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Neuro/Behavior I > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Embryology of the Thalamus

A

Forebrain (prosencephalon) –> diencephalon –> Thalamus

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2
Q

The Thalamus consists of:

A
  • Thalamus
  • Subthalamus
    -Hypothalamus
  • Pineal gland
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3
Q

Interthalamic adhesion

A

connects the two halves of the thalamus, however no communication/axons between the two

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4
Q

Relay Nuclei

A

Thalamus nuclei that relays specific sensory, motor, or limbic information to specific regions of the cortex

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5
Q

Association nuclei

A

Thalamus nuclei that relays information to/from multiple regions of cortex

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6
Q

Intralaminar nuclei

A

Thalamus nuclei that projects to cortex and Basal Ganglia
- Encased in the internal medullary lamina
- Example: centromedian nucleus

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7
Q

Thalamic Reticular nucleus

A
  • gates the output of the thalamus to cerebral cortex
  • Does not have direct connection to cortex
  • GABAergic terminals inhibit thalamic neurons to reduce the flow of information when it is not needed or beneficial
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8
Q

Anterior nucleus of the relay nuclei

A

relaying information to the Limbic cortex –> cingulate gyrus

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9
Q

Ventral lateral/anterior nucleus of the relay nuclei

A

relaying information to the motor cortex

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10
Q

Ventral posterior lateral/medial nucleus of the relay nuclei

A

relaying information to the somatosensory cortex

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11
Q

Medial geniculate nucleus of the relay nuclei

A

relaying information to the auditory cortex

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12
Q

Lateral geniculate nucleus of the relay nuclei

A

relaying information to the visual cortex

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13
Q

Association nuclei

A
  • inputs from and outputs to association cortex
  • Medial dorsal nucleus: prefrontal association cortex (From PFC–>PFC)
  • Pulvinar nucleus: parietal/occipital/temporal –> association cortex (Large, off the back of the Thalamus
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14
Q

Thalamic cortical projections are:

A

ipsilateral (NEVER contralateral)

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15
Q

Internal capsule

A
  • a superhighway of axons entering and exiting the cortex
  • Axons ascend and descend to and from the Thalamus/cortex here
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16
Q

Thalamic blood supply: Medial thalamus

A

Thalamosubthalamic (paramedian thalamic) artery

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17
Q

Thalamic blood supply: Anterior thalamus

A

Tuberothalamic (polar) artery

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18
Q

Thalamic blood supply: Ventrolateral thalamus

A

Inferolateral (Thalamogeniculate) artery

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19
Q

Thalamic blood supply: Posterior thalamus (pulvinar nucleus)

A

Lateral posterior choroidal artery

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20
Q

Lesions causing thalamic stroke

A
  • ex. small: VPL/VPM: acute paresthesia, chronic spontaneous pain
  • ex. large: potentially including the internal capsule: signs of upper motor neuron lesion, positive Babinski sign
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21
Q

Very large thalamic lesion: Dejerine-Roussy Syndrome

A

A condition of central neuropathic pain caused by thalamic stroke. Characterized by severe, burning, sharp, and/or stabbing pain involving the areas affected by stroke, and motor symptoms related to loss of cerebellar input to thalamus. Occurs due to damage to the ventral posterolateral nucleus, which relays sensory information from the lateral spinothalamic tract. Also known as “Thalamic pain Syndrome”

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22
Q

What is the energy budget of the brain?

A
  • Synaptic transmission (44%)
  • Housekeeping (axoplasmic transport (25%)
  • Action potential (16%)
  • Resting potential (15%)
  • Neurotransmitter recycling (4%)
  • Ca2+ entry and vesicle recycling (3%)
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23
Q

What is the energy used for in the brain?

A

Function activity: Somatosensory system, movement and motor control, cognitive functions, homeostatic regulation– particularly from cellular signaling and ion pumping

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24
Q

Major pathways for energy metabolism in the brain

A

Neurometabolic coupling- brain work
- Synapses, axonal transport, nodes of ranvier

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25
Q

Glycogen in the brain

A

Stored within astrocytes ONLY, only 1% of glycogen storage in the body. Also used in hypoxia and cofactor deficiency situations

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26
Q

Global brain metabolism and how its measured

A

Cerebral metabolic rate (CMR = (Arterial-Venous) Blood flow/Weight (g)

A-V = (+) = consumed
A-V = (-) = Produced
CMR units: moles/g/min

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27
Q

For each mole of glucose consumed by the brain, how much is converted to lactate?

A
  • A small amount in normal differentiated cells
  • The majority in tumor cells of highly proliferative cells
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28
Q

Warburg effect

A

Excessive glycolysis in the presence of O2 by tumor cells or highly proliferative cells because it is faster than mitochondrial respiration. The mechanism is thought to promote growth, survival, and proliferation of cancer cells.

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29
Q

Astrocyte-Neuron Lactate Shuttle

A

The ANLS operates under normal physiological conditions with astrocytes responding to glutamatergic activation (increased brain activity) by increasing their rate of glucose utilization and release of lactate in the extracellular space, making the lactate available for neurons to sustain their energy demands, and to replenish the neurotransmitter pool of glutamate and completes the glutamate–glutamine cycle

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30
Q

How is energy produced in the brain?

A

1.) with oxygen, mitochondrial respiration ( electron transport chain)
2.) glycolysis / TCA cycle
3.) Glycogen storages (rare, emergent, only lasts for minutes before depletion)
4.) Ribose PPP– more common in babies (5-7%) compared to adults (~2%)
5.) Ketone body production (neonates because milk=fat, fasting, keto diet, heavy exercise)

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31
Q

Regional metabolism theory (Sokoloff method/ 2-DG)

A

At the occipital lobe, glucose metabolism was measured by injecting 2-DG into monkeys.
Both eyes open: Grey matter using glucose
Both eyes closed: No firing, no use of glucose
One eye open: Zebra pattern, half the occipital lobe space metabolizing glucose

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32
Q

FDG PET scan

A

fluorodeoxyglucose (FDG)-positron emission tomography (PET). The role of this procedure is to detect metabolically active malignant lesions by measuring glucose metabolism (Malignancy cells have a higher rate)

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33
Q

CMRG and CMRO2 in different situations

A

Epilepsy: CMRG increase, CMRO2 increase

Drowning: CMRG increase, CMRO2 decrease

Anesthesia: CMRG decrease, CMRO2 decrease

Cardiac Arrest: CMRG increase (glycogen) then decrease, CMRO2 decrease –> Post CA sees increase in both

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34
Q

Oxidation of Glucose equations:

A

1 glucose + 6O2 = 6CO2 + 6H2O

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35
Q

Why does the brain use more glucose than needed for oxidation?

A

-additional for astrocyte glycogen storage
-additional for production of NTs (glutamate, etc)

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36
Q

Why is 2-DG used to understand glucose metabolism?

A

2-DG is transported into the cells through glucose transporters and phosphorylated by hexokinase to Gluc-6-P without further processing. Therefore, it can be used as a radioactive marker for uptake

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37
Q

Cranial nerves and where they arise from

A
  1. olfactory, telencephalon
  2. optic, diencephalon
  3. oculomotor, midbrain
  4. trochlear, midbrain
  5. trigeminal, pons
  6. Abducens, pons
  7. Facial, pons
  8. vestibulocochlear, medulla
  9. glossopharyngeal, medulla
  10. vagus, medulla
  11. spinal accessory, spinal cord
  12. hypoglossal, medulla
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38
Q

Pathway of the Facial nerve, CN7

A

Fibers leave from the pons–> internal acoustic meatus–> stylomastoid foramen–> lateral aspect of the face

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39
Q

Motor/sensory function of facial nerve CN7

A

Motor: facial expression, transmittal of autonomic impulses to lacrimal and salivary glands
Sensory: taste from the anterior 2/3 of the tongue

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40
Q

Facial nerve motor nuclei in the pons (SVE): CN7

A

as the motor fibers of the facial nerve loop posteriorly over the abducens nerve nucleus (facial colliculi) in the fourth ventricle that controls the muscles of facial expression

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41
Q

Superficial salivary nucleus (GVE): CN7

A

next to facial nucleus, supplies secremotor parasympathetic fibers as nervus intermedius, and innervates salivary glands (Submandibular, sublingual)

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42
Q

Nucleus of solitary tract (SVA): CN7

A

lateral to the dorsal nucleus of the vagus nerve, supplies taste fibers that eventually end up in the chorda tympani (anterior 2/3 of tongue). Fibers travel with nervus intermedius

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43
Q

Spinal nucleus of the trigeminal nerve (GSA): CN7, CN10

A

somatic sensation to part of the skin, external ear canal, and certain parts of the throat

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44
Q

Bell’s Palsy

A

temporary weakness or paralysis of the muscles of the face when cranial nerve 7 becomes inflamed, swollen, or compressed. Symptoms include: sudden weakness of half of the face, drooping/stiffness. Can be from rxn to viral infection and usually resolves on its own

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45
Q

Cranial nerve 9: glossopharyngeal

A
  • Fibers emerge from medulla, and leave via the jugular foramen
  • Motor: innervates tongue, pharynx, parotid salivary gland
  • Sensory: Taste and general sensory impulses from the tongue and pharynx
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46
Q

Nucleus of the solitary tract (SVA) CN9

A

Taste of posterior 1/3 of the tongue

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47
Q

Nucleus of the solitary tract (GVA): CN9

A

Innervates the oropharynx. carotid body and sinus, middle ear cavity, and eustachian tube

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48
Q

Nucleus ambiguous (SVE): CN9

A

Innervates the stylopharyngeus muscle of the pharynx

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49
Q

Inferior salivary nucleus (GVE): CN9

A

Provides parasympathetic innervation to the parotid gland

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50
Q

Glossopharyngeal nerve (CN9) injury

A
  1. Loss of gag reflex (pharyngeal reflex)
  2. hypersensitive carotid sinus reflex (Syncope)
  3. Loss of general sensation in the oropharynx
  4. loss of taste in the posterior 1/3 of the tongue
  5. Glossopharyngeal neualgia
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51
Q

Glossopharyngeal neuralgia

A

extreme pain in the back of the throat, tongue, and/or ear. Attacks of intense. electric shock-like pain can occur randomly or with swallowing. May be from a blood vessel compressing the nerve inside the skull

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52
Q

Vagus nerve: CN10

A
  • Only cranial nerve that extends beyond the head and neck
  • Fibers emerge from the medulla via the jugular foramen
  • Motor: parasympathetic fibers to the heart, lungs, and visceral organs
  • Sensory: taste
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53
Q

Nucleus of the solitary tract (GVA): CN10

A

Visceral sensation information for the larynx. esophagus, lungs, trachea, heart, and most of the digestive tract

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54
Q

Nucleus of the solitary tract (SVA): CN10

A

A small role in the sensation of taste near the root of the tongue

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55
Q

Nucleus ambiguus tract (SVE): CN10

A

Stimulating muscles in the pharynx, larynx, and soft palate (motor)

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56
Q

Dorsal nucleus of the vagus nerve (GVE)

A

stimulating muscles in the heart, lowers resting heart rate, stimulates involuntary contractions in the digestive tract (stomach, esophagus, and intestines) allowing food to move through the tract.

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57
Q

Vagus nerve lesion

A
  • ipsilateral paralysis of the soft palate, pharynx, larynx, muscles
  • Dysphonia, Dyspnea. dysarthria, dysphagia
  • inability to raise the palate
  • loss of gag reflex (efferent limb)
  • inability to generate the reflex upon touching the lateral pharyngeal wall
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58
Q

Paralysis of muscles with a resultant loss of the ability to speak could indicate damage to what nerve?

A

Vagus nerve (CN10)

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59
Q

The vagus nerve regulates major elements of which part of the nervous system?

A

Parasympathetic nervous system

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60
Q

The four nuclei connected to the vagus nerve:

A

1.) Dorsal nucleus of vagus (GVE)
2.) Nucleus ambiguus (main motor of vagus-branchial)
3.) Tractus solitarius (GA fibers)
4.) Spinal nucleus of CN5 (SA fibers)

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61
Q

Loss of somatic sensation over the anterior 2/3 of the tongue indicates damage to:

A

Lingual branch of mandibular nerve of CN5

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62
Q

CN7 nerve supplies

A

Muscles of facial expression

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63
Q

What nerve affects heart rate?

A

Vagus nerve

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64
Q

Homeostasis

A

The state of a steady internal environment maintained by living systems

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65
Q

Three ways homeostasis is maintained:

A

1.) Structural: physical feature changes, long term
2.) Functional: metabolism changes, fast change
3.) Behavioral: actions and interactions, immediate change

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66
Q

Feedback mechanisms

A

general mechanisms of nervous or hormonal regulation in animals

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67
Q

Stimulus

A

the change from ideal or resting conditions

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68
Q

Receptor

A

the cells or tissue which detects the change due to the stimulus

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69
Q

Relay

A

the transmission of the message from stimulus –> brain (effector) via nerves, hormones, or both

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70
Q

Feedback

A

The consequences of the response on the stimulus.
- Positive: when the response enhances the original stimulus
- Negative: when the response diminishes the original stimulus (back to homeostasis)

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71
Q

Homeostasis three components that interact

A

Receptor –> Integrator –> effector –> response (fed back to the receptor, positive or negative)

Example: Nerve ending in skin –> brain –> muscle/gland

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72
Q

Example of negative feedback

A

Eat carbs (stimulus) –> increase in glucose –> increase in insulin –> decrease in glucose

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73
Q

Example of positive feedback

A

(less common)

Baby suckles –> increase hormone in mom –> increase milk release

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74
Q

Somatic nervous system

A
  • sensory and motor neurons
  • voluntary ( cerebral cortex)
  • one neuron pathway
  • Acetylcholine
  • effectors: Skeletal muscles
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75
Q

Autonomic nervous system

A
  • sensory
  • involuntary (limbic, hypothalamus)
  • two neurons pathway (autonomic ganglion)
  • pre-acetylcholine
  • post-sympathetic: norepinephrine (except sweat)
  • post-parasympathetic: acetylcholine (except adrenal)
  • Effectors: smooth muscle, cardiac, glands
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76
Q

Brain involvement of ANS

A

Afferent input (GVA) –> Limbic system, hypothalamus, reticular formation, spinal level –> ANS pheripheral changes

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77
Q

Sympathetic nervous system

A
  • fight or flight
  • thoracolumbar (T1-L2)
  • From spinal cord
  • short preganglionic and long post-ganglionic
  • global responses
  • postganglionic transmitter: NE
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78
Q

Parasympathetic nervous system

A
  • rest and digest
  • craniosacral (CN3, 7, 9, 10, S2-4)
  • From medulla
  • long preganglionic and short post-ganglionic
  • discrete/local responses
  • postganglionic transmitter: acetylcholine
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79
Q

Effects of activation of SNS

A
  • increased heart rate
  • increased sweating
  • dilates pupils
  • inhibits GI movement
  • closes sphincters
  • diverts blood from skin and GI tract to skeletal muscles
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80
Q

Effects of activation of PSNS

A
  • digestion and GI tract peristalsis
  • slows heart rate
  • constricts pupils
  • empties bladder
  • relaxes sphincters
  • mediates genital erection
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81
Q

Mechanisms of thermoregulation

A

1.) afferent sensing
2.) central control
3.) efferent responses
– hypothalamus is the central controller of thermoregulation

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82
Q

Regulation of blood pressure

A

Baroreceptors: act via the brain to influence the nervous system and endocrine systems. Detects high pressure in arterial zones, and low pressure in in veins.

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83
Q

Renin-angiotensin system:

A

results in an increase in blood volume which results in an increased cardiac output by the Frank-Starling law of the heart, and in turn increases arterial blood pressure

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84
Q

Aldosterone release:

A

releases from adrenal cortex in response to angiotensin II or high serum potassium levels to stimulate sodium retention and potassium excretion by kidneys. (increase fluid retention)

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85
Q

Regulation of respiratory system

A

parasympathetic: vagus nerve. Responsible for bronchoconstriction, mucus secretion, and bronchial vasodilation mediated by muscarinic acetylcholine (M2 and M3) receptors.
sympathetic: symp trunk of upper thoracic and cervical ganglia. Responsible for bronchodilation mediated by beta2-andrenergic receptors

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86
Q

H1-receptors

A

mediate the bronchoconstrictive effect of histamine and increase vascular permeability, which leads to plamsa exudation. Present in T cells, B cells, monocytes, lymphocytes– pro-inflammatory effects

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87
Q

Neural regulation of the bladder

A

parasympathetic: contractions and bladder emptying, (S2-S4)
Sympathetic: internal urethral sphincter closing, (T10-L2)
– voluntary control of the external sphincter mediated by alpha-motor neurons of the ventral horn in (S2-S4)

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88
Q

Central governance of bladder regulation

A

stems from the rostral pons

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89
Q

Located on target organs, when stimulates can cause an increase in the force of contraction of the heart, increase heart rate, and bronchial dilation

A

beta-adrenergic receptors

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90
Q

Adult derivative of pharyngeal groove

A

I: External ear/external auditory meatus
II III IV: cervical sinus

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91
Q

Adult derivatives of pharyngeal pouch and lining structures

A

I: middle ear auditory tube
II: supratonsillar fossa
III: thymus, inferior parathyroid gland
IV: superior parathyroid gland, post-branchial body

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92
Q

branchial grooves

A

First groove: persists as the external acoustic meatus
Subsequent grooves: obliterated with the overgrowth of arch 2 and the closure of the cervical sinus

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93
Q

Branchial cyst

A

spherical or elongated cysts that are remnants of 2nd pharyngeal groove (often associated with branchial structures), developing along the anterior border of sternocleidomastoid muscle

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94
Q

Branchial sinuses

A

openings along the anterior border of SCM muscles due to failure of 2nd pharyngeal groove and cervical sinus to obliterate

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95
Q

Branchial fistulas

A

canal opening internally into tonsillar sinus and externally onto side of neck, resulting from persistence of 2nd pharyngeal groove and pouch

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96
Q

Branchial Vestiges

A

cartilaginous or bony remnants of branchial arch cartilages which do not fully transform/disappear (typically found anterior to the inferior third of SCM muscle)

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97
Q

In development, the midline of the face begins:

A

Laterally

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98
Q

Thyroid development

A
  • thyroid begins in the floor of the pharynx
  • descends via the thyroglossal duct formed via the thyroid diverticulum
  • passes anterior to the hyoid
  • Remains connected to the tongue via thyroglossal duct during development, and then obliterates before birth
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99
Q

1st branchial cleft anomaly: type I

A
  • Duplication of the external ear canal, lined by squamous epithelium
  • runs parallel to ear canal and has a pit/fistula which terminates in the post-auricular or pre-tragal regions
  • recurrent parotiditis
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100
Q

1st branchial cleft anomaly: type II

A
  • between angle of mandible and external ear canal
  • crosses mandible–> through parotid–> terminates at nearby junction of EAC
    -cyst or opening in the neck superior to hyoid bone– deep, lateral, or between branches of nerve (CN7)
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101
Q

A neck mass in adults >50 years old

A

presumed malignant until proven otherwise. Biopsy because HPV+ oropharynx cancers look similar to branchial cleft cyst

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102
Q

2nd branchial cleft anomaly

A
  • most common (>90%)
  • 2nd arch forms hyoid
    -2nd pouch becomes palatine tonsil and supratonsillar fossa
  • begin in neck, travel between internal and external carotid, over CN 9, 12, and end at supratonsillar fossa
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103
Q

3rd branchial cleft anomaly

A
  • neck–> behind internal carotid–> over Cn12–> through superior pole of thyroid–> superior to superior laryngeal nerve–> pierce thyrohyoid membrane–> enters piriform sinus
  • Cysts occur anywhere along this tract
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104
Q

4th branchial cleft anomaly

A
  • RARE, presents as recurrent left sided acute suppurative thyroiditis or recurrent cervical abscess
  • low in neck–> thyroid gland–> around thyroid cartilage ala–> enter piriform sinus and apex
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105
Q

Treacher Collins syndrome

A
  • autosomal dominant, TCOF1 in 80%
  • features include downslanting eyes, underdeveloped midface, small ears, hard time breathing, hearing loss in 50%
  • normal intelligence
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106
Q

Goldenhar syndrome

A

-affects 1st and 2nd arch
- features include: facial asymmetry, microtia/anotia/hearing loss, facial weakness, cleft lip/palate, dental abnormalities, eye cancer/malformations
- may be associated with intellectual disability and many other physical malformations

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107
Q

Moebius syndrome

A
  • weakness or paralysis of CN6 and 7
  • unilateral or bilateral
  • mask-like face (doesn’t move) and excessive head movements
  • facial skeleton is normal
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108
Q

Pierre-Robin sequence

A
  • underdeveloped jaw–> retrodisplacement of the tongue (glossoptosis)–> u-shaped cleft palate
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109
Q

Cleft lip and palate

A
  • maxillary prominences do not fuse in the 4th-6th week of development
  • risk factors: smoking, diabetes, medications (topamax, valproic acid), and genetics
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110
Q

22q deletion syndrome (AKA DiGeorge or Velocardiofacial syndrome)

A
  • small deletion of chromosome 22 at 11.2
  • failure of neural crest cell migration into arches –> 3rd and 4th pouch failure (no thymus or parathyroid)
  • many symptoms associated, slightly dysmorphic in appearance
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111
Q

Thyroglossal duct cyst

A
  • 3rd and 4th arches, can develop anywhere in the neck when thyroid is descending
  • most common midline neck mass, presenting at any age either randomly or after URI
  • Sistrunk procedure (remove middle hyoid bone) required to prevent recurrence
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112
Q

Lingual thyroid

A
  • failure of thyroid to descend in embryogenesis, resulting in difficultly breathing in babies, especially on their back
  • most common ectopic location: base of the tongue (90%), others: cervical lymph nodes, submandibular glands, trachea
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113
Q

Ankyloglossia (tongue tie)

A
  • failure of involution, tongue remains attached to the bottom of the mouth
  • presents as failure to latch, heart-shaped tongue appearance, speech impediments
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114
Q

Branches of the superior vena cava v

A
  • internal jugular
  • subclavian
  • right and left brachiocephalic
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115
Q

Branches of aortic a arch

A
  • brachiocephalic trunk
  • left common carotid
  • left subclavian
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116
Q

Thoracic outlet syndrome

A

Space between clavicle and 1st rib, compression of artieries, veins, and nerves in the area typically causing weakness and tingling in the arm and fingers

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117
Q

Branches of the thyrocervical trunk

A
  • transverse cervical
  • suprascapular
  • inferior thyroid
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118
Q

thyroidea ima artery

A

artery to midline of the thyroid (esp. when there is a pyramidal lobe) that can cause danger for tracheotomy or cricothyrotomy

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119
Q

Ludwig’s Angina

A
  • submandibular/ submental infection stemming from rapidly spreading cellulitis often from tooth abscess of M2 or M3 whose roots reach below the mylohyoid line
  • Symptoms: neck mass, swelling over left mandibular space, trismus (difficulty opening mouth)
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120
Q

Spinal accessory nerve (CN11)

A
  • purely motor nerve formed by the confluence of LMNs from C1-C5
  • originates from spinal cord and travels through foramen magnum and jugular foramen
  • motor innervation to upper trapezius (contralateral) and SCM (ipsilateral) descending within the CORTICOSPINAL tract
  • accessory nucleus located in the gray matter of the ventral horn of the spinal cord
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121
Q

Cranial branch of CN 11, spinal accessory nerve

A
  • smaller branch that exits from the nucleus ambiguus in the medulla
  • briefly joins spinal accessory and exits jugular foramen
  • joins vagus nerve to create pharyngeal plexus for CN9/10
    -considered to be a part of CN10
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122
Q

Accessory nucleus (CN11) is present in

A

C1-C5/6, approximately in line with nucleus ambiguus in the medulla

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123
Q

Jugular foramen

A
  • formed by the jxn of temporal and occipital bones
  • holds inferior petrosal sinuses, jugular bulb, and CN 9, 10, 11
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124
Q

Peripheral accessory nerve

A

Exits the jugular foramen and goes over the transverse process of C1
- 80% of the time it travels superficially to the IJV
- travels posterolaterally to enter the SCM on its deep surface, remaining fiber pass through posterior triangle to the anterior border of the trap

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125
Q

Erb’s point

A

Point along the posterior SCM at the jxn of the lower 2/3 and upper 1/3 where many sensory nerves exit – important surgical landmark to identify CN11 easily

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126
Q

SCM

A
  • extends from the mastoid process of the temporal bone to the sternum (sternal head) and clavicle (clavicular head)
  • responsible for rotating the head to the OPPOSITE, flexion and extension of the neck
  • Gatekeeper to the neck
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127
Q

Trapezius muscle

A
  • elevates, retracts, and rotates scapula
  • CN11 innervates upper fibers, C3/C4 rootlets innervate the rest
  • allows for shrugging and abduction of the arm above 90 degrees
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128
Q

Hypoglossal nerve (CN12)

A
  • purely somatic motor, providing innervation to genioglossus, hyoglossus, styloglossus
  • exits at the level of the medulla between the olive and pyramid
  • innervation to CN12 nuclei is CORTICOBULBAR tract, and bilateral
    -EXCEPTION: genioglossus muscles receives contralateral innervation only
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129
Q

Genioglossus

A

Extrinsic muscle that protrudes tongue: contralateral innervation from CN12

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130
Q

Styloglossus

A

extrinsic muscle that elevates and retracts the tongue: innervation from CN12 bilaterally

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131
Q

Hyoglossus

A

Extrinsic muscle that depresses and retracts the tongue: innervation from CN12 bilaterally

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132
Q

Palatoglossus

A

Extrinsic muscle that elevates the posterior tongue: innervation from CN10 bilaterally

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133
Q

Obstructive sleep apnea and INSPIRE

A
  • collapse of upper airway causing obstruction and desaturation
  • independent risk factor for sleep apnea: insulin resistance, vascular disease, dyslipidemia, and death
  • C-PAP gold standard for AHI >15
    -INSPIRE: hypoglossal nerve stimulator causing contraction of the genioglossus and opening of the airway
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134
Q

The arches support the lateral walls of the primordial pharynx which is derived from the

A

cranial aspect of the foregut

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135
Q

Stomodeum

A

Future oral cavity

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136
Q

Buccopharyngeal membrane

A

Facial separation from the pharynx by a bilaminar membrane. Ectoderm externally and endoderm internally– ruptures at 26 days and makes the foregut and pharynx communication with the amniotic cavity

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137
Q

Facial development

A

-4-8th weeks
- neural crest cells migrate into the future head and neck regions
-the NCCs invade mesenchymal core of each arch which will then produce mandibular and maxillary processes

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138
Q

Paired maxillary prominence

A
  • 1st pharyngeal arch
  • Form lateral boundary of stomdeum
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139
Q

Paired mandibular arch

A
  • 1st pharyngeal arch
  • forms caudal boundary
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140
Q

Frontonasal prominence

A

Surrounds ventrolateral surface of forebrain. Frontal part develops into the forehead, and nasal part develops from the rostral portion of the prominence boundaries of the stomodeum

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141
Q

Placodes

A

Ectodermal thickenings with neurogenic potential that appear in pairs on the developing head. They contribute to the special senses

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142
Q

Lens placode

A

lens of the eye, vision

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143
Q

Otic placode

A

inner ear, hearing

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144
Q

Nasal placode

A

nasal cavity, olfactory epithelium, part of upper lip, smell. Appears during the 5th week, becomes depressed and forms the nasal pits.
– Surrounding mesenchyme from frontonasal prominence gives rise to medial and lateral nasal prominences–> deepens nasal pit and forms the primordial nasal sac

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145
Q

What keeps the maxillary process and lateral nasal process separate at week 5?

A

Nasolacrimal groove

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146
Q

Where do maxillary prominence and lateral nasal prominence merge together?

A

Nasolacrimal groove– creates the continuity of medial cheek and lateral nasal wall (nasolabial fold) and groove becomes nasolacrimal duct (drains tears into nasal passage)

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147
Q

Nasal Lacrimal Duct Obstruction (NLDO)

A
  • congenital NLDO: 5% of neonates, secondary to persistent membranes at distant valve of Hasner
  • treatment: observation, massage, probing, puncturing membrane (young babies only)
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148
Q

Epiphora

A

Excessive watering of the eyes

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149
Q

Dacryocystocele

A
  • dilation of the nasal lacrimal duct that can extend into the nasal cavity
  • bluish mass, inferior to the medial canthus
  • dacryocystitis and rspiratory distress because babies are nose-breathers and it impinges the nasal airway
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150
Q

Cartilage that appears between weeks 5-8 and produces the foundation for endochondral ossification

A

Meckel’s cartilage

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151
Q

Nasal development

A

Nasofrontal prominence mesenchyme at margins of the placode proliferate –> horseshoe elevations–> medial and lateral nasal prominences–> nasal pits deepen–> nasal sac that separates from oral cavity (oronasal) ruptures and develops primordial choanae

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152
Q

Medial nasal prominences migrate towards each other and fuse to form

A

nasal septum and intermaxillary segment (philtrum, pre-maxilla, gingiva, and primary palate)

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153
Q

Ectodermal epithelium on roof of each nasal cavity form:

A

specialized olfactory epithelium

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154
Q

Choanal Atresia

A
  • congenital narrowing of the posterior aspect of the nose (choana) due to oronasal membrane not breaking down
  • 75% unilateral, 25% bilateral
  • Right> left
  • 70% membranous, 30% bony
    Symptoms: Cyanotic during breastfeeding, and pink during crying
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155
Q

Choanal atresia is commonly associated with:

A

CHARGE syndrome:
- Coloboma
- Heart defects
- Atresia (choanal)
- Growth retardation
- GU abnormalities
-Ear abnormalities

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156
Q

3 components of Palate development

A

Primary palate: develops from intermaxillary segment
Secondary palate: develops from palatal shelves of the maxillary prominences
Nasal septum: develops from the medial nasal prominences

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157
Q

Primary palate

A
  • From intermaxillary segment
  • develops by merging of the medial nasal prominences
  • forms the anterior and midline aspect of the maxilla
  • creates small part of hard palate (anterior to incisive fossa)
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158
Q

Secondary palate

A

-Definitive palate- hard and soft
- lateral palatine processes initially project inferomedially on each side of tongue, and then assume the horizontal position above the tongue
- posterior parts do not ossify but extend to form the soft palate and uvula

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159
Q

unilateral cleft lip

A
  • failure of the maxillary prominences on the affected side to unite with the merged medial nasal prominences
  • persistent labial groove develops from lack of mesenchyme and then breaks down
  • “complete” if it goes through the alveolus
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160
Q

Bilateral cleft lip

A
  • failure of mesenchymal masses in both maxillary prominences to meet and untie with the merged medial nasal prominences
    -“Complete” if the median palatal process hangs freely and projects anteriorly
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161
Q

Complete cleft palate

A

Extends through the soft palate and incisive fossa

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162
Q

Clefts of anterior palate

A

Anterior to incisive fossa (primary palate), lateral palate processes fail to fuse with the primary palate

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163
Q

Cleft of posterior palate

A

Posterior to incisive fossa (secondary palate), lateral palatal processes fail to fuse together with the nasal septum

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164
Q

Cleft of anterior or posterior palate

A

lateral palatal processes fail to meet and fuse with each other, with the primary palate, and with the septum

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165
Q

Fetal alcohol spectrum disorder

A

FAS: infants with classical facial features, growth impairment, and cognitive disability
- Classic findings: Microcephaly, short palpebral fissures, underdeveloped maxilla, short nose, thin upper lip, abnormal palmer creases, growth retardation, congenital heart disease
– Spectrum classified by growth deficiency, cognitive deficits, and facial dysmorphia

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166
Q

Fibers of nociception

A

A-delta: 1-5um diameter, fast (3-30m/s), myelinated
C: <2.5um diameter, slow (<1m/s), unmyelinated

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167
Q

Fast nociception

A

sharp, pricking, burning. Usually due to mechanical or thermal stimuli. Precisely localized and modality-specific (mechanical, chemical, thermal).
– Found primarily in the skin

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168
Q

Slow nociception

A

Dull, achy, throbbing. usually due to chemical stim associated with TISSUE DAMAGE. Poorly localized, radiates, and can be referred pain
– Found in every tissue

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169
Q

Neuropathic pain

A

Abnormal pain due to neuron damage or loss in the PNS or CNS that triggers remodeling of pain pathways in the CNS.
Characterized by: spontaneous pain, numbness, hyperalgesia, or allodynia (allodynia and hyperalgesia are independent of one another)

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170
Q

Allodynia

A

A sensation of pain triggered by a stimulus that is not ordinarily considered painful. It is about MODALITY, not intensity

171
Q

Platypus venom:

A

triggers hyperalgesia

172
Q

Ciguatoxin from fish:

A

triggers allodynic response

173
Q

Male transmission of nociception

A

With testosterone: Microglia signaling
Pregnant females/lack T cells: microglia signaling

174
Q

Female transmission of nociception

A

T cell pain signaling

175
Q

Reciprocal signaling between the body and brain means that:

A

emotional pain can cause physical damage that results in physical pain (and vice versa)
– a pathological positive feedback loop

176
Q

Broken heart syndrome

A
  • Takotsubo cardiomyopathy
  • 90% women 58-75
  • psychological stressors causing physical injuries and ailments - esp. heart damage
177
Q

Total pain model includes:

A

1.) physical (co-morbidity/treatment/etc)
2.) social ( loss of job/financial security/etc)
3.) spiritual (fear of unknown, faith, etc)
4.) psychological ( anxiety, depression, experiences/etc)

178
Q

Afferent brings information:

A

to a structure– afferent from body–> spinal cord = sensory neurons (ascends)

179
Q

Efferent carries information:

A

from a structure– efferent from spinal cord–> body = motor neurons (descends)

180
Q

Sensory pathways are:

A

multidirectional and have terminating branches that have multiple effects. Pain system has ascending and descending components

181
Q

Glutamate receptors mediate synaptic plasticity in the pain pathway by:

A
  • NMDA receptors strengthening synapses (LTP)
  • Substance P inhibiting/modulating signals and actions of NMDA receptors
182
Q

Gate Theory of Pain

A

The Gate Control Theory of Pain is a mechanism, in the spinal cord, in which pain signals can be sent up to the brain to be processed to accentuate the possible perceived pain, or attenuate it at the spinal cord itself. The ‘gate’ is the mechanism where pain signals can be let through or restricted.

183
Q

Mechanoreceptors and nociceptor interaction

A

Mechanoreceptors can activate inhibitory GABA interneuron via NMDA and AMPA receptors, which will inhibit the pain signal

184
Q

Enkephalin receptors

A

NE via NA receptor and serotonin via 5HT receptor can activate ENK receptor activate inhibitory meu (u) receptors pre-synaptically (causing decreased NT release) or post-synaptically (opening K+ channels and hyperpolarizing cell to inhibit AP) to decrease response to pain

185
Q

Four steps to pain:

A

1.) initiation by local stimulus
2.) transmission to the brain
3.) perception as pain
4.) reaction of individual

186
Q

Opioids affect:

A
  • the patient’s reaction to pain
  • the way the pain is perceived
187
Q

Pain pathways:

A

Ascending: stimulus via nociceptor –> STT–> Thalamus–> somatosensory cortex

Descending: inhibitory pathways, signals from cortex modulating perception of pain by inhibiting signal between primary and secondary afferent neurons (mediated by endogenous opioids)

188
Q

Opiate

A

drug derived from opium poppy (opium, morphine, codeine)

189
Q

Opioid

A

generic term, all substances, endogenous and exogenous, that bind opioid receptors (endorphins-endogenous, morphine, fentanyl)

190
Q

Narcotic

A

a legal term encompassing many illicit drugs and their use (opioids, cannabinoids, stimulants, etc)
– do not use this term

191
Q

Mu (u) receptors

A

opioid receptor causing analgesia, respiratory depression, decreased GI motility, and physical dependence

endogenous opioids: endorphins, endomorphins, enkephalins

192
Q

Kappa (k) receptors

A

opioid receptor causing analgesia, sedation, and decreased GI motility

endogenous opioids: dynorphins

193
Q

Delta receptors

A

opioid receptor causing modulation of Mu (u) activity – complex

endogenous opioids: enkephalins, endorphins, dynorphins

194
Q

endogenous opioid pathways

A

Periaqueductal gray (has tonic GABA that can be inhibited by opioids)–> RVM/Raphe nucleus (has tonic GABA that can be inhibited by opioids)–> dorsal horn (has 5-HT and opioid that can inhibit pre and post-synaptic).

195
Q

Locus Coeruleus

A
  • Major source of norepinephrine (NE) projections throughout the CNS.
  • receives input from many regions (PAG, hypothalamus, amygdala, cingulate cortex, medial PFC)
196
Q

Norepinephrine:

A

1.) activates opioid interneurons
2.) inhibits primary afferent neurons (pre-synaptic inhibitor)

197
Q

Opioid receptors are:

A

G-protein coupled receptors that inhibit pre-synaptic Calcium efflux (low Ca = no NT release), and increase post-synaptic potassium influx (hyperpolarize= no AP)

– they also inhibit adenylyl cyclase to inhibit NT release

198
Q

Presynaptic inhibition of afferent neurons

A

1.) receptor-activated blocks voltage-gated Ca2+ channels
2.) reduced release of glutamate and substance P

199
Q

postsynaptic inhibition of afferent neurons

A

1.) receptor activation opens K+ channels
2.) inhibit excitation of postsynaptic neuron

200
Q

Putative sites of action for opioids:

A
  • peripheral tissues (afferent nociceptor)
  • spinal cord (dorsal horn)
  • thalamus (ventral caudal thalamus)
201
Q

Descending pain pathway and opioids:

A
  • Disinhibition: pain inhibitory neurons indirectly activated
  • opioid receptor activation blocks release of GABA from inhibitory neuron resulting in enhanced inhibition of the ascending pathway
  • greater inhibition of nociceptive processing in dorsal horn of spinal cord
202
Q

Agonist opioid drugs

A
  • receptor binding produces effect
  • ex. morphine, methadone, fentanyl, oxycodone, meperidine, heroin
203
Q

Antagonist opioid drugs

A
  • receptor binding produces no effect, reverse effect of morphine-like opioids
  • ex. naloxone, naltrexone
204
Q

partial agonist opioid drugs

A
  • less efficacy than full agonist (ceiling effect), lower abuse potential
  • ex. codeine, hydrocodone
205
Q

Mixed agonist-antagonist opioid drugs

A
  • agonist at one receptor (mu) and antagonist at another (kappa)
    -ex. buprenorphine, suboxone (bup with naloxone), pentazocine, nalbuphine, butorphanol
206
Q

Mu agonists (u)

A

morphine, oxycodone, meperidine, fentanyl, heroin, methadone, hydromorphone, oxymorphone

207
Q

Weak/partial mu (u) agonists

A

codeine, hydrocodone

208
Q

Mixed agonist/antagonists

A

buprenorphine, pentazocine, nalbuphine, butorphanol

209
Q

Dextromethorphan

A

OTC, antitissuve, weak mu agonist, limited abuse potential

210
Q

Loperamide

A

OTC, antidiarrheal, mu agonist, action most limited to gut, limited abuse potential

211
Q

Oral route of administration for opioids

A
  • high first pass metabolism is limiting (requires 3-6x higher dose than parenteral)
  • slower onset, delayed peak effect, longer duration
  • better for chronic treatment
212
Q

IV route of administration for opioids

A
  • precise and accurate dosing
  • rapid onset, increased adverse effects
  • bolus vs continuous
  • patient controlled (PCA)
213
Q

IM/subcutaneous route of administration for opioids

A
  • rapid onset
  • duration between oral and IV
214
Q

Spinal route of administration for opioids

A
  • longer duration at lower doses that systemic
  • can avoid brain-mediated adverse effects
215
Q

Buccal/sublingual route of administration for opioids

A
  • Faster onset than oral, avoids first pass metabolism
  • convenient
  • ex. suboxone, fentanyl lollipop
216
Q

transdermal route of administration for opioids

A
  • convenient, avoids first pass metabolism
  • better for chronic treatment
  • ex. fentanyl, buprenorphine
217
Q

Methadone and first pass metabolism

A

Less effected by it, only need 1.5-2x higher dose, compared to the avg 3-6x

218
Q

Lipid solubility

A

more lipid soluble= rapidly crosses BBB, producing a faster euphoria/rush

  • ex. heroin more lipid soluble than morphine
219
Q

Pharmacologically active metabolites

A
  • morphine-6-glucuronide
  • analgesic activity similar to morphine
  • impacted effect if renal fxn is compromised
220
Q

Toxic metabolites

A
  • Normeperidine
  • excitotoxic: tremor, twitching, convulsions
  • only use acutely
221
Q

Excretion of metabolites

A

Metabolites primarily excreted in urine, some glucuronides excreted in feces

222
Q

Site of action and effect in CNS for opioids: Cortex

A

pain perception, reaction to pain, euphoria, sedation

223
Q

Site of action and effect in CNS for opioids: medulla

A

respiratory distress, antitussive effects, nausea, vomiting, thermoregulation (hyperthermia)

224
Q

Site of action and effect in CNS for opioids: spinal cord

A

depressed pain reflexes

225
Q

Site of action and effect in CNS for opioids: eye, oculomotor nerve

A

miosis (pinpoint pupils)- little tolerance means it is a good indicator of opioid use

226
Q

Site of action and effect outside CNS for opioids: GI tract

A
  • constipation, decreased gastric emptying, cramping
    -slow tolerance, always an issue with opioids
227
Q

Site of action and effect outside CNS for opioids: Heart/lungs/other

A

bradycardia, bronchiolar constriction (high doses), histamine release (flushing and itching of the skin)

228
Q

Site of action and effect outside CNS for opioids: uterus/ureters/bladder

A
  • reduced smooth tone of uterus (prolongation of labor)
  • bladder increased smooth tone (difficulty urinating)
229
Q

Physical/psychological dependence

A

adaption to drug such that removal or administration of antagonist (ex. naloxone) leads to withdrawal syndrome. psych caused craving and seeking

230
Q

Substance misuse

A

use of a drug in a manner other than how prescribed/indicated

231
Q

Substance abuse

A

unlawful use, results in failure to fulfill major obligations or patterns of legal, social, and interpersonal problems

232
Q

Addiction

A

compulsive, resulting in physical, social, and psychological harm. Chronic with underlying neurobiological dysfunction. Unable to abstain, impaired behavior control, dysfunctional emotion

233
Q

Maintenance therapy for opioid addiction

A
  • methadone (OD still possible- highly variable PK)
  • buprenorphine (agonist/antagonist)
  • Suboxone (lower abuse potential bc naloxone addition)
234
Q

Tension Headache

A
  • Most common type of HA seen in population studies
  • gradually developing, constant bilateral dull ache or squeezing band-like HA
  • typically starts midday, more common in women
    -associated symptoms: fatigue, pericranial muscle tenderness, sleep disturbances
  • treated with analgesics and stress relief
235
Q

Migraine headache

A
  • Most common type presenting in primary care
  • unilateral throbbing HA with sudden onset, more common in women and younger people
  • associated symptoms: fatigue, NAUSEA, photophobia, vomiting
  • treated with dark room, meds, sleep
236
Q

Cluster headache

A
  • Most debilitating
  • Sudden onset, unilateral, severe HA lasting 15-180 minutes and occurring at the same time each day
  • more common in men, 20-40 years old
  • ipsilateral cranial autonomic symptoms
  • treated with activity, meds, oxygen, and pacing
  • comorbidities with depression, sleep apnea, restless legs, asthma, and smoking
237
Q

Paroxysmal hemicrania

A
  • unilateral HA lasting 2-30 minutes
  • more common in women, 34-41 years old
  • reliably responds to indomethacin
238
Q

Short-lasting unilateral neuralgiform headaches with conjunctival injection and tearing

A
  • unilateral HA lasting 5-240 seconds occurring 3-200 times per day
  • more common in men, 35-65 years old
  • usually refractory to treatment, ipsilateral eye symptoms, RARE
239
Q

Trigeminal neuralgia

A
  • paroxysmal, electrical, sharp, stabbing pain in trigeminal nerve distribution lasting a few seconds. episodes last weeks to months
  • more common in women, onset after 50 years old
  • treatment is carbamazepine (tegretol)
  • inconsistent patterns of HAs, triggered by cold air, light tough in the distribution area of CN5
240
Q

Classic presentation of tension headaches

A

bilateral, described as pressure, tightening sensation, no more than moderate severity, not exacerbated by routine of physical activity – no associated symptoms. Sensitivity in the nociceptors in the pericranial myofascial tissues

241
Q

Classification of tension headaches

A

1.) infrequent-episodic: occurs > 1 day/month
2.) frequent episodic: episodes occur 1-14 day/month
3.) chronic: occur > 15 days/month

242
Q

Migraine differences that separate it from a tension HA

A
  • nausea, photophobia, phonophobia, physical activity makes it worse
  • can be with or without an aura
  • pain is moderate to severe

think POUND:
- Pulsatile
- hOurs (4-72hr duration)
- Unilateral
- Nauseating
- Disabling

243
Q

Mechanisms of migraines

A

1.) cortical spreading depression
2.) trigenminovascular system
3.) sensitization

244
Q

Cluster headaches proposed mechanism

A

1.) hypothalamic activation leading to secondary activation of the trigeminal-autonomic reflex
2.) neurogenic inflammation in the cavernous sinus impacting intracranial internal carotid

245
Q

Presentation of cluster HAs and autonomic symptoms

A
  • severe, “suicide headache”
  • AN symptoms: ipsilateral tearing or conjunctival redness, nasal congestion/rhinorrhea, eyelid edema, forehead/facial sweating, miosis or ptosis, restlessness
246
Q

Tension HA acute treatment

A

Anti-inflammatories (NSAIDs) - limit to 15 days/month
- combination analgesics (acetaminophen, caffeine, aspirin, ibuprofen) - limit to 9 days/month

247
Q

Tension HA chronic/prophylactic treatment

A
  • tricyclic antidepressants
  • mirtazapine
  • SNRIs (venlafaxine)
  • anticonvulsants (topiramate, gabapentin)
  • muscle relaxant (tizanidine)
  • triggerpoint injections: botox or lidocaine
248
Q

Migraine acute/abortive treatment

A
  • NSAIDs, tylenol
  • dihydroergotamine
  • triptans
  • anti-emetics
  • calcitonin-gene related peptide antagonists
  • dexamethasone
  • lidocaine, intranasal
249
Q

Migraine chronic/prophylactic treatment

A
  • Beta blockers
  • calcium channel blockers
  • antidepressants
  • anticonvulsants
  • CGRP antagonists
  • lidocaine, trigger point injections
  • botulinum injections
250
Q

Cluster HA treatments

A
  • abortive: triptans, 100% O2, nasal lidocaine
  • transitional treatments: suboccipital steroid injections, PO/IV steroids
  • prophylactic options
  • neurostimulation or somatostatin receptor agonist (octreotide)
251
Q

Secondary headache types

A

1.) abnormal build-up of pressure on the meninges

2.) from an inflammatory response/ trauma

252
Q

History headache red flags

A

1.) sudden and severe HA, “worst HA of my life!”
2.) New pattern to a HA with increase in frequency or severity
3.) steady or rapid change in mental status or personality change
4.) associates symptoms of fever, neck stiffness, neurologic symptoms
5.) associated trauma
6.) immunocompromised, h/o cancer, pregnant, over age 50

253
Q

Physical exam headache red flags

A

1.) focal neurologic signs, rapid change in exam
2.) papilledema
3.) fever
4.) asymmetric pupil size

254
Q

Red flags for headaches: SNNOOP10

A

Systemic symptoms
Neoplasm- current/historic
Neurologic deficit
Onset- sudden or abrupt
Older age (>50)
Pattern: new/change
Position
Posttraumatic (acute/chronic)
Precipitated- sneezing/coughing
Painful eye + autonomic feature
Painkiller overuse
Papilledema
Pathology (immune system)
Pregnancy
Progressive

255
Q

Work-up for headaches

A

History/exam: consider HA diary

Labs indicated by history: ESR, TSH, CBC

if Red Flags: non-contrast CT, lumbar puncture and CSF analysis, potential MRI, MRA (vascular)

256
Q

Bones of the orbit

A

Frontal, zygomatic, sphenoid, maxilla, lacrimal, ethmoid, and sometimes palatine

257
Q

Fragile areas of the orbit that can have blow-out effects

A

1.) Maxillary to the sinus
2.) Ethmoid to the sinus
- Will feel like severe pressure. orbital contents may enter sinus

258
Q

What layer of the eye has vasculature?

A

Choroid/uvea

259
Q

Superior root branches of V1

A
  1. Frontal
  2. Supraorbital
  3. Supratrochlear
  4. Lacrimal n. to lacrimal gland
260
Q

Inferior root branches of V1

A
  1. nasociliary
  2. long ciliary
  3. short ciliary
  4. posterior ethmoidal
  5. anterior ethmoidal
261
Q

H test:

A

Lateral rectus (CN6): abduction
Superior rectus (CN3): abduction and raise
Inferior rectus (CN3): abduction and depress
Medial rectus (CN3): adduction
Superior oblique (CN4): adduction and depress
Inferior oblique (CN3) adduction and raise

262
Q

Every eye muscle attaches to the Common Tendinous Ring (Annulus of Zinn) except:

A

Inferior oblique (CN3), which originates from maxilla

263
Q

Long ciliary nerve

A

post-ganglionic sympathetic info from internal carotid plexus –> dilator pupillary m. to widen eye/pupil

264
Q

Short ciliary nerve

A

parasympathetic info to sphincter muscle to constrict eye/pupil from ciliary ganglion

265
Q

Horner’s syndrome

A
  • interruption of sympathetic on ipsilateral (same side) in the Cervical sympathetic trunk and sympathetic fibers in brain stem and spinal cord
  • Clinical features: Ptosis (eyelid droop), miosis (pupillary constriction), anhidrosis (absence of sweating), vasodilation (redness and flushing)
266
Q

NSAIDs vs opioids

A

NSAIDs:
Pros- loss of pain from inflammation, fewer AE
Cons- only mild/moderate pain control

Opioids:
Pros- high intensity pain relief, helps sharp and intense pain
Cons- drowsiness, tolerance, physical dependence, abuse potential, respiratory depression

267
Q

Pathway of arachidonic acid–> effectors

A

Lipoxygenase: LTB4, LTC4/D4/E4 leading to phagocyte chemotaxis, inflammation, and bronchial constriction, increased secretion, and edema

Cyclooxygenase: Prostaglandins (platelet aggr., inflammation), Thromboxane (platelet aggr., inflammation), and Prostacyclin ( inhibits platelet aggr., vasodilation, GI cytoprotection)

268
Q

NSAIDs inhibit:

A

COX1 and COX2 from cyclooxygenases.

COX1: normal physiology, gastric protection, vasodilation, platelet aggr.
COX2: inducible, acute inflammation, inhibited by glucocorticoids

269
Q

Prostaglandins

A

-PGE2, PGD2, PGF2a
-modify nociception thresholds (more sensitive)

270
Q

Thromboxanes

A

-TXA2
-increase platelet aggregation

271
Q

Prostacyclin

A

-PCI2
-decreases platelet aggregation

272
Q

Which NSAIDs is a suicide inhibitor, permanently inhibiting platelets’ COX1 and COX2?

A

Aspirin

273
Q

All NSAIDs are:

A
  • analgesic
  • antipyretic
  • anti-inflammatory
274
Q

Adverse effects of NSAIDs (esp aspirin)

A

1.) GI distress
2.) GI bleeding
3.) nephrotoxicity (not bypasses by selective COX2 drugs)
4.) impact on clotting time (2x increase for 7 days after single 650mg dose)
5.) respiratory and electrolyte disturbances (toxic doses)

275
Q

Mild toxicity aspirin overdose

A
  • tinnitus
  • HA
  • nausea, vomiting
  • sweating, thirst, hyperventilation
  • hearing loss (reversible)
276
Q

Severe toxicity aspirin overdose

A
  • hyperventilation
  • acid-base imbalance
  • dehydration
  • agitation, hyperactivity, slurred speech, tremor, seizures, coma
  • fever (esp. in children)
277
Q

Treatment of aspirin overdose

A

1.) gastric decontamination: vomiting, lavage, activated charcoal
2.) correct acid-base imbalance: sodium bicarbonate
3.) additional measures: transfusion, dialysis

278
Q

Aspirin hypersensitivity is likely due to:

A

shunting of arachidonic acid into leukotriene, lipoxygenase pathway

279
Q

Reye’s syndrome

A
  • Swelling of the liver and brain contributing to confusion, seizures, and LOC
  • Children at highest risk
  • aspirin use in presence of viral infection
  • may be from underlying fatty acid oxidation disorder
280
Q

Ibuprophen

A
  • analgesic, antipyretic, anti-inflammatory
  • fewer GI adverse effects than aspirin
  • clotting effects are reversible
281
Q

Naproxen

A
  • analgesic, antipyretic, anti-inflammatory
  • fewer GI adverse effects than aspirin
  • clotting effects are irreversible
  • effects last longer then ibuprophen
282
Q

Indomethacin

A
  • analgesic, antipyretic, anti-inflammatory
  • The most potent COX inhibitor
  • used when other NSAIDs are ineffective (esp in fever or arthritis)
  • has significant toxicity
283
Q

Patent ductus arteriosus

A

-congenital disorder where embryological duct in the heart fails to close after birth
- mediated by PGE2, use indomethacin to close duct

284
Q

Ketorolac

A
  • NSAID, injected IV or IM
  • replace morphine if addiction is an issue
    -combine with opioid to decrease opioid requirement by 25-50%
285
Q

Celecoxib

A
  • selective COX2 inhibitor
  • increased risk of MI and stroke because prostacyclin inhibition = pro-platelet aggregation = clots
286
Q

Acetominophen

A
  • NOT anti-inflammatory
  • analgesic, antipyretic
  • Weak, but very few AE
  • therapeutic index is small- toxic metabolite produced especially in the presence of alcohol leading to cell death
  • Overdose treatment: N-acetylcysteine as a scavenger drug (like glutathione)
287
Q

What are local anesthetics?

A
  • the loss of sensation in a limited region of the body
  • complete loss of all sensory modalities
  • delivered directly to target region (systemic distribution diminishes effect)
  • weak bases (pH ~ 8-9)
288
Q

Three structural components of a local anesthetic

A

1.) hydrophobic component: increases potency, plasma binding protein, duration of action, toxicity
2.) Intermediate linker component: ester bond or amide bond, and determines metabolic rate
3.) Hydrophilic component: amine, determines pK of drug

289
Q

Local anesthetics are

A

weak bases, ionized when protonated

  • unlike weak acids which are ionized when unprotonated
290
Q

Local anesthetics block:

A

Sodium channels (therefore the conduction of APs)

291
Q

Mechanism of action for local anesthetics:

A
  • need equal amount of ionized and unionized because un-ionized crosses plasma membrane, but ionized required to interact with and block Na+ channels from the inside of the cell
292
Q

Lower pK drugs have:

A

more rapid onset of action (more uncharged form of drug at physiological pH, and more rapid diffusion into cytoplasm)

293
Q

Three stages of AP

A

1.) resting/closed (resting membrane potential)
2.) open (depolarization)
3.) inactive (channel closes whole cell is depolarized)

Drug affinity: Low for resting state, high for open or inactive states

294
Q

LAs preferentially block

A

Smaller diameter nerve fibers, and myelinated nerves before unmyelinated

295
Q

Order in which sensations are blocked/affected:

A
  1. pain
  2. cold
  3. warmth
  4. touch
  5. deep pressure
  6. motor function
296
Q

CNS toxicity in LAs

A
  • tongue numbness, metallic taste
  • dizziness
  • visual disturbances
  • tinnitus
  • slurred speech
  • generalized convulsions
  • eventual coma
297
Q

Cardiovascular toxicity in LAs

A
  • hemodynamic instability
  • decreased myocardial electrical excitability
  • cardiovascular collapse
298
Q

Hypersensitivity rxns are more likely to be seen with which LAs?

A

Esters – allergy to para-aminobenzoic acid (PABA), a metabolite

299
Q

Methemoglobinemia

A
  • Some LAs, metabolites can oxidize iron/heme –> methemoglobin
  • causes decreased O2 binding capacity and Decreased O2 release (hypoxia, cyanosis, etc)
300
Q

Metabolism of different LAs

A
  1. Esters: are rapidly hydrolyzed in plasma by pseudocholinesterase
  2. Amides: are hydrolyzed in liver by mixed function oxidases
    – metabolites excreted in urine
301
Q

EMLA

A
  • eutectic mixture of local anesthetics
  • Lidocaine + prilocaine
  • effective for LP, venipuncture, skin graft harvesting
302
Q

infiltration anesthesia

A

-subQ or submucosal
- common for dental, minor procedures– avoid IV injection on accident

303
Q

Minor nerve block

A

blocks small periphery, such as digit blocking

304
Q

Major nerve block

A

injection of relatively large volume to block whole extremity (ex. brachial plexus)

305
Q

Intravenous regional (Bier) block

A
  • IV anesthetic + tourniquet – usually only for arms
306
Q

Procaine

A
  • ester-type
  • short-acting- commonly given with vasoconstrictor
  • rapid metabolism in plasma
  • not useful as a topical anesthetic
307
Q

Lidocaine

A
  • amide-type
  • one of the most widely used
  • metabolized in liver
  • intermediate duration
  • used for all types of local anesthesia
308
Q

Mepivacaine

A
  • amide-type
  • action similar to lidocaine
  • tendency toward vasoconstriction, and longer lasting
309
Q

Bupivacaine

A
  • amide type
  • long-acting and potent
  • used for: epidurals, and prolonged surgeries
310
Q

Ropivacaine

A
  • amide-type
  • long-acting local anesthetic
  • less CV and CNS toxicity than bupivacaine
311
Q

Prilocaine

A
  • amide type
  • intermediate-acting local anesthetic, less vasodilation
  • causes methemoglobinemia
312
Q

Tetracaine

A
  • ester type
  • used primarily for topical anesthesia of the eye, nose, throat and for spinal anesthesia
313
Q

Benzocaine

A
  • ester type
  • pK 3.5 (LOW)
  • lacks amino terminus, range of action is pH-independent
  • limited to topical anesthesia
  • causes methemoglobinemia so not used often
314
Q

Cocaine

A
  • ester type
  • good penetration of tissues and vasoconstrictor action
  • Primarily used for URI, and mucosal membranes
  • abuse potential, controlled substance, inconvenient
315
Q

pathway of vision

A

Rods and cones –> bipolar cells –> ganglion cells –> optic nerve –> optic chiasm –> optic tract –> lateral geniculate nucleus –> optic radiation –> visual cortex (Calcarine dividing cuneus and lingual)

316
Q

Temporal/nasal hemiretina

A

UTQ: upper temporal quadrant
LTQ: lower temporal quadrant
UNQ: upper nasal quadrant
LNQ: lower nasal quadrant

317
Q

Visual field

A

area seen by a patient without movement of the head with eyes fixed on a single spot

318
Q

Monocular visual field

A

what is seen through one eye when the other is covered

319
Q

Binocular visual field

A

includes the monocular field of each eye

320
Q

Contralateral visual fields and brain

A
  • Left visual field projects to the right thalamus and cortex
  • Right visual field projects to the left thalamus and cortex
321
Q

The optic chiasm is located:

A

just anterior to the pituitary gland - clinically significant – only nasal half crosses the midline in the chiasm (contralateral), temporal fibers do not decussate (ipsilateral)

322
Q

Axons that visualize temporal fields are

A

nasal retinal axons (and cross in the chiasm)

323
Q

Axons that visualize the nasal fields are

A

temporal retinal axons (and do not cross)

324
Q

Damage at the optic tract causes

A

homonymous damage– only to left or right visual field

325
Q

Damage at the optic nerve or chiasm causes

A

heteronymous damage– involves parts of both visual fields so defects are non-overlapping

326
Q

Lateral geniculate nucleus

A
  • in the thalamus/just below it
  • most axons from retinal ganglion terminate here
  • each LGN receives information from only one visual field (contralateral)
  • retinotopic mapping
327
Q

pupillary response is mediated through:

A

Edinger-Westphal nucleus

328
Q

Geniculocalcarine Tract (optic radiation)

A

projections split into two pathways in the internal capsule on the way to the occipital lobe

329
Q

Sublenticular

A

fibers from the upper visual field traveling through the TEMPORAL LOBE as MEYERS LOOP

330
Q

Retrolenticular

A

fibers from the lower visual field travel directly through the PARIETAL LOBE to the occipital cortex

331
Q

Primary visual cortex, V1, Area 17

A

Macular representation: caudal 1/3
peripheral field: rostral 2/3

  • Myers loop (upper visual) projects to lingual gyrus (below calcarine sulcus)
  • lower visual projects to cuneate gyrus
  • cells respond to visual stimuli such as color, location, shape, and motion
332
Q

What deals with complexity of vision?

A

Visual cortex Area 18,19 with input from Area 17

333
Q

Dorsal stream, Magnocellular

A
  • association cortex projection stream
  • projects to parietal and upper temporal cortex
  • information about the WHERE of a visual stimulus (Location, movement, position in space)
334
Q

Ventral stream, Parvocellular

A
  • association cortex projection stream
  • projections to inferior temporal cortex
  • information about the WHAT of a visual stimulus (form, color, object, recognition, memory)
335
Q

What is consciousness?

A

Awareness of the self and the environment. Internal stream of thought that involves memory, reflection, symbolic representations, and synthesis of life events.
– requires wakefulness and awareness
– waking state, experience and the mind

336
Q

Coma

A

state of acute unconsciousness: NOT awake, NOT aware, transitional state.
DO NOT: wake, open eyes or track objects, follow verbal commands, show purposeful movements
DO: show reflexive movements

337
Q

Vegetative state

A
  • persistent or permanent state of unconsciousness; awake but NOT aware
  • they have sleep/wake cycles
  • open eyes when awake, but do not track
  • movements are reflexive
  • cannot think or feel, including NO PAIN
  • unconscious because they are unaware
338
Q

Anatomical location of consciousness

A

reticular formation (brainstem) + thalamus + cortex and their connection

339
Q

Quinlan case

A
  • Quinlan overdosed –> received CPR –> became vegetative
  • father removed ventilation, hospital worried about liability
  • SCOTUS: substituted judgement okay with ethics committee agrees no regained consciousness
  • died 10 years later of pneumonia, extensive thalamus and cortex degeneration
340
Q

Cruzan case

A
  • car accident, arrested and resuscitated–> vegetative
  • weaned ventilator, tube fed, nutrition removed based on friends and family (best expressed in writing)
  • Patient Self-determination act: require federally-funded facilities to inquire about written wishes or help prepare them
341
Q

vegetative vs minimally conscious state

A

MCS: limited awareness of self and environment, can feel pain, purposeful movement. CAN FEEL PAIN
Coma–> VS–> MCS: continuum in brain injured patients

342
Q

Substituted judgement

A

relatives make decisions based on what they believe the patient would want, limited information

343
Q

Neuroimaging features of disorders of perturbed consciousness (DPC)

A

1.) CT/MRI: evidence of diffuse or multifocal brain damage
2.) serial images: improvement vs atrophy
3.) <50% glucose metabolism (PET)
4.) PET: primary visual or auditory cortices are stimulated in VS and MCS
5.) neural networks connecting to secondary cortices are disrupted in VS, but normal in MCS

343
Q

Neuroimaging features of disorders of perturbed consciousness (DPC)

A

1.) CT/MRI: evidence of diffuse or multifocal brain damage
2.) serial images: improvement vs atrophy
3.) <50% glucose metabolism (PET)
4.) PET: primary visual or auditory cortices are stimulated in VS and MCS
5.) neural networks connecting to secondary cortices are disrupted in VS, but normal in MCS

344
Q

Noxious stimulus activates thalamus and cortex in MCS but no in:

A

VS– no pain perception in VS

345
Q

Locked-in sydrome

A

pontine injuries that result in tetraplegia. Normal cognition in sleep/wake cycles. Can open the eyes and move them vertically

346
Q

NO activity EEG

A
  • brain death, sporadically seen in coma and VS
347
Q

Vegetative state EEG

A
  • slow activity during wakefulness, no change with stimulation
  • no changes in wave patterns from wake/sleep, no REM or slow wave sleep
348
Q

MCS EEG

A
  • slow wave activity during wakefulness
  • near normal sleep (REM and slow wave sleep)
349
Q

Neocortical death

A

loss of higher cortical function alone– no capacity for consciousness

350
Q

Treatments for disorders of perturbed consciousness (DPC)

A
  • hypothermia
  • intense rehab
  • deep brain stimulation
  • drugs (stimulants, antidepressants, anticonvulsants)
351
Q

Prognosis of DPC

A

TBI > stroke

Young > old

352
Q

ACA: cost-cutting panels vs Americans with disabilities act

A

Vegetative patients cannot be denied their preferred treatment

353
Q

prosopagnosia

A

Cannot recognize faces – facial blindness

354
Q

Sensation

A

the stimulation of sensory receptors and transmission of sensory information to the CNS
- bottom-up processing (raw material, entry level, data driven)
- occurs in the peripheral NS

355
Q

Perception

A

the process by which sensations are organized and interpreted to form an inner representation of the world
- top-down processing (concept driven, use preexisting knowledge to interpret information)
- occurs in the brain

356
Q

Perception key concepts

A
  1. selection
  2. organization
  3. interpretation
  4. subliminal (subconscious) and extrasensory (ESP)
357
Q

Three major factors of selection

A
  1. selective attention
  2. feature detectors
  3. habituation
358
Q

Four major factors of organization

A
  1. Form (Gestalt, dynamic wholes)
  2. Constancy (size, shape, color, brightness)
  3. Depth
  4. Color
359
Q

Gestalt principles

A

Rules that summarize how we tend to organize bits and pieces of information into meaningful wholes

360
Q

Gestalt psychology of form

A
  • figure ground
  • proximity
  • closure
  • contiguity
  • similarity
361
Q

Constancy examples

A

size, shape, color, brightness

362
Q

Four major factors of interpretation

A
  1. perceptual adaption
  2. perceptual set
  3. individual motivation
  4. frame of reference
363
Q

Types of extrasensory perception

A

Subliminal perception: stimuli that occur below the threshold of our conscious awareness, but have a weak effect on behavior
Types: telepathy, precognition (future seeing), clairvoyance, psychokinesis

364
Q

Stimulus

A

• all objects in the environment are available to the observer
• observer, selectively attends to objects
• stimulus impinges on receptors resulting in internal representation

365
Q

Perceptual process: electricity

A

Transduction: changes, environmental energy to nerve impulses

Transmission : occurs when signals from the receptors travel to the brain

Processing: occurs during interactions among neurons in the brain

366
Q

Recognition

A

After conscious perception of experience, an object is placed in a category giving it meaning

367
Q

Pathway of stimulus to action

A

Environmental stimulus—> attended stimulus—> stimulus on the receptors—> transduction—> transmission—> processing—> perception—> recognition—> action

368
Q

Bottom up processing

A

• processing based on incoming stimuli from the environment
• also called databased processing

369
Q

Top down processing

A

• processing based on the perceivers previous knowledge (cognitive factors)
• also known as knowledge based processing

370
Q

Study of PP (stimulus—> experience, and action)

A

• links stimuli and perception
• present stimulus, and get subjects response of perception

371
Q

Study of PH1 (stimulus—> physiological processes)

A

• present stimulus, and measure neurons firing (brain response)

372
Q

Study of PH2 (physiological processes—> experience, and action)

A

• present stimulus and measure both brain response and subject response (verbal)

373
Q

The process by which our brain organizes and interpret sensory information, sorting it into useful information is?

A

Perception

374
Q

The concepts of sensation and perception are different, because:

A

Sensation is something that happens to your sense organs and neurons; perception of something that happens in consciousness

375
Q

Phenomena, such as change blindness and perceptual set are evidence that perception is:

A

At least partly dependent on expectations and biases about the world

376
Q

Perceptual set

A

A predisposition to perceive things in a certain way

377
Q

Change blindness

A

A perceptual phenomenon that occurs when a change in visual stimulus is introduced and the observer does not notice it

378
Q

3 layers of the eye

A
  1. Sclera and cornea
  2. Uvea (Choroid, ciliary body, iris) and lens
  3. Retina (innermost layer)
379
Q

2 fluids of the eye

A

Aqueous humor (anterior and posterior chambers) and vitreous humor

380
Q

Retina “floaters”

A

The vitreous humor gradually shrinks with age and collagen components can clump and cast shadows on the retina
– sudden increase in floaters, accompanied by light flashes may indicate RETINAL DETACHMENT

381
Q

Eye muscles

A

striated: Almost all, nicotinic ACh receptors innervated by CN7

Smooth: superior tarsal muscle: alpha1 adrenergic innervated by CN3

382
Q

Blinking functions

A

corneal lubrication, eye protection, visual information processes

383
Q

Blinking rhythm

A

Forceful, contraction and relaxation or orbicularis oculi and levator palpebrae superioris
- can be spontaneous or reflexive

384
Q

Spontaneous blinking

A
  • periodic, symmetrical (precisely conjugated- both eyes), brief
  • wide variation (10-20 per minute, children less)
  • pattern generator in brainstem reticular formation highly influenced by dopaminergic activity
385
Q

corneal reflex

A

touch of the cornea to activate the blink reflex

386
Q

Optic reflex

A

bright light/ rapidly approaching objects activate the blink reflex

387
Q

Consensual response

A

normal, with both eyes at the same time. afferents impinge on pattern generator in the brainstem to control motor neuron on both sides

388
Q

Tear composition

A
  1. lipid secrete by sebaceous glands
  2. Aqueous based solution from lacrimal gland (contains lysozyme and enzymes to protect against infection
  3. mucous from conjuntiva
    – composition and basal tear production vary with stimulus and age
389
Q

Stye

A

blocked sebaceous gland as a result of staph infection.

390
Q

Epiphora

A

overflow of tears, under the control of ANS (parasympathetic CN7)
Produced by: increasing tear production, and decreasing outflow
Induced by: corneal stimulation (CN5) or strong emotional response (limbic system)

391
Q

The only eye movement that is not conjugate:

A

Convergence led by the co-contraction of the medial rectus muscles

392
Q

Diplopia

A
  • Double vision
  • one extraocular eye muscle is functionally weaker than the other eye, objects are projected to different parts of the retina
393
Q

Refraction

A
  • Bending of light when media changes density
  • Image on the retina is inverted and reversed
  • cornea has greater refractive power, but focusing power of the lens can be adjusted to allow near vision (accommodation)
394
Q

Lens is connected to ciliary muscle by

A

Zonular fibers

395
Q

Accommodation pathways

A

Relaxation of ciliary muscle—> tightened zonule—> pull on lens—> lens flattens (Less refractive power)

Contraction of ciliary muscle —> loosened zonule—> Less pull on lens—> lens round (more refractive power)

396
Q

Distance vision requires:

A

A flat lens

397
Q

Focal length

A

Distance from the lens to the place where the image is in focus

398
Q

Axial length

A

Physical distance between the lens and the retina

399
Q

When the focal length is equal to the axial length:

A

The image is in focus on the retina

400
Q

Hyperopia

A

Farsightedness: axial length < focal length, so the image is behind the retina
• short axial length or weak, refractive power
• corrected by convex lenses (+D)

401
Q

Myopia

A

Nearsightedness: axial length > focal length, so the image is in front of the retina
• long axial length or strong, refractive power
• corrected by concave lenses (-D)

402
Q

Presbyopia

A

Decrease in accommodative power of the lens with age

403
Q

Astigmatism

A

Unequal refraction—> portion of the images out of focus

404
Q

Cataracs

A

opacity of the lens is increased due to physical trauma, radiation, high glucose concentration in aqueous humor, and age

405
Q

Pupil size: mydriasis

A

sympathetic, neurons, release NE—> alpha1 —> contraction of dilator muscle (dilation, lowlight, sympathetic activation)

406
Q

Pupil size: Miosis

A

Parasympathetic neurons release ACh—> M3 —> contraction of sphincter muscle (constriction, high light)

407
Q

Pupillary light reflex

A

1.) light stimulates one retina—> optic nerve/tract bilaterally to upper midbrain (pretectal nucleus)
2.) midbrain neurons—> bilaterally to Edinger westphal nucleus
3.) Edinger westphal neurons—> preganglionic parasympathetic neurons of ocular motor nerves—> ipsilaterally to ciliary ganglion
4.) ciliary ganglion neurons—> postganglionic neurons in ciliary nerves—> ipsilateral Iris sphincter muscle—> pupil constriction

408
Q

Ciliary body and aqueous humor flow

A

Ciliary body—> posterior chamber—> pupil—> anterior chamber—> trabecular, meshwork canal of Schlemm

409
Q

Glaucoma

A

• increased intraocular pressure
• equation: intraocular pressure = flow X resistance

410
Q

Macula lutea

A

•Location of the fovea centralis (concentration of cones)
• appears colored because of blue pigment Lutein and zeaxanthin

411
Q

Optic disc

A

Exit of optic nerve fibers = axons of ganglion cells (on nasal side)

412
Q

Papilledema

A

• swelling of the optic nerve, increased intracerebral pressure— causes optic disc to look less clear and bigger

413
Q

Retinal layers

A
  1. Photo receptors (rods and cones)
  2. Horizontal cells (modulate activity)
  3. Bipolar cells (receptor potential)
  4. Ganglion cells (action potential)
  5. Amacrine cells (modulate activity)
414
Q

The 10 retina layers

A
  1. Sclera
  2. Choroid (RPE)
  3. Rods and cones
    ( external limiting membrane)
  4. Outer nuclear layer
  5. Outer plexiform layer
  6. Inner nuclear layer (bipolar cells)
  7. Inner plexiform layer
  8. Ganglion cell layer
  9. Nerve fiber layer
  10. Inner limiting membrane
415
Q

Some ganglion cells have:

A

• photopigments (melanopsin) and can transduce light
• they connect to the regions of the brain that generate the dominant circadian rhythm

416
Q

Visual transduction

A

1.) activation of receptor protein rhodopsin (visual purple)
2. Activated receptor stimulates G protein (transducin) where GDP is exchanged for GTP, and the alpha subunit dissociates
3. Transducin alpha, subunit, activates phosphodiesterase to convert cGMP—> GMP
4. Decrease in cGMP closes cyclic nucleotide dependent cat ion channels
(Decrease in Na= hyper polarization)

417
Q

Spatial visual acuity

A

Ability to distinguish two points in space. Changes depending upon location of stimulus and light intensity (rods versus cones)

418
Q

Spectral visual acuity

A

Ability to distinguish two colors as different

419
Q

Temporal visual acuity

A

Ability to distinguish two events as separate (critical fusion frequency ~ 50 Hz = 20ms to have continuous picture movement)

420
Q

Most common color blindness

A

Red/green

• due to defect in OPN1LW or OPNIMW genes
• x-linked, recessive

421
Q

Achromatopsia

A

Complete lack of color vision— rare. Due to defect in conversion of transducin, or a defect in cone CNG channels.

422
Q

Retinal pigment epithelium (RPE)

A

• opsin
• Vitamin A—> 11-cis-retinal (chromophore)
• for rods: dark adaptation, increased sensitivity in low light conditions

Neuro/Behavior I (3 decks)

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