Week 4 (Test 2) Flashcards

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1
Q

What’s the function of CN XII?

A

hypoglossal: motor innervation of all intrinsic and extrinsic skeletal muscles of tongue

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2
Q

What’s the function of the nucleus ambiguus?

A

this nucleus contains special “visceral” efferent neurons that innervate skeletal muscle of the larynx and pharynx as cranial nerves IX, X, and a small part of 11

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3
Q

What’s the function of the inferior salivatory nucleus?

A

contains preganglionic parasympathetic neurons that exit the brainstem as part of CN IX to innervate the parasympathetic neurons in the otic ganglion

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4
Q

What’s the function of the dorsal motor nucleus of Vagus nerve?

A

contains preganglionic parasympathetic neurons that send their long axons out of the brainstem with the vagus nerve to innervate the parasympathetic ganglia in the walls of the esophagus, trachea, bronchi, heart, and gastrointestinal tract down to the transverse colon

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5
Q

What’s the function of the nucleus of the solitary tract?

A

1) contains primary afferent axons of CN’s 9 and 10 that carry visceral sensation from carotid body to CN 9 and the pharynx, larynx, viscera in thorax and abdomen to CN 10 2) ALL TASTE AFFERENTS

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6
Q

What’s the function of the nucleus of the Spinal Trigeminal Tract?

A

this nucleus receives all somatic afferent info that comes from the face and also the oral and nasal cavities

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7
Q

Which artery is blocked in Wallenberg’s Syndrome?

A

PICA

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8
Q

What’s the function of the inferior olivary nucleus?

A

contains neurons whose axons (“climbing fibers”) enter the contralateral inferior cerebellar peduncle to travel to the cerebellum

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9
Q

What’s the function of the dorsal and ventral cochlear nuclei?

A

contain the secondary special sensory neurons for the special sense of hearing

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10
Q

What’s the function of pyramids?

A

contain cortical upper motor neurons, axons destined for the spinal cord, i.e., corticospinal fibers

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11
Q

What’s the function of the medial longitudinal fasciculus (MLF) tract?

A

they are composed of the axons of interneurons which interconnect the cranial nerve nuclei involved with movement of the eyes and balance. THEY ARE CLINICALLY IMPORTANT BECAUSE WHEN LESIONED, CONJUGATE EYE MOVEMENTS ARE LOST

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12
Q

What’s the function of the dorsal (posterior) longitudinal fasciculus (DLF) tract?

A

its axons carry signals from the hypothalamus to autonomic nuclei in the brainstem and spinal cord

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13
Q

When looking in the brainstem, what is the name commonly used for the spinothalamic tract?

A

Anterolateral system

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14
Q

What’s the function of the ventral spinocerebellar tract? (VSCT)?

A

it carries unconscious proprioceptive info from groups of muscles to the cerebellum

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15
Q

What’s the function of the dorsal spinocerebellar tract?

A

it carries unconscious proprioceptive info from single muscles to the cerebellum

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16
Q

What’s the function of the trigeminal thalamic tract?

A

it carries all somatic sensory modalities for the FACE and oral and nasal cavities

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17
Q

What’s the function of the spinal trigeminal tract?

A

carries primary somatic sensory axons from the trigeminal ganglion to the spinal trigeminal nucleus

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18
Q

What’s the function of the central tegmental tract?

A

contains ascending and descending fibers of the reticular formation and connects the inferior olivary nucleus of the medulla with the red nucleus of the midbrain

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19
Q

What do substantia nigra neurons produce?

A

dopamine

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20
Q

Which cranial nerves are found in the midbrain?

A

CN III and IV

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21
Q

Which cranial nerves are found in the pons?

A

CN 5, 6, 7, & 8

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22
Q

Which cranial nerves are found in the medulla?

A

CN 9, 10, 11, & 12

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23
Q

Which arteries supply the medulla?

A

vertebral arteries, PICA, anterior spinal artery, and posterior spinal artery

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24
Q

Which arteries supply the pons?

A

pontine arteries off of the basilar artery supply middle and AICA supplies lateral portion

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25
Q

Which arteries supply the midbrain?

A

posterior cerebral arteries

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26
Q

What does the upper part of the nucleus solitarius do?

A

taste

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27
Q

Why is the lower part of the nucleus solitarius important?

A

it contains cardio respiratory neurons; if these get damaged you can die

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28
Q

Which two muscles open the eye?

A

Mueller’s muscle and levator occuli

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29
Q

paralysis of one side of the body

A

hemiplegia

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30
Q

weakness of one side of the body

A

hemiparesis

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31
Q

pseudounipolar neurons =

A

general sensory

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32
Q

bipolar neurons =

A

special sensory

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33
Q

What is the function of the nucleus solitarius?

A

visceral sensory info (taste, baroreceptors, gut distention) [vagal nuclei]

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34
Q

What is the function of the nucleus ambiguus?

A

motor innervation of pharynx, larynx, and upper esophagus [vagal nuclei]

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35
Q

What is the function of the dorsal motor nucleus?

A

sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI [vagal nuclei]

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36
Q

How would a lesion in cranial nerve 6 present clinically?

A

no lateral gaze of the eye on the same side as the lesion

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37
Q

How would a lesion in the nucleus of cranial nerve 6 present clinically?

A

no lateral gaze of the eye on the same side as the lesion and no conjugate contralateral medial gaze

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38
Q

Describe the pathway involved in the corneal reflex.

A

afferent signal is sent from V1 (trigeminal) to rostral spinal nucleus (trigeminal); efferent signal is then sent from facial motor nucleus to orbicular oculi muscle and you blink

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39
Q

Describe the pathway involved in the jaw jerk reflex.

A

afferent signal is sent to mesencephalic nucleus (trigeminal) and efferent signal is then sent from the motor nucleus (trigeminal) to masseter and temporal muscles

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40
Q

What are the common signs of a lesion to the trochlear nerve?

A

SIGNS: 1) Extorsion (Can’t Look Down & In) 2) Vertical Diplopia (Double Vision) when Reading or Walking Down Stairs 3) Head Tilt + Chin Down Contralat. to Affected SO

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41
Q

pin point pupil

A

miosis

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42
Q

dilated pupil

A

mydriasis

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43
Q

What do you see in Horner’s syndrome?

A

Sympathetics Lost: Partial Ptosis (Muller’s m.) Miosis (Pin Point Pupil) Anhydrosis

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44
Q

What do you see in a lesion of CN III?

A

Somatic Motor Lost: - Full Ptosis (Levator m.) –Eye closes all the way -Down and Out Parasympathetics Lost: - Mydriasis (Dilated Pupil)

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45
Q

What is the blood supply of brainstem nerves and nuclei for CN 1 & 2?

A

anterior cerebral artery

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46
Q

What is the blood supply of brainstem nerves and nuclei for CN 3 & 4?

A

posterior cerebral artery

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47
Q

What is the blood supply of brainstem nerves and nuclei for CN 5, 6, &7?

A

AICA

48
Q

What is the blood supply of brainstem nerves and nuclei for CN 8, 9, & 10?

A

PICA

49
Q

What is the blood supply of brainstem nerves and nuclei for CN 11 & 12?

A

anterior spinal artery

50
Q

Where is norepinephrine made?

A

locus Ceruleus

51
Q

Where is serotonin (5-HT) made?

A

Raphe Nuclei

52
Q

Blockage of the aqueous flow can cause a disease called ____

A

Glaucoma; excess fluid cannot flow out of the eye properly, causing the intraocular pressure (IOP) to increase. Over time, raised IOP causes damage to the nerve fibers.

53
Q

List the coverings of the eye from outermost to innermost.

A

Sclera–> choroid–> trabecular meshwork

54
Q

usually occurs beginning at around age 40, when people experience blurred near vision when reading, sewing or working at the computer

A

presbyopia

55
Q

which type of lens corrects myopia (nearsightedness)?

A

concave lens

56
Q

Which type of lens corrects presbyopia?

A

convex lens

57
Q

Over time, yellow-brown pigment is deposited in the lens, and this, together with disruption of the lens fibers, reduces the transmission of light and leads to visual problems

A

cataract

58
Q

This is the major glia in retina. Note it extends the whole thickness of the retina.

A

Mueller supporting cell

59
Q

In which layer of the retina do you find photoreceptor cell bodies ?

A

external nucleus layer

60
Q

High intracranial pressure can cause abnormal optic disc appearance known as _____.

A

Papilledema

61
Q

Bottom line: When light hits a photoreceptor, it _____.

A

it decreases its glutamate release

62
Q

Describe the biochemical events that happen in the photoreceptors when light hits them.

A

light –> confirmational change in rhodopsin –> transducin binds GTP –> PDE (phosphodiesterase) activity increased —> cGMP levels decreased –> close Na+ channels —> hyperpolarization –> reduce glutamate release

63
Q

Rods are importnat for ___.

A

night vision and peripheral vision

64
Q

Cones are important for ____.

A

daylight vision and central vision

65
Q

In retinitis pigmentosa there is severe degeneration of rod photoreceptors.

The patient thus has:

A
  • Impaired night vision
  • Impaired peripheral vision
66
Q

Which Broadmann’s areas are part of the visual cortex?

A

17, 18, 19

67
Q

What does atropine do?

A

muscarinic receptor blocker (used clinically to block postganglionic parasympathetics–> use with wild mushroom poisoning)

68
Q

What does botulinum toxin do?

A

blocks release of acetylcholine from presynaptic cell

69
Q

What does cocaine do?

A

blocks monamine re-uptake at synapse to prolong action of NTs

70
Q

What does curare do?

A

blocks binding of ACh to its nicotinic (ion channel linked) receptor on skeletal muscle

71
Q

What does neostigmine do?

A

inhibits acetylcholinesterase activity, proloing ACh activity

72
Q

What do organophosphates (insecticides) do?

A

irreversibly inactivates acetylcholinesterase

73
Q

What do tricyclic antidepressants do?

A

block monamine reuptake (much like cocaine)

74
Q

What are the five classes of autonomic drugs?

A
  • Direct-acting cholinomimetics
  • Cholinoceptor blockers
  • Indirect-acting cholinesterase inhibitors
  • Sympathomimetics (direct/indirect)
  • Adrenoceptor blockers
75
Q

What are the toxicities for muscarininc agonists

A

SLUDGE:

Salivation, Lacrimation, Urination, Defecation, GI upset (diarrhea), Emesis (vomiting)

76
Q

What occurs with atropine toxicity?

A

•Dry as a bone: blocks thermoregulatory sweating, salivation, lacrimation

• Red as a beet: Dilation of blood vessels “atropine flush” (unknown mechanism)

• Mad as a hatter: CNS effects leading to delirium and hallucinations

77
Q

What is the antidote for cholinesterase inhibitors?

A

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atropine (cholinoreceptor blocker)

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78
Q

What role does the anterior hypothalamus play in the ANS?

A

regulates the parasympathetic nuclei (cholinergic postsynatpic)

**ALSO**, it contains the area that regulates cholinergic sweating

79
Q

What role does the posterior hypothalamus play?

A

it regulates the sympathetic nuclei (adrenergic postsynaptic)

80
Q

What type of neurogenic bladder is seen with CNS lesions above the pons?

A
  • No desire to control micturition or urgency to urinate but can’t delay- both leading to incontinence
  • uninhibited reflex bladder (infantile)
81
Q

What type of neurogenic bladder is seen with bilateral lesion of the sacral spinal cord?

A
  • LMN type lesion
  • Areflexic, “flaccid” bladder
  • Incontinence
  • Severe urinary tension
82
Q

What type of neurogenic bladder is seen with a CNS lesion between the lumbar cord and the pons?

A
  • UMN type lesion
  • Loss of voluntary control, hyperreflexia, “spastic” bladder
  • Does not empty fully (cysitits), incontinence
83
Q

Describe the nicotinic ACh receptor.

A
  • Five protein subunits
  • Two α; single β,δ and ε subunits
  • Only two α subunits bind Ach molecules
84
Q

Describe the structure of Succinylcholine?

A

two ACh molecules attached to each other

85
Q

How do depolarizing NM blockers like succinylcholine work?

A

–Rapidly bind to Ach receptor and generate action potential (act as if Ach receptor agonists)

–NOT metabolized by Acetylcholinesterases → level does not fall at receptors → prolonged depolarization of muscle end plate

86
Q

How do non-depolarizing NM blockers work?

A

–Bind to Ach receptors but can NOT produce conformational changes for action potential

–Competitive antagonists

–Compete with the existing levels of Ach for the Ach receptors

87
Q

Succinylcholine isn’t broken down by AChE, so how does it get degraded?

A

once it enters the blood, pseudocholinesterase metabolizes it

88
Q

Succinylcholine has a typical duration of less than 10 minutes. What might cause this duration to be prolonged?

A

–High dose
–Hypothermia (decreased hydrolysis)
–Low Pseudocholinesterase levels (modest prolongation of block by 2-20 minutes)
•Pregnancy
•Liver dz
•Kidney dz
•Drugs (neostigmine, metoclopramide, esmolol, oral contraceptives)

89
Q

When is succinylcholine avoided?

A

***Sch is AVOIDED in pediatric patients due to high incidence of undiagnosed mypopathies and resulting severe hyperkalemia and associated complications***

–This can cause arrhythmias and death

90
Q

Woman are 30% more sensitive to this non-depolarizing muscle relaxant.

A

•Vecuronium

91
Q

Why does increased solubility of an agent increase its equilibration time?

A

the more soluble the agent, the more easily dissolved in the blood. Once in the blood, it has a reduced ability to exit the blood and enter tissues where it will have its effect

92
Q

What’s the definition of minimum alveolar concentration (MAC), the primary measure of potency for inhaled anesthetics?

A

–equilibrium concentration required to prevent movement to skin incision at 1 ATM in 50% of patients

93
Q

What is MAC (minimum alveolar concentration) not changed by?

A

hyper/hypo-thyroidism

94
Q

What are the predictable CNS effects of inhaled anesthetics?

A

–Hypnosis
–Amnesia
–Analgesia (questionable)
–Inhibition of autonomic reflexes
–Muscle relaxation (except N2O)

95
Q

List 3 factors that increase MAC requirements

A

–Hyperthermia
–Elevated CNS catecholamine neurotransmitter release (anxiety)
–Chronic alcohol use
–Acute amphetamine use
–Hypernatremia
[he listed more than 3, sorry]

96
Q

List 3 factors that decrease MAC requirements.

A

–Hypothermia
–Pregnancy
–Shock
–Increasing age
–Acute alcohol ingestion
–CNS-depressant drugs
–Chronic amphetamine use

97
Q

What is the mosts likely mechansim of action of inhaled anesthetics?

A

ligand gated ion channels are the most likely targets [be aware he talked a lot about GABA-a receptors, which when activated hyperpolarize membranes, but he then went on to say that theory had major short comings]

98
Q

IV anesthetic that protects the brain best from hypoxic/ischemic injury.

A

thiopental

99
Q

What’s the mechanism of action of Thiopental?

A

-Binds to GABA-A receptor
–->Increases chloride ion flux into cell
–»Increases the duration of channel opening

100
Q

What are the common Benzodiazepines?

A

Midazolam and lorazepam

101
Q

What’s the best amnestic IV anesthetic?

A

benzodiazepines

102
Q

What’s the mechanism of action for benzodiazepines?

A
  • Bind to GABA-A receptor

–Increase Cl- flux, affinity for GABA, frequency of channel opening

103
Q

raises seizure threshold and is therefore a good antivconvulsant

A

Midazolam

104
Q

What’s the mechansim of action of opioids?

A
  • Analgesic action is via µ receptors

–G-protein linked receptors

105
Q

What are some side effects of opioids?

A

pruritis (itching), chest wall rigidity, patients “forget to breathe”

106
Q

only indicated for shivering

A

Meperdine (an opioid)

107
Q

shortest acting opioid; termination of action is due to elimination, not redistribution

A

Remifentanil

108
Q

“dissociative” anesthetic: an individual’s cognitive function is ‘separated’ from his physical being

A

Ketamine

109
Q

What’s the mechanism of action of Ketamine?

A

it’s a non-competitive NMDA antagonist

110
Q

What’s the mechanism of action of etomidate?

A

activates GABA-a receptors (inceasing chloride influx–> hyperpolarizing the membrane)

111
Q

Good for short procedures because it is a minimal ventillatory depressant

A

etomidate

112
Q

What’s the mechanism of action of Propofol?

A
  • Some action at GABAA complex

–Binds to a distinct site

  • May enhance Cl- conductance at glycine receptors
113
Q

Wha’ts the mechanism of action for Dexmedetomidine?

A
  • alpha-2 agonist

–Central alpha-2 stimulation results in sedation and analgesia
–Excellent sedative for administration by infusion

114
Q

Persistence of the choroid fissure results in what developmental defect?

A

Coloboma

115
Q

What is unique about the smooth muscles of the pupil as regards their developmental origin?

A

they are derived from neurectoderm of the optic cup

116
Q

What is Aniridia?

A

absence of the iris

117
Q

what is aphakia?

A

absence of the lens