BECOM Exam #5 (Week 2) Flashcards
volume and frequency are measured in
volume: decibels (amplitude of wave)
frequency: hertz (frequency of wave)
Tensor tympani vs stapedius
Tensor tympani: muscle that is attached to the malleus that can contract to lessen transduction of sound to the inner ear
-CN VII (fascial)
Stapedius:
-CN V (trigeminal - mandibular division)
low frequency vs high frequency sound transduction
low: detected in wider region near the apex
higher: detected in narrower region near the base
Endolymphatic hydrops (Meniere’s Disease)
when you have too much endolymph
inner hair cells vs. outer hair cells
Inner hair cells: perceive sounds ( >90% of afferent fibers)
outer hair cells: amplify sound wave propagation
41/42 vs. 22 (Brodmann’s areas)
41 and 42: basic properties of sound, like rainfall vs thunderclap
22 (wernickes): pitch, intensity, melody, prosody – important for interpreting emotional state of a speaker
Descending hearing pathways
Superior olivary nucleus receives afferent input, send efferent outputs:
- Lateral olivocochlear efferents go to IHCs (through spiral ganglion)
- Medial olivocochlear efferents go to OHCs (bypassing spiral ganglion)
Loud noise reflex
Loud noise reflex: hair cells and vestibulocochlear cranial nerve are (primarily) afferents (CN VIII), facial (CN VII) and trigeminal nerves (CN V) are efferents to the stapedius and tensor tympani (respectively)
-L and R sup olivary nucleus -> CN VII nuclei –CN VII–> L and R stapedius
Contraction of these muscles dampens/mitigates conduction and amplification of the stapes and malleus – your built-in ‘volume limiter’
Conductive hearing loss
Sensorineural hearing loss
Conductive hearing loss: dysfunction of a structure in the outer or middle ear
Sensorineural hearing loss: dysfunction of hair cells
-Conductive loss will be able to hear a tuning fork when placed on the skull but sensorineural will not
modiolus
Central axis of the cochlea containing spiral ganglion and cochlear nerve
Ascending hearing pathway
hair cell stimulation -> CN VIII -> synapse at cochlear nuclei (some fibers decussate at sup oliv nuc, some don’t) -> synapse at inferior colliculus -> auditory cortex
-END RESULT: both L & R auditory cortices are ALWAYS receiving input from BOTH EARS
Low vs high frequency processed where
Low frequency sounds are processed superficially/laterally
High frequency sounds are processed deep/medially
Fungiform vs. foliate vs. circumvallate
innervation
location
Fungiform (have taste buds)
Innervation: facial
Location: ant. 2/3 on sides and tip
Foliate (don’t have taste buds)
Innervation: mainly glossopharyngeal and some fascial
Location: on side of tongue
Circumvallate (have taste buds)
Innervation: glossopharyngeal
Location: post. tongue
Taste Receptor Communication (2 separate ways)
- Tastant interacts with microvilli
- Depolarization of receptor potentials
- Na+ channels -> ATP released through Ca2+ independent mechanisms, into extracellular space via gap junction channels (released to extracellular space) -> firing of nerve
- Ca2+ channel -> ATP release onto peripheral nerve ending (directly to neuron) -> firing of nerve
Salt taste
No receptors involved.
Na+ ions increase outside and move into the cell through cation channels, causing depolarization
-ATP released to extracellular space
Sour taste
Weak organic acids diffuse across membrane, dissociate and increase intracellular acidity and cause cation channels to open
Stronger acids act as a ligand that will open pH-sensitive cation channels
Sweet, Umami, and bitter taste
-atp release
Bind to GPCR, cause a second messenger cascade that results in cation channels being opened
-ATP released directly onto peripheral nerve ending
Gustatory Information Pathway
Nerves from taste buds travel through respective ganglia and synapse in the nuclei of the solitary tract
- Reflex: CN X will synapse will synapse with reticular fibers allowing reflex activities of salivation, swallowing, coughing
Connections with reticular formation (RF) - Interpretation of taste: Ipsilateral travel to the thalamus to synapse in the most medial portion of the ventral posteromedial nucleus
Then to the gustatory cortex
Olfactory Receptors transduction mechanism
1 – cation channels that are closed when there is no odorant
2 – odorant binds, the G-protein dissociates from the GPCR and activates adenylate cyclase. That triggers the activation of the cAMP
3 – cAMP causes Na+ and Ca2+ in and K+ out
4 – increase in Ca2+ binds Cl- channel causes it to open and depolarize the cell
Depolarization triggers action potential
mitral cells
mitral cells make up the olfactory bulb and receive stimulation from incoming olfactory receptor cells preceding to pass down the olfactory tract
-Different odorants activate different glomeruli (mitral cell dendrites)
Prostacyclin (PGI2) NO Heparan sulfate Thrombomodulin Tissue factor pathway inhibitor Ectonucleotidase Adenosine
Prostacyclin (PGI2): inhibits platelet activation, aggregation, and vasodilates
NO: inhibits platelet activation, aggregation, and vasodilates
Heparan sulfate: activates antithrombin
Thrombomodulin: modifies thrombin activation
Tissue factor pathway inhibitor: inhibits tissue factor not allowing blood coagulation
Ectonucleotidase: destroys nucleotides resulting in the breakdown of ADP which is needed for coagulation
Adenosine: binds to the ADP receptors in the coagulation pathway blocking it
-all released by endothelial cells
GP Ib-V-IX
binds to von wilibrand factor (vWF) that is attached to collagen
-vWF must be bound to collagen for 159 to recognize it
GP IIb/IIIa (integrin alpha IIb beta3)
binds to loose fibrinogen and loose vWF
GP Ia/IIa and GP VI
bind directly to collagen
Platelet secretions upon activation
- Thromboxane A2 (AA derivative using COX), diffuses through the platelet membrane: activates platelet and also secreted by platelets
- Alpha granules exocytosis -> fibrinogen, vWF, coagulation factor V
- Dense granules exocytosis -> ADP, Ca2+
ADAMTS13
breaks down vWF multimers
P2Y1 and P2Y12 receptors
receptors that bind ADP resulting in autocrine and paracrine activation of platelets
shortage of vWF will cause what intrinsic factor def.?
VIIIa
-increases VIIIa half-life
thrombomodulin causes
binds to thrombin making a inhibitory complex that activates Protein C -> inactivation of Va and VIIIa
- secreted by normal endothelium
- Protein S (cofactor) is needed by thrombin/thrombomodulin to activate protein C
Antithrombin
Serine protease inhibitor (serpin) when it binds to heparan it inactivates thrombin, IXa, Xa and XIa
Tissue factor pathway inhibitor
Circulating or attached to vascular endothelium, inhibits Xa and VIIa-TF complex
Role of calcium (IV) in coagulation cascade
- platelet morphological changes
- activation of several coagulation factors
plasmin
active enzyme that breaks up clot by cleaving fibrin threads resulting in the degradation products D-DIMERs
-associated with fibrinolysis
Hemophilia
Excessive bleeding caused by deficiency of one of the factors in the clotting cascade
MOTION DETECTION
semicircular ducts
utricle’s macula
saccule’s macula
semicircular ducts: rotational movement of the head
utricle’s macula: side to side movement (ant. to post. movement)
saccule’s macula: vertical movement
otoconia
Enables continued sensation of head’s position in absence of acceleration
-head is put sideway but you know you head is still sideways although the movement is no longer occurring
loss of one vs loss of two vestibule system sources (eyes, inner ears, body’s proprioceptors)
Loss of one of these systems usually does not produce problems (especially if temporary)
Loss of two of these systems usually results in dizziness/vertigo/system failure
Vestibuloocular reflex
allows eyes to stay fixed with movement of the head
dorsal column medial lemniscal tract issue vs. cerebellar dysfunction (Romberg test)
Medial lemniscal tract/dorsal column: can stand normally with eye open but will fall when eyes are closed
-Cerebellar dysfunction: can’t stand when eyes are open or closed
Nystagmus
-ABNORMAL nystagmus issue
“snapping back”
- jumping from one object to another while driving
- ABNORMAL nystagmus: tracking finger and left eye follows but right eye stops but then snaps back to following (CN VIII)
Benign paroxysmal positional vertigo
Forceful, abrupt head movement (trauma ) cause the otoconia to dislodge -> loose otoconia can cause vertigo when the head is in certain, specific positions
alc effect on hearing
Relaxation of stapedius and tympani -> inc sound transduction
alc effect on vestibulocochlear system
alc infiltrates the endolymph causing a drop in density of cupulae relative to endolymph -> body is more sensitive to movement
as alc exfiltrates the cupulae density increases leading to slower movement of hair cells -> slow/exaggerated movements
scala vestibule
scala media
scala tympani
Scala vestibule (starts with oval window) -perilymph (Na+) Scala media -endolymph (K+) Scala tympani (ends with round window) -perilymph (Na+)
stria vascularis
pushes K+ and Ca2+ out of the cells into endolymph
- K+ has a strong gradient into cell
- it produces endolymph gradient for the scala media
prestin
once OHC is stimulated causes contraction and elongation of leading to amplification of sound
depolarization route in IHC
Tip link: connects stereocilia
- also connected to a cation gate that can be physically opened when stereocilia are displaced
- allows K+ in depolarizing cell -> activate Ca2+ channles -> neurotransmitter released
olfactory pathway
cilia on olfactory receptor cell -> glomeruli -> mitral cells -> olfactory tract