Block 3 More plz Flashcards
sympathetic NS
mydriasis a1 contracts pupillary dilator muscle a1 contracts superior tarsal muscle b2 relax ciliary muscle = increase long distance vision b increase aq humor formation
parasympathetic NS
miosis ptosis muscarinic receptors: M3 contract pupillary sphincter M3 contract ciliary muscle = increase near vision M3 increase drainage of aq humor
mydriatic agents
ATROPINE: muscarinic receptor antagonist > cycloplegia (paralysis of ciliary muscle)
PHENYLEPHRINE a1 agonist, reverts ptosis in Horner’s syndrome
EPINEPHRINE a1 agonist, increases aq humor outflow, inhibits aq humor formation*
COCAINE blocks axoplasmic pump, inc NE
AMPHETAMINE release of NE
miotic agents
PILOCARPINE muscarinic agonist
ACETYLCHOLINE muscarinic agonist
NICOTINE activates para sympathetic nerves
PHYSOSTIGMINE anticholinesterase AChE
TERAZOSIN a1 antagonist
RESERPINE depletes NE
Tx for glaucoma
ECOTHIPHATE and PHYSOSTIGMINE anticholinesterases
PILOCARPINE muscarinic agonist
= increase outflow of aqueous humor
APROCLONIDINE a2 agonist
ACETAZOLAMIDE CA inhibitor
TIMOLOL b antagonist/blocker
= suppress aq humor formation
alpha agonists
phenylephrine a1
epinephrine a1
aproclonidine a2
muscarinic agonists
pilocarpine
acetylcholine
anticholinesterases
physostigmine
ecothiophate
botulism toxin
suppresses ACh release from neurons
optic nerve pathway
retinal ganglia > optic nerve > optic chiasm > optic tract > lateral geniculate nucleus > optic radiation > visual cortex (occipital lobe)
Meyer’s Loop/sublenticular
upper visual field fibers –> temporal lobe –> visual cortex
retrolenticular
lower visual field fibers –> parietal lobe –> visual cortex
Area 17
and 18 and 19
visual cortex in occipital lobe
then 18 and 19 association cortex
CN I special neurons
BIPOLAR
bipolar neurons through
cribriform plate to olfactory bulb
receptors and 1* neuron process
- activate receptor protein
- activates G protein (G-olf)
- inc cAMP
- cAMP opens ligand gated Na+ channel > DEPOLARIZATION
2* olfactory neuron called
mitral neuron, in olfactory bulb, which goes to synapse a bunch of places
primary olfaction cortex
piriform “pear shaped” cortex
orbital frontal cortex
where taste and smell meet to produce “flavor”
gustation involves which CN
CN V (touch and temp), VII (taste), IX (taste touch temp), X
gustation receptor cells are not
primary neurons
they are RECEPTOR CELLS
(100 receptor cells per taste bud, each cell does one of five tastes, receptor cells turn over q10days)
gustation process/pathway
- receptor is activate
- G protein (sweet, omami, bitter) / Na channel or proton closes K channel (sour, salty)
- 2nd mess (sweet, umami, bitter)
- open channel for DEPOLARIZATION
- open VG Ca++ or release intracellular Ca++
- AP
gustation receptor cell types
sweet, sour, bitter, omami, salty
taste buds (tip to back of tongue)
fungiform, foliate, circumivallate
CN XI origin
C 1-5 of spinal cord
CN XI stroke on right
Sx
weak SCM same side (can’t turn to opposite side)
CN IX glossopharyngeal supplies
tonsillar area and TM
retropharyngeal space
worry about infeciton
adenoidectomy
pharyngeal tonsils
cough afferent reflex
CN VII
cricothyroid muscle innervation
external branch of superior laryngeal nerve of vagus
piriform recess innervation
internal branch of superior laryngeal nerve of vagus
CN X vagus
cough swallow speech
PALATOGLOSSUS
4 gaze systems
- saccadic movements (rapid, jerky movements, scan to find salience)
- smooth pursuit (moving image centered on fovea)
- VOR (steady fovea during head movement)
- vergence (image on fovea when object is nearer or farther away)
MLF medial longitudinal fasciculus
nerves that supply pairs of eye muscles yoke together through this column of axons
UMN vs LMN anatomy
UMN: cortex to nucleus
LMN: nucleus to wherever (innervating or synapse)
anisocoria
pupils of different size
uveitis
iris
ciliary body
choroid
chorioretinitis
choroid
retinal layers
endophthalmitis
aqueous and vitreous humor
RECENT INTRAOCULAR SURGERY esp cataracts
normal flora: pseudomonas, staph, candida
Tx: fluoroquinolone or vance injected into eye
eye infections: route of infection
trauma paranasal sinuses IC anatomical abnormalities (dysfxn tear states) blood born sexually transmitted
tear include
sIgA and lysozome
lubrication
sIgA (secretory IgA = dimer) protects IgA from being degraded
why not use corticosteroids during eye infections?
corticosteroids facilitate corneal penetration
Chlamydia trachomatis serotypes
INCLUSION conjunctivits serotypes D-K
TRACHOMA serotypes A-C *leading cause of blindness worldwide (due to multiple inf and non lasting immunity, scar cornea each time)
Chlamydia trachomatis Dx
direct fluorescent ab
Chlamydia trachomatic inf
*co-infection with N. gonorrhea
BASOPHILIC INCLUSION BODIES
elementary bodies (rigid membrane) enter epithelia cell > change into reticulate bodies > replicates binary fission > leaves as EB
Tx chlamydia
AZITHROMYCIN
adenovirus
ds DNA non enveloped lytic in epithelial cells latent in lymphoid highly contagious
*infects epithelia cells of RESPIRATORY TRACT, CONJUNCTIVA, ENTERIC ORGANS because antigen and ability to act on certain receptors > Sx
path: migration into (HOST CELL) microtubules > induce cell cycle > block apoptosis > block host mRNA transport and translation > disrupt cytokeratin network
(HOST ORG) antagonize interferon, TNF
how Dx adenovirus
ADENOPLUS test
detects hexon proteins (part of viral capsid)
chronic conjunctivitis associated with
blepharitis
staphylococcus
hordeolum
STYE Tx: erythromycin ointment warm compress massage open keep clean
allergic rhinoconjunctivitis
IgE response
Tx: antihistamines, avoid steroids
viral conjuctivitis
neonatal
adult
HSV adenovirus Tx: cold compress topical vasoconstrictors
acute bacterial conjunctivitis
kids
adults
staph aureus+
strep pneumo+
h flu-
staph aureus+
Tx:
EMPIRIC (gram - and gram +)
TRIMETHOPRIM
POLYMYXIN OPHTHALMIC DROPS = POLYTRIM*
hyperacute bacterial conjunctivits
Neisseria gonorrheae
preauricular adenopathy
copious yellow/green PURULENT DISCHARGE
Tx:
CEFTRIAXONE
newborns receive prophylactic
erythromycin ointment
to prevent ophthalmia neonatorum
keratoconjunctivitis HSV
topical trifulridine and system acylovir
trifluridine
pyrimidine analog
*effective aginst acyclovir resistant virus bc can be phosphorylated BY HOST KINASES
TOXIC, TOPICAL ONLY
pseudomonas aeroginosa
gram -, rod, flagella
PYOCYANIN inhibits mto enz, disrupts ciliary beating
biofilms
adherence factors
secreted cytotoxins (destroy corneal epithelium)
host imm resp damages cornea > scarring, loss visual acuity
Tx:
POLYMYXCIN B
acanthamoeba
single cell, EUK
cysts and trophozoites in tissue
Tx: AZOLES
CMV retinitis
BRUSHFIRE
Toxoplasma
Dx: IgM serology
Tx: pyrimethamine and sulfadiazine
keratitis Sx
vision defects
photophobia
pain (cornea has lots nerve endings)
foreign body sensation
keratitis Tx
acyclovir and trifluridine VIRAL
moxifloxacin eyedrops
iritis (anterior uveitis)
notn infectious
chorioretinitis
IC or HIV: toxoplasma or CMV
conjunctivitis bilateral
allergic (usually)
conjunctivitis discharge type
viral, serous
Chlamydia, mucoid/mucopurulent
bacterial, mucopurulent
preauricular adenopathy
viral
chlamydia
neisseria gon
labyrinthitis
inner ear infection
associate recurrent OM (otitis media) with
conductive HL
meningitis
mastoiditis
commonly occur together, similar agents
bacterial conjunctivitis
otitis media
sinusitis
Moraxella catarrhalis
gram - diplococcus OXIDASE + FASTIDIOUS CHOCOLATE AGAR 95% produce BETA-LACTAMASES* HOCKEY PUCK TEST
Haemophilus influence NTHi
gram - LPS > rash CHOCOLATE AGAR NONENCAPSULATED BETA-LACTAMASES*
Strep pneumo
gram + lancet shape diplococcus
many virulence
suscept: alcoholism, DM, chronic RD
strep pneumo virulence
resistance
capsule
choline-biding prot (bind carb on surface epithel)
neuramoinidases (cleave host mucins)
pneumolysis (pore forming toxin, disrupts host cilia > HL, causes apoptosis
iron acquisition A (compete with host for iron)
OM Tx
- amox
- augmentin (amok with clavulanate)
- azithromycin
- eartube insertion to drain fluid (8PM TM)
Otitis externa Tx
cleanse with acetic acid topical abx: NEOMYCIN + POLYMXYIN - HYDROCORTISONE itch
*avoid flushing unless TM intact
otitis media with effeusion
NOT AN INFECTION
fluid in eustachian tube > resolves on own
complications of OM
CHOLESTEATOMA cyst of epithelial cells > erode IE or bone or brain, eardrum sucked inward
CONDUCTIVE HL
MASTOIDITIS red, hot, swollen behind ear
otitis externa micro
staph +
pseudomonas -
aspergillus
candida
otitis externa Sx and issues
Sx: unilateral, inflam ear canal, pain, itch, purulent ear draiage
- pustule with hair follicle
- itches, red canal, pain
(can progress to) - invasion adj bone and cartilage –> CN PALSY/DEATH
(more common in elderly, poorly controlled DM, IC)
Olfactory projections
Olfactory bulb > olfactory tract >
- olfactory tuburcle/amygdala > hypothalamus VISCERAL RXNS, HOMEOSTASIS, EMOTIONAL
- piriform cortex pear > MD thalamus > orbitofrontal cortex CONSCIOUS PERCEPTION, FLAVOR
- entorhinal cortex > hippocampus MEMORIES
Gustatory projections
CN VII, IX, X (1*) > solitary tract > SOLITARY NUCLEUS >
- hypothalamus
- amydala (emotions)
- nucleus ambiguus (gag reflexes to stop intake of spoiled foods)
- salivatory nucleus
- hypoglossal nucleus
- BILATERAL (2) to VPM > (3) gustatory cortex (insula) > orbitofrontal cortex (combination of taste and smell = flavor)
sense of taste tells: salt sweet umami sour bitter
salt content high-energy carbs proteins pH toxic substances
Spinal accessory nerves is special because
it is the only cranial nerve to both enter and exit the skull
CN XII damage
when protrude the tongue…
deviates TOWARDS side of damaged NERVE
deviates AWAY side of lesioned CORTICOBULBAR TRACT
rate of blinking can be diagnostic because
descengin control from basal ganglia and cortex is regulated by DOPAMINERGIC CIRCUITS
epiphora
produced by
induced by
over-tearing
increased tear production
decreased outflow
CORNEAL STIMULATION reflex
strong emotional responses LIMBIC SYSTEM
Refraction definition
bending light
inverted and reversed
light when hits cornea gets bent > lens is adjustable for refraction
emmetropic
perfect vision: refracting normally, infinity in focus
refractive power measured in
diopters
cornea + lens
diplopia
oculomotor damage (or abducens or trochlear)
what is happening when lens is flat?
see long-distance (sympathetic)
ciliary muscle relaxed
zonules tight
what is happening when lens is FAT?
see close (parasympathetic)
ciliary muscle contracted (M3 Rec)
zonules relaxed
hyperopia
myopia
farsightedness
eyeball too short
nearsightedness
eyeball too long
presbyopia
decreased accommodative power with age
cataract
glycoslylation of LENS proteins
associate SYMPATHETIC EYE
superior cervical ganglion
NE and a1
superior tarsal (injury: ptosis)
pupillary DILATOR (injury: miosis)
associate PARASYMPATHETIC EYE
ciliary ganglion
ACh and M3
pupillary SPHINCTER/CONSTRICTOR (injury: mydriasis)
pupillary light reflex pathway
CN II > optic chiasm > optic tract > optic radiations > edinger westphal nucleus in midbrain > PREganglionic PARAsympathetic to ciliary ganglion > synapse at ciliary ganglion > POSTganglionic PARAsympathetic to pupillary sphincter > miosis
aqueous humor production in
absorbed in
posterior chamber
anterior chamber (canal of Schlemm)
increase outflow of aqueous humor by
MIOSIS: give AChE
b2 increases concentration of
cAMP > increase aq humor volume > increased intraocular pressure
Beta blockers decrease aqueous humor formation
inflow of aqueous humor
- b2 sympathetics increase [cAMP]
2. CA incrases osmotic bleh so Cl- secretion
outflow of aqueous humor
- paraysmpathetics > miosis (AChEs)
2. PGF2 > relaxation of ciliary muscle
glaucoma
open angle
closed angle
increased INTRAOCULAR PRESSURE
OPEN: common, slow progression, late symptoms
increased production, decreased outflow
normal angle
CLOSED: MEDICAL EMERGENCY
acute, suden onset
SEVERE PAIN, BLURRY, RED EYE
iris moves and blocks Schlemms canal
closed angle glaucoma progression >
edema and decreased transparency = “halo effect”
damages PRs
neural conduction of CNII affected
Muller cells (of eye)
specialized glial cells
Retina 3 nuclear layers
most inner: ganglion cell bodies (axons form optic nerve)
middle: INNER NUCLEAR LAYER bipolar cell bodies
outer: OUTER NUCLEAR LAYER PRs cell bodies
3 neurons that begin the process of visual perception
1* PRs
2* bipolar neurons
3* ganglion cells
ganglion axons go to form the optic nerve (CN II) > optic chiasm > optic tract > optic radiation > visual cortex
___% cones are in fovea
90%
blind spot
optic disk, where all ganglion cell axons leave to go to brain
no PRs
PRs adequate stimulus
LIGHT
350-750nM
PRs encode
frequency = color intensity = brightness
scotopic vision
photopic vision
can see in dark, RODS
vision in bright lights, CONES
RODS
scopotic vision more pigment more sensitive to single photon saturate sooner RHODOPSIN integrated: low spatial and temporal resolution slower
CONES
photopic vision less pigment less sensitive to detecting photons bright light color vision per certain wavelengths precise, high temporal and spatial resolution faster
color vision wavelengths
blue: short wave
green: medium wave
red: long wave
* red doesn’t overlap -> red vision from cones
types visual acuity
- spatial ( two points in space, eye chart)
- temporal (two events as separate, critical fusion freq: 50Hz)
- spectral (two colors as different)
rhodopsin
light activated > change conformation > G protein > PDE > cGMP to GMP > CLOSE cAMP depending Na channels > HYPERPOLARIZATION
rhodopsin/rod vision special because
stimulus CLOSES channel, not open it
HYPERPOLARIZATION
2nd messenger: get AMPLIFICATION > increased sensitivity > CAN SEE IN DARK
Retinitis Pigmentosa and Retinopathy
neither involved in inflammation
both STOP PRs from working
NIGHT BLINDNESS FIRST
Vitamin A deficiency
NIGHT BLIND because rods don’t work well
Macular degeneration (Fitz)
degeneration in RPE
rhodopsin cycle with RPE
light > rod > rhodopsin to opsin > all transretinal > all transretinol > TO RPE CELL > all transretinol > 11-cis-retinal > TO ROD > makes more rhodopsin
adaptation definition
dark adaptation
decreased response to sustained stimulus
RPE pumps retinal components into rods > more rhodopsin > more sensitive
upper visual fields project to
lower visual fields project to
lingual gyrus (of occipital)
cuneate gyrus (of occipital)
macular representation in area 17
peripheral field representation in area 17
macular = most caudal = towards back of head
peripheral = rostral 2/3 of area 17 = back of head towards eyes
dorsal stream (parietal and upper temporal visual association cortex)
ventral stream (inferior temporal visual association cortex)
“where”
(lying on back/dorsally in ocean, where am I?)
“what”
(lying on stomach/ventrally in ocean, what am I looking at?)
projections to superior colliculus
via optic radiation and brachium of superior colliculus
i. SCANNING movement
ii. ACCOMMODATION/ CONVERGENCE reflex
homonymous defects
right POST-CHIASMATIC defects
left homonymous hemianopsia
left upper homonymous quadrantanopsia
left homonymous hemianopsia with macular sparing
heteronymous defects
OPTIC CHIASM (can't see periphery) bitemporal heteronmymous hemianopsia
hemianopsia
defective vision or blindness in one half of visual field
bitemporal heteronymous hemianopsia, left homonymous (with and without macular sparing)
accommodation reflex
(initiated when gaze is shifted from distant object to near one and image becomes blurred)
OCULAR CONVERGENCE both MR contract
MIOSIS constrictor pupillae sharpen image
LENS THICKENING ciliary muscle contracts, increasing refractive power of lens
Horner’s Sx
ptosis
miosis
vasodilation (flushing of face)
anhidrosis (absence of sweating)
Argyll Robertson pupil
pupil ACCOMMODATES to near objects but DOES NOT REACT TO LIGHT
(issues with pretectal area)
tabes dorsalis/tertiary syphilis, SLE, DM
strabismus
squint: failure of coordination of extra ocular eye muscle, resulting in deviation of affected eye and diplopia
amblyopia
lazy eye
decreased visual acuity in absence of anatomical defects in visual pathway
to avoid diplopia, vision in one eye is suppressed at level of the visual cortex
scotoma
island of visual loss within visual field
sphenoid sinus does not open into
middle nasal meatus
nasolacrimal duct communicates with
inferior nasal meatus
sensory neurons to roof of hard and soft palate
nasopalatine nerve of V
tympanosclerosis
calcium plaque in ME
perforation of TM
cholesteatoma
long standing retraction of TM into ME, negative pressure > skin cyst > cyst slowly erodes bone
Sx: facial paralysis, HL, dizziness, can erode brain cavity
hemotympanium
blood in middle ear
BAD
red eye, minor cold, clear eye drainage
adenovirus
visual field deficit, most common in HIV infected individuals
CMV
releases pnemolysin pore forming toxin
streptococcus pneumonea
green/yellow discharge from eyes
neisseria gonorrhea
ototoxic drugs
gentamicin, lasix, cisplatin, ASA/NSAIDS, antimalarials
presbycusis
most common cause of loss of hair cells, progressive
Otosclerosis
autosomal dominant
poor conduction
stapes needs fixing
BPPV
most common
“roll out of bed, turn and room starts spinning”
Dix Hallpike
Ostemoa
benign growth in ear canal
cold water exposure
nothing to do about it
looks like cholesteatoma
Meniere’s
inner ear
spontaneous VERTIGO lapses
ENDOLYMPH LEAKING
Acute Otitis Media
2nd most common disease in children Eustachian tube dysfunciton s. pneumo h. flu moraxella
Allergic rhinitis
IgE mediated hypersensitivity of nasal mucosa to foreign substances
affects 20% US pop
DOESN’T HAPPEN BEFORE AGE 2, BUT BY 20YO
M>F
Sx: sneezing, rhinorrhea, nasal congestion, lacrimation
macular degeneration
dry
wet
DRY DRUSEN, can get wet
WET, BLOOD Subretinal hemorrhage, grayish = bad
wet macular degneration Tx
anti-VEGF
glaucoma
optic nerve cupping: ENLARGED OPTIC CUP
LOSS OF OPTIC NERVE FIBERS
diabetic retinopathy
can cause BLINDNESS
NONPROLIFERATIVE
microanurysms, blot hem, exudates, macular edema, cotton wool spotaj
PREPROLIFERATIVE
venous beading, intraretinal microvascular changes, ischemic areas (cotton wool spots)
PROLIFERATIVE
BOAT HEMORRHAGE
diabetic retinopathy Tx
anti-VEGF
proliferative; panretinal photocoagulation
hypertensive retinopathy
silver wiring
cotton wool spots
amaurosis fugax
sudden vision loss
no pain
vascular insufficiency
CARDIAC WORKUP
ophthalmic migraine
hallmark: SCINTILLATINGN SCOTOMA: aura, colorful/shimmery aura
20-30 minutes
Spasm of arteriol in occipital cortex
retinal arterial occlusion
CHERRY RED SPOTS sudden vision loss one eye painless BREATHE CO2 TIMOLOL ACETAZOLAMIDE IV
retinal vein occlusion
SQUASHED TOMATO
temporal arteritis
history is key
EXTREME TENDER SCALP
STEROIDS IMMEDIATELY
CN III palsy
“down and out”
mydriatic
ptosis
diplopia
CN IV palsy
common
one eye slightly higher than other
vertical diplopia (not horizontal)
CN VI palsy
one eye in “down and in”
alkali eye injury
irrigate forever
hyphema
DON’T MISS THIS
blood in anterior chamber
subconjunctival hemorrhage
blood on surface of sclera, under conjunctiva
harmless
sudden painless loss of vision
retinal detachment
retinal vein occlusion - squashed tomato
retinal artery occlusion - cherry red
vitreous hemorrhage
sudden painful loss of vision
corneal abrasion
uveitis
traumatic hyphema
acute glaucoma
sudden BILATERAL vision loss
painless: meds
painful: toxins, chemical exposure
gradual vision loss
macular degeneration
cataracts