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Block VIII, Week II


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what types of anesthesia are available?
1. general
2. regional (spinal, epidural, caudal)
3. local
drug induced reversible depression of the CNS is what type of anesthesia?
what three modalities are blocked in regional anesthesia?
what is the cutoff line for regional anesthesia, where any higher of a blockage will cause decreased HR and respirations?
T4 (nipple line)
what is the difference between a spinal and an epidural block?
spinal - must be performed below L1, denser block with profound sensory, motor and sympathetic block
epidural - can be performed at any level, less dense, don't get motor block
why must a spinal block be performed below L1?
to prevent spinal cord trauma
which type of block (spinal or epidural) uses a larger needle and therefore more commonly has spinal H/A as a result?
examples of when you would use a:
1. spinal block
2. epidural block
1. hysterectomy, C-section, lower extremity ortho, urology
2. operative, post-op, OB, chronic pain
what type of block would be used for procedures on shoulder, arm, trunk, legs?
peripheral nerve block
what are some complications of regional anesthesia?
injection into vascular system
spinal hematoma
T/F: general anesthesia can be accomplished with one drug
6 goals of general anesthesia?
1. analgesia
2. amnesia
3. loss of consciousness
4. lack of patient movement
5. attenuation of autonomic response
6. maintain health and safety of patient
what is done to provide analgesia?
opioids are added separately (GAs are poor analgesics)
do GAs provide amnesia?
NO (benzo usually added)
do GAs provide loss of consciousness?
lack of patient movement is accomplished by administering a?
neuromuscular blockade
what is administered to attenuate the autonomic response?
benzo or opioid
(don't want a spike in BP or HR)
what are the five steps in administration of general anesthesia?
1. Pre-Op
2. Induction of anesthesia
3. Maintenance of anesthesia
4. Emergence from anesthesia
5. Post-anesthesia care (PACU)
if an adverse incident is going to occur, during which stage of administration of GA is it most likely to occur?
MC MOA of anesthetic agents?
modulate GABAergic neuronal transmission (interfering with transmembrane electrical activity)
in general, how are most inhalational general anesthetic agents believed to work?
membrane expansion on and at ion channels
what is the method of administration of most induction agents?
(children can use inhalational)
name two barbituates used in induction of anesthesia
Sodium Pentothal (Thiopental)
Brevital (Methohexital)
MOA of barbituates as anesthetic inducers?
inhibits excitatory transmission, facilitates inhibitory (GABA) transmission
vital sign effects of barbituates?
reduced BP and CO
increased HR
why are barbituates contraindicated in shock patients?
risk of severe hypotension
which barbituate is the MC used as an anesthetic inducer?
brevital has an increased risk of what adverse effect?
(in susceptible patients)
name two benzodiazepines used as anesthesia inducers
two "attributes" of benzodiazepenes in relation to anesthesia?
preoperative sedation
MOA of benzodiazepenes?
facilitate GABA transmission
effects of benzodiazepenes on respiratory system?
respiratory depression
(dose dependent and synergistic with opioids)
benzodiazepenes are antagonized by?
MC opioid used in anesthesia induction?
other opioids used as anesthesia adjuncts?
MOA of opioids
bind to mu, kappa and gamma receptors: close N type voltage-gated calcium channels and open calcium dependant K+ channels RESULTING IN HYPERPOLARIZATION AND DECREASED NEURONAL EXCITABILITY IN THE SPINAL CORD
physiological effects of opioids binding to the mu receptor?
respiratory depression
supraspinal analgesia
physiological effects of opioids binding to the kappa receptor?
spinal analgesia
physiological effects of opioids binding to the delta receptor?
physiological effects of opioids binding to the sigma receptor?
opioids are antagonized by?
specifics for opioids:
1. MC used pre or post op
2. used to specifically treat what post-op condition?
1. commonly used post-op
2. post-op shivering
which opioid would most likely be used in cardiac surgery? why?
which misc. anesthetic agent is known for providing "clear-headedness" upon awakening and therefore is used in anesthesia induction for short, ambulatory procedures?
besides anesthetic properties, what other advantages does propofol have?
MOA of propofol?
facilitates inhibitory (GABA) transmission, also inhibits NMDA (glutamate) receptors
effect of propofol on respirations, BP and HR?
respiratory depression
decreases BP
not much effect on HR
etomidate is used in what kind of patients?
impaired CV functioning
MOA of etomidate?
facilitates inhibitory (GABA)transmission by increasing the # of available GABA receptors.
adverse effects of etomidate?
pain on injection
decreased stress response, therefore increased mortality with long term infusion
effect of etomidate on adrenal steroid production?
inhibits 11-B hydroxylase -> inhibits steroid production
which misc. anesthetic would be used in shock patients and pts with reactive airway disease?
MOA of ketamine?
blocks NMDA receptors
ketamine results in dissociative anesthesia. what does that mean?
eyes are open but anesthesia is complete
effect of ketamine on vital signs?
(tachycardia, hypertension)
what can be administered to decrease the likelihood of emergence delerium when coming out of ketamine anesthesia?
methods of ketamine administration?
why is ketamine not used in neurosurgery?
it is a vasodilator
which anesthesia adjunct is a depolarizing neuromuscular blocking agent?
MOA of succinylcholine?
mimics ACh, binds to ACh receptor generating an AP. result is fasciculations of the muscle followed by paralysis as long as there are adequate concentrations
why should succinylcholine NOT be used in children or crush/denervation injuries?
increased K+ is released --> may result in CV failure
name three nondepolarizing neuromuscular blockers
MOA of nondepolarizing neuromuscular blockers?
competes with ACh and prevents it from binding to its receptor -> no end plate potential -> no depolarization
which is longer acting: a polarizing or depolarizing neuromuscular blocker?
(45 min. vs. 5)
define the MAC in relation to inhalational anesthetics
the alveolar concentration that inhibits movement in 50% of patients.
physiological factors that would increase MAC?
physiological factors that would decrease MAC?
acute alcohol
four volatile liquids used as inhalational anesthetic agents?
gas form of inhaled anesthetic?
nitrous oxide
compare the solubility of volatile liquids and their relative onset of action
low solubility (desflurane, secoflurane) - quick onset, quick wake up
high solubility (halothane) - slow onset, slow wake up time
three types of central/neuraxial anesthesia?
1. epidural
2. spinal blocks
3. caudal blocks
what is the upper spinal segment that is the limit for a spinal block?
T4 (nipple line)
what is the MC spinal region for an epidural?
describe the onset of an epidural compared to a spinal block
which is more "dense" - an epidural or a spinal block?
spinal block
spinal blocks must be performed below which spinal level? why?
avoid needle trauma to cord
(usually performed L2-L5)
which uses larger needles: epidural or spinal block?
(smaller needles in a spinal block decrease the chance of a spinal H/A)
what is the MC block in peds?
caudal blocks
where is the needle inserted in a caudal block?
through the sacral hiatus
what is the anesthesia procedure of choice for procedures on the arm, shoulder, legs?
peripheral nerve block
MC complications of regional blocks?
backache (MC)
hypothermia (due to vasodilation and inhibition of shivering)
spinal hematoma (backache followed by numbness and/or lower extremity weakness)
the level of sympathetic block may extend how many dermatomes beyond the sensory level?
the sensory block may be how many dermatomes from the motor block?
2-3 dermatomes HIGHER
in regards to local anesthetics, what is the nomenclature for an:
1. esther
2. amide
1. --CAINE
2. -I--CAINE
in regards to local anesthetics, lipophilicity has what effect on the potency, duration of action and toxicity?
potency - increased
duration of action - increased
toxicity - increased
1. esthers are metabolized where?
2. amides are metabolized where?
1. hydrolyzed very rapidly in the blood (very short half life)
2. liver (CYP-450)
MOA of local anesthetics
*primary site of action is the cell membrane
*prevent voltage gated channels from opening, threshold is not reached, nerve segments are not depolarized
describe the order of inhibition of the 3 nerve fiber types.
1st: C-fibers (get blockage of SNS, decr. BP and HR)
2nd: A-delta fibers (get loss of pain and temp)
3rs: A-alpha (get loss of pressure, touch)
identify the order of modality loss in local anesthetics
pain -> cold, warmth, touch, deep pressure, motor function
major adverse effects of local anesthetics?
1. stimulation of the CNS (restlessness, tremors, convulsions)*CNS depression can follow stimulation*
2. CV - decr. excitability, conduction rate and force of contraction
what can we administer to decrease CNS stimulation seen as an adverse effect of LAs?
which LAs have the greatest CV adverse effects?
MCC of death as an adverse reaction to LAs?
respiratory depression
signs of LA toxicity?
visual disturbances
tongue numbness
how would a hypersensitivity rxn to local anesthesia present?
allergic dermatitis
asthma attack
hypersensitivity rxns to LAs are MC due to what?
esther type (PABA metabolite)
Rx. of a LA hypersensitivity?
1. use an amide LA, not an esther
2. use preservative free LAs
benefits of adding epinephrine to LAs?
1. prolongs duration of anesthesia
2. reduces systemic absorption
3. increases intensity of blockade (vasoconstriction, reduces sensory neuron firing)
additional benefit of cocaine ontop of being a topical anesthetic?
produces vasoconstriction -> reduces surgical bleeding
avg. onset and duration of topical anesthetics?
onset: 2-5 min
duration: 30-45 min
EMLA is a mixture of?
lidocaine and prilocaine
what can be done to prolong (double) the duration of topical anesthetics?
add epinephrine
3 MC topical anesthetics?
the choice of which LA to use is often based on?
duration of action
name a long acting amide and ester LA.
amide - bupivacaine
ester - tetracaine
name a short acting ester LA
stimulation of skin nociceptors will result in what types of pain sensation?
stimulation of muscle, joint, and skeletal receptors results in what type of pain sensation?
deep aching pain
what is the difference between A-delta and C nerve fibers?
A-delta: myelinated
C: unmyelinated
where are the cell bodies of A-delta and C nerve fibers found?
dorsal root gangla or trigeminal ganglion
what are the 4 ascending pain pathways?
spinothalamic (MC recognized)
dorsal column
do the pain pathways cross in the spinal cord?
most cross, but some remain ipsilateral
(this is why cutting one side of the ascending pathway to relieve pain is ineffective)
pain pathways project to a variety of brain regions. what do they all have in common?
high concentration of opioid receptors
define hyperalgesia
enhanced responsiveness of nociceptors
(often due to extreme tissue stress or damage)
excess firing of ascending neurons and reduced activity of descending neurons results in?
persistent pain or abnormal pain perception
normal function of NMDA?
*helps regulate influx of Ca++ into neuron
*helps regulate plasticity in dorsal horn area of SC
how is NMDA associated with persistent pain or abnormal pain perception?
overactivity of the NMDA Ca++ channel is believed to produce excess firing of the ascending nociceptive pathways

(Ca++ facilitates NT release, results in prolonged depolarization, produces persistent or abnormal type of sensation)
clinical manifestations of pain that effects the spinoreticular system?
arousal, pain wakes you up or grabs your attention
clinical s/s of pain that effects the central gray and hypothalamic sites?
autonomic activation
(sweats/chills, vision fluctuation)
clinical s/s of pain that effects the thalamus, amygdala, mesencephalic, spinoreticular system?
affective change
what is the difference between nociceptive and neuropathic pain?
nociceptive - appropriate to stimulus
neuropathic - not neccessarily stimulus related, see damage of nervous system
give an example of nociceptive pain and neuropathic pain
nociceptive pain - OA
neuropathic pain - radiculopathy
5 meds for chronic pain in order you would prescribe them?
2. NSAIDs (also COX II)
3. Anticonvulsants
4. muscle relaxants
5. opioids
give an example of an anticonvulsant that is prescribed for neuropathic pain
what do all arboviruses have in common as far as their vector?
four viral families that belong to the arbovirus group?
what is the arbovirus genome like?
RNA genome
are arboviruses naked or enveloped?
all (but reoviridae) are enveloped
name four diseases caused by flaviviriae
1. Yellow fever
2. Dengue
3. St. Louis encephalitis
4. West Nile
two diseases caused by togaviridae
1. eastern equine encephalitis (EEE)
2. western equine encephalitis (WEE)
two diseases caused by bunyaviridae?
1. LaCrosse encephalitis
2. California encephalitis
disease caused by reoviridae?
colorado tick fever
describe the extrinsic incubation period
the period between infection of the vector until the time the vector becomes infectious
what is transovarial transmission and why is it important?
transisison of the virus to insect progeny (vertical transmission)
important for overwintering
pathogenesis of encephalitis
1. SQ inoculation, virus replicates in local tissue and regional lymph nodes
2. virus transported to lymphatics
3. virus seeded to distant organs, larger amounts are shed into blood due to incr. replication (viremia)
4. virus breaches BBB to enter CNS, infection spreads rapidly
what are some factors that could compromise the BBB, thereby leading to the potentiation of encephalitis?
old age
most arboviral encephalitis infx. are asymptomatic. what are some clinical manifestations of mild disease?
febrile H/A
aseptic meningitis
does WNV more commonly produce meningitis or encephalitis?
what is the most significant risk for developing severe neurological disease from WNV?
advanced age
in relation to St. Louis encephalitis:
1. primary host?
2. primary vector?
1. birds
2. mosquitoes
what is the most significant risk for developing St. Louis encephalitis?
advanced age
LaCrosse encephalitis is endemic where?
in relation to LaCrosse Encephalitis:
1. principal host
2. principal vectors
1. chipmunks, squirrels
2. mosquitoes
90% of cases of LaCrosse encephalitis are in which age group?
*only encephalitis that is associated with youth*
in relation to Western Equine encephalitis (WEE):
1. primary host?
2. primary vector?
1. birds
2. mosquito
WEE causes clinical symptoms in what species?
humans, horses, emus
which is worse to have: WEE or EEE?
*EEE is the most severe arboviral CNS disease in the USA*
mortality of EEE is highest in which age group?
in regards to EEE:
1. coma and death occur in what fraction of patients?
2. permanent brain damage occurs in what fraction of patients?
1. 1/3
2. 1/3
two tick borne encephalitises?
powassan virus
colorado tick fever
hosts for colorado tick fever?
two flaviviruses that cause hemorrhagic disease?
yellow fever virus
dengue virus
two filoviruses that cause hemorrhagic disease?
two bunyaviruses that cause hemorrhagic disease?
crimean-congo HF
two arenaviruses that cause hemorrhagic disease?
lassa virus
junin/machupo virus
3 classic features of dengue fever?
1. fever
2. arthralgia "break-bone fever"
3. rash
how many antigenically distinct dengue virus serotypes are there?
(DEN-1 through 4)
dengue is transmitted by?
host of dengue virus in urban areas?
*more than one serotype can circulate in a geographic region at the same time - what is the significance of this?
increased incidence of hemorrhagic fever where there are two or more circulating serotypes
which two serotypes are most responsible for hemorrhagic fever?
DEN-2 and 3
(DEN-1 rarely causes hemorrhagic fever)
what is the exact sequence of dengue serotype infection that causes DHF?
previous infx by one serotype and subsequent infection by a second serotype
(antibody directed against previous serotype binds but doesn't neutralize 2nd serotype. these complexes are ingested by macrophages - macr. are lysed by CTLs - this releases vasoactive mediators)
diagnostic test for dengue virus?
RT-PCR of CSF (rapid and specific)
*also can detect specific IgM in acute phase CSF using antibody capture ELISA (MC method)
vaccines are available for which arboviruses?
Yellow fever virus
japanese encephalitis virus
what is the best prophylaxis for arbovirus infection?
control of vector population
what is the MC type of skull fracture?
(due to broad based impact - traffic, falls)
three types of basilar skull fractures?
1. comminuted fractures of orbital roof
2. hinge fractures
3. ring fractures
when are fractures of the orbital roof seen?
in falls to the back of the head, temple to temple gunshot wounds
clinical presentation of an orbital roof fracture?
perioribtal ecchymosis
which basilar fractures are always fatal?
hinge fracture
ring fracture
describe the gross findings in a hinge fracture
deep linear fracture across both sides of the middle cranial fossa. (implies massive impact to head)
describe the gross findings in a ring fracture
roughly circular fracture surrounding the foramen magnum (seen in forcible hyperextension of the neck - traffic accidents, or falls from great heights with landing on buttocks or feet)
which skull fracture am I?
bone is pushed inward often causing CNS trauma. associated with severe CNS injury.
seen with forceful impact striking skull over a small surface area
depressed fracture
what type of skull fracture is generally seen with a forceful heavy object striking the head over a wide surface area?
comminuted fracture
(see bone breaking into multiple fragments)
what is a diastatic fracture?
fracture line extends along and opening a suture line
(MC in children)
define a compound fracture
any type of fracture associated with an overlying scalp laceration
which are MC: coup or counter-coup contusions?
what types of contusions are MC seen in GSW?
herniation contusion

(explosive force thrusts a portion of the brain against a bony ridge or dural boundary)
what is a "burst lobe"
severe contusion/cerebral laceration with tearing of the pia
*MC in frontal and temporal lobes
injury of white matter in the brain that is diffuse and often surrounded by hemorrhage is known as?
diffuse axonal injury (DAI)
what is the early morphology of DAI?
axonal retraction bulbs in neuronal processes
mid-range morphology of DAI (weeks-months)?
microglial proliferation around damaged area
late morphology of DAI (months to years)?
reduced mass of white matter with compensatory cerebral atrophy/hydrocephalus
mechanism of DAI?
tearing/stretching of axon allows Ca++ influx
*Ca++ activated protease, cytoskeleton trauma
*continued axonal transport produces the retraction bulbs
what is diffuse vascular injury characterized by?
petechial hemorrhage throughout the white matter, brainstem and thalamus
(thought to be the mechanism of injury for patients who die within minutes of injury)
what type of emboli are commonly seen after trauma (esp. arm trauma)?
fat/marrow emboli
(may be fatal or full recovery)
what are the 2 MC primary complications of CNS injury?
cerebral edema
epidural hemorrhages usually result from laceration of?
middle meningeal artery
(requires a direct blow to the head)
where does bleeding occur in a subdural hemorrhage?
between the dura and the brain
where does the bleeding occur in an epidural hemorrhage?
between the skull and dura
subdural hemorrhages result from tearing of?
the bridging veins
CT differences between an epidural and subdural hemorrhage?
epidural - lens shaped
subdural - crescent shaped
three secondary complications of CNS injury?
1. hypoxic brain injury due to increased intracranial pressure
2. infections
3. aeroceles
describe hypoxic brain injury due to increased intracranial pressure
when intracranial pressure = blood pressure blood flow to brain stops, brain dies w/i minutes. Hypoxic injury is 1st seen in watershed areas
what is an aerocele?
trapping of air w/i the cranial cavity. may manifest as mass effect or increased intracranial pressure
what types of CVAs are associated with loss of consciousness?
bilateral hemispheric & vertebralbasilar system infarcts
the Dolls eye phenomenon tests the integrity of which brain structure?
(extremely poor prognosis if absent)
some causes of metabolic encephalopathy?
1. hyponatremia
2. hypomagnesemia
3. renal failure
4. hypothyroidism
5. B-12 deficiency
6. lead intoxication
7. multifactorial (meds)
what is pseudotumor cerebri?
overproduction of CSF or broken resorptive mechanism - results in increased intracranial pressure
visual manifestations of pseudotumor cerebrii?
blurred vision that improved during the day
*also see bilateral papilledema*
three risk factors for developing pseudotumor cerebri?
1. female
2. obesity
3. tetracycline
treatment for pseudotumor cerebri?
(CA inhibitor diuretic)
what is amaurosis fugax?
temporary loss of vision
(can be uni or bilateral)
what is the prognositic difference between a unilateral and bilateral case of amaurosis fugax?
unilateral - serious, due to atherosclerosis of internal carotid a.
bilateral - benign, cause unknown
visual manifestations of motor impersistence of gaze?
unable to maintain fixation of eyes while looking towards one side
cause of motor impersistence of gaze?
occlusion of one carotid a. - other has severe stenosis
*unable to hold persistent gaze to side OPPOSITE of completely occluded a.
in homonymous hemianopsia due to acute infarction: which side is the visual defect on in relation to the cerebral lesion?
visual defect is on opposite side of cerebral lesion
seeing twinkling lights and geometric shapes is characteristic of?
clinical s/s of temporal arteritis
*bitemporal headaches
*temporary partial loss of vision in one or the other eye
*jaw claudication while eating
*tender, pulseless, nodular temporal arteries
treatment for temporal arteritis?
(must treat immediately to avoid permanent damage)
in forced deviation of gaze - eyes look which way in relation to:
1. a destructive lesion
2. an irritative lesion
1. look TOWARD a DESTRUCTIVE lesion
2. look AWAY FROM an IRRITATIVE lesion
describe optic neuritis
subacute vision loss in one or both eyes - indicative of current or future MS
what other ocular defect is seen in MS (but only in alreadyestablished MS)?
internuclear opthalmoplegia
progressive supranuclear palsy has symptoms that resemble?
(can be differentiated b/c here impairment of downward gaze is characteristic)
what is the triad seen in low pressure hydrocephalus?
1. balance problem
2. cognitive disturbance (rapid progressive memory loss)
3. urinary incontinence
presenting s/s of Friedrich's ataxia?
increasing imbalance
incoordination of extremities
dysarthria (speech impairment)
inheritance pattern of Friedrich's ataxia?
paraneoplastic ataxia is MC seen with which cancer?
SCC of the lung
s/s of vestibular neuronitis?
acute onset vertigo
trouble focusing vision due to nystagmus
aggravated by head mvmt
transient, but may be recurrent
may be hereditary
triad commonly seen in Meniere's disease?
1. vertigo
2. tinnitus
3. high frequency hearing loss
differentiate positional from non-positional vertigo
positional - gets better in certain positions
non-positional - no position helps vertigo
positional vertigo is MC due to? (2)
1. tumors of the 4th ventricle
2. large cerebellar infarcts
red flags for secondary headaches?
1. abrupt onset
2. anticoagulant use
3. recent Hx. of head trauma
4. fever/immunosuppression
5. neck pain/stiffness
6. altered LOC
7. focal neurologic s/s
three primary H/A disorders?
s/s of a migraine?
unilateral throbbing
what is the initiating factor in the development of migraine H/As?
vasodilation of dural blood vessels
what explains the referral of migraine pain to various locations in the head and the face?
connections with the trigeminal nucleus caudalis
what explains the neck pain seen in migraines?
the trigeminal nucleus caudalis extends to the dorsal horn for C2, 3, and 4 -> result is neck and posterior head pain
what explains the autonomic sx. seen in migraines?
the superior salivatory nucleus is close to the trigeminal nucleus caudalis and leads to initiation of ANS symptoms
why are symptoms found in the sinus cavities and tear ducts?
cranial parasympathetic NS extends into the sinus cavities and tear ducts. this leads to sinus sx. that often get misdiagnosed as a sinus H/A
describe a tension H/A
*no associated disability
*always bilateral (never unilateral)
*no throbbing or assoc. sx.
what frequency in the use of analgesics increases risk of medication induced H/As
>3 doses/wk
does any sort of analgesic increase the risk of medication induced H/A?
short T1/2
are cluster H/As unilateral or bilateral?
unilateral and periorbital
describe the duration and recurrence of cluster H/As
short duration
occur in clusters over weeks to months, then dissapear for long periods of time
name 4 acute medications to treat H/As
name 5 preventative medications for H/A
1. beta blockers
2. CCBs
3. anticonvulsants
4. TCAs
5. serotonin modulators

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