El Hefnawy - week 1 Flashcards
adequate vs. inappropriate stimulus
adequate - stimulus that receptor was designed for; low threshold
inappropriate - irritation of the stimulus; not the normal
what occurs with increasing the stimulus intensity?
increase the frequency of the coded AP
TRPM8
menthol activates this channel
- inward cations (Na+, Ca++)
- sensitive over temps 10-35 degrees C
tonic vs. phasic receptors
tonic - slow or non-adapting; ex. proprioception, chemoreceptors
phasic - fast adapting; on or off response; ex. tactile
variation in conduction
- thick, myelinated fibers fastest
- thin, unmyelinated fibers slowest
A fibers
conduct fast pain
- pacinian and Ruffini use the Abeta fibers
- tactile and fast pain use the Adelta fibers
C fibers
conduct slow pain
temporal vs. spatial summation
- spatial = multiple graded potentials from different neurons reach threshold –> fire AP
- temporal = multiple repetitive signals from the same neuron reaches threshold –> fire AP
how can an intense stimulus fire more neurons?
higher # of facilitated zone neurons are activated leading to the stronger stimulus
convergence
many inputs entering exciting a single neuron
-point discrimination/localization is lost with increasing convergence
dorsal column medial lemniscus
- large myelinated fibers
- transmit only mechanoreceptor info.
- crosses at medulla (2nd order)
- 3rd order in thalamus
amorphysis
loss of association cortex (complex sensory experience)
2 point discrimination
block lateral spread of synaptic transmission by inhibiting adjacent neurons
- increases contrast b/w stimulus
- can use interneurons to suppress adjacent
anterolateral pathway aka spinothalamic tract
- info. goes straight to thalamus
- transmits: pain, temp, crude touch, sex
substance P vs. glutamate
substance P - chronic pain
glutamate - fast/acute pain (hyperexcitability with activation of NMDA)
fast pain conduction (neospinothalamic pathway)
- 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
slow pain conduction (paleospinothalamic pathway)
- 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
what are the chemicals used as analgesics?
- endorphine
- enkephalin
- dynorphin
analgesia system components
- periaquaductal gray
- raphe Magnus nucleus
- pain inhibitory complex in dorsal horn
how can you inhibit the neurons?
descending inhibitory neurons from brainstem
-can inhibit postsynaptic neuron or presynaptic neuron by releasing endorphins, enkephalins
referred pain
when 2nd order neurons in dorsal horn receive mixed signals from viscera and skin
visceral pain
localized damage (ex. ischemia, ulcer, spasm, over distention) --> severe pain -stab wounds do not cause much pain
how do you get hyperalgesia?
- primarily from burn
- secondarily from spinal cord or thalamic lesions
what happen with excess production of glutamate due to damage?
activates both AMPA and NMDA –> Ca++ release –> more production of AMPA and glutamate –> hyperalgesia
capsaicin
- uses TRPV1 channel –> Ca2+ influx –> pain and burning
- other activators: bradykinin, adenosine, piperine, camphor, venoms, jellyfish extract
how do local anesthetics work?
membrane stabilizing drugs by inhibiting Na+ channel –> no AP
-acidosis from inflammation protonates the drugs inhibiting them from entering
refraction
bending of light as it passes from optic density to another
-air to cornea has the most bending
diopteric power
the power of refraction
- excess refraction in myopia (high cornea)
- less refraction in hypermetropia (flat cornea)
cornea and sclera of eye
- cornea - REFRACTION; avascular; receive O2 and nutrients from aqueous humor and lacrimal fluid; only free nerve endings, no tactile
- sclera - white part; exoskeleton of the eye; attachment for extrinsic eye muscles
formation of aqueous humor
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
glaucoma cause and effects
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
accommodation reflex
change in dioptric power of lens
- contracting ciliary muscle relaxing suspensory ligament –> increase curvature (convexity,thickness) of lens - more power
- signal travels to CORTEX
vision pathway
optic nerve –> LGN –> primary visual cortex –> pretectal area –> Edinger Westphal –> ciliary ganglion –> contract ciliary muscle and constrictor pupillae
refraction defects
- myopia (nearsighted) = focus anterior to retina
- hypermetropia (farsighted) = focus posterior to retina
- astigmatism = uneven curvature
- presbyopia = lens sclerosis - lose accomodation
- cycloplegia = paralysis - lose accommodation
- anisometropia = unequal refraction in both eyes
pupillary reactions
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
pupillary reflex
info. travels to thalamus, not cortex
- pretectal area –> thalamus (LGN) –> edinger westphal –> ciliary ganglion –> ciliary muscles –> pupil constriction (miosis)
depth perception - stereopsis (binocular)
- determined by size of object and angle
- moving parallax (moving eye changes angle)
layers and receptors of eye
- pigment (outer) - no synapse, prevent light scattering w/ melanin, phagocytosis, store vit. A
- photoreceptor layer
- outer nuclear - nuclei of receptors
- outer plexiform - synapses
- inner nuclear - bipolar
- inner plexiform - 2nd synapse b/w bipolar and ganglion cells
where does retinal detachment occur?
b/w pigment layer and receptor layer
retina
- 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
importance of fovea centralis
- least convergence - cones only (high density)
- no blood vessels –> macula and fovea 1st to degenerate if deprived of nutrients
cones vs. rods
- cones
- in center (fovea), low sensitivity, high acuity, day vision, color, blue red green light - rods
- periphery, high sensitivity, low acuity (high convergence), night vision, black/white, monochromatic (don’t respond to red)
rods - rhodopsin
- 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
where does the excess retinal go?
store as retinol (vitamin A) in pigment layer
-pull from stores and convert back to retinal by isomerase if needed
excitation of rods in response to metarhodopsin II
- 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
how can viagra lead to blindness?
inhibit PDE5 –> continued depolarization –> light distortion
color vision by cones
- photopsin protein
- different combinations b/w retinal and proteins determines the wavelengths detected
- combine different receptors for color variety
why don’t rods see red?
prevent from losing dark adaptation when looking at Xray films under red light for ex.
light vs. dark adaptation
- light adaptation
- faster than dark but low sensitivity, breaks pigments-proteins and converts pigments to vit. A for storage - dark adaptation
- slower, synthesize pigment to increase sensitivity, pull from vit. A stores
horizontal cells
- inhibitory (always) - lateral inhibition –> prevents distortion and provides contrast
- inhibit neurons less stimulated
- most active neuron passes signal to bipolar cell
bipolar cells
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
amacrine cells
interneurons - control many NTs
- communication with neurons, control light sensitivity, detect direction, paracrine (ACh, dopamine)
- some provide lateral inhibition
ganglion cells
- on/off centers - respond to different illuminations
- melanopsin protein
- stimulate suprachiasmatic nuclei regulating circadian rhythm
P (parvocellular) vs. M (magnocellular) ganglion cells
- P cells
- smaller, color sensitive, fine details, slow movement, sustained response - M cells
- larger, color insensitive, low contrast, rapid movement, transient response
eye centers in brain
- suprachiasmatic = input from ganglion cells - circadian rhythm
- superior colliculi = rapid movement of eyes (moving object)
- pretectal nuclei = eye reflex, light reflex
- VLN = behavior
- LGN = fibers to midbrain (Edinger westphal)
oculocephalic reflex
brain dead if eyes fail to fixate on object when head is being moved
