Principles in Neurology_3 Flashcards
1
Q
clinical features of CJD?
A
rapidly progressive dementia with myoclonus
2
Q
what are the histologic/gross findings in CJD?
A
spongiform cortex • prions (PrPc→PrPsc sheet [β-pleated sheet resistant to proteases])
3
Q
what is MS?
A
autoimmune inflammation and demyelination of CNS
4
Q
Patients with MS can present how?
A
optic neuritis • MLF syndrome • hemiparesis • hemisensory symptoms • bladder/bowel incontinence
5
Q
what is the course in MS?
A
relapsing and remitting
6
Q
MS most often affects who?
A
women in their 20’s and 30’s; more common in whites
7
Q
what is Charcot’s classic triad of MS?
A
a SIN: • Scanning speech • Intention tremor/Incontinence/INO • Nystagmus
8
Q
what are the findings in MS?
A
↑ protein (IgG) in CSF • Oligoclonal bands are diagnostic • MRI is gold standard • Periventricular plaques with destruction of axons
9
Q
what is the treatment for MS?
A
β-interferon, immunosuppression, natalizumab • symptomatic tx for neurogenic bladder, spasticity, and pain
10
Q
what is the most common variant of Guillain-Barre syndrome?
A
Acute Inflammatory demyelinating polyradiculopathy
11
Q
what is acute inflammatory demyelinating polyradiculopathy?
A
autoimmune condition that destroys Schwann cells → inflammation and demyelination of peripheral nerves and motor fibers
12
Q
acute inflammatory demyelinating poly radiculopathy results in what?
A
symmetric ascending muscle weakness/paralysis beginning in lower extremities • facial paralysis in 50% of cases • autonomic dysfunction
13
Q
prognosis of acute inflammatory demyelinating polyradiculopathy?
A
almost all patients survive; majority recover completely after weeks to months
14
Q
what are the findings in acute inflammatory demyelinating polyradiculopathy?
A
↑CSF protein with normal cell count (albuminocytologic dissociation). • ↑protein →papilledema
15
Q
acute inflammatory demyelinating polyradiculopathy is associated with which infections?
A
Campylobacter jejuni and CMV
16
Q
how does infection cause acute inflammatory demyelinating polyradiculopathy?
A
autoimmune attack of peripheral myelin due to molecular mimicry, inoculations, and stress, but no definitive link to pathogens
17
Q
Tx for acute inflammatory demyelinating polyradiculopathy?
A
respiratory support is critical until recovery. • additional: plasmapharesis, IV immune globulins
18
Q
what is progressive multifocal leukoencephalopathy?
A
demyelination of CNS due to destruction of oligodendrocytes
19
Q
PML is associated with what?
A
JC virus
20
Q
PML is seen in which patients?
A
2-4% of AIDS patients
21
Q
prognosis of PML?
A
rapidly progressive, usually fatal
22
Q
what is acute disseminated (postinfectious) encaphalomyelitis?
A
multifocal perivenular inflammation and demyelination after infection (measles or VZV) or vaccination (rabies, small pox)
23
Q
what is metachromatic leukodystrophy?
A
autosomal recessive lysosomal storage disease, most commonly due to aryl sulfatase A deficiency.
24
Q
what causes demyelination in metachromatic leukodystrophy?
A
build up of sulfatides leads to impaired production of myelin sheath
25
Charcot-Marie-Tooth disease is AKA what?
hereditary motor and sensory neuropathy
26
what is HMSN?
group of progressive heeditary nerve disorders related to the defective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath
27
What is Krabbe's disease?
AR lysosomal storage disease due to deficiency of galactocerebrosidase
28
how does Krabbe's disease cause demyelination?
build up of galactocerebroside destroys myelin sheath
29
seizures are characterized by what?
synchronized high frequency neuronal firing
30
partial seizures affect what?
1 area of the brain
31
partial seizures most commonly originate where?
medial temporal lobe
32
partial seizure is often preceded by what?
seizure aura
33
secondary consequence of some partial seizures?
can secondarily generalize
34
what are the types of partial seizure?
simple partial • complex partial
35
what is a simple partial seizure?
consciousness intact: • motor, sensory, autonomic, psychic
36
what is a complex partial seizure?
partial seizure with impaired consciousness
37
what is epilepsy?
a disorder of recurrent seizures- excluding febrile seizures
38
what is status epilepticus?
continuous seizure for >30 min or recurrent seizures without regaining consciousness between seizures for >30min
39
what are the causes of seizures in children?
genetic • infection (febrile) • trauma • congenital • metabolic
40
what are the causes of seizures in adults?
tumors • trauma • stroke • infection
41
what are the causes of seizures in the elderly?
stroke • tumor • trauma • metabolic • infection
42
what are the types of generalized seizures?
Absence (petit mal) • myoclonic • tonic-clonic (grand mal) • tonic • atonic
43
features of absence seizure?
3Hz • no postictal confusion • blank stare
44
features of myoclonic seizure?
quick repetitive jerks
45
features of tonic-clonic seizure?
alternating stiffening and movement
46
features of tonic seizure?
stiffening
47
features of atonic seizure?
drop' • commonly mistaken for fainting
48
head aches are all characterized by what?
pain due to structures such as the dura, cranial nerves, or extracranial structures
49
localization of cluster HA?
unilateral
50
duration of cluster HA?
15min-3hr; repetitive
51
clinical presentation of cluster HA?
repetitive brief HA. excruciating periorbital pain with lacrimation and rhinorrhea
52
cluster HA may induce what?
Horner syndrome
53
cluster HA is more common in whom?
males
54
what is the treatment for cluster HA?
inhaled O2 • sumatriptan
55
localization of tension headache?
bilateral
56
duration of tension HA?
>30 min (~4-6hr); constant
57
clinical presentation of tension HA?
steady pain. no photophobia or phonophobia. no aura
58
localization of migraine HA?
unilateral
59
duration of migraine HA?
4-72hr
60
clinical features of migraine?
pulsating pain with nausea, photophobia, phonophobia, aura
61
what causes migraine?
irritation of CN V, meninges, or blood vessels (release of substance P, GCRP, vasoactive peptides)
62
what are the abortive therapies for migraine?
triptans
63
what are the prophylactic therapies for migraine?
propanolol • topiramate
64
what is vertigo?
sensation of spinning while stationary
65
what is the more common type of vertigo?
peripheral vertigo
66
what causes peripheral vertigo?
inner ear etiology: • semicircular canal debris • vestibular nerve infection • Menieres disease
67
what is the finding of positional testing in peripheral vertigo?
delayed horizontal nystagmus
68
what causes central vertigo?
brainstem or cerebellar lesion: • stroke affecting vestibular nuclei • posterior fossa tumor
69
what are the findings in central vertigo?
directional change of nystagmus • skew deviation • diplopia • dysmetria
70
results of positional testing in central vertigo?
immediate nystagmus in any direction; may change directions
71
what are the neurocutaneous disorders?
1. Sturge-Weber syndrome • 2. Tuberous sclerosis • 3. NF1 • 4. Von Hippel-Lindau disease
72
what is Sturge-Weber syndrome?
congenital disorder with port-wine stains (nevus flammeus) typically in V1 ophthalmic distribution
73
what tumors are seen with Sturge-Weber syndrome?
leptomeningeal angiomas • pheochromocytomas
74
Sturge Weber syndrome can cause what?
glaucoma • seizures • hemiparesis • MR
75
inheritance of Sturge-Weber syndrome?
occurs sporadically
76
clinical features of Tuberous Sclerosis?
HAMARTOMAS: • Hamartomas in CNS and skin • Adenoma sebaceum (cutaneous angiofibroma) • Mitral regurgitation • Ash-leaf spots • cardiac Rhabdomyoma • Tuberous sclerosis • autosomal dOminant • Mental retardation • Angiomyolipoma • Seizures
77
what are the clinical features of NF1?
Cafe-au-lait spots • Lisch nodules • neurofibromas in skin • optic gliomas • pheochromocytomas
78
genetic features of NF1?
AD • 100% penetration • variable expressivity • mutated NF1 gene on chromosome 17
79
what are the clinical features of VonHippel-Lindau disease?
Cavernous hemangiomas in skin, mucose, organs; • bilateral RCC • hemangioblastoma in retina, brainstem, cerebellum; • pheochromocytomas
80
genetic features of VonHippel-Lindau disease?
AD • mutated tumor suppressor VHL gene on chromosome 3
81
what is the most common 1° brain tumor in adults?
GBM/ Grade IV astrocytoma
82
prognosis for GBM?
malignant with <1yr life expectancy
83
where is GBM found?
cerebral hemispheres • can cross corpus callosum (butterfly glioma)
84
how do you stain GBM?
stain astrocytes for GFAP
85
histologic findings in GBM?
pseudopalisading pleomorphic tumor cells- border central areas of necrosis and hemorrhage
86
what is the 2nd most common 1° brain tumor in adults?
meningioma
87
meningioma most commonly occurs where?
in convexities of hemispheres (near surfaces of brain) and parasagital region
88
morphologic features of meningiomas?
1. arise from arachnoid cells • 2. are extra-axial (external to brain parenchyma) • 3. may have a dural attachment (tail)
89
prognosis of meningioma?
typically benign and resectable
90
clinical presentation of meningioma?
often asymptomatic; may present with seizures or focal signs
91
what is the 3rd most common 1° brain tumor in adults?
Schwannoma
92
morphologic features of Schwannoma?
Schwann cell origin; often localized to CNIII →acoustic neuroma
93
treatment for Schwannoma?
resectable or treated with stereotactic radiosurgery
94
Schwannoma is usually found where?
cerebellopontine angle
95
how does a Schwannoma stain?
S-100 positive
96
bilateral acoustic neuromas found in what?
NF2
97
frequency of oligodendroglioma?
relatively rare, slow growing
98
oligodendroglioma is most often located where?
frontal lobes
99
morphologic features of oligodendroglioma?
chicken wire capillary pattern • oligodendrocytes= fried egg cells- round nuclei with clear cytoplasm • often calcified in oligodendroglioma
100
pituitary adenoma is most commonly what?
prolactinoma
101
symptoms of prolactinoma?
bitemporal hemianopia and hypo/hyperpituitarism
102
what are the childhood primary brain tumors?
1. pilocytic (low-grade) astrocytoma • 2. medulloblastoma • 3. ependymoma • 4. hemangioblastoma • 5. craniopharyngioma
103
morphologic features of pilocytic astrocytoma?
well circumscribed • cystic and solid
104
where is pilocytic astrocytoma most often found in children?
posterior fossa/cerebellum • may be supratentorial
105
how does pilocytic astrocytoma stain?
GFAP positive
106
prognosis of pilocytic astrocytoma?
benign • good prognosis
107
histologic findings in pilocytic astrocytoma?
Rosenthal fibers- eosinophilic corkscrew fibers
108
what is a medulloblastoma?
highly malignant cerebellar tumor • form of primitive neuroectodermal tumor
109
medulloblastoma can compress what?
4th ventricle → hydrocephalus
110
how does medulloblastoma metastasize?
can send drop mets to spinal cord
111
morphologic findings in medulloblastoma?
Horner-Wright rosettes • Solid • small blue cels
112
treatment of medulloblastoma?
radiosensitive
113
ependymal cell tumors are most commonly found where?
in 4th ventricle
114
ependymal cell tumors can cause what?
hydrocephalus
115
prognosis of ependymal tumors?
poor
116
morphologic findings in ependymoma?
characteristic perivascular pseudorosettes. rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus
117
hemangioblastomas in the brain are most often where?
cerebellum
118
hemangioblastomas are associated with what condition when seen with retinal angiomas?
VonHippel Lindau disease
119
hemangioblastomas can produce what?
erythropoietin→2° polycythemia
120
what findings are characteristic of hemangioblastoma?
foamy cells and high vascularity
121
what is a craniopharyngioma?
benign childhood tumor, confused with pituitary adenoma (can also cause bitemporal hemianopia)
122
what is the most common childhood supratentorial tumor?
craniopharyngioma
123
craniopharyngioma is derived from what?
Rathke's pouch
124
morphological features of craniopharyngioma?
calcification is common (tooth enamel like)
125
what are the herniation syndromes?
1. cingulate (subfalcine) herniation under falx • 2. downward transtentorial (central) herniation • 3. uncal herniation • 4. cerebellar tonsillar herniation into the foramen magnum
126
cingulate herniation under falx can do what?
compress ACA
127
where is the uncus?
medial temporal lobe
128
complications of cerebellar tonsilar herniation into the foramen magnum?
coma and death result when these herniations compress the brain stem
129
what do glaucoma drugs do?
↓ IOP via ↓ amount of aqueous humor (inhibit synthesis/secretion or increase drainage)
130
what are the classes of glaucoma drugs?
α1-agonists • β-blockers • diuretics • cholinomimetics • prostaglandin
131
what are the α agonists used to treat glaucoma?
Epinephrine • Brimonidine (α2)
132
what is the MOA of epinephrine for glaucoma?
↓ aqueous humor via vasoconstriction
133
what is the MOA of brimonidine for glaucoma?
↓ aqueous humor synthesis
134
what are the side-effects of epinephrine for glaucoma?
mydriasis; do not use in closed angle glaucoma
135
what are the side effects of brimonidine for glaucoma?
Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus
136
what are the β-blockers used for glaucoma?
timolol • betaxolol • carteolol
137
what is the MOA of timolol, betaxolol, and carteolol for glaucoma?
↓ aqueous humor synthesis
138
what are the side effects of timolol, betaxolol, and carteolol for glaucoma?
no pupillary or vision changes
139
what are the diuretics used for glaucoma?
acetazolamide
140
what is the MOA of acetazolamide for glaucoma?
↓aqueous humor synthesis via inhibition of carbonic anhydrase
141
what are the side effects of acetazolamide for glaucoma?
no pupillary or vision changes
142
what are the direct cholinomimetics used for glaucoma?
pilocarpine, carbachol
143
what are the indirect cholinomimetics used for glaucoma?
physostigmine • echothiophate
144
what is the mechanism of action of cholinomimetics for glaucoma?
↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
145
what are the side effects of cholinomimetics for glaucoma?
miosis and cyclospasm
146
which drug should be used for glaucoma emergency?
pilocarpine- very effective at opening meshwork into canal of Schlemm
147
what is the prostaglandin used for glaucoma?
Latanoprost (PGF2α)
148
what is the MOA of latanoprost?
↑ outflow of aqueous humor
149
what are the side effects of latanoprost for glaucoma?
darkens color of iris
150
which drugs are opioid analgesics?
1. morphine • 2. fentanyl • 3. codeine • 4. heroin • 5. methadone • 6. meperidine • 7. dextromethorphan • 8. diphenoxylate
151
what is the MOA of opioid analgesics?
agonists at opioid receptors to modulate synaptic transmission- open K+ channels, close Ca2+ channels→ ↓ synaptic transmission • - inhibit release of ACh, NE, 5-HT, glutamate, substance P
152
what is the clinical use of opioid analgesics?
pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone)
153
what happens in opioid analgesic toxicity?
addiction • respiratory depression • constipation • miosis (pinpoint pupils) • additive CNS depression with other drugs
154
there is no tolerance to which side effects of opioids?
miosis • constipation
155
opioid toxicity is treated with what?
naloxone or naltrexone (opioid receptor antagonist)
156
what stimulates opioid mu receptor?
morphine
157
what stimulates opioid delta receptor?
enkephalin
158
what stimulate opioid kappa receptor?
dynorphin
159
what is the MOA of Butorphanol?
mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia
160
what is the clinical use of Butorphanol?
severe pain (migraine, labor, etc.) causes less respiratory depression than full opioid agonists
161
what happens in butorphanol toxicity?
can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors). overdose not easily reversed with naloxone
162
what is the MOA of tramadol?
very weak opioid agonist; also inhibits 5HT and NE reuptake (works on multiple neurotransmitters)
163
what is the clinical use of tramadol?
chronic pain
164
what happens in tramadol toxicity?
similar to opioids. decreases seizure threshold
165
What kind of seizures do you treat with phenytoin?
- 1st LINE: Tonic-Clonic + Prophylaxis of status epilepticus • - Simple and complex partial
166
what type of seizures do you treat with carbamazepine?
1st LINE: Simple and complex partial + Tonic-Clonic
167
which types of seizures do you treat with lamotrigine?
- Simple and complex partial • - Generalized tonic-clonic
168
which types of seizures do you treat with gabapentin?
- Simple and complex partial • - generalized tonic-clonic
169
which types of seizures do you treat with topiramate?
- Simple and Complex Partial • - Generalized Tonic-clonic
170
which types of seizures do you treat with phenobarbital?
- Simple and complex partial • - generalized tonic-clonic
171
which types of seizures do you treat with Valproate?
1st LINE: Tonic-Clonic • - Simple and Complex partial • - absence
172
which types of seizures do you treat with ethosuxamide?
1st LINE: absence
173
which types of seizures do you treat with Benzodiazepines?
1st LINE: acute status epilepticus
174
which types of seizures do you treat with tiagabine?
simple and complex partial seizures
175
which types of seizures do you treat with vigabatrin?
simple and complex partial
176
which types of seizures do you treat with levetiracetam?
- simple and complex partial • - generalized tonic clonic
177
what is the first line treatment for prohpylaxis of Status epilepticus?
phenytoin
178
what is the 1st line treatment for acute status epilepticus?
benzodiazepines
179
what is the first line treatment for absence seizures?
ethosuxamide
180
what are the first line treatments for tonic-clonic seizures?
phenytoin • carbamazepine • valproic acid
181
what are the first line treatments for simple and complex partial seizures?
carbamazepine
182
MOA of phenytoin?
use dependent blockade of Na channels; inhibition of glutamate release from excitatory presynaptic neuron
183
how do you give parenteral phenytoin?
Fosphenytoin
184
MOA of carbamazepine?
↑ Na+ channel inactivation
185
which drug is the 1st line treatment for trigeminal neuralgia?
carbamazepine
186
MOA of lamotrigine?
blocks voltage gated Na+ channels
187
what is the MOA of gabapentin?
designed as GABA analog, but primarily inhibits high-voltage-activated Ca++ channels
188
gabapentin is used for what other than seizures?
peripheral neuropathy • postherpetic neuralgia • migraine prophylaxis • bipolar disorder
189
MOA of topiramate?
blocks Na+ channels • ↑GABA action
190
topiramate is used for what other than seizures?
migraine prevention
191
MOA of phenobarbital?
↑GABAa action
192
when is phenobarbital 1st line?
in children
193
MOA of valproic acid?
↑Na+ channel inactivation, • ↑ GABA concentration
194
valproic acid can be used for which unusual type of seizure?
myoclonic seizure
195
MOA of ethosuxamide?
blocks thalamic T-type Ca++ channels
196
MOA of diazepam/lorazepam?
↑GABAa action
197
benzodiazepines are used for what in pregnancy?
seizures in eclampsia, but 1st line is MgSO4
198
MOA of tiagabine?
inhibits GABA reuptake
199
MOA of vigabatrin?
irreversibly inhibits GABA transaminase →↑GABA
200
MOA of levetiracetam?
may modulate GABA and glutamate release
201
Benzodiazepine toxicity?
Sedation • Tolerance • Dependence
202
Carbamazepine toxicity?
Diplopia • ataxia • blood dyskrasias (agranulocytosis, aplastic anemia) • liver toxicity • teratogenesis • P450 induction • SIADH • SJS
203
ethosuxamide toxicity?
GI distress • fatigue • headache • urticaria • SJS
204
phenobarbital toxicity?
Sedation • tolerance • dependence • induction of P450
205
Phenytoin toxicity?
nystagmus • diplopia • ataxia • sedation • gingival hyperplasia • hirsutism • megaloblastic anemia (↓folate absorption) • teratogenesis (fetal hydantoin syndrome) • SLE like syndrome • induction of P450 • lymphadenopathy • SJS • osteopenia
206
Valproic acid toxicity?
GI distress • rare but fatal hepatotoxicity • NTD • tremor • weight gain • CI in pregnancy
207
toxicity of lamotrigine?
SJS
208
gabapentin toxicity?
sedation • ataxia
209
topiramate toxicity?
sedation • mental dulling • kidney stones • weight loss
210
clinical presentation of SJS?
prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules • skin lesions progress to epidermal necrosis and sloughing
211
Clinical use of phenytoin?
tonic-clonic seizures • class 1B antiarrhythmic
212
which drugs are the barbiturates?
phenobarbital • pentobarbital • thiopental • secobarbital
213
mechanism of action of Barbiturates?
facilitate GABAa action by *↑ duration* of Cl channel opening→↓ neuron firing
214
what is the clinical use of barbiturates?
sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
215
Barbiturate toxicity?
Respiratory and cardiovascular depression (can be fatal) • CNS depression (↑ by EtOH) • dependence • induces P450
216
when are barbiturates contraindicated?
porphyria
217
what is the treatment for barbiturate overdose?
supportive (assist respiration and maintain BP)
218
which drugs are benzodiazepines?
diazepam • lorazepam • triazolam • temazepam • oxazepam • midazolam • chlordiazepoxide • alprazolam
219
what is the mechanism of action of benzodiazepines?
facilitates GABAa action by ↑ frequency of Cl channel opening
220
effect of benzodiazepines on REM sleep?
↓
221
t1/2 of benzodiazepines?
most have long half lives and active metabolites except for triazolam, oxazepam, and midazolam which are short acting →higher addictive potential
222
what do benzos barbs and EtOH all have in common?
all bind GABAa receptor= ligand gated Cl channel
223
clinical use of benzodiazepines?
anxiety • spasticity • status epilepticus • detoxification • night terrors • sleepwalking • general anesthesia (amnesia, muscle relaxation) • hypnotic
224
which benzos can be used for status epilepticus?
lorazepam and diazepam
225
toxicity of benzodiazepines?
dependence • additive CNS depression FX with EtOH • less risk of respiratory depression and coma than with barbiturates
226
treat overdose of benzodiazepines with what?
flumazenil (competitive inhibitor at benzodiazepine GABA receptor)
227
which drugs are the nonbenzodiazepine hypnotics?
Zolpidem (Ambien) • zalephon • eszopiclone
228
mechanism of nonbenzodiazepine hypnotics?
act via the BZI subtype of the GABA receptor
229
how are effects of Zolpidem, zalephon, and eszopiclone reversed?
flumazenil
230
what is the clinical use of zolpidem and other non benzodiazepine hypnotics?
insomnia
231
toxicity of zolpidem, zalephon, eszopiclone?
ataxia • HA • confusion
232
duration of non BZD hypnotics?
short because of rapid liver metabolism
233
difference between zolpidem and older sedative hypnotics?
cause only modest day after psychomotor depression and few amnestic effects • lower dependence risk than benzos
234
what is necessary for a drug to work on the CNS?
lipid soluble (cross BBB) • or • be actively transported
235
features of anesthetics with ↓ solubility in blood?
rapid induction and recovery times
236
features of anesthetics with ↑ solubility in lipids?
↑ potency= 1/MAC
237
what is MAC?
minimal alveolar concentration at which 50% of the population is anesthetized
238
MAC varies with what?
age
239
solubility properties of N2O?
↓ blood and lipid solubility, and thus fast induction and low potency
240
solubility properties of halothane?
↑lipid and blood solubility, and thus high potency and slow induction
241
which drugs are inhaled anesthetics?
halothane • enflurane • isoflurane • sevoflurane • methoxyflurane • nitrous oxide
242
what is the mechanism of inhaled anesthetics?
unknown
243
what are the effects of inhaled anesthetics?
myocardial depression • respiratory depression • nausea/emesis • ↑ cerebral blood flow (↓cerebral metabolic demand)
244
toxicity of halothane?
hepatotoxicity
245
toxicity of methoxyflurane?
nephrotoxicity
246
toxicity of enflurane?
proconvulsant
247
which inhaled anesthetics carry risk of malignant hyperthermia?
all but N2O; rare life threatening inherited susceptibility
248
toxicity unique to N2O?
expansion of trapped gas in a body cavity
249
what are the intravenous anesthetics?
Barbiturates • Benzodiazepines • Arylcyclohexylamines (Ketamine) • Opioids • Propofol
250
MC barbiturate IV anesthetic?
Thiopental
251
PK of thiopental as IV anesthetic?
high potency, high lipid solubility, rapid entry into brain
252
thiopental is used as an IV anesthetic for what?
induction of anesthesia and short surgical procedures
253
effect of thiopental as IV anesthetic is terminated by what?
rapid redistribution into tissues (MSK + Fat)
254
effect of IV thiopental on cerebral blood flow?
↓cerebral blood flow
255
which IV benzodiazepine is most common anesthetic used for endoscopy?
midazolam
256
how is midazolam used as IV anesthetic?
adjunctively with gaseous anesthetics and narcotics
257
risk of IV midazolam for anesthesia?
may cause severe post/op respiratory depression, ↓BP and amnesia
258
what are arylcyclohexylamines like ketamine?
PCP analogs that act as dissociative anesthetics
259
PD of IV ketamine in anesthesia?
blocks NMDA receptors
260
effect of IV ketamine on Cardiovascular system?
cardiovascular stimulant
261
congitive effects of arylcyclohexylamines?
cause disorientation, hallucination, and bad dreams
262
effect of arylcyclohexylamines on cerebral blood flow?
↑ cerebral blood flow
263
use of IV opioids in anesthesia?
morphine, fentanyl used with other CNS depressants during general anesthesia
264
propofol is used for what?
sedation in ICU • rapid anesthesia induction • short procedures
265
PD effects of IV propofol?
potentiates GABAa
266
difference in side effects between propofol and thiopental?
propofol has less postoperative nausea than thiopental
267
what are the local anesthetic esters?
procaine • cocaine • tetracaine
268
what are the aminde local anesthetics?
lidocaine • mepivacaine • bupivacaine
269
MOA of local anesthetics?
block Na+ channels by binding to specific receptors on inner portion of channel
270
local anesthetics preferentially bind to what?
activated Na+ channels, so most effective in rapidly firing neurons
271
PK of 3° amine local anesthetics?
penetrate membrane in uncharged form, hen bind to ion channels as charged form
272
Local anesthetics can be given as what combination?
can be given with vasoconstrictors (epi) to enhance local action= • ↓bleeding, ↑anesthesia by ↓systemic concentration
273
what happens when you use an alkaline anesthetic in infected tissue?
in acidic tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively →need more anesthetic
274
what is the order of nerve blockade by local anesthetics?
small diameter myelinated > small unmyelinated> large myelinated fibers > large unmyelinated
275
what is the order of loss of sensation in local anesthesia?
1 pain • 2 temperature • 3 touch • 4 pressure
276
what is the clinical use of local anesthetics?
minor surgical procedures, spinal anesthesia. If allergic to esters, give amides
277
toxicity of local anesthetics?
CNS excitation, severe cardiovascular toxicity (bupivacaine), HTN, arrhythmia (cocaine)
278
neuromuscular blocking drugs are used for what?
muscle paralysis in surgery or mechanical ventilation. selective for motor vs autonomic nicotinic receptor
279
prototypical depolarizing neuromuscular blocker?
succinylcholine
280
MOA of succinylcholine?
strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction
281
steps in reversal of succinylcholine blockade?
Phase I (prolonged depolarization) no antidote. block potentiated by cholinesterase inhibitors • Phase II (repolarized but blocked) antidote consists of cholinesterase inhibitors
282
complications of succinylcholine use?
hypercalcemia • hyperkalemia • malignant hyperthermia
283
what are the nondepolarizing neuromuscular blockers?
tubocurarine • atracurium • mivacurium • pancuronium • vecuronium • rocuronium
284
MOA of nondepolarizing neuromuscular blockers?
competitive antagonists- compete with ACh for receptors
285
how do you reverse blockade by nondepolarizing neuromuscular blockers?
neostigmine • edrophonium • and other cholinesterase inhibitors
286
what is the MOA of dantrolene?
prevents the release of Ca++ from the sarcoplasmic reticulum of skeletal muscle
287
what is the clinical use of dantrolene?
used in the treatment of malignant hyperthermia and neuroleptic malignant syndrome
288
what are the strategies for the treatment of Parkinson's disease?
1. Dopamine agonists • 2. ↑dopamine • 3. prevent dopamine breakdown • 4. Curb excess cholinergic activity
289
what is the mnemonic for the treatment of Parkinson's?
BALSA • Bromocriptine • Amantadine • Levodopa • Selegiline • Antimuscarinics
290
what are the dopamine agonists used for Parkinson's?
Bromocriptine (ergot) • pramipexole • ropinirole (non-ergot) • Non ergot are preferred
291
what are the agents used to ↑dopamine in Parkinson's?
Amantadine (may ↑dopamine release) • L-dopa/carbidopa
292
Amantadine is also used for what?
antiviral against influenza A and rubella
293
toxicity of Amantadine?
ataxia
294
MOA of Ldopa?
converted to DA in CNS
295
what agents prevent dopamine breakdown in Parkinson's?
Selegiline • entacapone • tolcapone
296
MOA of selegiline?
selective MAO type B inhibitor which preferentially metabolized dopamine over NE and 5HT
297
MOA of entacapone, tolcapone?
COMT inhibitors- prevent Ldopa degradation
298
which agents curb excess cholinergic activity in Parkinson's?
Benztropine
299
MOA of benztropine?
Antimuscarinic; • improves tremor and rigidity but has little effect on bradykinesia
300
difference between Ldopa and DA?
L dopa can cross BBB and is converted by dopa decarboxylase in the brain to DA
301
MOA of carbidopa?
a peripheral decarboxylase inhibitor, is given with Ldopa to ↑bioavailability of Ldopa in the brain and to limit peripheral side effects
302
toxicity of Ldopa/carbidopa?
arrhythmia from increased peripheral formation of catecholamines • long term use can lead to dyskinesia following administration, akinesia between doses
303
clinical use of selegiline?
adjunctive agent to L dopa in Tx of Parkinsons
304
toxicity of selegiline?
may enhance adverse effects of Ldopa
305
what are the Alzheimer's drugs?
Memantine • Donepezil, galantamine, rivastigmine
306
MOA of memantine?
NMDA receptor antagonist; helps prevent excitotoxicity
307
toxicity of memantine?
dizziness • confusion • hallucinations
308
MOA of donepezil, galantamine, rivastigmine?
acetylcholinesterase inhibitors
309
toxicity of AChE inhibitors in AD?
nausea • dizziness • insomnia
310
what are the neurotransmitter changes in Huntington's disease?
↓GABA • ↓ACh • ↑DA
311
what are the treatments for Huntingtons?
Terbenazine and reserpine • Haloperidol
312
MOA of terbenazine and reserpine in huntingtons?
inhibit VMAT; limit DA vesicle packaging and release
313
MOA of haloperidol for huntingtons?
DA receptor antagonist
314
MOA of sumatriptan?
5HT1B/1D agonist- • inhibits trigeminal nerve activation • prevents vasoactive peptide release • induces vasoconstriction
315
t1/2 of sumatriptan?
<2h
316
clinical use of sumatriptan?
acute migraine • cluster HA attacks
317
toxicity of sumatriptan?
coronary vasospasm (CI in patients with CAD or prinzmental's angina) • mild tingling
