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BECOM II Exam 5 > El Hefnawy - week 1 > Flashcards

El Hefnawy - week 1 Flashcards

1
Q

adequate vs. inappropriate stimulus

A

adequate - stimulus that receptor was designed for; low threshold
inappropriate - irritation of the stimulus; not the normal

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2
Q

what occurs with increasing the stimulus intensity?

A

increase the frequency of the coded AP

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3
Q

TRPM8

A

menthol activates this channel

  • inward cations (Na+, Ca++)
  • sensitive over temps 10-35 degrees C
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4
Q

tonic vs. phasic receptors

A

tonic - slow or non-adapting; ex. proprioception, chemoreceptors
phasic - fast adapting; on or off response; ex. tactile

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5
Q

variation in conduction

A
  • thick, myelinated fibers fastest

- thin, unmyelinated fibers slowest

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6
Q

A fibers

A

conduct fast pain

  • pacinian and Ruffini use the Abeta fibers
  • tactile and fast pain use the Adelta fibers
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7
Q

C fibers

A

conduct slow pain

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8
Q

temporal vs. spatial summation

A
  • spatial = multiple graded potentials from different neurons reach threshold –> fire AP
  • temporal = multiple repetitive signals from the same neuron reaches threshold –> fire AP
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9
Q

how can an intense stimulus fire more neurons?

A

higher # of facilitated zone neurons are activated leading to the stronger stimulus

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10
Q

convergence

A

many inputs entering exciting a single neuron

-point discrimination/localization is lost with increasing convergence

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11
Q

dorsal column medial lemniscus

A
  • large myelinated fibers
  • transmit only mechanoreceptor info.
  • crosses at medulla (2nd order)
  • 3rd order in thalamus
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12
Q

amorphysis

A

loss of association cortex (complex sensory experience)

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13
Q

2 point discrimination

A

block lateral spread of synaptic transmission by inhibiting adjacent neurons

  • increases contrast b/w stimulus
  • can use interneurons to suppress adjacent
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14
Q

anterolateral pathway aka spinothalamic tract

A
  • info. goes straight to thalamus

- transmits: pain, temp, crude touch, sex

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15
Q

substance P vs. glutamate

A

substance P - chronic pain

glutamate - fast/acute pain (hyperexcitability with activation of NMDA)

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16
Q

fast pain conduction (neospinothalamic pathway)

A
  • Adelta fibers
  • terminate in lamina marginalis in dorsal horn containing 2nd order neuron
  • ascending fibers - some terminate in reticular formation but most in thalamus
  • glutamate as NT
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17
Q

slow pain conduction (paleospinothalamic pathway)

A
  • C fibers
  • terminate in substantia gelatinosa in dorsal horn containing 2nd neuron
  • ascending fibers - terminate in brainstem mainly (1/4 in thalamus)
  • substance P as NT
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18
Q

what are the chemicals used as analgesics?

A
  • endorphine
  • enkephalin
  • dynorphin
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19
Q

analgesia system components

A
  • periaquaductal gray
  • raphe Magnus nucleus
  • pain inhibitory complex in dorsal horn
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20
Q

how can you inhibit the neurons?

A

descending inhibitory neurons from brainstem

-can inhibit postsynaptic neuron or presynaptic neuron by releasing endorphins, enkephalins

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21
Q

referred pain

A

when 2nd order neurons in dorsal horn receive mixed signals from viscera and skin

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22
Q

visceral pain

A 
localized damage (ex. ischemia, ulcer, spasm, over distention) --> severe pain 
-stab wounds do not cause much pain
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23
Q

how do you get hyperalgesia?

A
  • primarily from burn

- secondarily from spinal cord or thalamic lesions

24
Q

what happen with excess production of glutamate due to damage?

A

activates both AMPA and NMDA –> Ca++ release –> more production of AMPA and glutamate –> hyperalgesia

25
Q

capsaicin

A
  • uses TRPV1 channel –> Ca2+ influx –> pain and burning

- other activators: bradykinin, adenosine, piperine, camphor, venoms, jellyfish extract

26
Q

how do local anesthetics work?

A

membrane stabilizing drugs by inhibiting Na+ channel –> no AP
-acidosis from inflammation protonates the drugs inhibiting them from entering

27
Q

refraction

A

bending of light as it passes from optic density to another

-air to cornea has the most bending

28
Q

diopteric power

A

the power of refraction

  • excess refraction in myopia (high cornea)
  • less refraction in hypermetropia (flat cornea)
29
Q

cornea and sclera of eye

A
  1. cornea - REFRACTION; avascular; receive O2 and nutrients from aqueous humor and lacrimal fluid; only free nerve endings, no tactile
  2. sclera - white part; exoskeleton of the eye; attachment for extrinsic eye muscles
30
Q

formation of aqueous humor

A

formed by Na+ secretion from ciliary body

  • pulls Cl- and H2O in w/ it; also sugar and AAs
  • ciliary body –> post. chamber –> pupil –> angle of ant. chamber –> trabecular meshwork –> canal of schlemm –> venous/choroid plexus
  • increased intraocular pressure w/ insufficient drainage –> glaucoma
31
Q

glaucoma cause and effects

A

increased intraocular pressure –> damage optic nerve causing blindness

  • open or closed angle
  • closed = dilation of pupil in dark closing chamber of ant. angle –> acute red eye
32
Q

accommodation reflex

A

change in dioptric power of lens

  • contracting ciliary muscle relaxing suspensory ligament –> increase curvature (convexity,thickness) of lens - more power
  • signal travels to CORTEX
33
Q

vision pathway

A

optic nerve –> LGN –> primary visual cortex –> pretectal area –> Edinger Westphal –> ciliary ganglion –> contract ciliary muscle and constrictor pupillae

34
Q

refraction defects

A
  1. myopia (nearsighted) = focus anterior to retina
  2. hypermetropia (farsighted) = focus posterior to retina
  3. astigmatism = uneven curvature
  4. presbyopia = lens sclerosis - lose accomodation
  5. cycloplegia = paralysis - lose accommodation
  6. anisometropia = unequal refraction in both eyes
35
Q

pupillary reactions

A

constriction (miosis)

  • increases ant. angle –> more iridial crypt absorption of aqueous humor preventing glaucoma
  • controls depth of focus of lens
  • squinting reduces distortion of light
36
Q

pupillary reflex

A

info. travels to thalamus, not cortex
- pretectal area –> thalamus (LGN) –> edinger westphal –> ciliary ganglion –> ciliary muscles –> pupil constriction (miosis)

37
Q

depth perception - stereopsis (binocular)

A
  • determined by size of object and angle

- moving parallax (moving eye changes angle)

38
Q

layers and receptors of eye

A
  1. pigment (outer) - no synapse, prevent light scattering w/ melanin, phagocytosis, store vit. A
  2. photoreceptor layer
  3. outer nuclear - nuclei of receptors
  4. outer plexiform - synapses
  5. inner nuclear - bipolar
  6. inner plexiform - 2nd synapse b/w bipolar and ganglion cells
39
Q

where does retinal detachment occur?

A

b/w pigment layer and receptor layer

40
Q

retina

A
  • contain photoreceptors - cones and rods (outer segment), mitochondria and nucleus (inner segment)
  • optic disc - blind spot, no photoreceptors
  • best visual acuity in fovea and macula
41
Q

importance of fovea centralis

A
  • least convergence - cones only (high density)

- no blood vessels –> macula and fovea 1st to degenerate if deprived of nutrients

42
Q

cones vs. rods

A
  1. cones
    - in center (fovea), low sensitivity, high acuity, day vision, color, blue red green light
  2. rods
    - periphery, high sensitivity, low acuity (high convergence), night vision, black/white, monochromatic (don’t respond to red)
43
Q

rods - rhodopsin

A
  • contains retinal (pigment) and scotopsin (protein)
  • stimulation by light converts cis retinal to trans retinal (unstable)
  • batho –> lumi –> metarhodopsin I –> metarhodopsin II (active) –> trans retinal + scotopsin –> cis retinal + scotopsin –> rhodopsin
  • converting enzyme isomerase
44
Q

where does the excess retinal go?

A

store as retinol (vitamin A) in pigment layer

-pull from stores and convert back to retinal by isomerase if needed

45
Q

excitation of rods in response to metarhodopsin II

A
  • default - depolarization –> Na+ influx/K+ efflux during dark current (cGMP) dependent –> high NT release
  • stimulated rods by light - metarhodopsin activates transducin –> activate PDE5 –> stop Na+ influx –> continue K+ efflux –> hyperpolarization –> less NT (glutamate)
  • rhodopsin kinase inactivates metarhodopsin II
  • faster changes in cones than rods
46
Q

how can viagra lead to blindness?

A

inhibit PDE5 –> continued depolarization –> light distortion

47
Q

color vision by cones

A
  • photopsin protein
  • different combinations b/w retinal and proteins determines the wavelengths detected
  • combine different receptors for color variety
48
Q

why don’t rods see red?

A

prevent from losing dark adaptation when looking at Xray films under red light for ex.

49
Q

light vs. dark adaptation

A
  1. light adaptation
    - faster than dark but low sensitivity, breaks pigments-proteins and converts pigments to vit. A for storage
  2. dark adaptation
    - slower, synthesize pigment to increase sensitivity, pull from vit. A stores
50
Q

horizontal cells

A
  • inhibitory (always) - lateral inhibition –> prevents distortion and provides contrast
  • inhibit neurons less stimulated
  • most active neuron passes signal to bipolar cell
51
Q

bipolar cells

A

ON/OFF response - inhibitory or excitatory

  • provide contrast and sharpen image by depolarizing one and hyper polarizing the other
  • 1st theory: depends on glutamate receptors
  • 2nd theory: horizontal cell inhibition of bipolar
52
Q

amacrine cells

A

interneurons - control many NTs

  • communication with neurons, control light sensitivity, detect direction, paracrine (ACh, dopamine)
  • some provide lateral inhibition
53
Q

ganglion cells

A
  • on/off centers - respond to different illuminations
  • melanopsin protein
  • stimulate suprachiasmatic nuclei regulating circadian rhythm
54
Q

P (parvocellular) vs. M (magnocellular) ganglion cells

A
  1. P cells
    - smaller, color sensitive, fine details, slow movement, sustained response
  2. M cells
    - larger, color insensitive, low contrast, rapid movement, transient response
55
Q

eye centers in brain

A
  1. suprachiasmatic = input from ganglion cells - circadian rhythm
  2. superior colliculi = rapid movement of eyes (moving object)
  3. pretectal nuclei = eye reflex, light reflex
  4. VLN = behavior
  5. LGN = fibers to midbrain (Edinger westphal)
56
Q

oculocephalic reflex

A

brain dead if eyes fail to fixate on object when head is being moved

BECOM II Exam 5 (24 decks)

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