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Brain and Behavior > Exam 1 (week 1) > Flashcards

Exam 1 (week 1) Flashcards

1
Q
  • 3 weeks of embryology - what happens in nervous system
A
  • surface ectoderm turns into neural groove
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2
Q
  • cavity in neural tube becomes what
A
  • ventricles in brain and cavity in spinal cord
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3
Q
  • what happens in 4 weeks of embryology
A
  • anterior end of neural tube starts to get bulges (Forebrain, midbrain and hindbrain)
    • flexures start happening
      • midbrain/cephalic flexure ventrally-down
      • cervical flexure at medulla/spinal cord ventrally/down
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4
Q
  • latin terms for parts of brain
A
  • forebrain = prosencephalon, midbrain = mesencephalon, hindbrain = rhombencephalon
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5
Q
  • what happens in 5 weeks of embryology
A
  • 5 brain vesicles - forebrain subdivides into cerebral hemispheres (Telencephalon) and diencephalon (major part is thalamus)
    • hindbrain also subdivides into (cerebellum and pons - mesencephalon) and (medulla oblongata - myelencephalon)
    • flexure:
      • at level of pons - neural tube bends dorsally (pontine flexure)
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6
Q
  • what part of brain is retina derived from
A
  • diencephalon
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7
Q
  • where are ventricles
A
  • 2 in each cerebellum (lateral), 1 in diencephalon, 1 in cerebellum,pons and medulla
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8
Q
  • where is the central aqueduct
A
  • in midbrain connecting 3rd ventricle and 4th ventricle
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9
Q
  • what happens at 3 months of developmentnt
A
  • cerebral hemispheres grow in all directions, diencephalon is completely covered
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10
Q
  • what happens at 6 months of development
A
  • midbrain gets covered by cerebral hemispheres - covered until the cerebellum
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11
Q
  • what happens at 9 months of development
A
  • gyri, fissures and sulci are formed
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12
Q
  • when is maximum weight of brain achieved
A
  • 8 years old
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13
Q
  • what is deeper, fissure or sulcus
A
  • fissure
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14
Q
  • what are the lobes and poles in the brain
A
  • frontal lobe and pole
    • temporal lobe and pole
    • occipital lobe and pole
    • parietal lobe
    • insular lobe (within lateral fissure)
    • limbic lobe
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15
Q
  • division between frontal and parietal lobes
A
  • central sulcus
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16
Q
  • division between temporal and parietal/frontal
A
  • lateral sulcus
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17
Q
  • division between parietal/temporal and occipital
A
  • laterally, arbitrary line between parietal occipital sulcus to pre occipital notch
    • medially parietal occipital sulcus
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18
Q
  • division between limbic lobe and rest
A
  • lyric lobe is made of 2 gyri, cingulate sulcus (separates cingulate gyrus and frontal/parietal) and collateral sulcus (separates parahippocampal gyrus and temporal lobe)
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19
Q
  • separation between cerebral hemispheres
A
  • superior longitudinal fissure until corpus collosum
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20
Q
  • separation between occipital pole and cerebellum
A
  • transverse cerebral fissure
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21
Q
  • how to identify central sulcus
A
  • look for 3 parallel sulci - middle is central. central doesn’t reach all the way down to lateral fissure
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22
Q
  • what sulcus runs within parietal lobe on lateral surface
A
  • intraparietal sulcus
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23
Q
  • what does intraparietal sulcus separate
A
  • superior and inferior parietal
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24
Q
  • frontal lobe gyri (4)
A
  • pre central gyrus (area 4, primary motor)
    • superior frontal
    • middle frontal
    • inferior frontal
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25
Q
  • parietal lobe gyri (4)
A
  • post central gyrus (primary somatosensory, areas 3,1,2)
    • superior parietal (paint temp touch)
    • inferior parietal (language)
    • precuneus (medially)
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26
Q
  • temporal lobe gyri (3)
A
  • superior temporal
    • middle temporal
    • inferior temporal
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27
Q
  • parahipocampal gyrus ending
A
  • uncus (close to temporal pole)
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28
Q
  • occipital lobe gyri (2)
A
  • on medial surface there’s calcarine sulcus - above is called cuneus
    • below is called lingual
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29
Q
  • anatomical parts of corpus coliseum
A
  • rostrum (nose), genu (knee), body and selenium (tail)
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30
Q
  • structures to identify on ventral surface of brain (6)
A
  • olfactory bulb
    • olfactory tract
    • optic nerve
    • optic chasm
    • pituitary stalk
    • mammary bodies
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31
Q
  • what structures does internal capsule run through
A
  • between thalamus and basal ganglia gray matter (caudate, putamen and globus pallidus)
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32
Q
  • brainstem subdivisions from dorsal to ventral
A
  • tectum (roof)
    • tegmenjtum (floor)
    • basilar region
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33
Q
  • where is tectum
A
  • only in midbrain, above cerebral acqdueduct
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34
Q
  • what does tegmenjtum contain
A
  • cranial nerve nuclei, reticular formation, and tracts to cerebrum
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35
Q
  • what does basilar region contain
A
  • descending motor tracks from cerebral cortex
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36
Q
  • what does tectum contain
A
  • superior colliculus (vision)

- inferior colliculus (hearing)

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37
Q
  • cranial nerve that exits dorsally
A
  • trochlear (4)
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38
Q
  • what nerves exit between midbrain and pons
A
  • 3rd - oculomotor

- 4th - trochlear

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39
Q
  • what nerve exits from basilar region of pons
A
  • 5th - trigeminal
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40
Q
  • what nerves exit between pons and medulla
A
  • 6th (abducens)
    • 7th (Facial)
  • 8th
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41
Q
  • what nerves exit from medulla
A
  • 9th - 12th
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42
Q
  • what is the demarcation between brainstem and spinal cord
A
  • pyramidal decussation
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43
Q
  • describe primitive neuroepithelium
A
  • pseudstratefied epithelium, with stem cells at the apical/luminal surface
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44
Q
  • what do neuroepithelial stem cells differentiate into
A
  • either neuroblasts or gliablasts
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45
Q
  • what are the cells that line the central canal, what are they derived from
A
  • ependymal cells (glial cells - also form the choroid plexus)
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46
Q
  • what are microglial cells and what are they derived from
A
  • phagocytes of CNS, monocyte derivative - mesodermally derived (Bone marrow)
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47
Q
  • what is mantle zone- what kind of matter does it become
A
  • down toward ventricle, contain lots of cell bodies that cell processes peripherally (GREY matter)
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48
Q
  • what is marginal zone - what kind of matter does it become
A
  • myelinated outer core - peripheral process from mantle zone (WHITE matter)
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49
Q
  • what does mantle layer get divided into
A
  • dorsal alar plates (eventually sensory horns)

- ventral basal plates (eventually motor horns)

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50
Q
  • division of grey and white in brain
A
  • deep grey, intermediate white, superficial grey (migrates up from deep manta layer)
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51
Q
  • how does grey matter neurons migrate in brain?
A
  • via radial glial cells - serve as train tracks from deep to periphery (like elevator)
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52
Q
  • genes important for nervous system stratification (motor, ibternueorns, sensory)
A
  • BMP (dorsal gradient - induces sensory neurons)
    • SHH (ventral gradient - induces motor neurons)
    • interneurons are induced by overlap
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53
Q
  • gene that regulates face development (and what over/under expression causes)
A
  • cyclopia - under expression of SHH

- facial duplication - over expression of SHH

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54
Q
  • most common developmental defect of forebrain
A
  • holoprosencephaly - single forebrain vesicle instead of two lateral. get mid facial defects - due to SHH defects
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55
Q
  • where does spina bifida generally occur (along spina cord)
A
  • lower lumbar/sacral (lower has better prognostic outcomes)
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56
Q
  • what superficial presentations occur with spina bifida occulta
A
  • hairy nevus overlaying area of spinal cord where this defect is occurring (lumbar)
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57
Q
  • difference between meningocele and meningomyleocele
A
  • meningocele is herniation of JUST cerebrospinal fluid, meningomyelocele also herniates spinal cord contents
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58
Q

rachiscesis

A
  • when spina bifida open neural tube to the outside world - causes paralysis (and possible infection)
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59
Q
  • what can you monitor in maternal serum to detect spina bifida in fetus
A
  • increased levels of alpha-fetoprotein
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60
Q
  • what can you provide women to reduce levels of spinal tube defects
A
  • folic acid supplementation (40mcg/day). because deficiency leads to abnormal cell division - can reduce incidence of neural tube defects by 70-80%
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61
Q
  • point where coronal and sagittal sutures meet
A
  • bregma
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62
Q
  • point where saggital suture meets occipital bone
A
  • lambda
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63
Q
  • junction of temporal, sphenoid, parietal and frontal bone
A
  • pterion (greater wing of the sphenoid)
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64
Q
  • junction of temporal, parietal and occipital bone
A
  • asterion
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65
Q
  • extra bones at sutures
A
  • wormion bones
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66
Q
  • fontanelles
A
  • anterolateral where pterion forms
    • posterolateral where astern forms
    • anterior at bregma
    • posterior at lambda
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67
Q
  • first and last fontanelles to close
A
  • first = posterior (1-2months after birth)

- last = anterior (2 years after birth)

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68
Q

what percentage of americans have some mental health disorder

A

18%

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69
Q

what type of opioid has recently been responsible for the most deaths

A

fentanyl

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70
Q

what percentage of homeless individuals living in shelters have a serious mental illness

A

26%

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71
Q

what percentage of homeless individuals living in shelters have substance use disorders

A

35%

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72
Q

what range of percentages of adult inmates have mental illnesses

A

45-64% in federal, state and local jails

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73
Q

what percentage of youth in juvenile justice systems have mental health conditions

A

20%

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74
Q

premature mortality in serious mental illness (decreases lifespan by how many years)

A

15-20 years

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75
Q

what percentage of illnesses contributing to early mortality in mental illness

A

40% (health behaviors)

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76
Q

what are 60% of premature schizophrenia deaths caused by (3)

A

cardiovascular, pulmonary and ID

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77
Q

first psychiatric drug approved by FDA

A

thorazine, chloramphetachol

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78
Q

componentts of the mental status exam (7)

A
  1. general appearance, behavior and attitude
  2. consciousness and orientation
  3. speech and language
  4. mood and affect
  5. thought content, form and perceptions
  6. memory and cognition
  7. judgement and insight
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79
Q

4 D’s in psychopathology

A
  1. danger
  2. distress
  3. dysfunction
  4. deviance

all have problems - not ideal markers

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80
Q

sections of the DSM diagnosis

A
  1. symptoms
  2. duration/time course
  3. ruling out medical conditions/substances
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81
Q

when does myelin form on axon

A

when axon gets a diameter more than 1 micrometer (micron)

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82
Q

what are nissl bodies

A

layers of rough ER and ribosomes in neuron cell bodies (NOT axons)

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83
Q

what direction and what protein does anterograde transport use

A

anterograde is from cell body down axon, uses kinesis

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84
Q

what direction and what protein does retrograde transport use

A

retrograde is back up to cell body from axon, uses dynein

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85
Q

what do synapses look like on EM

A

fuzzy catterpillars

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86
Q

what is euthymic mood

A

normal range of mood, absence of depressed or elevated mood

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87
Q

what is expansive mood

A

expression of feelings without restraint

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88
Q

what is anhedonia

A

loss of interest and withdrawal from regular and pleasurable activities

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89
Q

what is alexithymia

A

inability or difficulty in describing or being aware of one’s emotions

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90
Q

what is diurnal variation in mood

A

mood is worst in the morning, immediately after awakening and improves as the day progresses

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91
Q

what is echopraxia

A

pathologial immitation of movements of one person by another

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92
Q

what is catalepsy

A

immobile position that is constantly maintained

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93
Q

what is catatonic excitement

A

agitated, purposeless motor activity

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94
Q

what is catatonic stupor

A

markedly slower motor activity - seeming unawareness of surroundings

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95
Q

what is catatonic rigidity

A

assumption of rigid posture,held against all efforts to being moved

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96
Q

what is catatonic posturing

A

assumption of an inappropriate or bizarre posture, maintained for long periods

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97
Q

what is cerea flexibilitas

A

waxy flexibility - person can be molded into a position that is then maintained

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98
Q

what is negativism

A

resistance to all attempts to be moved or to instructions

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99
Q

what is cataplexy

A

temporary loss of muscle tone and weakness due to an emotional state

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100
Q

what is stereotypy

A

repetitive fixed pattern of physical action or speech

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101
Q

what is mannerism

A

ingrained, habitual involuntary movement

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102
Q

what is akathisia

A

subjective feeling of muscular tension, causing restlessness, pacing, repeated sitting and standing

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103
Q

what is aggression

A

the motor counterpart of the affect of rage, anger or hostility

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104
Q

what is a formal thought disorder

A

disturbance in form of thought, not content of thought - characterized by loosened associations, neologisms, illogical constructs

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105
Q

what is magical thinking

A

form of illogical thought similar to preoperational phase in children in which thoughts, words or actions assume power (can cause or prevent events)

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106
Q

what is neologism

A

new word created by patient by combining syllables of other words

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107
Q

what is circumstantiality

A

indirect speech that is delayed in reaching the point but eventually gets to desired goal

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108
Q

what is tangentiality

A

inability to have goal-directed associations of thought - never gets to desired goal

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109
Q

what is perseveration

A

persisting response to a prior stimulus after a new stimulus has been presented

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110
Q

what is verbigeration

A

meaningless repetition of specific words or phrases

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111
Q

what is echolalia

A

repeating of words or phases of one person by another

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112
Q

what is flight of ideas

A

rapid, continuous verbalizations or plays on words that produce constant shifting from one idea to another that tend to be connected

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113
Q

what is clang association

A

association of words with similar sounds not meanings

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114
Q

what is blocking

A

abrupt interruption in train of thought before its finished. after a while the person has no recall of the previous thought (AKA thought deprivation)

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115
Q

what is a systematized delusion

A

false beliefs united by a single event or theme (persecuted by the CIA)

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116
Q

what is a bizarre delusion

A

invaders from space planted electrodes in my brain - totally implausible

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117
Q

what is a mood-congruent delusion

A

delusion with content that has no association with mood, or is mood-neutral

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118
Q

what is a nihilistic delusion

A

false feeling that self, others or the world is nonexistent or ending

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119
Q

what is somatic delusion

A

false belief involving functioning of one’s body (brain is melting)

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120
Q

what is a delusion of reference

A

false belief that the behavior of others refers to oneself (belief that persons on the television are talking to our about you)

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121
Q

what is thought withdrawal

A

delusion that one’s thoughts are being removed from on’es mind

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122
Q

what is thought broadcasting

A

delusion that one’s thoughts can be heard by others

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123
Q

what is thought control

A

delusion that one’s thoughts are being controlled by others

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124
Q

what is pseudologia phantastica

A

associated with munchausen’s, a type of lying in which the person appears to believe in the reality of his/her fantasies and acts on them

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125
Q

what is non-spontaneous speech

A

no self-initiation of speech - only speaks when spoken to

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126
Q

what is poverty of speech vs poverty of content of speech

A

poverty of speech = restriction of amount of speech (monosyllabic responses)

poverty of content of speech = adequate amount of speech, but conveys too little information

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127
Q

what is dysprosody

A

loss or normal speech melody

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128
Q

what is dysarthria

A

difficulty in articulation (not word finding or grammar)

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129
Q

what is motor aphasia

A

understanding remains intact, but ability to speak is impaired (Broca’s, nonfluent, expressive)

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130
Q

what is sensory aphasia

A

loss of ability to understand, but speech is fluid (Wernicke’s, fluent, repetitive)

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131
Q

what is nominal aphasia

A

difficulty in finding correct name for an object

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132
Q

what is syntactical aphasia

A

inability to arrange words in proper sequence

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133
Q

what is jargon aphasia

A

words are totally neologistic, nonsense words repeated with various intonations and inflections

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134
Q

what is global aphasia

A

combination of nonfluent aphasia with fluent aphasia

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135
Q

what is hypnagogic hallucination

A

false sensory perception while falling asleep (non-pathological)

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136
Q

what is hypnopompic hallucination

A

false perception occurring while awaking from sleep (non-pathological)

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137
Q

what is somatic hallucination

A

false sensation of things occuring in or to the body

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138
Q

what is illusion

A

misperception or misinterpretation of real external sensory stimuli

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139
Q

what is anosognosia

A

ignorance of illness

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140
Q

what is somatopagnosia

A

ignorance of the body - inability to recognize a body part as one’s own

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141
Q

what is prosopagnosia

A

inability to recognize faces

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142
Q

what is apraxia

A

inability to carry out specific tasks

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143
Q

what is visual agnosia

A

inability to recognize objects or persons

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144
Q

what is depersonalization

A

subjective sense of being unreal, strange or unfamiliar to oneself

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145
Q

what is derealization

A

sense that the environment is strange, unreal

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146
Q

what is anterograde amnesia

A

amnesia for events occuring AFTER a point in time

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147
Q

what is retrograde amnesia

A

amnesia for events occurring BEFORE a point in time

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148
Q

difference between immediate, recent, recent past, and remote memory

A

immediate = seconds to minutes
recent = past fes days
recent past = past few months
remote = distant past

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149
Q

IQ for mild mental retardation

A

50 or 55 - 70

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150
Q

IQ for moderate mental retardation

A

35 or 40 - 50 or 55

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151
Q

IQ for severe mental retardation

A

20 or 25 - 34 or 40

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152
Q

IQ for profound mental retardation

A

below 20 or 25

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153
Q

what is dyscalculia

A

inability to do calculations not caused by anxiety or impairment in concentration

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154
Q

what is dysgraphia

A

loss of ability to write in cursive style, loss of word structure

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155
Q

what is alexia

A

loss of previously possessed reading facility

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156
Q

what is pseudodementia

A

clinical resemblance to dementia but caused by depression

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157
Q

what is concrete thinking

A

literal thinking - one-dimensional thought

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158
Q

what is abstract thinking

A

ability to appreciate nuances of meaning - multidimensional thinking

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159
Q

excitatory neurotransmitter in CNS

A

glutamate

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160
Q

inhibitory neurotransmitter in CNS

A

GABA (brain)

glycine (spinal cord)

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161
Q

which astrocytes are in white matter

A

fibrous

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162
Q

which astrocytes are in grey matter

A

protoplasmic

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163
Q

which cell can myelinate more than one neuron

A

oligodendrocytes

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164
Q

difference between unmyelinated neurons in PNS vs CNS

A

PNS is still surrounded by cytoplasm of schwann cell

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165
Q

what does leptomeninges incldue

A

dura and arachnoid

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166
Q

what mater is most close tot he spinal cord

A

pia

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167
Q

what mater has innervation

A

dura only

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168
Q

what is falx cerebri and what innervates it

A

dura mater right down the hemispheres, in the anterior cranial fossa, is innervated by ophthalmic and maxiillary branches of trigeminal CN V

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169
Q

innervation of middle cranial fossa

A

ophthalmic and maxilary V1, V2 and some V3 mandibular

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170
Q

posterior cranial fossa innervation

A

vagus X
C1, C2 and C3 dorsal rami
(maybe glossopharyngeal)

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171
Q

what is subarachnoid space

A

between arachnoid and pia, contains CSF and vasculature

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172
Q

what is epidural space

A

between bone and dura, only a potential space in the skull

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173
Q

what is subdural

A

not naturally occuring space, between dura and arachnoid

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174
Q

where is superior saggital sinus

A

along middle of hemispheres - top of falx cerebri

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175
Q

where is transverse sinus, and where does it receive blood from

A

meets up with superior saggital sinus and straight sinus (which is inferior sagittal sinus and great cerebral vein combination) into confluence and then transverse

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176
Q

what does transverse sinus become

A

sigmoid, which then becomes internal jugular

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177
Q

what are arachnoid granulations and where are they

A

little mushrooms of arachnoid into superior sagittal sinus - how CSF gets recycled

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178
Q

what is in cavernous sinus and what’s around it

A

around pituitary and sphenoid, contains CN 3, 4, V1 V2, 6 and internal carotid

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179
Q

if you have a supratentorial lesion/tumor, what could happen

A

temporal lobe can be pushed through tenrtorial notch and impinge on cn3

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180
Q

if you have a pituitary adenoma, where could it go and what could it do

A

it could push up through the diaphragma sellae and impact the optic chiasm, causing tunnel vision (bitermporal hemianopsia)

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181
Q

STUDY THE FORAMEN

A

separate piece of paper

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182
Q

lefort 1

A

transverse maxillary fracture -“floating palate”

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183
Q

lefort 2

A

pyramidal fracture- through orbital rim, “floating maxilla”

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184
Q

lefort 3 and 4

A

craniofacial disjunction - through orbital walls “floating face”

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185
Q

on what bone are the nuchal lines

A

occipital bone

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186
Q

a tumor that presses on jugular foramen would impact which nerve

A

glossopharyngeal

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187
Q

parts of sphenoid bone (4)

A
  1. lesser wing (above superior orbital fissure)
  2. greater wing (below superior orbital fissure, extends laterally to side of face)
  3. sella turcica - depression above body where pituitary is
  4. lateral and medial pterygold plates - muslce attachments
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188
Q

muscles associated with functino of eustacian tube (4)

A
  1. levator veli palatini (elevates palate - innervated by vagus)
  2. saslpingopharyngeus (closes eustacian tube)
  3. tensor tympani (tenses tympanic membrane)
  4. tensor veli palatini (flattens palate)
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189
Q

why do kids get ear infections

A

eustacian tube is more horizontal and it’s shorter

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190
Q

what’s the problem with emissary veins

A

can bring infection from scalp to brain through emissary veins

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191
Q

where do bringing veins go

A

cerebral veins to sinus

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192
Q

skull fracture at pterion would cause epidrual hematoma from which artery

A

middle meningial artery (MMA)

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193
Q

scalp acroynym

A 
skin
connective tissue
aponeurosis (connects to muscles)
loose areolar tissue
periosteum (dura mater reflection)
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194
Q

dermatomes of C2 - ventral vs dorsal ramus

A

C2 dorsal ramus on back of scalp

C2 ventral is neck and ear

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195
Q

what movements are along the vertical axis of eye

A

abduction and adduction

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196
Q

what movements are along the horizontal axis of eye

A

elevation and depression

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197
Q

what muscles do oculomotor nerve innervate in eye (extrinsic)

A

superior rectus
medial rectus
inferior rectus
inferior oblique

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198
Q

what muscle does trochelar lnerve innervate in eye

A

superior oblique

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199
Q

what muscle does abducens innervate in eye

A

lateral rectus

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200
Q

what movements are along the visual axis of eye

A 
intorsion = eyeball rotates towards nose
extosion = eyeball rotates away from nose
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201
Q

what is convergence in terms of eyes

A

medial rectus (oculomotor CN3) work to make eyes crossyeed

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202
Q

how to test SR and IR eye muscles

A

put eye laterally then elevate or depress the eye

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203
Q

how to test superior oblique

A

bring eye medially and then down

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204
Q

how to test eye muscles generally

A

first line up line of pull with visual axis then

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205
Q

how to test inferior oblique

A

bring eye medially and then up

206
Q

oculomtor nuclei tracks where do they go and come out

A

motor nucleus
edinger-westphal nucleus

through interpeduncular fossa through cavernous sinus

207
Q

what does edinger-westphal contain

A

parasympathetic to ciliary ganglion

208
Q

when someone has unilateral damage to CN3, what will the eye look like

A
  1. drooping eyelid
  2. eye is down and out “lateral strabismus”
  3. mydriasis (dilated pupil)
209
Q

ptosis due to sympathetic - what will pupil look like

A

smaller - myosis

210
Q

ptosis due to CN3 damage - what will pupuil look like

A

dilated - mydriasis

211
Q

slight ptosis caused by what muscle

A

superior tarsal

212
Q

what are the intrisnci muscles of the eye that CN3 innervates (and what motion do they control)

A
  1. sphincter pupillae (constricts pupil) - parasympthathetics
  2. ciliary bodies (accommodation reflex)
213
Q

where does dilator pupillae innervation coem from

A

from sympathetic trunk to superior cervical ganglion - leads to pupil dilation

214
Q

what nuclei are involved in pupillary reflex - path from optic nerve to pupil contraction

A

optic nerve to pretectal nuclei, to EW nuclei, to oculomotor nerve, to ciliary ganglion to pupil contraction

215
Q

what are the components of the accomodation reflex - what things need to change

A
  1. convergence
  2. pupil constriction
  3. rounding of lens (via ciliary bodies)
216
Q

what motions of eye does trochlear control

A
  1. depression
  2. intorsion
    OF OPPOSITE EYE

due to innervation of superior oblique

217
Q

what will the eye look like with trochlear damage

A

eye will be slightly up and medial

218
Q

what kind of double vision will you have

A

vertical double vision

219
Q

how do people with trochlear nerve

A

tilt away from affected eye (so that the affected eye can extort)

220
Q

when abducens is damaged, what will the eye look like

A

affected eye will be medially rotated - medially strabismus

221
Q

what is reticular formation, where is it housed

A

cells packed in meshwork of tracks.

housed in the tegmentum

222
Q

what does ascending reticular system do and where does it go

A

projects to cortex - maintains brain at appropraite level of arousal – reticular activating system

223
Q

what does descending reticualr system do and where does it go

A

pass to spinal cord in reticulospinal tract

modulates spinal reflex activity

224
Q

what structures are in tegmentum (4)

A
  1. reticular formation
  2. cranial nerve nuclei and tracts
  3. ascending pathways from spinal cord
  4. some descending pathways
225
Q

what senses are carried in visceral sensory

A

taste

visceral

226
Q

what senses are carried in special sensory

A

vision
hearing
balance

227
Q

where in brainstem are sensory nuclei grouped - dorsal, ventral, medial or lateral

228
Q

where in brainstem are motor nuclei grouped - dorsal, ventral, medial or lateral

229
Q

what sensory info decussates in the internal arcuate fibers

A

touch, vibration, proprio

230
Q

what replaces substantia gelatinosa in medulla cross section

A

spinal tract and nucleus of V (recieves SENSORY info from 5, 7, and 9 from the head/face)

231
Q

what are the two most medial small structures at level in medulla, right dorsally to the decussation of the gracillis and cuneatus gracts

A

medial lemniscus

232
Q

once you get above the nucleas cuneatus/gracilis, what are the CN nuclei from medial to lateral

A
  1. hypoglossal (motor)
  2. dorsal motor nucleus of 10 (motor)
  3. solitary nucleus and tract (senosory)
  4. vestibular nuclei (sensory)
233
Q

where to hypoglossal axons exit

A

in pre olivary sulcus

234
Q

where do dorsal motor nucleus of 10 axons exit

A

in post olivary sulcus

235
Q

what info does dorsal motor nucleus contain/carry

A

preganglionic parasympathetics to thorax and abdominal viscera

236
Q

what info does solitary nucleus contain

A

taste from 7, 9 and 10

237
Q

what nucleus is ventral to the rest of the bunch of nuclei in the medulla at the level of the 4th ventricle

A

nucleus ambiguus

238
Q

what does the nucleus ambiguus do

A

controls swallowingn and vocalization from 9 and 10

239
Q

what is lateral to nucleus ambiguus

A

reticular formation that controls heart rate

240
Q

what CNs does medial longitudinal fasciculus play a role in communicating between

241
Q

what facial deficits would you see with medial medullary lesion

A

eye is down and out

tongue deviates away from affected ey

242
Q

3 structures in base of pons

A
  1. pontine nuclei most medial and dorsal
  2. pontocerebellar fibers, running lateral to medial ventral to the pontine nucleus
  3. corticospinal tracts most ventral, which will become pyramids
243
Q

what percentage of american suffer from an anxiet disorder

244
Q

what are the primary anxiety disorders (5)

A
  1. generalized anxity disroder
  2. panic disorder
  3. agoraphobia
  4. specific phobia
  5. social phobia
245
Q

what are four medical conditions that can cause anxiety

A
  1. hyperthyroidism
  2. COPD
  3. congestive heart failure
  4. arrhythmia
246
Q

what are 2 substances that canc ause anxiety

A
  1. caffeine

2. stimulants (amphetamines, cocaine)

247
Q

what are the neurotransmitters involved in anxiety (3)

A
  1. GABA
  2. NE
  3. serotonin
248
Q

what are the 3 components or sides to anxiety (and the 3 A’s)

A
  1. cognitive (anticipation)
  2. physiologic (arousal)
  3. behavioral (avoidance)
249
Q

hormone involved in anxiety

250
Q

why is axiety worse when you’re lying down

A

carbon dioxide - your tidal volume decreases and your trigger mechanism in carotids goes off

251
Q

what drug don’t you give in anxiety

A

alprazolam (xanax) - tends to have more reinforcing or addictive effects

252
Q

how to treat specific phobias therapeutically

A

systemic desensitization

253
Q

what are the 3 parts to systemic desnsitization

A
  1. stimulus hierarchy (start with thinking, then photo, then removed, then touching)
  2. learn coping mechanisms
  3. learn to connect stimulus to response and coping mechanisms
254
Q

what percentage of population has social anxiety disorder

255
Q

what are the therapeutic treatments for social anxiety disorder (2)

A
  1. social skills training/exposure (group therapy)

2. cognitive behavior therapy

256
Q

what are the medications for social anxiety disorder (4)

A
  1. SSRI
  2. SSNI
  3. MAOI
  4. benzos
257
Q

what are the medications for generalized anxiety disroder

A
  1. SSRI/SNRI
  2. benzos

might have to start with benzos to get the initial symptoms controlled, because ssris take some time. also ssri’s can cause initial worsening of symptoms

258
Q

steps in cognitive behavior therapy (3)

A
  1. identify thought
  2. identify that it is distorted (unlikely)
  3. make thought more logical
259
Q

how long do panic attacks have to persist to be classified as panic attacks

A

1 month or more

260
Q

what percentage of population has panic disorder

261
Q

what two things are often comorbid with panic disorder

A
  1. major depressive disorder

2. substance dependence

262
Q

what percentage of individuals with panic disorder are treatment responsive

263
Q

how long out of the day does a person do their compulsions in ocd

A

more than an hour

264
Q

etiologies of OCD (3)

A
  1. genetics
  2. infections
  3. PANDAS - autoimmune
265
Q

treatments for OCD (pharm and therapy) (5)

A
  1. high dose SSRI/SNRI
  2. exposure therapy (virtual reality)
  3. systematic desensitization
  4. deep brain stim
  5. bilateral cingulotomy neurolosurgery
266
Q

where is the abducens nucleus in the tegmentum of the pons

A

just ventral to the 4th ventricle

267
Q

where is the facial motor nucleus to the abducens nucleus

A

just ventral and lateral to the abducens nucleus - the fibers from the facial motor nucleus wrap around the nucleus and form the facial colliculus (bump in 4th ventricle)

268
Q

where do the abducens fibers exit

A

just over pyramids

269
Q

where do facial motor nucleus fibers exit

A

lateral to the pyramids

270
Q

where is the trigeminal nucleus in the pons

A

sensory is lateral, motor is medial

271
Q

where do trigeminal nerve fibers exit

A

through transverse fibers, lateral to pyramids

272
Q

what is basis of cereral peduncles also called

A

crus cerebri

273
Q

what do you find in crus cerebri (3)

A

decsneding tracks of

  1. corticospinal
  2. corticobulbar
  3. corticopontine
274
Q

what cranial nerve nuclei will you find in midbrain

A

CN3 oculomotor and Edinger Westphal

CN4

275
Q

where si the oculomotor nuclei in midbrain

A

just ventral to cerebral aqueduct

276
Q

what nuclei (NON-CN nuclei) are also in midbrain

A
  1. red nucleus

3. substantia nigra

277
Q

superior colliculi controls relates to what sense

278
Q

inferior colliculi controls relates to what sense

279
Q

symptoms of lateral medullary syndrome- what nuclei/tracks are disrupted (7)

A
  1. vertigo (vestibular)
  2. coordination issues (cerebellar peducnles)
  3. dysphagia and dysarthria (n. ambiguus)
  4. glossopharyngeal
  5. vagal
  6. spinothalamic track (pain and temp sensation)
  7. descending sympathetic
280
Q

how long do you have to have symptoms for depressioin

A

at least 2 weeks

281
Q

what symptoms do you have to have for depression

A

5 of the following

  1. depressed mood
  2. loss of interest or pleasure
  3. weight loss or weight gain
  4. insomnia or hypersomnia
  5. psychomotor agitation/retardation
  6. loss of energy
  7. decreased concentration
  8. inappropriate guilt
  9. thoughts of death or suicide
282
Q

is anxiety episotic or chronic

283
Q

is depression episodic or chronic

284
Q

what do you see with depression with “mixed features” (2)

A

elevated mood

inflated self esteem

285
Q

what kind of sleep disturbances do you see with melancholic depression

A

early morning awakening

286
Q

what are atypical features in depression (4)

A

mood reactivity
increased apetite (Carbs)
hypersomnia
rejection sensitivity

287
Q

what cancer is specifically linked to depression

A

pancreatic

288
Q

difference between persistent depressive disorder, depressive personality disorder, and major depressive disorder

A

timecourse and severity

MDD - 5 symptoms for 2 weeks, episodic
PDD - 3 symptoms for 2 years
DPD - constant

289
Q

what is adjustive disorder iwth depressed mood vs MDD

A

in reaction to stressor - does not meet criteria for MDD

290
Q

what is double depression

A

coexistance of MDD and PDD (persistent depressive disorder)

291
Q

diathesis

A

genetic vulnerability

292
Q

what nuclei produce seratonin

A

raphe nuclei

293
Q

problems with neocortex will cause what symptom in depression

A

concentration

294
Q

problems with striatum (reward center) will cause what symptom in depression

A

lack of interest

295
Q

problems with amygdaloid body will cause what symptom in depression

296
Q

problems with the hypothalamus will cause what symptoms in depression

A

sleep and appetite

297
Q

problems with the hippocampus will cause what symptom in depression

A

memory issues

298
Q

what percent of depressed individuals will go into remission after initial treatment

A

30% (60% respond to a drug, but only 30% are made better just by that first treatment)

299
Q

what percentage of people will go into remission after dedicated longer term treatment

300
Q

how may neurons in the brain, and how many synapses do eac make

A

100 billion neurons

each make 1,000 synapses

301
Q

how many glia per neuron

A

about 1:1, if not less - but it differes in different areas - more glia in cerebral cortex, fewer in cerebellar cortex

302
Q

how many seconds after blood supply stops to the brain do we lose consciousness

A

10 seconds

303
Q

how many minutes after blood supply stops to brain does irreparable brain damage occur

304
Q

what is the function of the spines on the dendrites (2)

A
  1. termination sites of glutamatergic input (#s incrase for more synapse formation)
  2. sites of memory storage
305
Q

what is the function of the axon hillock (2)

A
  1. screens out cellular organelles like Nissl bodies that shouldn’t be in axon
  2. summates synaptic potentials from dendrites and soma
306
Q

what is the function of the initial segment of the axon (2)

A
  1. highest density of voltage-gated Na+ channels

2. thus, is the site of AP generation and propagation along the axon

307
Q

what does botulinum toxin do to neurons

A

cut the synaptic vesile release machinery (SNARE complex - all 3 components) which allows for vesicle docking and fusion

308
Q

what does Tetanus toxin do to neurons

A

cut synaptobrevin part of SNARE complex to inhibit neurotransmitter vesicle docking and fusion

309
Q

what is molecular mechanism of lambert-eaton

A

autoimmune destruction of Ca2+ channels (in response to antigen in small-cell lung carcinoma) - causes reduced Ca2+ entry in response to AP, decreased Ach release, muscle weakness

310
Q

what is the most common cause of neurodegeneration, generally speaking

A

failures in axon maintenance

311
Q

what are neurofilaments in axon responsible for

A

caliber of axon and thus AP conduction along axon

312
Q

what are microtubules in axon responsible for

A

polarity, morphology (shape), transportation and scaffolding

313
Q

what does fast anterograde transport use, and what does it transport (3)

A 
uses kinesin
transports:
1. transmitter vesicles
2. neurotransmitters (NE, serotonin, dopamine)
3. mitochondria
314
Q

what neurotransmitters are NOT transported via fast anterograde transport

A

glutamate, GABA and Ach (those are synthesized and recycled in axon terminals)

315
Q

what does slow anterograde transport use, and what does it transport (3)

A

mechanisms not well known (involves microtubles and neurofilaments)
transports:
1. cytoskeletal/cytoplasmic proteins
2. organelles
3. neurotransmitter synthesizing enzymes (for GABA and Ach)

316
Q

what does retrograde axonal transport use and what does it transport (3)

A 
uses dynein
transports:
1. aging organelles and protein waste for destruction
2. nerve growth factors
3. viruses and toxins
317
Q

what does Taxol (paclitaxel) do to axons

A

stabilizes the microtubule and blocks cell division, but also leads to axonal degeneration

318
Q

Defects in what cause Charcot-Marie-Tooth diseases (not just one thing)

A

tubulins, dynein, kinesin or other microtubule-associated molecules

319
Q

what protein is disrupted in Alzheimers

A

Tau - microtubule associated protein - normally stablizes microtubules and blocks cargo transport. when phosphorylated, cargo can pass. aggregates of tau in alzheimers causes tangles and disrupts the axons

320
Q

where is tau usually at higher concentrations along axons

A

at distale end because they are needed for regulation at synaptic terminals for cargo loading and unloading

321
Q

what protein is disrupted in Lewy Body dementia and parkinson’s

A

alpha-synuclein - transports membrane vesicles to axon terminals for neurotransmitter vesicle formation. Aggregates disrupt mitochondria transport along the axon, causing axonal degeneration

322
Q

examples of diseases caused by mutations in mitochondrial fusion genes (Mfn2 and OPA1) (2 known, 4 speculated)

A
  1. axon degeneration in Charcot-Marie Tooth type 2A
  2. AD optic nerve atrophy - retinal ganglion axon degeneration
  3. speculated in Parkinson’s alzheimers, huntington’s and ALS
323
Q

overexpression and accumulation of what proteins causes ALS

A
  1. tau

2. neurofilaments

324
Q

5-10% of ALS cases caused by what genetic mutation

A

missense mutation in superoxide dismutase (SOD) - antioxidant enzyme, making aggretation more likely and causing axonal aggregation

325
Q

what marker do most astrocytes express in the hippocampus

A

GFAP (glial fibrillary acidic protein) only a few do in the thalamus

326
Q

what protein is expressed in astrocytes in gray matter

A

gap junction protein connexin 30 to connect among astrocytes

327
Q

how do astrocytes interact with glutamate (and what enzymes/transporters are used) (2)

A

they clear the synaptic cleft of glutamate, preventing epilepsy.

  1. they uptake glutamate via glutamate transporters, convert glutamate to glutamine via GLUTAMINE SYNTHETASE, transfer glutamine out. glutamine then gets converted back to glutamate in presynaptic neuron terminal via GLUTAMINASE
  2. They also release glutamate (gliotransmitter) into presynaptic terminal to modulate modulate synaptic transmission
328
Q

how do astrocytes interact with GABA (and what enzymes/transporters are used)

A

GABA is taken up via GABA transporters, converted to Glu, then Gln, then Gln is transported out of astrocyte and into GABAergic terminal of neuron, where it is reconverted to GABA via GLUTAMIC ACID DECARBOXYLASE (GAD)

329
Q

relationship between astrocytes and glycogen

A

they store glycogen and provide energy (via lactate) to neurons when blood glucose is limited

330
Q

relationship between astrocytes and potassium (2)

A
  1. removes excess potassium so that the brain doesn’t get hyperexcited (epilepsy) or have excess glutamate (excitotoxicity)
  2. this release of K+ into arteriolar smooth muscles leads to dilation and increased bloodflow which make active brain regions seen on functional MRI
331
Q

how does brain get more glucose and oxygen (2)

A
  1. increased neuronal activity causes increased CO2 which increases calcium in astrocytes, leading to COX1 generation and release of prostaglandin PGE2 to relax pericytes and dilate blood vessels - allowing more glucose and oxygen to be delivered to active brain regions
  2. increased neuronal activity also causes nitric oxide release which increases arteriolar smooth muscles and pericyte relaxation
332
Q

how are reactive astrocytes double edged swords (3 good, 2 bad)

A

Good:

  1. fill in the space caused by injury
  2. promote neuronal survival around injury site via antioxidant, growth factor and glutamate uptake
  3. uses inflammation (IL-1, TNF alpha, prostaglandins) to activate microglia

BAD:

  1. scar inhibits axonal regeneration
  2. excessive microglia activation exacerbate brain tissue damage
333
Q

what type of cancer results from proliferative capacity of astrocytes - and which subtype especially

A

astrocytoma

glioblastoma multiforme (GBM) in frontal or temporal lobe)

334
Q

what causes neuronal damage and dementia in HIV patients

A

infected microglia which release a bunch of stuff like ROS that damage neurons and cytokines that activate astrocytes

335
Q

role of microglia in development

A

50% of neurons have to undergo programmed cell death in early postnatal life and their corpses must be cleared

336
Q

role of microglia in promoting neuronal cell survival

A

microglia secrete insulin-like growth factor (IGF-1) - neurons that express IGF receptors survive, those that don’t undergo apopotosis

337
Q

relationship between microglia and Alzheimers/Parkinson’s

A

microglia come in contact with the tangles of tau, beta-amyloid or alfa-synuclein, get activated, release cytokines etc that cause neuronal cell death/damage, which then promotes more microglia activation (perpetual cycle)

338
Q

microglia and OCD/autism

A

autism/schizophrenia: increased microglial density in prefrontal cortex

OCD: microglia-related cause of trichotillomania (hair pulling)

339
Q

diseases that attack myelin producing cells (2)

A

MS= oligodentroglia

Guillain Barre= Schwann cells

340
Q

learning new skills does what to neurons in white matter

A

increases myelination

341
Q

which neurotransmitters in brain are composed of biogenic amines (6)

A
  1. serotonin
  2. acetylcholine
  3. norepineprhine
  4. dopamine
  5. histamine
  6. epinephrine
342
Q

what are the catecholamines (3)

A
  1. epi
  2. norepi
  3. dopa
343
Q

neurotransmitter small molecule (amino acids) (4)

A

GABA
glutamate
aspartate
glycine

344
Q

large molecule (peptide) neurotransmitters (3)

A

opioids:
enkephalin
endorphin
dynorphin

345
Q

excitatory amino acid

346
Q

inhibitory amino acid

347
Q

which way do glutamate projections go

A

descending (from cortex down)

348
Q

huntington’s and amino acid in brain

A

you see neurotoxicity via a subtype of glutamate receptor

349
Q

too little GABA activity causes what disease processes (3)

A
  1. epilepsy
  2. anxiety
  3. huntingtons
350
Q

what direction do dopa projections go (and from what nucleus)

A

ascending (from nucleus accumbens and ventral tegmental)

351
Q

dopa cell body death seen in what disease process

A

Parkinsons

352
Q

dopa cell body hyperactivity seen in what

A

schizophrenia

353
Q

where are dopa cell bodies and projections located that are affected in parkinsons

A

“mesolimbic” - substantia nigra projecting to striatum

354
Q

where are dopa cell bodies and projections located that are affected in schizophrenia

A

ventral tegmental area projecting to nucleus accumbens

355
Q

dopa and addiction correlation

A

dopa projections to nucleus accumbens related to addiction

356
Q

what direction do Ach projections go (and from what nucleus)

A

ascending (from septal nuclei and nucleus basalis)

357
Q

is Ach excitatory or inhibitory in CNS

A

excitatory

358
Q

where do Ach fibers project to, and what brain functions are they involved in

A
  1. cortex (learning)

2. hippocampus and amygdala (memory)

359
Q

Ach neurons degenerate in what disease

A

Alzheimer’s

360
Q

what kind of drug do you avoid in elderly to avoid confusion

A

anticholinergic

361
Q

what kind of neurons increase in tone in parkinsons

A

cholinergic

362
Q

how does GABA get increased in parkinsons and what symptom does it cause

A

because Ach tone is increased (due to decreased dopa tone), GABA gets stiumated by Ach, which is inhibitory, and causes “frozen” motion in patient

363
Q

what direction do NE projections go (and from what nucleus)

A

ascend (from locus coeruleus)

364
Q

what areas do NE project to (3)

A
  1. cortex
  2. hippocampus
  3. cerebellum
365
Q

role of NE in CNS (3)

A
  1. attentiveness
  2. mood (target for antidepressants)
  3. withdrawal (hyperactive)
366
Q

what direction do serotonin projections go (and from what nucleus)

A

ascending (from raphe)

367
Q

what areas do serotonin project to (3)

A
  1. cortex
  2. hippocampus
  3. cerebellum
368
Q

what disease processes are treated with increasing serotonin (4)

A
  1. depression
  2. migraine
  3. anxiety
  4. sleep
369
Q

what direction do histamine projections go (and from what nucleus)

A

ascending (from tuberomamillary nucleus of hypthalamus)

370
Q

role of histamine in CNS (1)

A

wakefulness (antihistamines make you sleepy)

371
Q

when do the pharyngeal arches appear - what week

372
Q

what is week of pregnancy for embryological week 4 of development

A

6 weeks of pregnancy

373
Q

what bones make up the orbit (superior, lateral, and inferior walls)

A

frontal
temporal
maxillary

374
Q

what is opening between eyelids called

A

palpebral fissure

375
Q

function of tarsal glands

A

secrete lipids that prevent eye from sticking together. can become clogged

376
Q

function of tarsal plates (3)

A
  1. provide structure for eyelids
  2. secrete lipids that prevent eye from sticking together.
  3. site of muscle attachment (LPS)
377
Q

what is sensory info to partoid gland

A

somatic sensory from cervical plexus

378
Q

functional innervation to parotid (2)

A

parasymp pvia glossopharyngeal

symp from spinal cord

379
Q

3 SSRI prototypes

A
  1. fluoxetine
  2. escitalopram
  3. seteraline
380
Q

3 SSRI prototypes

A
  1. fluoxetine (prozac)
  2. escitalopram (lexapro)
  3. seteraline (zoloft)
381
Q

1 SNRI prototype

A

duloxetine (cymbalta)

382
Q

1 MAOI prototype

A

tranylcypromine

383
Q

antidepresant drug timecourse - when do adverse effects occur and when do mood changes occur

A

mood changes don’t occur until ~6 weeks

adverse effects happen pretty immediately

384
Q

mech of action of buproprion (and trade name)

A

wellbutrin - dopa reuptake inhibitor (DAT) and NET

385
Q

mech of action of mirtaxapine (and trade name)

A

remeron - autoreceptor antagonist - enhances NE release and seratnonin release

386
Q

what does serotonin get converted into and where

A

melatonin, in pineal gland

387
Q

does GABA stimulation relate to depression

388
Q

what are the benzo receptor agonists (2)

A

zolpidem

eszopiclone

389
Q

what is a benzo receptor antagonist (1)

A

flumazenil

390
Q

what is a melatonin congener (1)

391
Q

what drug is a 5-HT1a receptor agonist/ non-sedative anxioloytic

392
Q

what receptors do the Benzos and barbituates work at

393
Q

difference between sedatives and hyptonics

A

sedaives = calming. at high enough doses can produce sleep

hypnotics = sleep-inducing. some hypnotics are NOT sedative

394
Q

dose response of benzos vs barbituates

A

barbituates (and alcohol) have linear dose response - easier to cause coma and death with increased dosage

benzos plateau so it’s a lot harder to cause coma or death (have to combine with other sedatives to do so)

395
Q

what GABA receptor subtype do the anxiolytic drugs bind to

A

GABA - A, pentamer:

always has 2 alpha subunits and 3 other subunits (beta or gamma)

most common subsubtype is
alpha1 (2) beta2 (2) gamma1

396
Q

mech of action of barbituates (2)

A
  1. enhance duration of GABA-mediated chloride flux)
  2. at high doses DIRECTLY open GABA-A chloride channels

this leads to neuronal inhibition (via hyperpolarization of neuron) and suppression of glutamate transmission

397
Q

how many pharygeal arches, clefts, and pouches are there

A

6 arches, 5 clefts and pouches

398
Q

what are the embryoogic cell derivaties for the pharyngeal arches, clefts and pouches

A

mesoderm/mesenchyme arches
ectoderm clefts
endoderm pouches

399
Q

what are the cartilagenous and skeletal structures from first arch (2)

A

from MECKEL’S cartilage - makes malleus and incus

400
Q

main muscle from first arch

A

muscles of mastication

401
Q

nerve in first arch

A

trigeminal

402
Q

second arch AKA

403
Q

innervation of second arch

404
Q

cartillage of second, and what skeletal structures (4) and ligamentous structure (1)

A

REICHERT cartilage, turns into:

  1. stapes
  2. styloid process
  3. lesser cornu of hyoid bone
  4. upper part of body of hyoid

ligament:
1. stylohyoid ligament

405
Q

what muscles from second arch

A

muscles of facial expression

406
Q

what innervation of third arch

A

glossopharyngeal

407
Q

what muscle in third arch

A

stylopharyngeus

408
Q

what bone from third (2)

A

greater cornus of hyoid

lower part of body of hyoid

409
Q

4th and 5th arches - what cartilage

A

cartilages of larynx (becomes thyorid, cricoid etc. ALL cartilage)

410
Q

4th and 5th arches - what innervation

A
  1. superior laryngeal branch of vagus

2. reccurent laryngeal branch of vagus

411
Q

mandibulofacial dystotosis - what is the mechanism

A

lack of neural crest migration to 1st pharyngeal arch

412
Q

mandibulofacial dystotosis - symptoms and intelligence

A

craniofacial abnormalities and conductive hearing loss

- normal intelligence

413
Q

what does the first pharyngeal POUCH become (2)

A
  1. typanic or middle ear (lateral/distal part)

2. auditory tube (medial/proxila part)

414
Q

what does the first pharyngeal MEMBRANE become

A

typanic membrane

415
Q

what does first pharyngeal CLEFT become

A

external auditory meatus

416
Q

what does second parhyngeal POUCH become

A

medial becomes tonsillar fossa and surface of palatine tonsil

417
Q

what does third pharyngeal POUCH become (2)

A
  1. dorsal becomes INFERIOR parathyroids
  2. ventral becomes thymus

they both migrate caudally

418
Q

what does fourth pharyngeal POUCH become (2)

A
  1. dorsal becomes SUPERIOR parathyroids

2. ultimobranchial body becomes C-cells of thyroid

419
Q

which bones in skull are formed by endochondral ossificaton (4)

A
  1. ethmoid
  2. sphenoid
  3. lower occipital
  4. petrous temporal bone
420
Q

see a kid with frontal bossing, syndactyly

A

plagiocephay

421
Q

2 types of plagiocelphaly

A
  1. synostotic - premature fusion or failure to form

2. deformational - too many babies in uterus etc. sleeping on the back of yor head

422
Q

what is Apert syndrome and symptoms (5)

A

GOF mutation in osteoblasts in suture mesenchyme:

see:

  1. craniofacial abnormalities
  2. hearing/vision disturbances
  3. syndactlyly
  4. sweating and acne
  5. normal to delayed intelligence
423
Q

how does nose change at 4.5, 5, and 6 weeks

A 
4.5 = nasal placode (dent)
5 = nasal pit
6 = nasal pit with medial and lateral nasal prominences
424
Q

how does nose/face change at 7 weeks (2)

A
  1. medial prominences fuse and form upper lip,

2. nasolacrimal duct forms from fusion of lateral prominences and maxillary prominence

425
Q

how does face change at 10 weeks

A

fusion of palatine shelves and primary palate from

426
Q

what is fusion point of palate where a little opening remains

A

incisive foramen

427
Q

gender predominance for rates of cleft lip and palate

A

lip more common in girls

palate more common in boys

428
Q

what is smooth philtrum indicative of

A

fetal alcohol exposure

429
Q

what is number 1 cause of cleft lip and palate (genetically)

A

22q11 deletion syndrome (for example digeorge’s)

430
Q

superior tarsal innervated by what?

A

sympathetic innervation

431
Q

damage to superior cervical sympathetic ganglion causes what

A

Horner syndrome - partial ptosis - lack of innervation to superior tarsal

432
Q

parts of outer (Fibrous) layer of eye (2)

A
  1. sclera

2. cornea

433
Q

parts of middle (vascular) layer of eye (4)

A
  1. choroid (from retina to ciliary body)
  2. ciliary body (from choroid to iris)
  3. iris
  4. ciliary muscle/ciliaris (changes thickness of lens)
434
Q

what structure is at the apex of the orbit (relates to the extraocular muscles)

A

common tendinous ring

435
Q

what nerve structures travel outside of common tendinous ring

A

“little fairy tots”
lacrimal nerve
frontal nerve
trochlear nerve

436
Q

which eye muscles attach on atnerior half of eye

A

rectus muscles (medial, lateral, superior, inferior)

437
Q

which eye muscles attach on posterior half of eye

A

oblique muscles

438
Q

which muscle controls intorsion

A

superior oblique

439
Q

which muscle controls extorsion

A

inferior oblique

440
Q

branches of V1 in eye, providing sensory innervation

A
  1. frontal
  2. lacrimal
  3. nasociliary
441
Q

components of neurological exam from start to finish

A
  1. general
  2. CN
  3. motor
  4. sensory
  5. reflexes
442
Q

what is the parasymp ganglion by the parotid gland

443
Q

infection and stones of parotid gland called what

A

sialoadenitis

sialolithiasis

444
Q

what are the 5 branches of the facial nerve

A

Ten Zebras Bit My Cupcake:

Temporal
Zygomatic
Buccal
Marginal Mandibular
Cervical
445
Q

where does the facial nerve exit the skull - what foramen

A

stylomastoid foramen (on inferior skull by bottom of ear)

446
Q

what are the muscles innervated by facial nerve (4)

A
  1. facial expression muscles
  2. sylohyoid muscle
  3. posterior belly of digastric
  4. tensor tympani
447
Q

what are the major muscles of facial expression (5)

A
  1. orbicularis oculi
  2. orbicularis oris
  3. occipitofrontalis
  4. buccinator
  5. platysma
448
Q

portions of orbicularis oculi (3)

A
  1. orbital (voluntary)
  2. palpebral (involuntary)
  3. lacrimal - tear movement
449
Q

where/how is damage caused by bells palsy

A

virally caused compression of facial nerve as it leaves sylomastoid foramen

450
Q

what fissure in skull does opthalamic branch (V1) go through

A

superior orbital fissure

451
Q

what foramen in skull does V2 go through

452
Q

what foremen in skull does V3 go through

453
Q

what is the branch of V3 that exits on chin

A

mental nerve - from mental foramen

454
Q

what is the branch of V3 that exits by temple

A

auriculotemporal nerve (innervates parotid parasymp)

455
Q

what main artery supplies the face and what is it a branch off of

A

facial artery - branch of the external carotid

456
Q

what artery is associated with parotid gland, and what artery does it come from

A

superficial temporal artery, which is a continuation of the external carotid

457
Q

what are 2 first branches off of the facial artery and what is facial artery called after nose

A
  1. inferior labial
  2. superior labial

facial becomes angular artery at hose

458
Q

what veins drain face (2) and what do they become

A

facial vein and retromandibular vein, become internal jugular

459
Q

what is “danger triangle”

A

around your nose - if an infection here happens it can drain into cavernous sinus and cause issues

460
Q

gradient of SSRI drug-drug interactions - most to least

A

all inhibit P450 enzymes (CYP2D6), so can have drug-drug

fluoxetine>sertraline>escitalopram

461
Q

fluoxetine and cancer tx relationship

A

fluoxetine decreases efficacy of tamoxifen (tx for breast cancer)

462
Q

adverse effects of SSRI (6)

A
  1. CNS stimulation (insomnia, headache)
  2. sexual dysfunction
  3. GI tract - nausea, diarrhea
  4. platelet - bleeds
  5. prolong QT - excitalopram
  6. serotonin syndrome (usually when in combo with TCA or MAOI)
463
Q

tolerance and adverse effects of SSRIs

A

all wane with time except for sexual dysfunction

464
Q

what transporters do SNRIs block

A

NET and SERT

465
Q

Adverse effects of duloxetine

A
  1. discontinuation syndrome because they’re shorter acting
  2. CNS stim
  3. sexual dysfunction
  4. increase BP at high doses (alpha 1)
466
Q

what is unique indication for duloxetine

A

neuropathic pain

467
Q

mech of action of TCAs

A

block NET and SERT, but block other neurotransmitters too

468
Q

difference between tertiary and secondary amines (TCAs) and where does amitryptyline fit

A

secondary amines block NET preferentially
tertiary amines block SERT preferentially

amitriptyline is a tertiary amine, but gets metabolized to noretryptyline which is a secondary amine

469
Q

cardiac adverse effects of TCAs (3)

A
  1. tachycardia from NET block
  2. conduction block from Ach block
  3. arrhytmias from non-receptor mechanism (can cause death in overdose)
470
Q

which antidepressive meds cause weight gain

A

TCAs, mirtazapine

471
Q

which antidepressive meds are sedative

A

TCAs (antihistaminergic effect)

472
Q

which antidepressive meds cause dry mouth and constipation

A

TCAs (anticholinergic effect)

473
Q

why is halflife of MAOIs so long, and what is a potential consequence of that

A

because they bind irreversibly to MAO- so you have to wait for the body to synthesize more.

can cause seratonin syndrome

474
Q

drug interactions with MAOIs

A
  1. alpha 1 agonist phenylephrine (cold med) cause HTN crisis due to increased NE
  2. sympathomimetics pseudoephedrine (cold med) or tyramine foods (wine and cheese) will also cause HTN crisis
  3. dextromethorphan (cough med), meperidine will cause seratonin syndrome
475
Q

timing of MAOI admin changes, and why is that important

A

give more than 2 weeks after stopping MAOI to give a new drug, and at least 2 weeks after stopping SSRI/SNRI/TCAs to start MAOI

because serotonin syndrome

476
Q

tyramine and MAOIs - what’s the risk

A

MAOI block tyramine breakdown. tyramine buildup causes enhanced NE release (hypertensive crisis)

477
Q

unique use of bupropion

A

smoking cessation (antagonist at nicotinic receptor)

478
Q

adverse effect of bupropion (2)

A
  1. CNS stim - ANXIETY

2. seizures at high doses

479
Q

mirtazapine side effects (3)

A
  1. sedation
  2. weight gain
  3. posteurl hypotension
480
Q

which anti-depressive drugs don’t have sexual side effects

A

burpropion and mirtazapine

481
Q

which is best choice of antidepressive drug in pregnancy

A

amitriptyline

482
Q

which is best choice of antidepressive drug in childhood (8-12)

A

fluoxetine (only FDA approved)

483
Q

which are best choices of antidepressive drug in adolescents (2)

A

escitalopram and fluoxetine

484
Q

what are the mood stabilizing maintenance drugs used to treat bipolar disorder (4)

A
  1. lithium
  2. olanzapine
  3. valproate
  4. lamotrigine
485
Q

what drugs would you use for ACUTE manic emergency (3)

A
  1. olanzapine (antypsychotic)
  2. benzos
  3. sodiul valproate (anticonvulsant)

lithium is too slow

486
Q

what mood stabilizer do you need to monitor when adjusting renal clearance

A

lithium - does what sodium does

487
Q

adverse effects of lithium (3)

A
  1. tremor (treat with beta-blockers)
  2. renal - polydipsia, polyuria or nephrogenic diabetes insipidus
  3. fetal cardiac anomalies
488
Q

what mood stabilizer do you use in pregnancy

A

lamotrigine

489
Q

anticonvulsants that are used in treatment of bipolar disorder

A
  1. lamotrigine

2. valproic acid (depakote)

490
Q

side effect of lamotrigine

A

stevens johnson syndrome

491
Q

adverse effect of barbituates

A

linear dose-response - can lead to coma and death due to respiratory depression

492
Q

drug interactions of barbituates (2)

A
  1. ethanol - additive CNS depression

2. induce CYP enzymes

493
Q

benzos to know (5)

A
  1. alprazolam (xanax)
  2. clonaxepam (klonapin)
  3. diazepam (valium)
  4. midaxolam (versed)
  5. triazolam (halcion)
494
Q

benzos mech of action

A

increase frequency of chloride channel opening

no direct effect on chloride channel (won’t work without GABA present)

495
Q

receptor specificity for benzos

A

benzos will only bind on GABA-A receptors that have alpha (1,2,3 or 5) and a gamma subunit

496
Q

alpha 1 subunit stimulation effect

A

sedation (zolpidem)

497
Q

alpha 2/3 subunit stiumation effect

A

anxiolysis

498
Q

alpha 5 subunit stimulation efect

A

cognitive impairmnt

499
Q

what disease is a contraindication for benzos

A

obstructive sleep apnea

500
Q

why don’t you use benzos chronically

A

tolerance, abuse and withdrawal (esp with alprazolam which has short halflife)

501
Q

which benzo is used in sleep disroders (1)

502
Q

which benzos are used in epilepsy (2)

A

clonazepam and diazepam

503
Q

which benzo is used in anesthesia (1)

504
Q

whcih benzos are long acting vs medium vs short acting

A

long: diazepam, clonazepam
medium: alprazolam
short: triazolam, midazolam

505
Q

flumazenil mech of action

A

competititve antagonist for benzo site on GABAa - can reverse effects of BENZOS to reverse overdose

506
Q

what do you give buspirone to treat

A

generalized anxiety - not useful in panic disorders

507
Q

buspirone and admin timing

A

may take a few weeks to start working

508
Q

ramelteon mech of action and use

A

binds melatonin receptors - long term use for sleep aid

509
Q

benzo receptor agonists mech of action

A

bind to GABA-a receptors with alpha1 subunit

510
Q

benzo receptor agonist use and benefit

A

sleep aid - don’t affect sleep stages (don’t have day after sedation

511
Q

examples of benzo receptor agonists (2)

A

zolpidem (ambien)

eszopiclone (lunesta)

Brain and Behavior (6 decks)

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