neuroanatomy exam #3

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what type of system is olfaction? how is smell transported to the brain and what is unusual about the system?: olfaction is a GVA system.

airborn molecules dissolve in nasal mucus and interact with long cilia overlying the olfactory mucosa.

cilia project to bipolar neuron whose cell bodies are located within the epithelium.

**no peripheral ganglion associated with smell**
how is CN I formed? where do the primary afferents synapse and what is unique about them?: CN I is formed from the bundles of unmyelinated central processes of the bipolar neurons pasing thru the cribriform.

they synapse on ipsilateral olfactory bulbs at the distal (A-R) end of the olfactory tract.

*olfaction is the only sensory system that passes directly to cortex without thalamic relay intermediate*
what is considered the first relay of the olfactory system?: the bulb is the first relay of the olfactory system.
the bulb and tract are projections of the ______.: TELENCEPHALON
what defines a glomeruli?: groups of primary afferent olfactory axons + the 3 types of dendrites(mitral, tufted and periglomerular) forming hemispherical morphological units within the bulb.
how many layers consitute an olfactory bulb? what is at the core of a bulb?: there are 5 layers to an olfactory bulb. white matter constitutes the core.
what are the output neurons of the olfactory bulb? what do they constitute the majority of?: mitral and tufted cells are the output neurons of the olfactory bulb, they are the majority of the olfactory tract. (WHITE MATTER)
what is the olfactory tract made of?: white matter(at core of bulb):
mitral axons
tufted axons
centrifugal afferent fibers (from several CNS locations TO bulb)
when does the olfactory tract divide? what are it's componenets?: the tract divides just A-L to the optic chiasm:

1.smaller medial olfactory stria (centrifugal axons TO bulb)

2.larger lateral olfactory stria (projection axons FROM bulb TO cortex)
what is the anterior perforated substance?: the gray matter just caudal to the diverging striae. it's "perforated" by bbr of ACA. it supplies the olfactory trigone formed by the striae.
what nucleus is associated with the olfactory tract?: the anterior olfactory nucleus is within the tract. they project to IL & CL bulbs. decussating fibers utilize medial olfactory stria and anterior commisure.
how are fibers carried to the olfactory tubercle?: at the divergence, a small # of fibers form the intermediate olfactory stria which carries fibers to the tubercle (w/in anterior perforated substance.
where do fibers from the lateral olfactory stria project to?: 1.amygdala: deep to uncus. limbic, endocrine, visceral odor response.

2.piriform cortex: over uncus. orbitofrontal cortex, odor perception.

3.entorhinal cortex: rostral parahippocampal gyrus. odor memory.
what is considered the primary olfactory cortex? what are all olfactory structures collectively called?: piriform and entorhinal cortices.

all olfactory structures: rhinencephalon
what are gustatory receptor neurons? where are they found?: gustatory receptor neurons:

cells WITHOUT processes in specialized organs - TASTE BUDS - found on tongue, epiglottis, soft and hard palates.
how does a taste bud work?: dissolved substances gain access to apical microvilli of the taste receptor cells thru surface pore.

response depolarizes the cell; impulse is transmitted thru basal synapse to PERIPHERAL process of PSEUDOUNIPOLAR primary afferent neuron.
what cranial nerves are involved in taste? how is the innervation delineated and what ganglion are involved?: VII: anterior 2/3 of tongue. (lingual n & chorda tympani) geniculate ganglion at genu of VII in medial wall of middle ear cavity.

IX: posterior 1/3 of tongue to inferior petrosal ganglion near jugular foramen.

X: epiglottis to inferior (nodose) ganglion near jugular foramen.
what is the path of the central taste processes (CTP)thru the brainstem?: CTP course in their respective CNs TO the brainstem but within it, they make the SOLITARY TRACT of the DORSAL MEDULLA. (surrounded by solitary nucleus)

taste fibers exit ROSTRAL half of solitary nucleus.
how is the solitary nucleus divided?: caudally: receives visceral afferents of IX and X (cardiorespiratory nucleus)

rostrally: receives taste fibers (gustatory nucleus)
describe the path of taste fibers from the gustatory nucleus. what type of taste does this constitute?: from the rostral solitary nucleus, gustatory nucleus projects 2nd order axons IL via CTT to the VPM.

VPM projects 3rd order axons via PLIC to gustatory cortex of insula and adjacent operculum.

solitaryâ†’gustatoryâ†’VPMâ†’
gustatory cortexâ†’insula/operculum = conscious discriminative taste
name the borders, origin and composition of the thalamus.: medially: 3rd ventricle
laterally: PLIC

origin: diencephalon

composition: gray matter(mostly neurons)
what is the general function of the thalamus?: thalamus receives all precortical sensory input (NOT SMELL) and projects/receives from most areas of cortex.

thalamus acts as integrating center at nucleus level.
name the "nonspecific" thalamic nuclei, their locations, inputs and outputs.: 1.midline: medial thalamus, adjacent to 3rd ventricle.
input - hypothalamus, amygdala
projection - limbic cortex, parahippocampal gyrus
function - visceral and emotional response.

2.centromedian: part of int.medullary lamina (& intralaminar nucleus), passes rostrally thru middle thalamus.
input - spinal cord, brainstem, basal ganglia
projection - widespread cerebral cortex
function - regulates arousal
name the associative nuclei and their respective functions.: 1.mediodorsal (MD or DM): interpretation, integration and response to odor.

2.lateral posterior nucleus (LP/PL): interpretation of complex visual stimulus and formation of response.

3.pulvinar nucleus: visual integration. interpret stimuli and form response. heterogeneous (has other functions).
what are the inputs and outputs to the associative nuclei?: MD:
input - entorhinal cortex
output - prefrontal cortex

LP:
input - s.colliculus and pretectum
output - prefrontal cortex

Pulvinar:
input - retina, pretectum, striate cortex, visual assoc. cortex.
output - occipital, temporal and parietal lobes.
what are the limbic relay nuclei? list input, projections and function.: anterior:
i - mamillary nuclei
p - cingulate gyrus
f - emotion and memory (papez circuit)

lateral dorsal (LD):
i - hippocampal formation
p - cingulate gyrus
f - limibic/emotion
what are the motor relay nuclei? give input, projections and function.: VA:
i - pallidum
p - frontal lobe; premotor and supplementary motor areas
f - motor planning of complex behaviors

VL:
i - pallidum and cerebellum (dentate)
p - primary motor (precentral gyrus), premotor and supplementary motor
f - planning and modulation of commands to motor neurons
name the sensory relay nuclei and their functions.: 1.VPL: relay for somatic sensation.
2.VPM: relay for somatic sensation and taste.
3.LGN: relay in primary perception pathway of vision.
4.MGN: relay in primary perception pathway of sound.
what are the inputs and projections of VPL and VPM?: VPL:
i - somatosensory; CL trunk & limbs: ML and ALS
p - primary somatosensory cortex (postcentral gyrus) and gustatory cortex (insula)

VPM:
i - somatosensory; CL head & taste: trigeminal system
p - primary somatosensory cortex: postcentral gyrus
what is the 'gatekeeper' nuclei?: RETICULAR NUCLEUS:
i - thalamocortical and corticothalamic collaterals

p - thalamic nuclei

f - modulate (regulate) communication between thalamus and cortex
what is the arterial supply of the thalamus?: 3 primary sources:
Pcomm
PCA
MCA (a.choroidal esp.)

*all thalamic aa originate BELOW it and either ascend to it or arch around toward the top and descend**
what is a lacunar stroke?: a small, deep infarct of penetrating aa. causes deep necrosis.
what are some of the mechanisms of thalamic stroke?: embolus (cardiogenic)
atherosclerotic dz
hemorrhage (high BP)
what thalamic lesion produces CL hemianesthesia and homonymous hemianopsia?: ventral p. lateral lesion:
hemianesthesia - VPM, VPL, IC
h.hemianopsia - LGN
what is dejerine - roussey syndrome?: thalamic lesion interrupts ascending sensory pathways to cortex = hemianesthesia. any contact with the numbed areas results in hyperpathia (neuropathic pain).
how is alcoholism related to thalamic lesions?: alcoholics are often thiamine deficient; lesions and microhemorrhages of thalamus and brainstem are common. use T2 MRI scan.
what is thalamic hand?: motor lesion of the thalamus resulting in athetosis, a form of dyskinesia.
what are the contents of the lateral hypothalamic nucleus? what is it's function and what happens if it is lesioned?: lateral hypothalamic nucleus contains all of the scattered cells of the lateral region.

most fibers belong to rostrocaudally running medial forebrain bundle which runs thru it.

APPETITE: neurosecretory molecules which stimulate food-seeking behavior.
stimulative lesions = obesity
destructive lesion = anorexia
what is the function of the suprachiasmatic nucleus? where is it found?: the suprachiasmatic nucleus is immediately above the optic chiasm. it's neurons are the link between environmental cycles and internal biorhythms.

it receives DIRECT BILATERAL input from retina & acts as master biological clock for circadian rhythms.

*signals from this nucleus are responsible for melatonin production of pineal gland*
which nuclei are involved in thermoregulation?: the anterior and posterior nucleus of the hypothalamus. they coordinate info from cutaneous thermoceptors and thermosensitive neurons in hypothalamus to orchestrate autonomic, endocrine and behavioral responses.
how does the anterior nucleus of the hypothalamus regulate body temperature?: anterior nucleus responds to â†‘ temperature by DISSIPATING heat:

autonomic - thermogenesis, peripheral vasoconstrict (sympathetic) or vasodilate.

endocrine - regulate thyroid hormone production.
what does a preoptic lesion cause? what can the anterior hypothalamic nucleus generally be associated with?: preoptic lesion = hyperthermia

anterior nucleus =
â†‘parasympathetic activity.
bilateral lesion of what nucleus results in hyperphagia? what else is associated with this lesion?: the ventromedial nucleus of the hypothalamus. it's the satiety center; stimulation INHIBITS desire to eat but BILATERAL LESION causes OVEREATING.

**â†‘ aggresion also found with bilateral lesion**
what type of hypothalamic nuclei stimulation results in rage and/or savage behavior?: stimulation of the dorsomedial nucleus.
what is the posterior hypothalamus associated with? what does a lesion cause?: generally, posterior hypothalamus â†‘ sympathetics.

mediates thermoregulation at low temperatures via production (shivering) and conservation (vasoconstriction).

lesion = POIKILOTHERMIA
what are the functions of the mamillary nuclei?: the larger medial and smaller lateral mamillary nuclei have few if any intrahypothalamic connections.

afferents:
1.most = hippocampal formation via fornix.
2.brainstem via mamillary peduncle.

efferents:
1.anterior nucleus of thalamus via mamillothalamic tract.
2.brainstem via mamillotegmental tract.
what is the pars nervosa? what is unusual about it's development and what are it's nuclei?: pars nervosa is posterior pituitary, it is an extension of the hypothalamus.

1.supraoptic nucleus (above optic chiasm)

2. paraventricular nucleus (mid medial hypothalamus)
L:magnocellular is neuroendocrine.
M:parvocellular projects to brainstem and spinal cord.
what is the supraoptico (hypothalamo) hypophyseal tract?: large cells of supraoptic and paraventricular nuclei projections, thru infundibulum to posterior lobe of pituitary.

axons do NOT synapse! terminals are close to fenestrated capillaries. cell bodies make oxytoxcin & vasopressin which is stored in terminals. AP causes rls into the blood.
what is the function of oxytoxcin and vasopressin?: o: uterine contraction and milk ejection

v: â†‘BP and â†“urine production
what is the arterial supply of the posterior pituitary?: inferior hypophyseal a. (br of ICA)

*provides fenestrated capillary network*
what are the nuclei of the pars distalis?: pars distalis = anterior pituitary.

1.medial preoptic nucleus: above optic chiasm. gonadotrophic hormones from anterior lobe.

2.arcuate (infundibular; tuberal): above median eminence near entrance of infundibulum. MOST INFERIOR NUCLEUS OF HYPOTHALAMUS
multiple hormones from anterior lobe.
which anterior pituitary cells are neurotransducers? what is the function of their axons?: small-cells (parvocellular) are neuroendocrine transuducers. project to median eminence, releasing/inhibiting hypophyseal regulatory hormones.

arcuate nucleus forms tuberoinfundibular tract
what is the distribution of the hypothalamo-hypophyseal portal circulation?: FIRST capillary bed: median eminence, from superior hypophyseal aa (ICA)

portal vv carry hormones to 2nd capillary bed in ANTERIOR lobe (hormones act directly on pituitary secretory cells).

endocrine cells of anterior lobe secrete into systemic circulation.
how are visceral efferents set up in the hypothalamus?: upper visceral motor neurons originate in the hypothalamus(or brain stem nuclei).

descending visceral motor tracts regulate lower visceral motor neurons
(lower = preg neurons of 2 neuron chains constituting lower motor pathway of autonomics).
where are lower visceral motor neurons (preganglionic)located?: sympathetic: intermediolateral cell column of spinal gray, T1-L2.

para: brainstem nuclei of III, V, VII, IX and X & intermediolateral horn (column) of cord gray matter at spinal segments S2-S4.
what is the paraventricular nucleus?: paraventricular nucleus is the main regulator of autonomics.

fibers descend (distinct from the fibers projecting to posterior pituitary) LATERALLY thru hypothalamus in MFB.

MFB originates in frontal olfactory areas, coursing caudally thru lateral hypothalamus to brainstem tegmentum and PAG.

fibers leave MFB & course in dorsolateral tegmentum of midbrain, pons and medulla.
how is the hypothalamus connected with the parasympathetic nuclei of the brainstem?: the dorsal longitudinal fasciculus. it courses thru the brainstem in PAG ventral to cerebral aqueduct and 4th ventricle.

*conveys ascending viscerosensory and descending autonomic fibers*
what does interuption of the hypothalamospinal tract cause? where can this lesion occur?: horner's syndrome b/c hypothalamospinal tract = SYMPATHETICS

lesion may occur in dorsolateral pons or medulla due to PICA occlusion.

symptoms are IL
what is the arterial supply of the hypothalamus?: bbr of circle of willis:

Acomm
ACA
ICAâ†’superior and inferior hypophyseal aa.
Pcomm
PCA
what is another name for the inner eyelid surface? what is it composed of?: inner eyelid = palpebral conjunctiva.

it is composed of two layers; stratified columnar epithelium (2-7) and lamina propria with lymphoid and fibrous tissue.

meibomian glands are found near free edge (sebaceous).
what are the glands of the eyelid?: 1.sebaceous of zeis: open to hair follicles.

2.large sweat glands of moll: open into follicles or directly onto eyelid margin.

3.meibomian glands open onto eyelid margin.
what is a hordoleum?: hordoleum: common infection of LID GLANDS. red, swollen & tender. STY.

etiology: s.aureus

INNER: meibomian glands (point to conjunctival or skin side)

EXTERNAL:points to skin, Zeiss or Moll.
what is an eyelid infection characterized by STERILE granulomatous inflammation of a meibomian gland? what else is unique about it?: CHALAZION = sterile granulomatous inflammation of meibomeian.

unknown etiology
localized swelling; upper or lower eyelid. NO ACUTE inflammation.
majority point toward conjunctiva.
UNILATERAL.
what is a common CHRONIC BILATERAL inflammation of lid margins.: marginal blepharitis (granulated eyelids)

irritation, burning and itching of lid margins. scales.

staph blepharitis:
ULCERATIVE, dry scales, lashes fall out. S.AUREUS. tx with topical antibiotic.

seborrheic blepharitis:
NO ULCERATION, greasy scales.
malassezi furfur & demodex folliculorum present. seborrheic dermatitis of scalp!
what is meibomainitis?: meibomianitis is a BILATERAL chronic inflammation of the meibomian glands.

etiology? but usually assoc. w/blepharitis.

complicated by 2nd infection via g- (p.aeruginosa)
what are some infections of the lacrimal apparatus?: 1.chronic adult dacryocystitis:
s.pneumonia & candida albicans. tearing & some mucoid. surgery.

2.acute adult dacryocystitis
s.aureus or beta-hem strep. inflammation, pain, swell. chronic usually first.

3.infantile dacrocystitis
h.influenzae. failure to canalize nasolacrimal duct.

4.canaliculitis: ADULTS!
uncommon chronic unilateral
actinomyces israeli, candida albicans, aspergillus.
2nd purulent conjunctivitis.

5.dacryoadenitis
rare acute inflamed LACRIMAL GLAND.
via mumps/measles/influenza or gonococcal conjunctivitis.
adults or children.
via retrograde of bacterial conjunctivitis.
what is dacryocystitis?: dacryocystitis: infection of lacrimal sac. infants & adults > 40.

UNILATERAL, 2nd to obstruction of nasolacrimal duct.

s: tearing and discharge

path: tear fluid collects in sac, bacteria multiplies.

dx: stain conjunctival smear
what are the symptoms and etiology of preseptal cellulitis?: preseptal cellulitis: infxn of subcutaneous tissue of eyelid ANTERIOR to orbital septum.

most common <5yrs old:
trauma: s.aureus

extension: s.aureus or strep pyogenes

<3 y/o: h.influenzae b (this may penetrate orbit!)

anaerobes may be involved, usually does NOT penetrate orbit.
what causes orbital cellulitis? give it's symptoms, pathology and diagnosis.: orbital cellulitis: often extension of sinusitis.

e: pneumococci, strep, staph, h.influenzae b (<3 y/o). fungi: mucor and rhizopus in pt with acidosis (uncontrolled diabetics and immunocompromised)

s: swell, red eyelids, chemosis, exophthalmos, dull pain. unilateral.

path: sinuses. rupture eyeball or cavernous sinus thrombosis, meningitis or brain abscess.

dx: sample conjunctiva or blood if systemic rxn.
what are the natural defenses of the conjunctiva?: 1.tears
2.lysozyme: degrades peptidoglycan, kills SOME g+, NOT g-.
3.IgA: neutralize virus, inhibit bacterial adherence to surface.
4.IgG: promotes phag and complement mediated bacterial lysis.
5.lactoferrin: binds iron. antibacterial to some pathogens.
6.lymphoid elements in adenoidal layer of conjunctival stroma.
7.epithelial exfoliation.
what types of organisms are commonly pathogenic for conjunctiva? which are NOT?: pathogenic for genitourinary = pathogenic for conjunctiva

nasal mucosa organisms do NOT grow well in conjunctival sac
what are the signs and symptoms of conjunctivitis?: symp:
1.foreign body sensation
2.scratching/burning
3.sensation of fullness
4.itching (allergies)
5.cornea = photophobia + pain

signs:
1.hyperemia
2.tearing, exudate, edema
3.papillary hypertrophy
4.follicles
how is conjunctivitis diagnosed?: usually no culture taken!
sample conjunctival surface:
1.gram stain (bacteria)
2.giemsa stain (human cell)
3.wet mount (fungi)
what are the findings of normal and bacterial conjunctival scrapings?: 1.normal: epithelial + goblet

2.acute bacterial: >neutrophils + bacteria

3.chronic bacterial: <neutrophils, > lymphocytes and large mononuclear cells
what are some of the findings of a viral conjunctivitis scraping?: lymphocytes and monocytes predominate.

HSV: multinucleated epithelial.

DNA: intranuclear inclusion bodies.

psuedomembrane: neutrophils.
what are some of the culture findings for chlamydial conjunctivitis? allergic?: chlamydial: basophilic intracytoplasmic inclusion bodies in epithelial cells. early stages - exudate rich in neutrophils and plasma cells.

allergic: eosinophils
what is the etiology of acute catarrhal conjunctivitis?: acute catarrhal: mucopurulent conjunctivitis. fomites.

1.strep pneumonia: MOST common adults and children

2.h.aegyptius (koch weeks) & h.influenzae (kids)

3.s.aureus: NEWBORNS

4. viridans, e.coli, proteus
what are the causes of acute purulent conjunctivitis?: 1.n.gonorrhea: can cause corneal damage and iritis. if cornea perforates - endophthalmitis & panophthalmitis. newborns get it during birth. adults via complication of g.urethritis/vaginitis.

2.n.meningitidis: milder than gonorrhea. cause corneal damage. conjunctiva as entry to bloodstream and meninges.
what causes chronic bacterial conjunctivitis? pseudomembranous or membranous conjunctivitis?: chronic:
1.s.aureus
2.mixed (s.pneumonia + h.influenzae or s.aureus)
3.moraxela lacunata (g-): localized angular conjunctivitis + dermatitis, fissuring of canthi and scant conjunctival discharge.

pseudomembranous/membranous conjunctivitis:
1.cornyebacterium diptheriae
2.streptococcus pyogenes
what are the signs/symptoms and pathology of chlamydial conjunctivitis?: trachoma: a chronic follicular conjunctivitis.

e: c.trachomatis A-C: SUDAN
t: fomites & flies
s: 1.early - bacterial
2. later - papillary hypertrophy, lymphoid hyperplasia + follicles on upper tarsus
3. late: scarring. pannus, opacification of corneal stroma.

path:
1.chronic, 20% heal spontaneously
2.tx early with antib
3.common cause blindness in developing country
what is inclusion conjunctivitis?: e: c.trachomatis D-K (STD, US)
aka chlamydia oculogenitalis

t:
1.adults: GU to eye via fingers/fomites
2.indirectly from pool
3.newborn via birth

s/s:
1.red eye, pseudoptosis, profuse discharge in AM, BI.
2.acute follicular conjunctivitis
3.NEWBORN: papillary+exudate

dx: infant = scrapings
adult = culture
what is unique about viral conjunctivitis? what are some variants?: viral conjunctivitis discharge is watery, not purulent.

1.acute pharyngoconjunctival fever (PCF)
2.epidemic keratoconjunctivitis (EKC)
3.HSV
4.epidemic hemorrhagic conjunctivitis (EHC)
5.Molluscum contagiosum blepharoconjunctivitis (MCB)
6.varicella-zoster blepharoconjunctivitis (VZB)
7.measles keratoconjunctivitis (MK)
what is PCF?: acute pharyngoconjunctival fever: PCF

e: adenovirus type 3 (4 or 7). dsDNA virus, icosahedral, naked.

t: even in chlorinated swimming pools

s/s: fever, sore throat, acute follicular conjunctivitis, esp kids. maybe preauricular adenopathy.
what are the s/s of HSV? what tx should NOT be used?: HSV conjunctivitis usually associated with PRIMARY infection, usually I.
associated with HSV keratitis.

s/s: follicular or pseudomembranous. herpetic vesicles on eyelids/margins.

dx: conjunctival scrapings may be mononuclear if follicular. neutrophilic if pseudomembranous. multinucleated giant epithelial cells too.

tx: self limited! steroids PROLONG the dz by â†“ CMI!
what are the characteristics of a fungal conjunctivitis?: RARE. may be primary in conjunctival sac, secondary to mycotic obstruction. or via adjacent inflammation.
TRAUMA is factor in more than 1/2 cases (oculomycosis)
what are some examples of parasitic conjunctivitis?: 1.onchocerciasis: filarian
2.loa loa: filarian
3.phthirus pubis: louse
4.fly larva: ocular myiasis
5.caterpillar hair: ophthalmia nodosum
what is an immediate hypersensitivity reaction?: ALLERGIC rxn, ITCHING:

1.hay fever

2.vernal keratoconjunctivitis - may include papillary conjunctivitis and keratitis.
what are some delayed hypersensitivity infections?: 1.phlyctenulosis: mycobacterium, candida, staph. LIMBUS. usually result of staph blepharitis.

2.allergic contact: via topically applied meds
give an example of an autoimmune conjunctivitis. include symptoms.: keratoconjunctivitis sicca:
sjogren's
lacrimal gland infiltrated by lymphocytes = atrophy and destruction of glandular surface.
leads to much less effective tear film.
what types of conjunctivitis occur secondary to lacrimal obstruction?: 1.2nd to dacryocystitis via pneuomoccocus or b-hemolytic strep.

2.2nd to canaliculitis via actinomyces israeli or candida. scrapings = neutrophilic. cultures (unless done anaerobically) are negative.
what is ophthalmia neonatorum?: conjunctival infection of newborn within 10 days/via birth:

1.gonococcal: 2-3 incubation. crede or penicillin.

2.inclusion bennorrhea: c.trachomatis. 5-12 incubation. silver nitrate DOES NOT HELP! USE TOPICAL ERYTHROMYCIN.

3.HSVII: 2-3 incubation

4.staph, strep, pneumococcus, many g-s.

5.conjunctivitis from silver nitrate!! (w/in 24 hrs if it's going to happen at all)
why is the cornea transparent? what is an infection of the cornea called? what are it's defenses?: transparency due to uniform structure, avascularity and relative dehydration. has rich nerve supply.

infection: keratitis
defense: lids, antibody and lysozyme, epithelium.
what are some of the problems with the cornea, regarding infection?: 1.avascular
2.damaged stroma heals with permanent opacification
3.corneal neovascularization is part of normal inflammatory response.
4.conjunctiva and corneal epithelium are continuous
5.corticosteriods exacerbates fungi and HSV infection
what are some signs/symptoms of corneal infection?: 1.pain, photophobia
2.blurred vision/halos
3.NO DISCHARGE (no blood vv or glands)
4.tearing
5.circumcorneal vascular congestion
6.hypopyon (PMN in anterior chamber)
7.abnormal light reflex
what are some predisposing factors which can lead to corneal ulcers?: 1.dry eye
2.inability to close lids
3.trauma
4.inappropriate use of glucocorticoids
5.preexisting infxn of eye
6.contact lens overuse: g-rods (psuedomonas), some g+ rods, fungi or acanthamoeba
what is the etiology of keratitis?: bacteria:
1.strep pneumonia
2.s.aureus
3.p.aeruginosa
4.moraxella
5.n.gonorrhea
6.klebsiella pneumonia
7.serratia marcescens
8.viridans strep
9.chlamydia trachomatis

FUNGI:
1.fusarium
2.aspergillus
3.candida

VIRUS
1.HSV
2.H zoster
what is acute serpiginous ulcer?: PNEUMOCOCCAL ulcer:
e: strep pneumonia, used to be most common. some s.aureus.

1.follows coreal trauma
2.more likely if adjunct chronic pneumococcal dacryocystitis.
3.NO preceding conjunctivitis
4.RAPID development
what is necrotizing keratitis?: PSEUDOMONAS ulcer:

e: p.aeruginosa. ALWAYS most common g- causing ulcer.

1.follows corneal injury
2.contaminated fluids, makeup
3.RAPID via extracellular protease that degrades corneal proteoglycans.

**staph & strep viridans can cause more indolent corneal ulcers**
what is a viral corneal ulcer?: herpes simplex keratitis (dendritic):

MOST common cause of corneal ulcers/blindness in US!

1. usually HSV I, sometimes II
2. recurrence common. virus remains in trigeminal ganglion/cornea.
3. self-limited w.minimal scarring unless CORTICOSTEROIDS!

herpes zoster ophthalmicus also causes corneal dz/other eye problems.
what are some fungal corneal ulcers? how do they progress?: fungal corneal ulcers follow damage to epithelium. ulcers are slowly progressive, fungi may penetrate anterior chamber.

1.acanthamoeba keratitis: fresh water, daily wear soft contact lens. dx via giemsa. clinically resembles HSkeratitis.

2.hypersensitivity:
a. marginal - MOST common. >1/2 staph marginal blepharitis via allergic rxn to bacterial antigens.

b. herpes disciform keratitis - cmi response against infected stromal fibroblasts w.HSV antigen. MAY NOT BE DUE TO HERPES.
what is endophthalmitis? panophthalmitis?: endo: suppurative inflammation of intraocular contents. NO RUPTURE! NOT ALL LAYERS!

pano: acute suppurative inflammation of inner eye with necrosis of sclera/cornea. extension to orbit.
intraocular infections can proceed in two directions. explain.: ANTERIOR:
iritis, neutrophilic exudate leads to clouding of aqueous humor/hypopyon. pus-filled globe, loss of eye.

POSTERIOR:
via blood, blood vv in choroid dilate and exude fluid and cells. retinal necrosis/detachment.
what are some causes of chorioretinitis?: chorioretinitis is usually blood borne.

virus: torch (cytomegalovirus is most common in AIDS pt). HIV can affect retina directly.

toxicara canis or cati - nematodes acquired as eggs from dog/cat feces.

toxoplamsa gondii - especially if congenitally acquired.
what is iridocyclitis?: iridocyclitis is an intraocular infection.

inflamed iris and ciliary body.

1.autoimmune dz (juvenile rheumatoid arthritis, ankylosing spondylitis)

2.congenital syphilis

3.herpes simplex

4.herpes zoster
what is acute retinal necrosis?: see intraocular antibody formation to specific virus:
<20 HSV
>50 HZV

hemorrhagic edema leading to retinal tears, iritis, necrosis, inflammation of optic nerve.
when do you see post-operative endophthalmitis? what are the causes?: CATARACT SURGERY!

1.s.aureus, epidermidis = most common
2.g- esp psuedomonas and proteus
3.strep + pneumococcus
what are the causes of posterior segment enophthalmitis from endogenous metastasis?: virtually ANY bacterium that produces septicemia may produce this:

s.aureus is MOST common
strep and s.pneumonia too.
what is the prognosis for endophthalmitis and panophthalmitis?: endo: most pt experience vision loss

pano: eye often reduced to shrunken mass. focus more on preventing spread to brain or thru cavernous sinus.
what do the reticular fibers represent?: reticular fibers represent huge dendritic trees and highly collateralized axons.
what is the orientation of the reticular formation? how does this elevate the complexity of thought processes?: RF extends caudally into the intermediate zone of spinal gray matter and rostrally into parts of the diencephalon (thalamus).

RF fibers cover a large area in the TRANSVERSE PLANE. they are in a position to intercept ascending and descending tracts.
what are the two types of RF fibers? what is their function?: LARGE: Golgi I (long axons leaving cell body). fxn: rostrocaudal integration of output effects of RF.

SMALL: long dendrites.
fxn: penetrate cranial nuclei, sensory tracts and motor tracts. allows synaptic integration of systems projecting to or thru braintem.
*small RF axons project MEDIALLY*
what are the topographical subdivisions of the RF?: raphe: small neurons straddling entire length of brainstem median plane. (PAG included)

medial: gigantocellular in pontine and medullary tegmentum. OUTPUT.

lateral: parvicellular. INPUT.
what are the origins of the RF afferents? where do they synapse?: origins: spinal cord, brainstem, cerebellum, diencephalon and cerebral cortex

afferents synapse in LATERAL PARVICELLULAR, then relay to MEDIAL GIGANTOCELLULAR
what type of sensory information collaterals come to the RF?: secondary input which is involved in startle reactions to touch, light or sound.

**discriminative touch, vision and auditory senses BYPASS direct input to RF**
what spinal cord afferents synapse with the RF? brainstem afferents?: spinoreticular: originate at all levels of cord

spinothalamic: (ALS) send collaterals to RF (pain rxn)

CN nuclei (2nd and 3rd)
tectoreticular: from superior and inferior colliculi
reticuloreticular: exist btwn different parts of tegmentum
what are the cerebellar and limbic system inputs to the RF?: cerebellar: deep cerebellar nuclei (esp fastigial)

limbic: mamillary nuclei via mamillotegmental tract
what are the regions of RF output?: 1.CN nuclei via collaterals of LONG axons

2.descending reticulospinal fibers in ventral part of lateral funiculus and anterior funiculus (X and un-X fibers, excite and inhibit)

3.ascending axons to nonspecific intralaminar nuclei of thalamus (then to cortex)

4.cerebellum
what is the ARAS?: ARAS: ascending reticular activating system.

1.ROSTRAL RF
2.arousal, consciousness, sleep-wake, attn span.
3.anesthetics may act here
4.midbrain RF lesion = COMA
5.pontine RF lesion = insomnia
6.locus coeruleus: adjacent to PAG near pontomidbrain jct. melanin content, sleep phases. highly branched efferents reach ALL CNS (inc cortex) DIRECTLY.
what is the reticulospinal-reticulobulbar system? (RS-RB): RS-RB: LMN control

1.CAUDAL RF
2.motor and visceral control
3.relay for ALL descending motor commands EXCEPT DIRECT PYRAMIDAL TRACT
4.regulates hiccup, sneeze, yawn, swallow
5.RS tracts are major descending path in movement control
6.modulates normal postural tone and reflex
how is the RF involved in homeostasis and vegetative reflexes?: RF has CV and resp "centers"

breathing, HR, BP, GI & GU motility, electrolyte balance, pupillary size and ocular movements.

regulates fxns involving somatic and visceral coordination:
gagging, vomiting, laughing and crying.
how is the RF separated based on function?: ROSTRAL RF: mental activity (via tegmentum transection at mid-pons)

CAUDAL RF: vegetative and reflex activity
how are the raphe nuclei defined? what is their fxn?: raphe defined by serotonin use.

1.modulate ascending sensory transmission

2.receives limbic, olfactory and hypothalamic afferents

3.INPUT FROM PAG and OUTPUT TO dorsal horn = pain suppresion
what is the parabrachial area of the RF associated with? the PPRF? small cell zone? superficial medullary zone?: parabrachial: feeding and expiration

PPRF: eye reflexes

small cell zone: respiratory rhythm

superficial medullary zone: cardiac and respiratory regulation
what would happen if there was a lesion to the lateral RF?: loss of breathing regulation/rhythm (via small cell zone and superficial medullary zone)

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