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BECOM 2 > BECOM Exam #5 (Week 1) > Flashcards

BECOM Exam #5 (Week 1) Flashcards

1
Q

Long vs. short axon

A

Long axon: stimulus -> CNS (TOUCH and SMELL)

  • Somatic sensation (touch, pain, etc.)
  • Visceral sensation
  • Olfaction

Short axon: stimulus -> signal synapses primary afferent neurons’ peripheral processes -> CNS

  • Gustation (taste)
  • Photoreception
  • Hair cells of inner ear
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2
Q

Conscious proprioception (kinesthesia)

A

Joint position and movements – including direction and velocity

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3
Q

Nonconscious proprioception

A

Muscle spindles and golgi tendon organs (proprioception)

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4
Q

Pain: nociceptors (fast vs. slow)

  • type of pain
  • fibers
  • neurotransmitters
A

Fast pain: sharp, localized
-myelinated Aδ fibers (glutamate)

Slow pain: dull, burning, diffused
-unmyelinated C fibers (substance P)

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5
Q 
FUNCTION
Mechanoreceptor
Meissner corpuscles
Merkel discs
Hair follicle receptors
Ruffini endings
Pacinian corpuscles
Muscle spindles
A 
Meissner corpuscles (tactile shapes/surfaces)
Merkel discs (tactile indentations)
Hair follicle receptors (tactile in hairy skin)
Ruffini endings (stretching and shapes)
Pacinian corpuscles (vibrations)
Muscle spindles (proprioception)
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6
Q

Aδ mechanical vs C-polymodal (nociceptor)

  • type of pain
  • temp
A

Aδ mechanical: encapsulated/sheathed and detect discrete nocicept stimuli (pinprick)
-fast/acute pain
-cold
C-polymodal: free nerve ending that detect tissue damage)
-chronic pain
-heat

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7
Q

dorsal column (medial lemniscus system) mediates what? and cell body location

A

Tactile sensation and conscious proprioception

-cell bodies: dorsal root ganglia

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8
Q

Meissner’s, Pacinian, or joint receptor (dorsal column (medial lemniscus system)) pathway

A

primary neuron runs to dorsal root gang -> gracillis or cuneatus (decussation) -> VPL of thalamus -> sensory motor cortex
-same side of the body up through the spinal cord and crosses over at medulla

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9
Q

non conscious propreception pathway (posterior spinocerebellar tract)

A

muscle spindles and Golgi tendons enter and run to cerebellum without crossing (inferior peduncle)

  • proprioception
  • do not cross
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10
Q

non conscious propreception pathway (anterior spinocerebellar tract)

A

Golgi tendons enter and cross at level on the spinal cord and run up to pons where it crosses again and continues to cerebellum (superior peduncle)

  • Proprioception including skin stretch sensation
  • crosses twice
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11
Q

Cerebellar ataxia

A

Form of uncoordinated gait disturbance due in part because of the cerebellum not processing proprioceptive stimulus appropriately

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12
Q

Friedreich’s or spinocerebellar ataxia

A

Inherited neurodegenerative disease particularly affecting SPINOCEREBRAL tracts (proprioceptive tracts)
Symptoms: near total lack of upper limb coordination and reeling, wide-based gait

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13
Q

Special sensation with longest Axon

A

smell (olfactory)

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14
Q

Neospinothalamic tract

A

enters at spinal cord level and synapse with 1. substantial gelantinosa or 2. nucleus proprius -> crosses to lateral finiculus continues and synapsis at VPL of thalamus -> sensory cortex

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15
Q

Anterolateral cordotomy

A

a lesioning the spinalthalamic tract in order to stop pain transmission

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16
Q

Hyperalgesia and chemicals involved

A

enhancement of pain sensation (abnormally increased sensitivity to pain)

  • Either activate nociceptors themselves
  • Lower nociceptor threshold
  • Histamine, Substance P, Serotonin, Bradykinin increase ones sensitivity to pain
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17
Q

Allodynia

A

pain occurs after repetitive but typically non-painful stimulation
-ex. sunburn, sore throat

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18
Q

Causalgia

A

Burning sensation caused by increased sympathetic efferent activity after peripheral nerve injury

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19
Q

Paresthesia

A

Pricking, tingling, numbness, tingling, burning of skin with no apparent cause
-caused by nerve compression or PVD (peripheral nerve disease)

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20
Q

Meralgia paresthetica

A

compression of the lateral cutaneous nerve of the thigh causing numbness, tingling down the outside of the thigh

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21
Q

Tonic receptors

A

slow/non adaptive receptors (continue stimulation)
-proprioception, chemoreceptors, nociceptors, Golgi tendon apparatus, baroreceptors, receptors in vestibular apparatus (position)

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22
Q

Phasic (rate) receptors

A

fast adapting (loss of stimulation)

  • Display on/off response (feel hat when 1st put on and when taken off but not while wearing)
  • pacinian corpuscles most fast adapting
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23
Q

Lateral inhibition

A

Strongest neuron not only sends stimulus but also inhibits the surrounding weak stimuluses (via interneurons - neurons between neurons)
-allows brain to localize stimulus

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24
Q

First intention vs second intention wound healing

A

First Intention -> results in thin scar

  • Simplest type of cutaneous wound repair
  • Healing of a clean, uninfected surgical incision
  • Approximated by surgical sutures

Second Intention -> substantial scar

  • Excisional wounds
  • Repair process is more complicated
  • Create large defects on the skin surface
  • Extensive loss of cells and tissue
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25
Q

anterolateral (spinothalamic) pathway transmits

A 
pain
thermal
crude touch
tickle/itch
sexual sensation
-very little point discrimination
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26
Q

Pain neurotransmitters

A

neurotransmitters:

  • substance P (C fibers)
  • glutamate: activation of AMPA/NMDA (A delta)
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27
Q

Fast pain conduction route (anterolateral tract)

A

1st order: terminates in dorsal horn (lamina marginalis)

2nd order: crosses at lamina marginalis and ascend to thalamus and

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28
Q

Slow pain conduction route (paleospinothalamic pathway)

A

1st order: terminates in substantia gelatinosa (laminae II and III) in dorsal horn
2nd order: 1/4 to thalamus the rest terminate widely in the brainstem (reticular nuclei -> reticular activating system, tectum of midbrain, periaqueductal grey)

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29
Q

Pain suppression neurotransmitters

A
  • encephalin (pre- and post-synaptic inhibition of type C and Ad fibers)
  • serotonin
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30
Q

methanol stimulate

capsaicin (chilli)

A

TRPM8
TRPV1 (Ca2+ influx)
-(mild activator), adenosine, bradykinin, piperine, camphor, some venoms and jellyfish extract

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31
Q

MECHANISM
Prostaglandin
Anesthetics
Opiates

A

Prostaglandin: enhances/facilitate pain transmission
Anesthetics: blocks Na+ channels -> pain no AP
Opiates: inhibit at synapses via pre/post synaptic inhibition

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32
Q

Normal BMI

A

18.5-25

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33
Q

Marasmus

A

low protein and low carbohydrate intake leading to emaciation

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34
Q

Kwashiorkor

A

Calorie deprivation may be nearly adequate, but protein deprivation is severe

  • distended abdomen bc depletion of visceral protein
  • edema bc low albumin level = low oncotic pressure
  • fatty liver due to sparing of subcutaneous fat
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35
Q

Cachexia

A

is loss of weight, muscle atrophy, fatigue, weakness and significant loss of appetite in someone who is not actively trying to lose weight

  • PEM caused by advanced cancer, AIDs
  • PIF and proinflammatory cytokines cause skeletal muscle breakdown via NF-κB activation of ubiquitin proteasome pathway
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36
Q

Anorexia nervosa vs. bulimia

A

Anorexia nervosa: self-induced starvation that can lead to arrhythmiaandsudden death
Bulimia: binging on food and then induced vomiting (frequent vomiting leads to electrolyte imbalances)

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37
Q

Folic Acid (B9)

A

Megaloblastic anemia: bc enough protein but cells cannot divide

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38
Q

Cobolamin (B12)

A
  • pernicious anemia: B12 malabsorption due to def. in parietal cells that release intrinsic factor
  • neurologic dysfunction
  • megaloblastic anemi: needed for folate to function properly
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39
Q

Pyridoxine (B6)

A

Coenzyme especially for amino acid metabolism

  • active compound is pyridoxal phosphate (PLP)
  • microcytic anemia
  • ONLY water soluble vitamin with sufficient toxicity -> sensory neuropathy
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40
Q

Thiamine (B1)

A

Function in decarboxylation reactions related to the TCA cycle

  • Wernicke-Korsakoff syndrome: memory loss and loss of balance due
  • Beriberi: wet = cardiovascular, dry = nervous system
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41
Q

Niacin (B3)

A

Coenzymes in oxidation reduction reactions

-Pellagra: triple D (dermatitis, dementia, diarrhea)

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42
Q

Riboflavin (B2)
Biotin (B7)
Pantothenic acid (B5)

A

Riboflavin (B2): coenzymes of oxidation reduction reactions
Biotin (B7): coenzyme of carboxylation reactions
Pantothenic acid (B5): functions to transfer acyl groups

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43
Q

Vitamin A (retinol) and too much?

A

Maintenance of normal vision: synthesis of rhodopsin (night vision) and photopsins (color vision)
-buildup of keratin debris in small opaque plaques(Bitot spots)
Cell growth and differentiation: orderly differentiation of mucosal epithelium (def. causes epithelia metaplasia and keratinization)

Hypervitaminosis A: toxic level may produce liver cirrhosis
-synthetic retinoids in pregnancy should be avoided because of teratogenic effects

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44
Q

Vitamin D

A

maintain plasma calcium by absorption from intestines and kidneys

  • Deficiency causes bone demineralization (rickets in children and osteomalacia in adults)
  • Excess causes hypercalcemia and renal stones
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45
Q

Vitamin C

A

antioxidant and hydroxylation of collagen:Inadequately hydroxylated fibroblast procollagen cannot acquire stable helical configuration (in blood vessels, predisposes to hemorrhages)

  • Def.: scurvy
  • Toxicity: iron overload (inc absorption of iron)
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46
Q

Vitamin K

Vitamin E

A

Vitamin K: coenzyme for clotting factors

Vitamin E: deficiency is rare and may present with red blood cells sensitivity to oxidative stress (antioxidant)

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47
Q

Pear shape vs apple shape

A

Pear shape: lower risk of metabolic disease

Apple shape: excess central abdominal fat has an increased risk of morbidity and mortality

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48
Q

POMC/CART vs. NPY/AgRP

A

POMC/CART: promote energy expenditure and weight loss via MSH hormone -> TRH and CRH
-leptin activates (secreted by adipocytes to dec appetite)

NPY/AgRP: promote food intake and weight gain via Y1/5 receptor -> MHC and orexin

  • gherlin activates (released by stomach to inc appetite)
  • pYY, leptin, amylin inhibit (causes satiety)
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49
Q

Adiponectin

A

fat burning molecules that direct fatty acids to liver for B oxidation and decrease glucose production

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50
Q

Contraction of ciliary muscles results in

A

decreased tension on suspensory ligament and, in turn, allows the lens to increase its thickness, thereby focusing light rays from a NEAR object onto retina

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51
Q

constrictor vs dilator muscles of the iris (control)

A

constrictor: parasympathetic control
dilator: sympathetic control

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52
Q

glaucoma

A

Aqueous humor is constantly secreted and it is drained into the spaces of fontana, if drainage is block -> pressure on optic nerve resulting in glaucoma

53
Q

presbyopia

cataract

A

loss in lens elasticity as one ages resulting in farsightedness

cataract: opacification of the lens

54
Q

neural and non neural part of the retina

A

non-neural: pigment epithelium -> single layer of light-absorbing, pigmented cells lying adjacent to the choroid

neural: photoreceptors lie deepest within the retina and interdigitate with the pigment epithelium
- contains neurons

55
Q

retinitis pigmentosa

retinal detachment

A

retinitis pigmentosa: debris from photoreceptor cells accumulates between the photoreceptor cell layer and the pigment epithelial cell layer (normally phagocytosed by pigmented epithelial cells)

retinal detachment: detachment between the pigment epithelial cell layer and the photoreceptors

56
Q

rods vs cones

A

Rods: found around the periphery of the eye and are sensitive to light brightness (used to see in dim light)

Cones: found in the center of the eye and are used to confer high visual sharpness

57
Q

first order vs second order neurons of the eye

-pathway of light transmission

A

First-order neuron: bipolar cell (lies within retina)

Second-order neuron: ganglion cell (join to form optic nerve)

-light hits rods and cones -> bipolar cells -> ganglion cells

58
Q

Horizontal cells vs Amacrine cells

A

Horizontal cells modulate transmission between photoreceptors and bipolar cells

Amacrine cells modulate transmission between bipolar cells and ganglion cells

59
Q

Fovea

A

contain mainly rods that are directly exposed to light because of displacement of the others layers of the non neural part of the retina

60
Q

Optic Disc or Papilla

A

where unmyelinated optic nerve fibers exit from the retina

-contains no photoreceptors -> blind spot

61
Q

night blindness cause

A

On absorbing light, rhodopsin is broken down into retinal and opsin. After absorbing light, rhodopsin is then restored by a series of chemical reactions, some of which depend on vitamin A
-def. in vitamin A results in night blindness

62
Q

color blindness

A

absence of red, blue, or green cones

63
Q

disc edema, papilledema, or choked disc

A
  • optic nerve is surrounded by the dura as well as the arachnoid and pia mater
  • increased intracranial pressure can exert pressure via the cerebrospinal fluid-filled subarachnoid space onto the optic nerve
64
Q

Thalamic lesion result

A

complete all sensory loss (touch, pain, temp) on contralateral side of body

65
Q

Lateral Pontine lesion result

A
  • ipsilateral complete loss of facial sensory

- contralateral anterolateral (pain, temp) sensory loss

66
Q

Medial Medullary lesion results

A
  • no face sensory loss

- contralateral dorsal/post. column (vibration, touch, proprioception)

67
Q

pretectal area (light reflex) pathway

A

some optic nerve fibers branch off and terminate at the Edinger-Westphal nucleus (pretectal area) which mediates pupillary light reflex (constriction)

  • Edinger-Westphal nucleus -> pregang parasymp (oculomotor n.) -> ciliary gang -> postgang parasymp (short ciliary n.) -> constrictor muscle
  • one eye constricting will cause the other eye to also constrict
68
Q

damage to temporal lobe

A

will effect Meyer’s loop resulting in obstruction of superior visual field

69
Q

homonymous vs heteronymous

A

homonymous: same part of the visual field in each eye
- obstruction post. to optic chiasm
heteronymous: part of the visual field lost in each eye is different
- obstruction ant. to optic chiasm

70
Q

damage to optic chiasm

A

right eye: loss of left visual field
left eye: loss of right visual field
-bitemporal hemianopsia

71
Q

damage to right optic tract

A

loss of left visual field for left and right eye

72
Q

Pupillary Dilation Reflex pathway

A

post. hypothalamus -> ciliospinal center (C8) (pregang) -> superior cervical gang and synapse -> nasociliary and long ciliary nerves (carotid plexus) -> constrictor muscles

73
Q

dilator muscle vs constrictor muscle

A

d

74
Q

Accommodation Reflexes pathway

A

accommodation of lens, constriction of pupils, convergence of eyes

  • occipital cortex -> accommodation center (oculomotor nuclei) -> then
  • Edinger-Westphal (lens and pupil change) nucleus ->pregang parasymp (oculomotor n.) -> ciliary gang -> postgang parasymp (short ciliary n.) -> constrictor muscle
  • Somatic nuclei (convergence) -> medial rectus muscle
75
Q

Horner syndrome

A

miosis, mild ptosis (drooping of the eyelid) and anhidrosis (loss of sweating)
-lesions involving the lateral medulla; cervical spinal cord injuries, tumors, or syringomyelia; trauma to T1 and T2 ventral roots; cervical sympathetic trunk involvement by pulmonary carcinoma; and diseases of the internal carotid artery

76
Q

Path of light in the eye:

A 
Cornea (2/3 of refractive power occurs here)
Aqueous humor
Lens
Vitrous humor
Retina
77
Q

Route of aqueous humor

A

Flow through the pupil -> angle of anterior chamber -> trabecular meshwork -> canal of Schlemm -> aqueous veins -> choroidal plexus
-iredial crypts absorption some aqueous humor (iris)

78
Q

purpose of pigmented layer

A

Prevents light scattering
Reduces the risk of choroidal melanoma
Storage of vitamin A (required to make photopigments)
Phagocytosis

79
Q

cGMP phosphodiesterase (PDE5)

A

Metarhodopsin II -> transducen -> cGMP phosphodiesterase -> breaks down cGMP -> closure of the Na+ gates -> hyperpolarization -> cessation of glutamate release from the receptor

80
Q

Rhodopsin kinase

A

inactivates metarhodopsin II

81
Q

dark adaptation

A 
In dark (dim light), more cis retinal is formed from vitamin A -> more photopigment-protein combination -> enhanced sensitivity 
-takes time, why it takes a while before you can see better in the dark
In light rhodopsin is broken down and stored as vitamin A (trans retinol)
-FASTER
OTHERS:
-pupil size
-Ca2+ indirectly regulates Ca2+ channels
82
Q

Light through retina

A
  1. ganglion cells
    - amacrine cells
  2. Bipolar cells
    - horizontal cells
  3. Rods/Cones
  4. Pigmented epithelium (absorbs light so its not bouncing around eye distorting image, phagocytosis, stores vitamin A)
83
Q

macula brain part

A

most posterior part of visual cortex

84
Q

each optic tract, lateral geniculate nucleus and visual cortex receives information relating only to the contralateral half of the visual field This combination of images from both eyes is necessary for

A

stereoscopic vision (depth perception)

85
Q

myopia and cause

A

near sightedness

cause: over powerful cornea/lens, eye too long of axis

86
Q

hypermetropia and cause

A

far sightedness

-short eye axis

87
Q

Presbyopia
Cycloplegia
Anisometropia

A

Presbyopia: hardening of lens causing loss of lens accommodation
Cycloplegia: loss of accommodation bc ciliary m. paralysis
Anisometropia: two eyes have unequal refractive power

88
Q

Descending pain modulation pathways

A

Periaqueductal gray matter -> nucleus raphe manus -> down spinal cord -> interneurons at dorsal horn

OR

locus ceruleus neurons in upper pons -> down spinal cord -> interneurons at dorsal horn

89
Q

thalamus blood supply

A

perforating branches of posterior cerebral artery and posterior communicating artery

90
Q

ventral anterior (VA) nuclei

A

where basal ganglia can exert control over movement

  • medial segment of globus pallidus (3) and terminates-> principal part
  • pars reticulata of substantia nigra (4) and terminate -> magnocellular part
91
Q

ventral lateral (VL) nuclei

A

receives information from ipsilateral GPe, SNr and contralateral dentate nucleus

92
Q

ventral posterior (lateral, VPL; and medial, VPM) nuclei

  • ventral posterolateral nucleus
  • ventral posteromedial nucleus
A

general sensory information from contralateral half of body

ventral posterolateral nucleus (VPL): -> trance and limbs

  • spinothalamic tracts
  • medial lemniscus

ventral posteromedial nucleus (VPM):
-trigeminothalamic tracts

to —> primary somatosensory cortex

93
Q

Medial Geniculate Nucleus

A

Receives ascending fibers from -> inferior colliculus of midbrain -> primary auditory cortex (Transverse temporal (Heschl’s) gyrus)

94
Q

Anterior Nuclear Group

A

mammillary bodies –(mamillothalamic tract)–> ANG -> cingulate gyrus

Involved in:

  • control of instinctive drives (e.g., parenting)
  • emotional aspects of behaviors (e.g., fear)
  • memory
95
Q

Medial Nuclear Group controls

A

efferent to prefrontal cortexs

-mood and emotions

96
Q

Broca’s area

-brodmann’s area

A

speech production (can’t talk but can understand speech)

  • area 44, 45
  • found on dominant side, non dominant side responsible for variation in tone
97
Q

wernicke’s area (Auditory Association Cortex)

A

understanding spoken word (can talk but meaningless speech)

-found on dominant side, non dominant side appreciation of subliminal meanings and humor

98
Q

Layer III
Layer IV
Layer V

A

Layer III: commissural fibers
Layer IV: termination for afferent fibers from specific thalamic nuclei
Layer V: projection fibers to extracortical targets (basal ganglia, thalamus, brain stem and spinal cord)
-location of BETZ CELLS

99
Q

precentral gyrus

  • location
  • brodmann’s area
  • afferent fibers coming from
A

primary motor cortex: motor control to contralateral half of body

  • anterior to central sulcus
  • area 4
  • ventral lateral nucleus of the thalamus
100
Q

premotor cortex

  • location
  • brodmann’s area
A

less focused movements, posture, preparation of movements

  • anterior to primary motor cortex
  • area 6
  • includes SMA (postural control)
101
Q

Frontal Eye Field

  • location
  • brodmann’s area
  • lesion
A

Controls voluntary conjugate deviation of the eyes, as occur when scanning the visual field

  • inferior portion of premotor cortex
  • area 8
  • unilateral damage to this area causes conjugate deviation of the eyes towards the side of the lesion
102
Q

Prefrontal Cortex

A

Has cognitive functions that include:

  • Intellect
  • Judgment
  • Predictive faculties
  • Planning of behavior
103
Q

Left Frontal Lobe Lesions

A
  • Partial seizures: Paroxysmal jerking movements of the contralateral limbs are termed ‘simple motor’ or ‘Jacksonian’ seizures
  • Sensory/motor deficit: contralateral hemiplegia
  • Broca’s aphasia: Speech is produced with great effort and poor articulation
104
Q

Alzheimer’s disease

A
  • atrophy of the temporal and parietal lobes and the limbic system
  • disorientation in space, and loss of language (aphasia) and memory (amnesia)
105
Q

General paralysis of the insane (GPI)

A

-both frontal lobes are destroyed
total alteration of personality with loss of judgment

-planning and insight, and bizarre and uncharacteristic behavior

106
Q

Postcentral Gyrus

-brodmann’s

A

somatosensory cortex: sensory to contralateral half of body

-Brodmann’s areas 1, 2 and 3

107
Q

Right parietal lobe lesions vs. left parietal lobe lesions

A

SAME
-partial seizures: paroxysmal attacks of sensory disturbance affecting the contralateral side of the body (simple sensory seizures)

-sensory/motor deficit: contralateral hemisensory loss and an inferior visual field loss

DIFFERENT
RIGHT: psychological deficit: an inability to copy and construct designs because of spatial disorientation (constructional apraxia)

LEFT:Psychological deficit: inability to name objects (anomia) and a loss of literacy, with inability to read (alexia), to write (agraphia) and to calculate (acalculia)

108
Q

Left Temporal Lobe Lesions

A
  • Partial seizures: paroxysmal attacks of unresponsiveness (absences), purposeless behavior (automatism), olfactory and complex visual and auditory hallucinations, and disturbances of mood and memory (déjà vu)
  • Sensory/motor deficit: contralateral superior visual field loss
  • Psychological deficit: speech that is fluent and rapid but contains word errors (paraphasia) and is incomprehensible
109
Q

Occipital Lobe Lesions Cause

A

-Partial seizures: paroxysmal visual hallucinations of a simple, unformed nature, such as lights and colors (simple partial seizures)

-Sensory/motor deficit: contralateral visual field loss (contralateral homonymous hemianopia)
Bilateral occipital lobe lesions lead to:

-Bilateral occipito-parietal lesions can spare elementary vision, but prevent the recognition and depiction of objects (apperceptive visual agnosia)

110
Q

spatial summation vs temporal summation

A

spatial summation: multiple nuerons firing causing AP

temporal summation: 1 neuron firing multiple times causing AP

111
Q

C fibers and Adelta fibers terminate where in the dorsal horn

A

C fibers terminate in substantia gelatinosa

Ad fibers terminate in lamina marginalis

112
Q

Glutamate in hypersensitivity (hyperalgesia)

A

High glutamate primes neuron to express NMDA and inc AMPA resulting in any release of glutamate causing an exaggerated response

113
Q

Pos. Romberg test issue

A

Patients with dorsal column (medial lemniscal) tract dysfunction can stand still properly with eyes open
With eyes closed, they fall

114
Q

abnormal nystagmus cause

A

eye tracking finger slowly but stops tracking for a moment, then snaps to finger again
-CN VIII issues

115
Q

TRPM8

A
  • inward cations (Na+ and Ca++)
  • sensative to temperatures between 10-35 degrees Celsius
  • Menthol activates TRPM8
116
Q

Convergence high vs low

A

high: decrease localization
low: increase localization
- convergence can be from multiple sources (3 different neurons or multiple synapses from one neuron)

117
Q

Trigger pain:

A

Trigger pain: bradykinin, serotonin, histamine, K+, ACh and proteolytic enzymes
Increase pain sensitivity: Substance P and prostaglandin

118
Q

A alpha fibers:
A beta fibers:
A delta fibers:
C fibers:

A
  1. A alpha fibers: proprioception
  2. A beta fibers: touch
  3. A delta fibers: pain (acute)
  4. C fibers: pain (chronic)
    - 1 > 2 > 3 > 4 speed of transmission
119
Q

Reticular nucleus interaction with thalamus

A

sends inhibitory GABA to thalamic nuclei (regulatory input to thalamus)

120
Q

Primary auditory cortex brodmann’s

A

41 and 42

121
Q

eye constriction vs. dilation

A

Constriction: open angle, inc surface area for iridial crypts
Dilation: closed angle

122
Q

Rhodosin

  • proteins
  • unstimulated form
A

Light sensitive pigment in rods

  • scotopsin + retinal
  • unstimulated form: cis
123
Q

Rhodospin break down

A

bathorhodopsin (partially split rhodopsin) -> decays in ns to lumirhodopsin -> metarhodopsin I -> metarhodopsin II -> complete split to all-trans retinal and scotopsin

-metarhodopsin II active form

124
Q

Retinal isomerase

A

recycles all-trans back to cis retinal

125
Q

Horizontal cells
Bipolar Cells
Amacrine Cells

A

Horizontal cells: lateral inhibitory cells that provide contrast
-primary lateral inhibition
Bipolar Cells: inhibitory and excitatory cells that sharpen retinal image (photoreceptor cell -> bipolar cell)
Amacrine Cells: Interneurons between bipolar and ganglion cell
-some lateral inhibition
Ganglion Cells:

126
Q

Neurotransmitters

A
  • Glutamate is secreted by rods and cones

- GABA, ACh, glycine, dopamine and indolamine in amacrine cells play inhibitory roles

127
Q

Ganglion Cells (M and P)

A

-1 to 1 in fovea (sharp vision)
-200 to 1 in peripheral retina (light sensitivity)
-Few % of ganglion cells are sensitive to light and have melanopsin -> circadian rhythm regulation
M: sensitive to low contrast and rapid movement visual signals (not sensitive to color)
P: fine details, edges, color discrimination (sensitive to color)

128
Q

Upper visual field pathway

A

sweep into temporal lobe forming Meyer’s loop

-Damage to temporal lobe can effect meyer’s loop (sup. visual field)

129
Q

Miosis

ptosis

A

Miosis: pupil constriction
ptosis: drooping of eye

BECOM 2 (7 decks)

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