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► Med Notes > Principles in Neurology_3 > Flashcards

Principles in Neurology_3 Flashcards

1
Q

clinical features of CJD?

A

rapidly progressive dementia with myoclonus

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2
Q

what are the histologic/gross findings in CJD?

A

spongiform cortex • prions (PrPc→PrPsc sheet [β-pleated sheet resistant to proteases])

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3
Q

what is MS?

A

autoimmune inflammation and demyelination of CNS

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4
Q

Patients with MS can present how?

A

optic neuritis • MLF syndrome • hemiparesis • hemisensory symptoms • bladder/bowel incontinence

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5
Q

what is the course in MS?

A

relapsing and remitting

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6
Q

MS most often affects who?

A

women in their 20’s and 30’s; more common in whites

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7
Q

what is Charcot’s classic triad of MS?

A

a SIN: • Scanning speech • Intention tremor/Incontinence/INO • Nystagmus

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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

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9
Q

what is the treatment for MS?

A

β-interferon, immunosuppression, natalizumab • symptomatic tx for neurogenic bladder, spasticity, and pain

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10
Q

what is the most common variant of Guillain-Barre syndrome?

A

Acute Inflammatory demyelinating polyradiculopathy

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11
Q

what is acute inflammatory demyelinating polyradiculopathy?

A

autoimmune condition that destroys Schwann cells → inflammation and demyelination of peripheral nerves and motor fibers

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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

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13
Q

prognosis of acute inflammatory demyelinating polyradiculopathy?

A

almost all patients survive; majority recover completely after weeks to months

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14
Q

what are the findings in acute inflammatory demyelinating polyradiculopathy?

A

↑CSF protein with normal cell count (albuminocytologic dissociation). • ↑protein →papilledema

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15
Q

acute inflammatory demyelinating polyradiculopathy is associated with which infections?

A

Campylobacter jejuni and CMV

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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

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17
Q

Tx for acute inflammatory demyelinating polyradiculopathy?

A

respiratory support is critical until recovery. • additional: plasmapharesis, IV immune globulins

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18
Q

what is progressive multifocal leukoencephalopathy?

A

demyelination of CNS due to destruction of oligodendrocytes

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19
Q

PML is associated with what?

A

JC virus

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20
Q

PML is seen in which patients?

A

2-4% of AIDS patients

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21
Q

prognosis of PML?

A

rapidly progressive, usually fatal

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22
Q

what is acute disseminated (postinfectious) encaphalomyelitis?

A

multifocal perivenular inflammation and demyelination after infection (measles or VZV) or vaccination (rabies, small pox)

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23
Q

what is metachromatic leukodystrophy?

A

autosomal recessive lysosomal storage disease, most commonly due to aryl sulfatase A deficiency.

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24
Q

what causes demyelination in metachromatic leukodystrophy?

A

build up of sulfatides leads to impaired production of myelin sheath

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25
Q

Charcot-Marie-Tooth disease is AKA what?

A

hereditary motor and sensory neuropathy

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26
Q

what is HMSN?

A

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

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27
Q

What is Krabbe’s disease?

A

AR lysosomal storage disease due to deficiency of galactocerebrosidase

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28
Q

how does Krabbe’s disease cause demyelination?

A

build up of galactocerebroside destroys myelin sheath

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29
Q

seizures are characterized by what?

A

synchronized high frequency neuronal firing

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30
Q

partial seizures affect what?

A

1 area of the brain

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31
Q

partial seizures most commonly originate where?

A

medial temporal lobe

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32
Q

partial seizure is often preceded by what?

A

seizure aura

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33
Q

secondary consequence of some partial seizures?

A

can secondarily generalize

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34
Q

what are the types of partial seizure?

A

simple partial • complex partial

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35
Q

what is a simple partial seizure?

A

consciousness intact: • motor, sensory, autonomic, psychic

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36
Q

what is a complex partial seizure?

A

partial seizure with impaired consciousness

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37
Q

what is epilepsy?

A

a disorder of recurrent seizures- excluding febrile seizures

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38
Q

what is status epilepticus?

A

continuous seizure for >30 min or recurrent seizures without regaining consciousness between seizures for >30min

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39
Q

what are the causes of seizures in children?

A

genetic • infection (febrile) • trauma • congenital • metabolic

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40
Q

what are the causes of seizures in adults?

A

tumors • trauma • stroke • infection

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41
Q

what are the causes of seizures in the elderly?

A

stroke • tumor • trauma • metabolic • infection

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42
Q

what are the types of generalized seizures?

A

Absence (petit mal) • myoclonic • tonic-clonic (grand mal) • tonic • atonic

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43
Q

features of absence seizure?

A

3Hz • no postictal confusion • blank stare

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44
Q

features of myoclonic seizure?

A

quick repetitive jerks

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45
Q

features of tonic-clonic seizure?

A

alternating stiffening and movement

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46
Q

features of tonic seizure?

A

stiffening

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47
Q

features of atonic seizure?

A

drop’ • commonly mistaken for fainting

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48
Q

head aches are all characterized by what?

A

pain due to structures such as the dura, cranial nerves, or extracranial structures

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49
Q

localization of cluster HA?

A

unilateral

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50
Q

duration of cluster HA?

A

15min-3hr; repetitive

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51
Q

clinical presentation of cluster HA?

A

repetitive brief HA. excruciating periorbital pain with lacrimation and rhinorrhea

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52
Q

cluster HA may induce what?

A

Horner syndrome

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53
Q

cluster HA is more common in whom?

A

males

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54
Q

what is the treatment for cluster HA?

A

inhaled O2 • sumatriptan

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55
Q

localization of tension headache?

A

bilateral

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56
Q

duration of tension HA?

A

> 30 min (~4-6hr); constant

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57
Q

clinical presentation of tension HA?

A

steady pain. no photophobia or phonophobia. no aura

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58
Q

localization of migraine HA?

A

unilateral

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59
Q

duration of migraine HA?

A

4-72hr

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60
Q

clinical features of migraine?

A

pulsating pain with nausea, photophobia, phonophobia, aura

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61
Q

what causes migraine?

A

irritation of CN V, meninges, or blood vessels (release of substance P, GCRP, vasoactive peptides)

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62
Q

what are the abortive therapies for migraine?

A

triptans

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63
Q

what are the prophylactic therapies for migraine?

A

propanolol • topiramate

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64
Q

what is vertigo?

A

sensation of spinning while stationary

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65
Q

what is the more common type of vertigo?

A

peripheral vertigo

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66
Q

what causes peripheral vertigo?

A

inner ear etiology: • semicircular canal debris • vestibular nerve infection • Menieres disease

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67
Q

what is the finding of positional testing in peripheral vertigo?

A

delayed horizontal nystagmus

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68
Q

what causes central vertigo?

A

brainstem or cerebellar lesion: • stroke affecting vestibular nuclei • posterior fossa tumor

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69
Q

what are the findings in central vertigo?

A

directional change of nystagmus • skew deviation • diplopia • dysmetria

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70
Q

results of positional testing in central vertigo?

A

immediate nystagmus in any direction; may change directions

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71
Q

what are the neurocutaneous disorders?

A
  1. Sturge-Weber syndrome • 2. Tuberous sclerosis • 3. NF1 • 4. Von Hippel-Lindau disease
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72
Q

what is Sturge-Weber syndrome?

A

congenital disorder with port-wine stains (nevus flammeus) typically in V1 ophthalmic distribution

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73
Q

what tumors are seen with Sturge-Weber syndrome?

A

leptomeningeal angiomas • pheochromocytomas

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74
Q

Sturge Weber syndrome can cause what?

A

glaucoma • seizures • hemiparesis • MR

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75
Q

inheritance of Sturge-Weber syndrome?

A

occurs sporadically

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76
Q

clinical features of Tuberous Sclerosis?

A

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

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77
Q

what are the clinical features of NF1?

A

Cafe-au-lait spots • Lisch nodules • neurofibromas in skin • optic gliomas • pheochromocytomas

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78
Q

genetic features of NF1?

A

AD • 100% penetration • variable expressivity • mutated NF1 gene on chromosome 17

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79
Q

what are the clinical features of VonHippel-Lindau disease?

A

Cavernous hemangiomas in skin, mucose, organs; • bilateral RCC • hemangioblastoma in retina, brainstem, cerebellum; • pheochromocytomas

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80
Q

genetic features of VonHippel-Lindau disease?

A

AD • mutated tumor suppressor VHL gene on chromosome 3

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81
Q

what is the most common 1° brain tumor in adults?

A

GBM/ Grade IV astrocytoma

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82
Q

prognosis for GBM?

A

malignant with <1yr life expectancy

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83
Q

where is GBM found?

A

cerebral hemispheres • can cross corpus callosum (butterfly glioma)

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84
Q

how do you stain GBM?

A

stain astrocytes for GFAP

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85
Q

histologic findings in GBM?

A

pseudopalisading pleomorphic tumor cells- border central areas of necrosis and hemorrhage

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86
Q

what is the 2nd most common 1° brain tumor in adults?

A

meningioma

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87
Q

meningioma most commonly occurs where?

A

in convexities of hemispheres (near surfaces of brain) and parasagital region

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88
Q

morphologic features of meningiomas?

A
  1. arise from arachnoid cells • 2. are extra-axial (external to brain parenchyma) • 3. may have a dural attachment (tail)
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89
Q

prognosis of meningioma?

A

typically benign and resectable

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90
Q

clinical presentation of meningioma?

A

often asymptomatic; may present with seizures or focal signs

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91
Q

what is the 3rd most common 1° brain tumor in adults?

A

Schwannoma

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92
Q

morphologic features of Schwannoma?

A

Schwann cell origin; often localized to CNIII →acoustic neuroma

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93
Q

treatment for Schwannoma?

A

resectable or treated with stereotactic radiosurgery

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94
Q

Schwannoma is usually found where?

A

cerebellopontine angle

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95
Q

how does a Schwannoma stain?

A

S-100 positive

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96
Q

bilateral acoustic neuromas found in what?

A

NF2

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97
Q

frequency of oligodendroglioma?

A

relatively rare, slow growing

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98
Q

oligodendroglioma is most often located where?

A

frontal lobes

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99
Q

morphologic features of oligodendroglioma?

A

chicken wire capillary pattern • oligodendrocytes= fried egg cells- round nuclei with clear cytoplasm • often calcified in oligodendroglioma

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100
Q

pituitary adenoma is most commonly what?

A

prolactinoma

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101
Q

symptoms of prolactinoma?

A

bitemporal hemianopia and hypo/hyperpituitarism

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102
Q

what are the childhood primary brain tumors?

A
  1. pilocytic (low-grade) astrocytoma • 2. medulloblastoma • 3. ependymoma • 4. hemangioblastoma • 5. craniopharyngioma
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103
Q

morphologic features of pilocytic astrocytoma?

A

well circumscribed • cystic and solid

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104
Q

where is pilocytic astrocytoma most often found in children?

A

posterior fossa/cerebellum • may be supratentorial

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105
Q

how does pilocytic astrocytoma stain?

A

GFAP positive

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106
Q

prognosis of pilocytic astrocytoma?

A

benign • good prognosis

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107
Q

histologic findings in pilocytic astrocytoma?

A

Rosenthal fibers- eosinophilic corkscrew fibers

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108
Q

what is a medulloblastoma?

A

highly malignant cerebellar tumor • form of primitive neuroectodermal tumor

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109
Q

medulloblastoma can compress what?

A

4th ventricle → hydrocephalus

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110
Q

how does medulloblastoma metastasize?

A

can send drop mets to spinal cord

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111
Q

morphologic findings in medulloblastoma?

A

Horner-Wright rosettes • Solid • small blue cels

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112
Q

treatment of medulloblastoma?

A

radiosensitive

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113
Q

ependymal cell tumors are most commonly found where?

A

in 4th ventricle

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114
Q

ependymal cell tumors can cause what?

A

hydrocephalus

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115
Q

prognosis of ependymal tumors?

A

poor

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116
Q

morphologic findings in ependymoma?

A

characteristic perivascular pseudorosettes. rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus

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117
Q

hemangioblastomas in the brain are most often where?

A

cerebellum

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118
Q

hemangioblastomas are associated with what condition when seen with retinal angiomas?

A

VonHippel Lindau disease

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119
Q

hemangioblastomas can produce what?

A

erythropoietin→2° polycythemia

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120
Q

what findings are characteristic of hemangioblastoma?

A

foamy cells and high vascularity

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121
Q

what is a craniopharyngioma?

A

benign childhood tumor, confused with pituitary adenoma (can also cause bitemporal hemianopia)

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122
Q

what is the most common childhood supratentorial tumor?

A

craniopharyngioma

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123
Q

craniopharyngioma is derived from what?

A

Rathke’s pouch

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124
Q

morphological features of craniopharyngioma?

A

calcification is common (tooth enamel like)

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125
Q

what are the herniation syndromes?

A
  1. cingulate (subfalcine) herniation under falx • 2. downward transtentorial (central) herniation • 3. uncal herniation • 4. cerebellar tonsillar herniation into the foramen magnum
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126
Q

cingulate herniation under falx can do what?

A

compress ACA

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127
Q

where is the uncus?

A

medial temporal lobe

128
Q

complications of cerebellar tonsilar herniation into the foramen magnum?

A

coma and death result when these herniations compress the brain stem

129
Q

what do glaucoma drugs do?

A

↓ IOP via ↓ amount of aqueous humor (inhibit synthesis/secretion or increase drainage)

130
Q

what are the classes of glaucoma drugs?

A

α1-agonists • β-blockers • diuretics • cholinomimetics • prostaglandin

131
Q

what are the α agonists used to treat glaucoma?

A

Epinephrine • Brimonidine (α2)

132
Q

what is the MOA of epinephrine for glaucoma?

A

↓ aqueous humor via vasoconstriction

133
Q

what is the MOA of brimonidine for glaucoma?

A

↓ aqueous humor synthesis

134
Q

what are the side-effects of epinephrine for glaucoma?

A

mydriasis; do not use in closed angle glaucoma

135
Q

what are the side effects of brimonidine for glaucoma?

A

Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus

136
Q

what are the β-blockers used for glaucoma?

A

timolol • betaxolol • carteolol

137
Q

what is the MOA of timolol, betaxolol, and carteolol for glaucoma?

A

↓ aqueous humor synthesis

138
Q

what are the side effects of timolol, betaxolol, and carteolol for glaucoma?

A

no pupillary or vision changes

139
Q

what are the diuretics used for glaucoma?

A

acetazolamide

140
Q

what is the MOA of acetazolamide for glaucoma?

A

↓aqueous humor synthesis via inhibition of carbonic anhydrase

141
Q

what are the side effects of acetazolamide for glaucoma?

A

no pupillary or vision changes

142
Q

what are the direct cholinomimetics used for glaucoma?

A

pilocarpine, carbachol

143
Q

what are the indirect cholinomimetics used for glaucoma?

A

physostigmine • echothiophate

144
Q

what is the mechanism of action of cholinomimetics for glaucoma?

A

↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

145
Q

what are the side effects of cholinomimetics for glaucoma?

A

miosis and cyclospasm

146
Q

which drug should be used for glaucoma emergency?

A

pilocarpine- very effective at opening meshwork into canal of Schlemm

147
Q

what is the prostaglandin used for glaucoma?

A

Latanoprost (PGF2α)

148
Q

what is the MOA of latanoprost?

A

↑ outflow of aqueous humor

149
Q

what are the side effects of latanoprost for glaucoma?

A

darkens color of iris

150
Q

which drugs are opioid analgesics?

A
  1. morphine • 2. fentanyl • 3. codeine • 4. heroin • 5. methadone • 6. meperidine • 7. dextromethorphan • 8. diphenoxylate
151
Q

what is the MOA of opioid analgesics?

A

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
Q

what is the clinical use of opioid analgesics?

A

pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone)

153
Q

what happens in opioid analgesic toxicity?

A

addiction • respiratory depression • constipation • miosis (pinpoint pupils) • additive CNS depression with other drugs

154
Q

there is no tolerance to which side effects of opioids?

A

miosis • constipation

155
Q

opioid toxicity is treated with what?

A

naloxone or naltrexone (opioid receptor antagonist)

156
Q

what stimulates opioid mu receptor?

157
Q

what stimulates opioid delta receptor?

A

enkephalin

158
Q

what stimulate opioid kappa receptor?

159
Q

what is the MOA of Butorphanol?

A

mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia

160
Q

what is the clinical use of Butorphanol?

A

severe pain (migraine, labor, etc.) causes less respiratory depression than full opioid agonists

161
Q

what happens in butorphanol toxicity?

A

can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors). overdose not easily reversed with naloxone

162
Q

what is the MOA of tramadol?

A

very weak opioid agonist; also inhibits 5HT and NE reuptake (works on multiple neurotransmitters)

163
Q

what is the clinical use of tramadol?

A

chronic pain

164
Q

what happens in tramadol toxicity?

A

similar to opioids. decreases seizure threshold

165
Q

What kind of seizures do you treat with phenytoin?

A
  • 1st LINE: Tonic-Clonic + Prophylaxis of status epilepticus • - Simple and complex partial
166
Q

what type of seizures do you treat with carbamazepine?

A

1st LINE: Simple and complex partial + Tonic-Clonic

167
Q

which types of seizures do you treat with lamotrigine?

A
  • Simple and complex partial • - Generalized tonic-clonic
168
Q

which types of seizures do you treat with gabapentin?

A
  • Simple and complex partial • - generalized tonic-clonic
169
Q

which types of seizures do you treat with topiramate?

A
  • Simple and Complex Partial • - Generalized Tonic-clonic
170
Q

which types of seizures do you treat with phenobarbital?

A
  • Simple and complex partial • - generalized tonic-clonic
171
Q

which types of seizures do you treat with Valproate?

A

1st LINE: Tonic-Clonic • - Simple and Complex partial • - absence

172
Q

which types of seizures do you treat with ethosuxamide?

A

1st LINE: absence

173
Q

which types of seizures do you treat with Benzodiazepines?

A

1st LINE: acute status epilepticus

174
Q

which types of seizures do you treat with tiagabine?

A

simple and complex partial seizures

175
Q

which types of seizures do you treat with vigabatrin?

A

simple and complex partial

176
Q

which types of seizures do you treat with levetiracetam?

A
  • simple and complex partial • - generalized tonic clonic
177
Q

what is the first line treatment for prohpylaxis of Status epilepticus?

178
Q

what is the 1st line treatment for acute status epilepticus?

A

benzodiazepines

179
Q

what is the first line treatment for absence seizures?

A

ethosuxamide

180
Q

what are the first line treatments for tonic-clonic seizures?

A

phenytoin • carbamazepine • valproic acid

181
Q

what are the first line treatments for simple and complex partial seizures?

A

carbamazepine

182
Q

MOA of phenytoin?

A

use dependent blockade of Na channels; inhibition of glutamate release from excitatory presynaptic neuron

183
Q

how do you give parenteral phenytoin?

A

Fosphenytoin

184
Q

MOA of carbamazepine?

A

↑ Na+ channel inactivation

185
Q

which drug is the 1st line treatment for trigeminal neuralgia?

A

carbamazepine

186
Q

MOA of lamotrigine?

A

blocks voltage gated Na+ channels

187
Q

what is the MOA of gabapentin?

A

designed as GABA analog, but primarily inhibits high-voltage-activated Ca++ channels

188
Q

gabapentin is used for what other than seizures?

A

peripheral neuropathy • postherpetic neuralgia • migraine prophylaxis • bipolar disorder

189
Q

MOA of topiramate?

A

blocks Na+ channels • ↑GABA action

190
Q

topiramate is used for what other than seizures?

A

migraine prevention

191
Q

MOA of phenobarbital?

A

↑GABAa action

192
Q

when is phenobarbital 1st line?

A

in children

193
Q

MOA of valproic acid?

A

↑Na+ channel inactivation, • ↑ GABA concentration

194
Q

valproic acid can be used for which unusual type of seizure?

A

myoclonic seizure

195
Q

MOA of ethosuxamide?

A

blocks thalamic T-type Ca++ channels

196
Q

MOA of diazepam/lorazepam?

A

↑GABAa action

197
Q

benzodiazepines are used for what in pregnancy?

A

seizures in eclampsia, but 1st line is MgSO4

198
Q

MOA of tiagabine?

A

inhibits GABA reuptake

199
Q

MOA of vigabatrin?

A

irreversibly inhibits GABA transaminase →↑GABA

200
Q

MOA of levetiracetam?

A

may modulate GABA and glutamate release

201
Q

Benzodiazepine toxicity?

A

Sedation • Tolerance • Dependence

202
Q

Carbamazepine toxicity?

A

Diplopia • ataxia • blood dyskrasias (agranulocytosis, aplastic anemia) • liver toxicity • teratogenesis • P450 induction • SIADH • SJS

203
Q

ethosuxamide toxicity?

A

GI distress • fatigue • headache • urticaria • SJS

204
Q

phenobarbital toxicity?

A

Sedation • tolerance • dependence • induction of P450

205
Q

Phenytoin toxicity?

A

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
Q

Valproic acid toxicity?

A

GI distress • rare but fatal hepatotoxicity • NTD • tremor • weight gain • CI in pregnancy

207
Q

toxicity of lamotrigine?

208
Q

gabapentin toxicity?

A

sedation • ataxia

209
Q

topiramate toxicity?

A

sedation • mental dulling • kidney stones • weight loss

210
Q

clinical presentation of SJS?

A

prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules • skin lesions progress to epidermal necrosis and sloughing

211
Q

Clinical use of phenytoin?

A

tonic-clonic seizures • class 1B antiarrhythmic

212
Q

which drugs are the barbiturates?

A

phenobarbital • pentobarbital • thiopental • secobarbital

213
Q

mechanism of action of Barbiturates?

A

facilitate GABAa action by ↑ duration of Cl channel opening→↓ neuron firing

214
Q

what is the clinical use of barbiturates?

A

sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

215
Q

Barbiturate toxicity?

A

Respiratory and cardiovascular depression (can be fatal) • CNS depression (↑ by EtOH) • dependence • induces P450

216
Q

when are barbiturates contraindicated?

217
Q

what is the treatment for barbiturate overdose?

A

supportive (assist respiration and maintain BP)

218
Q

which drugs are benzodiazepines?

A

diazepam • lorazepam • triazolam • temazepam • oxazepam • midazolam • chlordiazepoxide • alprazolam

219
Q

what is the mechanism of action of benzodiazepines?

A

facilitates GABAa action by ↑ frequency of Cl channel opening

220
Q

effect of benzodiazepines on REM sleep?

221
Q

t1/2 of benzodiazepines?

A

most have long half lives and active metabolites except for triazolam, oxazepam, and midazolam which are short acting →higher addictive potential

222
Q

what do benzos barbs and EtOH all have in common?

A

all bind GABAa receptor= ligand gated Cl channel

223
Q

clinical use of benzodiazepines?

A

anxiety • spasticity • status epilepticus • detoxification • night terrors • sleepwalking • general anesthesia (amnesia, muscle relaxation) • hypnotic

224
Q

which benzos can be used for status epilepticus?

A

lorazepam and diazepam

225
Q

toxicity of benzodiazepines?

A

dependence • additive CNS depression FX with EtOH • less risk of respiratory depression and coma than with barbiturates

226
Q

treat overdose of benzodiazepines with what?

A

flumazenil (competitive inhibitor at benzodiazepine GABA receptor)

227
Q

which drugs are the nonbenzodiazepine hypnotics?

A

Zolpidem (Ambien) • zalephon • eszopiclone

228
Q

mechanism of nonbenzodiazepine hypnotics?

A

act via the BZI subtype of the GABA receptor

229
Q

how are effects of Zolpidem, zalephon, and eszopiclone reversed?

A

flumazenil

230
Q

what is the clinical use of zolpidem and other non benzodiazepine hypnotics?

231
Q

toxicity of zolpidem, zalephon, eszopiclone?

A

ataxia • HA • confusion

232
Q

duration of non BZD hypnotics?

A

short because of rapid liver metabolism

233
Q

difference between zolpidem and older sedative hypnotics?

A

cause only modest day after psychomotor depression and few amnestic effects • lower dependence risk than benzos

234
Q

what is necessary for a drug to work on the CNS?

A

lipid soluble (cross BBB) • or • be actively transported

235
Q

features of anesthetics with ↓ solubility in blood?

A

rapid induction and recovery times

236
Q

features of anesthetics with ↑ solubility in lipids?

A

↑ potency= 1/MAC

237
Q

what is MAC?

A

minimal alveolar concentration at which 50% of the population is anesthetized

238
Q

MAC varies with what?

239
Q

solubility properties of N2O?

A

↓ blood and lipid solubility, and thus fast induction and low potency

240
Q

solubility properties of halothane?

A

↑lipid and blood solubility, and thus high potency and slow induction

241
Q

which drugs are inhaled anesthetics?

A

halothane • enflurane • isoflurane • sevoflurane • methoxyflurane • nitrous oxide

242
Q

what is the mechanism of inhaled anesthetics?

243
Q

what are the effects of inhaled anesthetics?

A

myocardial depression • respiratory depression • nausea/emesis • ↑ cerebral blood flow (↓cerebral metabolic demand)

244
Q

toxicity of halothane?

A

hepatotoxicity

245
Q

toxicity of methoxyflurane?

A

nephrotoxicity

246
Q

toxicity of enflurane?

A

proconvulsant

247
Q

which inhaled anesthetics carry risk of malignant hyperthermia?

A

all but N2O; rare life threatening inherited susceptibility

248
Q

toxicity unique to N2O?

A

expansion of trapped gas in a body cavity

249
Q

what are the intravenous anesthetics?

A

Barbiturates • Benzodiazepines • Arylcyclohexylamines (Ketamine) • Opioids • Propofol

250
Q

MC barbiturate IV anesthetic?

A

Thiopental

251
Q

PK of thiopental as IV anesthetic?

A

high potency, high lipid solubility, rapid entry into brain

252
Q

thiopental is used as an IV anesthetic for what?

A

induction of anesthesia and short surgical procedures

253
Q

effect of thiopental as IV anesthetic is terminated by what?

A

rapid redistribution into tissues (MSK + Fat)

254
Q

effect of IV thiopental on cerebral blood flow?

A

↓cerebral blood flow

255
Q

which IV benzodiazepine is most common anesthetic used for endoscopy?

256
Q

how is midazolam used as IV anesthetic?

A

adjunctively with gaseous anesthetics and narcotics

257
Q

risk of IV midazolam for anesthesia?

A

may cause severe post/op respiratory depression, ↓BP and amnesia

258
Q

what are arylcyclohexylamines like ketamine?

A

PCP analogs that act as dissociative anesthetics

259
Q

PD of IV ketamine in anesthesia?

A

blocks NMDA receptors

260
Q

effect of IV ketamine on Cardiovascular system?

A

cardiovascular stimulant

261
Q

congitive effects of arylcyclohexylamines?

A

cause disorientation, hallucination, and bad dreams

262
Q

effect of arylcyclohexylamines on cerebral blood flow?

A

↑ cerebral blood flow

263
Q

use of IV opioids in anesthesia?

A

morphine, fentanyl used with other CNS depressants during general anesthesia

264
Q

propofol is used for what?

A

sedation in ICU • rapid anesthesia induction • short procedures

265
Q

PD effects of IV propofol?

A

potentiates GABAa

266
Q

difference in side effects between propofol and thiopental?

A

propofol has less postoperative nausea than thiopental

267
Q

what are the local anesthetic esters?

A

procaine • cocaine • tetracaine

268
Q

what are the aminde local anesthetics?

A

lidocaine • mepivacaine • bupivacaine

269
Q

MOA of local anesthetics?

A

block Na+ channels by binding to specific receptors on inner portion of channel

270
Q

local anesthetics preferentially bind to what?

A

activated Na+ channels, so most effective in rapidly firing neurons

271
Q

PK of 3° amine local anesthetics?

A

penetrate membrane in uncharged form, hen bind to ion channels as charged form

272
Q

Local anesthetics can be given as what combination?

A

can be given with vasoconstrictors (epi) to enhance local action= • ↓bleeding, ↑anesthesia by ↓systemic concentration

273
Q

what happens when you use an alkaline anesthetic in infected tissue?

A

in acidic tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively →need more anesthetic

274
Q

what is the order of nerve blockade by local anesthetics?

A

small diameter myelinated > small unmyelinated> large myelinated fibers > large unmyelinated

275
Q

what is the order of loss of sensation in local anesthesia?

A

1 pain • 2 temperature • 3 touch • 4 pressure

276
Q

what is the clinical use of local anesthetics?

A

minor surgical procedures, spinal anesthesia. If allergic to esters, give amides

277
Q

toxicity of local anesthetics?

A

CNS excitation, severe cardiovascular toxicity (bupivacaine), HTN, arrhythmia (cocaine)

278
Q

neuromuscular blocking drugs are used for what?

A

muscle paralysis in surgery or mechanical ventilation. selective for motor vs autonomic nicotinic receptor

279
Q

prototypical depolarizing neuromuscular blocker?

A

succinylcholine

280
Q

MOA of succinylcholine?

A

strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction

281
Q

steps in reversal of succinylcholine blockade?

A

Phase I (prolonged depolarization) no antidote. block potentiated by cholinesterase inhibitors • Phase II (repolarized but blocked) antidote consists of cholinesterase inhibitors

282
Q

complications of succinylcholine use?

A

hypercalcemia • hyperkalemia • malignant hyperthermia

283
Q

what are the nondepolarizing neuromuscular blockers?

A

tubocurarine • atracurium • mivacurium • pancuronium • vecuronium • rocuronium

284
Q

MOA of nondepolarizing neuromuscular blockers?

A

competitive antagonists- compete with ACh for receptors

285
Q

how do you reverse blockade by nondepolarizing neuromuscular blockers?

A

neostigmine • edrophonium • and other cholinesterase inhibitors

286
Q

what is the MOA of dantrolene?

A

prevents the release of Ca++ from the sarcoplasmic reticulum of skeletal muscle

287
Q

what is the clinical use of dantrolene?

A

used in the treatment of malignant hyperthermia and neuroleptic malignant syndrome

288
Q

what are the strategies for the treatment of Parkinson’s disease?

A
  1. Dopamine agonists • 2. ↑dopamine • 3. prevent dopamine breakdown • 4. Curb excess cholinergic activity
289
Q

what is the mnemonic for the treatment of Parkinson’s?

A

BALSA • Bromocriptine • Amantadine • Levodopa • Selegiline • Antimuscarinics

290
Q

what are the dopamine agonists used for Parkinson’s?

A

Bromocriptine (ergot) • pramipexole • ropinirole (non-ergot) • Non ergot are preferred

291
Q

what are the agents used to ↑dopamine in Parkinson’s?

A

Amantadine (may ↑dopamine release) • L-dopa/carbidopa

292
Q

Amantadine is also used for what?

A

antiviral against influenza A and rubella

293
Q

toxicity of Amantadine?

294
Q

MOA of Ldopa?

A

converted to DA in CNS

295
Q

what agents prevent dopamine breakdown in Parkinson’s?

A

Selegiline • entacapone • tolcapone

296
Q

MOA of selegiline?

A

selective MAO type B inhibitor which preferentially metabolized dopamine over NE and 5HT

297
Q

MOA of entacapone, tolcapone?

A

COMT inhibitors- prevent Ldopa degradation

298
Q

which agents curb excess cholinergic activity in Parkinson’s?

A

Benztropine

299
Q

MOA of benztropine?

A

Antimuscarinic; • improves tremor and rigidity but has little effect on bradykinesia

300
Q

difference between Ldopa and DA?

A

L dopa can cross BBB and is converted by dopa decarboxylase in the brain to DA

301
Q

MOA of carbidopa?

A

a peripheral decarboxylase inhibitor, is given with Ldopa to ↑bioavailability of Ldopa in the brain and to limit peripheral side effects

302
Q

toxicity of Ldopa/carbidopa?

A

arrhythmia from increased peripheral formation of catecholamines • long term use can lead to dyskinesia following administration, akinesia between doses

303
Q

clinical use of selegiline?

A

adjunctive agent to L dopa in Tx of Parkinsons

304
Q

toxicity of selegiline?

A

may enhance adverse effects of Ldopa

305
Q

what are the Alzheimer’s drugs?

A

Memantine • Donepezil, galantamine, rivastigmine

306
Q

MOA of memantine?

A

NMDA receptor antagonist; helps prevent excitotoxicity

307
Q

toxicity of memantine?

A

dizziness • confusion • hallucinations

308
Q

MOA of donepezil, galantamine, rivastigmine?

A

acetylcholinesterase inhibitors

309
Q

toxicity of AChE inhibitors in AD?

A

nausea • dizziness • insomnia

310
Q

what are the neurotransmitter changes in Huntington’s disease?

A

↓GABA • ↓ACh • ↑DA

311
Q

what are the treatments for Huntingtons?

A

Terbenazine and reserpine • Haloperidol

312
Q

MOA of terbenazine and reserpine in huntingtons?

A

inhibit VMAT; limit DA vesicle packaging and release

313
Q

MOA of haloperidol for huntingtons?

A

DA receptor antagonist

314
Q

MOA of sumatriptan?

A

5HT1B/1D agonist- • inhibits trigeminal nerve activation • prevents vasoactive peptide release • induces vasoconstriction

315
Q

t1/2 of sumatriptan?

316
Q

clinical use of sumatriptan?

A

acute migraine • cluster HA attacks

317
Q

toxicity of sumatriptan?

A

coronary vasospasm (CI in patients with CAD or prinzmental’s angina) • mild tingling

► Med Notes (62 decks)

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