
```
Simple:
Complex:
Tonic-Clonic:
Absence: Yes (First line)
Status Epilepticus:
```
26
What are Benzodiazepines (diazepam, lorazepam) used for?
```
Simple:
Complex:
Tonic-Clonic:
Absence:
Status Epilepticus: Yes (First line for acute)
```
27
What is Phenytoin used for?
```
Simple: Yes
Complex: Yes
Tonic-Clonic: Yes (First line)
Absence:
Status Epilepticus: Yes (First line for prophylaxis)
```
28
What is Carbamazepine used for?
```
Simple: Yes (First line)
Complex: Yes (First line)
Tonic-Clonic: Yes (First line)
Absence:
Status Epilepticus:
```
29
What is Valproic acid used for?
```
Simple: Yes
Complex: Yes
Tonic-Clonic: Yes (First line)
Absence: Yes
Status Epilepticus:
```
30
What is Gabapentin used for?
```
Simple: Yes
Complex: Yes
Tonic-Clonic: Yes
Absence:
Status Epilepticus:
```
31
What is Phenobarbital used for?
```
Simple: Yes
Complex: Yes
Tonic-Clonic: Yes
Absence:
Status Epilepticus:
```
32
What is Topiramate used for?
```
Simple: Yes
Complex: Yes
Tonic-Clonic: Yes
Absence:
Status Epilepticus:
```
33
What is Lamotrigine used for?
```
Simple: Yes
Complex: Yes
Tonic-Clonic: Yes
Absence: Yes
Status Epilepticus:
```
34
What is Levetiracetam used for?
```
Simple: Yes
Complex: Yes
Tonic-Clonic: Yes
Absence:
Status Epilepticus:
```
35
What is Tiagabine used for?
```
Simple: Yes
Complex: Yes
Tonic-Clonic:
Absence:
Status Epilepticus:
```
36
What is Vigabatrin used for?
```
Simple: Yes
Complex: Yes
Tonic-Clonic:
Absence:
Status Epilepticus:
```
37
What is the mechanism of Ethosuximide?
Blocks thalamic T-type Ca2+ channels
38
What are the Side Effects of Ethosuximide?
GI, fatigue, headache, urticaria, Steven-Johnson syndrome
39
What is the mechanism of Benzodiazepines
| (diazepam, lorazepam)?
↑ GABAA action
40
What are the Side Effects of Benzodiazepines
| (diazepam, lorazepam)?
Sedation, tolerance, dependence, respiratory depression
41
What else are Benzodiazepines used for?
Eclampsia seizures (1st line is MgSO4)
42
What is the mechanism of Phenytoin?
↑ Na+ channel inactivation; zero-order kinetics
43
What are the Side Effects of Phenytoin?
Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, teratogenesis (fetal hydantoin syndrome) SLE-like syndrome, induction of cytochrome P-450, lymphadenopathy, Stevens-Johnson syndrome, osteopenia
44
What is an additoinal fact about Phenytoin?
Fosphenytoin for parenteral use
45
What is the mechanism of Carbamazepine?
↑ Na+ channel inactivation
46
What are the Side Effects of Carbamazepine?
Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450, SIADH, Stevens-Johnson syndrome
47
What other condition is Carbamazepine a first line drug for?
Trigeminal neuralgia
48
What is the mechanism of Valproic acid?
↑ Na+ channel inactivation, ↑ GABA concentration
| by inhibiting GABA transaminase
49
What are the Side Effects of Valproic acid?
GI, distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain, contraindicated in pregnancy
50
What else is Valproic acid used for?
Myoclonic seizures, bipolar disorder
51
What is the mechanism of Gabapentin?
Primarily inhibits high voltage-activated Ca2+ channels; designed as GABA analog
52
What are the Side Effects of Gabapentin?
Sedation, ataxia
53
What else is Gabapentin used for?
Peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder
54
What is the mechanism of Phenobarbital?
↑ GABAA action
55
What are the Side Effects of Phenobarbital?
Sedation, tolerance, dependence, induction of cytochrome P-450, cardiorespiratory depression
56
When is Phenobarbital 1st line therapy?
For neonates
57
What is the mechanism of Topiramate?
Blocks Na+ channels, ↑ GABA action
58
What are the Side Effects of Topiramate?
Sedation, mental dulling, kidney stones, weight loss
59
What else is Topiramate used for?
Migraine prevention
60
What is the mechanism of Lamotrigine?
Blocks voltage-gated Na+ channels
61
What are the Side Effects of Lamotrigine?
Stevens-Johnson syndrome (must be titrated slowly)
62
What is the mechanism of Levetiracetam?
Unknown; may modulate GABA and glutamate release
63
What is the mechanism of Tiagabine?
↑ GABA by inhibiting re-uptake
64
What is the mechanism of Vigabatrin?
↑ GABA by irreversibly inhibiting GABA transaminase
65
What is Steven-Johnson Syndrome?
Prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital). Skin lesions progress to epidermal necrosis and sloughing.
66
What are the barbiturates?
Phenobarbital, pentobarbital, thiopental, secobarbital
67
What is the mechanism of barbiturates?
Facilitate GABAA action by ↑ duration of Cl− channel opening, thus ↓ neuron firing (barbidurates ↑ duration). Contraindicated in porphyria.
68
What is the clinical use of barbiturates?
Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
69
What is the toxicity of barbiturates?
Respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence; drug interactions (induces cytochrome P-450).
Overdose treatment is supportive (assist respiration and maintain BP).
70
What are the Benzodiazepines?
Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam.
71
What is the mechanism of Benzodiazepines?
Facilitate GABAA action by ↑ frequency of Cl− channel opening. ↓ REM sleep. Most have long half-lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting → higher addictive potential).
Benzos, barbs, and EtOH all bind the GABAA receptor, which is a ligand-gated Cl− channel.
72
What is the clinical use of Benzodiazepines?
Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
73
What is the toxicity of Benzodiazepines?
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor).
74
What are the Nonbenzodiazepine hypnotics?
Zolpidem (Ambien), Zaleplon, esZopiclone. “All ZZZs put you to sleep.”
75
What is the mechanism of Nonbenzodiazepine hypnotics?
Act via the BZ1 subtype of the GABA receptor. Effects reversed by flumazenil.
76
What is the clinical use of Nonbenzodiazepine hypnotics?
Insomnia
77
What is the toxicity of Nonbenzodiazepine hypnotics?
Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. ↓ dependence risk than benzodiazepines.
78
Anesthetics (General Principles) - What property must CNS drugs have to work?
CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.
79
Anesthetics (General Principles) - What property do drugs that have ↓ solubility in blood have?
Drugs with ↓ solubility in blood = rapid induction and recovery times.
80
Anesthetics (General Principles) - What property do drugs that have ↑ solubility in lipids have?
Drugs with ↑ solubility in lipids = ↑ potency = 1/MAC
81
Anesthetics (General Principles) - What is MAC?
Minimal Alveolar Concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (e.g., skin incision).
82
Anesthetics (General Principles) - Give examples of drugs that have ↑ and ↓ blood and lipid solubility.
N2O has ↓ blood and lipid solubility, and thus fast induction and low potency.
Halothane, in contrast, has ↑ lipid and blood solubility, and thus high potency and slow induction.
83
What are the inhaled anesthetics?
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
84
What is the mechanism of inhaled anesthetics?
Mechanism unknown.
85
What are the effects of inhaled anesthetics?
Myocardial depression, respiratory depression, nausea/emesis, ↑ cerebral blood flow (↓ cerebral
metabolic demand).
86
What is the toxicity of inhaled anesthetics?
Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas in a body cavity (nitrous oxide). Can cause malignant hyperthermia—rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene.
87
Intravenous anesthetics - What are the key features of Barbiturates?
Thiopental—high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue (i.e., skeletal muscle) and fat. ↓ cerebral blood flow.
88
Intravenous anesthetics - What are the key features of Benzodiazepines?
Midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, ↓ BP (treat overdose with flumazenil), and anterograde amnesia.
89
Intravenous anesthetics - What are the key features of Arylcyclohexylamines (Ketamine)?
PCP analogs that act as dissociative anesthetics. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. ↑ cerebral blood flow.
90
Intravenous anesthetics - What are the key features of Opioids?
Morphine, fentanyl used with other CNS depressants during general anesthesia.
91
Intravenous anesthetics - What are the key features of Propofol?
Used for sedation in ICU, rapid anesthesia induction, and short procedures. Less postoperative nausea than thiopental. Potentiates GABAA.
92
What are the Local Anesthetic esters?
Procaine, cocaine, tetracaine
93
What are the Local Anesthetic amides?
Lidocaine, mepivacaine, bupivacaine (amides have 2 I's in name)
94
What is the mechanism of Local Anesthetics?
Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. 3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.
95
Why are Local Anesthetics given with vasoconstrictors (usually epinephrine)?
Enhance local action— ↓ bleeding, ↑ anesthesia by ↓ systemic concentration.
96
What happens to Local Anesthetics in acidic tissue?
In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively → need more anesthetic.
97
What is the order of the nerve blockade?
Order of nerve blockade: small-diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers.
Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure.
98
What is the clinical use of Local Anesthetics?
Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.
99
What is the toxicity of Local Anesthetics?
CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine).
100
What are Neuromuscular blocking drugs used for?
Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
101
Neuromuscular blocking drugs (Depolarizing) - What are the features of Succinylcholine?
Strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction.
102
Describe the reversal of blockade of depolarzing neuromuscular blocking drugs?
Reversal of blockade:
▪ Phase I (prolonged depolarization)—no antidote. Block potentiated by cholinesterase inhibitors.
▪ Phase II (repolarized but blocked; ACh receptors are available, but desensitized)—antidote
consists of cholinesterase inhibitors.
103
What are the complications of Depolarizing Neuromuscular blocking drugs?
Complications include hypercalcemia, hyperkalemia, and malignant hyperthermia.
104
What are the nondepolarizing Neuromuscular blocking drugs and what are there features?
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium—competitive antagonists—compete with ACh for receptors.
105
Describe the reversal of blockade of nondepolarizing Neuromuscular blocking drugs.
Reversal of blockade—neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.
106
What is the mechanism of Dantrolene?
Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.
107
What is the clinical use of Dantrolene?
Used to treat malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).
108
What is Parkinsonism due to?
Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity.
109
Parkinson disease - What are the dopamine agonists?
Bromocriptine (ergot), pramipexole, ropinirole (non-ergot); non-ergots are preferred
110
Parkinson disease - What drugs ↑ dopamine?
Amantadine (may ↑ dopamine release); also used as an antiviral against influenza A and rubella; toxicity = ataxia
L-dopa/carbidopa (converted to dopamine in CNS)
111
Parkinson disease - What drugs prevent dopamine breakdown?
Selegiline (selective MAO type B inhibitor); entacapone, tolcapone (COMT inhibitors — prevent L-dopa degradation → ↑ dopamine availability)
112
Parkinson disease - What drugs curb excess cholinergic activity?
Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia)
113
Parkinson disease - What do you use for essential of familial tremors?
β-blocker (e.g., propranolol)
114
What is the mechanism of L-dopa (levodopa)/carbidopa?
↑ level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier and is
converted by dopa decarboxylase in the CNS to dopamine. Carbidopa, a peripheral decarboxylase
inhibitor, is given with L-dopa to ↑ the bioavailability of L-dopa in the brain and to limit peripheral
side effects.
115
What is the clinical use of L-dopa (levodopa)/carbidopa?
Parkinson's disease
116
What is the toxicity of L-dopa (levodopa)/carbidopa?
Arrhythmias from ↑ peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration (“on-off” phenomenon), akinesia between doses.
117
What is the mechanism of Selegiline?
Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, thereby ↑ the availability of dopamine.
118
What is the clinical use of Selegiline?
Adjunctive agent to L-dopa in treatment of Parkinson disease.
119
What is the toxicity of Selegiline?
May enhance adverse effects of L-dopa.
120
Alzheimer drugs - What is the mechanism of Memantine?
NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+).
121
What is the clinical use of Memantine?
Dizziness, confusion, hallucinations.
122
Alzheimer drugs - What is the mechanism of donepezil, galantamine, and rivastigmine?
AChE inhibitors.
123
What is the clinical use of Memantine?
Nausea, dizziness, insomnia.
124
What are the neurotransmitter changes in Huntington's disease?
↓ GABA, ↓ ACh, ↑ dopamine
125
Huntington's disease - What is the mechanism of tetrabenazine and reserpine?
Inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.
126
Huntington's disease - What is the mechanism of Haloperidol?
Dopamine receptor antagonist
127
What is the mechanism of Sumatriptan?
5-HT1B/1D agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half-life < 2 hours.
128
What is the clinical use of Sumatriptan?
Acute migraine, cluster headache attacks
129
What is the toxicity of Sumatriptan?
Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild tingling.
130
What drug is used to treat bedwetting (sleep enuresis)?
Oral desmopressin acetate (DDAVP), which mimics ADH; Benzodiazepines are useful for night terrors and sleepwalking.
131
What drug is useful for night terrors and sleepwalking?
Benzodiazepines
132
What do you treat Essential termor (postural tremor) with?
β-blockers, primidone
133
What do you treat Ischemic stroke with?
tPA (if within 3-4.5 hours of onset and no hemorrhage/risk of hemorrhage). Reduce risk with medical therapy (e.g., aspirin, clopidogrel); optimum control of blood pressure, blood surgars and lipids; and treat conditions that ↑ risk (e.g., atrial fibrillation).
134
What drug helps treat Amyotrophic lateral scleorsis (ALS)?
Riluzole treatment modestly ↑ survival by ↓ presynaptic glutamate release.
135
What drug is used to treat Facial nerve palsy?
Corticosteroids
136
What is used to treat Diabetic retinopathy?
Peripheral retinal photocoagulation, anti-VEGF injections
137
What is used to treat Age-related macular degeneration?
Anti-vascular endothelial growth facto injections (anti-VEGF) or laser
138
What is used to treat Multiple sclerosis?
β-interferon, immunosuppression, natalizumab. Symptomatic treatment for neurogenic bladder (catherization, muscarinic antagonists), spasticity (baclofen, GABA receptor agonist), and pain (opioids)
139
What drug is associated with a ↑ risk of Progressive multifocal leukoencephalopathy?
Natalizumab
140
What is the treatment for Cluster headaches?
Inhaled O2, sumatriptan
141
What is the treatment for Tension headaches?
Analgesics, NSAIDs, acetaminophen; amitriptyline for chronic pain
142
What is the treatment for Migraine headaches?
Abortive therapies (e.g., triptans, NSAIDs) and prophylactic (propranolol, topiramate, calcium channel blockers, amitriptyline)
