Exam 1 (week2) Flashcards
which transmitters are dysregulated in schizoprhenia (2)
serotonin
dopamine
which dopamine receptor is blocked in drugs that work for antipsychotics
D2
how could amphetamies cause psychotic symptoms
amphetamines come in to presynaptic neuron via trasmporter, kicks out dopamine, dopamine in synaptic cleft is increased - stimulates D2 channel causing symptoms
why do you need to wait 4-6 weeks for antispychotics (D2 blockers) to work
“depolarization inactivation” - initially the presynaptic nerve fires harder because of autoreceptors - some are inhibited so the neuron thinks there’s less dopamine and wants to release more
eventually it wears out and will stop firing (chronic treatment)
what happens to dopamine pathways during schizoprenia
for some reason, the connections between ventral tegmental to cortex die off, but the connections between ventral tegmental to limbic (nucleus accumbens) remain. there is a positive feedback loop from cortex to limbic because the cortex doesn’t sense enough stimulation. ramps up dopa firing to limbic system (nucleus accumbens)
when do you see tardive dyskinesia (iatrogenic)
too much dopanie block - prolonged treatment with D2 receptor blockers – causes D2 receptor supersensitivity
endocrine side effects of dopaine block
if you block D2, you increase PRL release, causing gynecomastia
dopamine blockade and eating/weight
motor neurons around ventricles involved in eating behavior, D2 blockade around ventriles cause weight gain
dopamine blockade and nausea
antiemetic because it blocks chemotrigger zone
first gen antipsychotic drug types and prototype for each (2)
- phenothiazines (chlorpromazine)
2. butyrophenones (haloperidol)
phenothiazine mech of action
like tricyclic - binds to a bunch of receptors, not just D2
butyrophenones mech of action
way more potent D2 block than alpha 1
second gen antipsychitic drugs - how did they change from first gen with respect to receptor blockade
increased the ratio of serotonin (5-HT2):D2 receptor blockade (less chance for tardive dyskinesia)
clozapine mech of action
caused selective depolarization inactivation in limbic system
blocks 5-HT2 receptors
adverse for clozzapine
- have to check blood because of risk for agranulocytosis - can’t give in patients with dyscrasia
- diabetes risk
what are the atypicals/second gen antipsychotics (6)
- clozapine
- risperidone
- olanzepine
- quetiapine
- ziprasidone
- aripiprazole
side effect ofs risperidone
dose-dependent - will cause extrapyramidal symptoms like first gen if dose is too high
NO risk of agranulocytosis or diabetes
side effect of olanzepine (2)
- risk for diabetes and weight gain
2. increased serum prolactin
side effect of quetiapine
diabetes risk
side effect of ziprasidone
widens QT interval
mech of action of aripiprazole
partial agonist at D2
damp down nucleus accumbens, incrase frontal cortex
whats the super bad early side effect of antipsychotic drugs that could be fatal
neuroleptic malignant syndrome - causes catatonia, stupor, fever, HTN, myoglobinemia
what’s the deal with antipsychotics and epilepsy
can lower seizure threshold
what’s rabbit syndrome
perioral “chewing” syndrome - late neurological side effect of antipsychotic drug
what do you absolutely not give someone with tardive dyskinesia due to antipsychotics
anticholinergic, will suppress GABA activity even more by removing Ach tone
which antipsychotics have increased risk for diabetes, weight gain and hyperlipidemia 92)
olanzepine
clozapine
alpha block is bad for which patient population
elderly (anatihypertensive - falls)
when can you give an anticholinergic to HELP side effects
with EPS symptoms from haliperidol, let’s say
glutamate and dopamine relationship
glutamate directly increases dopa
and indirectly regulates dopa via regulation of GABA which inhibits dopa
NMDA and schizophrenia
hypofunction in glutamate receptor is responsible for neurocognitive symptoms of schizophrenia - same process for PCP
what is timecourse for diagnosis of schizophrenia
1 month of active symptoms - 2 or more symptoms (one has to be positive)
and 6months of social dysfunction
what percentage of patients with schizophrenia commit suicide
10%
what chromosome might have relevance in schizophrenia
C4 component of 6
C4A causes synaptic pruning in prefrontal areas
what are the extrapyramidal side effects of D2 blockade (4)
- acute dystonia (forceful muscle contractions)
- akathisia (motor restlessness)
- drug-induced parkinsonism (bradykensia, rigidity, tremors)
- tardive dyskinesia (hyperkineic movement of head, limbs, tongue)
when do the EPS symptoms occur
hours to days - acute dystonia
days to weeks - akasthisa
weeks to months - parkinsonism
months to years - tardive dyskinesia
timecourse for brief psychotic disorder
1 day to 1 month
timecourse for schizophreniform disorder
1 month to 6 months
what symptoms are NOT present in delusional disorder
disorganized thought and behavior
functionality is not generally affected too much
diagnostic criteria for schizoaffective disorder (2)
- features of schizophrenia AND mood disorder
2. psychotic symptoms for at least 2 weeks WITHOUT mood symptoms (to differentiate between MDD with psychosis etc.)
whats the beginning of the retina (near the lens) called
ora serrata
developmental stages of eye (5)
from forebrain:
- optic sulcus
- optic vesicle
- lens placode
- optic cup
- neural epitheilum of retina (in contact with layer behind - pigment epithelium of retina)
function of retinal pigment epihtelium cells (4)
- support rots and cones
- phagocytose 7,500 rod and cone outer segment discs
- reconvert trans retinal to 11-cis retinal
- make melanin
what disease occurs when there are mutations in genes that control reconversion of trans retinal to 11-cis retinal
retinitis pigmentosum - results in blindness
what do you see in fundus for RP
pigment deposition in patches
what do patients see with retinitis pigmentosum
lose peripheral vision
what do you see with retinal detachment
see sudden increase in floaters
what do you see in fundus for retinal detachment
“horseshoe tear”
what are the 3 layers of retina from inner to outer
ganglion cells, bipoarl cells, phtoreceptors
what nuclear layer are the rods and cones
outer nuclear layer
what are the synapse layers between nuclear layers in retina called (2)
plexiform layers
(outer is between inner and outer nuclear layers)
(inner is beween gancglion and inner nuclear layer)
what layers do mueller cells make
inner limiting and outer limiting membranes
what is nerve fiber layer made of
axons of ganglion cells
where are the nuclei of the mueller cells
in inner nuclear layer
which cells (rods or cones) contain color vision
cone
where are most of your cones
macula
difference between macula, fovea and foveola
foveola ONLY has cones - tiny central area (200 microns)
fovea more cones than macula (1.5mm)
macula (5.5mm - can appreciate on photo)
what do people see if they have macular degeneration
loss of central vision
what do you see on fundus for macular degeneration
destruction at macula - difference between wet (blood) and dry
what layer does uveitis affect
middle/choroid layer
what are 4 parts of middle layer
- choroid (under retina)
- ciliary body
- ciliary processes
- iris
what are layers of chroid beneath retina (2)
- Bruch’s membrane - small capillaries
2. choriocapillaris - larger vessels
what part of ciliary body actually pulls on lens
the zonule fibers produced by ciliary body and processes
functions of ciliary body and processes (3)
- produce aqueous humor
2 produce zonules to attach to lens - ciliary muscles contract during accommodation
layers of outer eye (4)
- mostly sclera (posterior to ora serrata)
- lamina cribosa (where white meets clear)
- corneoslceral junction/limbus
- cornea
function of lamina cribosa
supports the optic nerve
if pressure is too high, axons of optic nerve get pinched, those retinal gangion cells will die, and you lose vision from hundreds of photoreceptors
what ratio do you measure in glaucoma
disc:cup ratio
what is special about corneoscleral jucntion
- contain canals of schlemm
- contain trabecular meshwork that can close vessels when sclerosed
- contain corneal epithelial stem cells
layers of cornea from out to in (5)
- stratefied squamous non-keratinizing epithelium
- bowman’s layer (specialized BM)
- stroma
- descemet’s membrane (specialized BM)
- endothelium
functions of cornea(3)
- smooth surface over which tears can spread for vision
- barrier to microbes
- glial support for intraepithelial corneal sensory nerves (when you feel like something is in your eye)
what do fibroblasts in corneal stroma do (2)
- synthesize collagen and proteoglycans that provide strength to cornea
- pump out excess water to maintain clarity in cornea
what cells HAVE to be present in corneal transplant
endothelial cells
where in lens does proliferation occur
in anterior lens epithelial cells (they move posteriroly and differentiate into lens fibers)
when lens is flat, do you see close or far
far
when ciliary muscles contract, what happen to lens
rounds up
what are the layers of tears (3)
lipid outer, then acqueous, then mucin
after optic chiasm, where do optic tracts synapse
lateral geniculate nucleus (LGN) of thalamus
do you get convergence/binocular vision from thalamus?
no - the inputs from R and L eye are separated
after lateral geniculate nucleus, where do they go
optic radiations/ geniculocalcarine tract project to visual/calcarine cortex via EITHER retrolenticular internal capsule through parietal lobe
OR sublenticular internal capsule through temporal lobe
what’s the difference between sublenticular and retrolenticular
(meyer’s loop) sublenticular detect upper part of visual field (detects bottom of retina)
retrolenticular detect lower part of visual field (detects upper part of retina)
what are the lenticular nuclei
putamen and globus pallidus
what are the Brodmann’s area numbers for vision
area 17 = primary visual cortex
areas 18 and 19 are visual association cortex (above and below calcarine sulcus
homonymous visual field defect
means corresponding halves of visual field for both eyes (L for both, R for both)
what is hemionospia
half of vision lost
blood supply to visual cortex, and what kind of vision losses do you have with issues with this vessel
posterior cerebral artery, get macular sparing because of collateral blood supply from middle cerebral artery
what are the components of the “ventral stream” of image processing and what kinds of vision processing does it do
V1 is light, detects a lot of things, projects to V2, which detects fewer, but more specific things, V3 which detects even fewer and more specific things
pathway used for object recognition
what are components of the “dorsal stream” of image processing and what kinds of vision processing doe sit do
V1 to V2 to MT (which detects movement)
pathway used for spatial vision
when are photoreceptors hyper or depolarized
in the dark, cGMP is constituately produced, which causes Na+ influx and K+ efflux, DEPOLARIZING the cell
in the light, decreased cGMP is hydrolyzed (due to opsin coupled to cis retinal) causes closing sodium channel, reducing Na+ influx and K+ efflux, causing HYPERPOLARIZATION
how long do manic symptoms have to last for a diagnosis
at least 1 week (OR requiring hospitalization)
how many symptoms do people need to express for diagnosis of mania
3 (or 4 if irritable)
time course for hypomania
4 days (could be less)
diagnostic criteria for bipolar 1 (in terms of episodes)
one manic episode
diagnostic criteria for bipolar 2 (in terms of episodes)
one hypomanic plus one major depressive episode
in bipolar 1 and 2, which episodes are more common, manic or depressive
depressive by a lot
definition of rapid cycling in bipolar disorder
4 or more episodes in a y ear
which cranial nerves have parasympathetic function
3
7
9
10
what does gag reflex test
CN9 (sensation/afferent)
CN10 (motor/efferent)
what does “open and say ah” test
CN10
what does sticking out your tongue test
CN12
what 3 things does dysfunction of CNX cause
- loss of gag/swallow reflex
- loss of carotid sinus (heart rate control)
- loss of oculocardiac reflex causing dysphagia
what are the nuclei of CNX (4)
- dorsal motor nucleus (parasymp output)
- nucleus ambiguus (skeletal motor output)
- nucleus solitaris (visceral sensory input and taste input)
- spinal trigeminal nucleus (general sensory input)
what does visceral sensory function of CN10 control (2)
- cough reflex
2. nausea and vomitting reflex
what is skeletal motor nucleus of CN10 called
nucleus ambiguus
what specific nerve branch is responsible for cough reflex
internal laryngeal nerve (branch of vagus nerve)
what’s the medical term for hoarseness
dysphonia
what’s the medical term for “losing your voice”
dysarthria
which branch of which nerve can cause dysfunction of vocal cords
recurrent laryngeal branch of vagus
where is the general sensory location (on skin) of vagus
small area of skin of external ear canal
where is taste location of vagus
epiglottis and pharynx
patient with bilateral loss of smell and taste for 7mo and headache for 5mo
meningioma
patient with unilateral painful loss of vision and otpic neuritis
MS
patient with papilledema and horizontal diplopia
brain tumor causing increased ICP
patient with syncope, shaking, confusion, numbness over left jaw for past 2 years
lesion impacting CN5 as it exits cerebellar/pontine angle in medial temporal lobe (epileptic location)
facial weakness in upper vs lower motor neuron lesion
lower motor - can’t more upper or lower facial muscles (whole face)
upper motor - deficits in lower facial ONLY
if someone complains of things being really loud, what CN are you thinking about
CN7 (stapedius in innervated by CN7 - doesn’t dampen stapes)
Rinne and Weber testing - how to do it, and what does it test
tuning fork (512 Hz)
Weber: place fork in middle of center head on top (should hear on both sides equally, conducive (blockage) louder on affected ear)
Rinne: compare air and bone (normally air is louder than bone, conducive bone is louder than bone, sensorineural air is louder than bone)
someone with unilateral sensorineural hearing loss, vertigo, and tinnitis
Meniere’s (increased endolymph production)
when neurons need to regenerate, what structural components are upregulated and downregulated
upregulate microfilaments and microtubules (which are more dynamic), downregulate intermediate filaments, neurofilaments (which are more stable)
what is the most common way to damage neurons
upregulation of glutamate that triggers caspase elevation and apoptosis
functional recovery vs regeneration
functional recovery = getting function back via recruitment of OTHER neurons, versus repairing the damaged neurons themselves
what are neurotrophins
growth factors that bind to neurons to promote growth
3 things that happen in CNS in response to neuronal injury
- astrocyte proliferation and expression of GFAP, resulting in “glial scar”
- proliferation of oligodendroglial precursors and oligodendrocytes
- microglial recruitment and activation
what do olfactory unsheathing cells do
cells like Schwann cells that can be transplanted into CNS to promote recovery
animal examples of neuronal stem cells (2)
1) fish retinas that get bigger as fish grows
2) song birds learning new songs each year
2 areas of human brain where stem cell populations reside
- subventricular zone (SVZ) that give rise to olfactory bulb
- dentate gyrus in hippocampus (memory and learning?)
symptoms of lateral medullary syndrome and what areas are affected (4)
- dizziness (vestibular)
- hoarseness, difficulty swallowing (nucleus ambiguus of CN9,10,11)
- loss of pain and temp ipsilaterally in face (CNV)
- loss of pain and temp contralaterllly in body (spinothalamic)
lateral medullary syndrome caused by issue in what blood vessel
PICA
symptoms and areas affected by medial medullary syndrome
- deviation of tongue, tongue atrophy, speech problems (hypoglossal nerve)
- contralateral hemiplegia in body (corticospinal tract)
- loss of discriminative touch contralaterally in body (medial lemniscus)
what blood vessel causes medial medullary syndrome
anterior spinal artery from vertebral artery
oculocardiac reflex
pressure on orbit due to sx or tumor, travels along opthalmic V1 through trigeminal ganglion to sensory nucleus in pons, where INTERNUCLIAL FIBERS in RETICUALAR FORMATION connect to DORSAL MOTOR nucleus of 10 which SLOWS HEART
what CN does special sensory to posterior 1/3 of tongue
CN9 - glossopharyngeal
what is parasymp nucleus of glossopharyngeal nerve and what does it control?
inferior salivatory nucleus - controls parotid gland function
middle ear sensory i smediated by what nerve
glossopharyngeal 9
visceral sensory of CN9 - what nucleus and what function
into nucleus solitaris, sensory from carotid body and sinus
which part of carotid body/sinus senses what (chemo/baro)
body = chemo sinus = baro
skeletal motor component and nucleus for CN9
nucleus ambiguus - stylopharyngeal muscle for swallowing
what is general sensation for CN9 - what nucleus and what sensation (4)
through spinal trigeminal nucleus
sensation for:
- soft palate
- pharynx
- posterior 1/3 of tongue
- middle ear cavity
what does CN11 do
motor only- innervates trapezius and sternocleidomastoid
where is CN12 nucleus
most ventral and medial
what does CN12 do
innervates muscle of tongue - protrusion
what side does tongue deviate to with CN12 injury
lower motor neuron - flaccid paralysis, deviates to the side of injury
what muscle attaches to coronoid process of mandible
temporalis
what bones articulate to form TMJ
condyloid process of mandible with zygomatic arch - articular tubercle prevents anterior dislocation
what ligament stabilizes TMJ
lateral ligament to prevent posterior dislocation
what movement does superior compartment of TMJ allow for
gliding/translation - jutting chin out when you open very wide
what movements does inferior compartment of TMJ allow for
elevation
depression
what is the blood supply to the infratemporal fossa and what is it a branch from
superficial temporal artery - branch of external carotid
what is the sensory innervation of the infratemporal fossa and what is it a branch of
auriculotemporal nerve - branch of V3
movements of temporalis muscle (2)
- elevation of mandible
2. retraction of mandible
movements of masseter
- elevation of mandible
2. protrusion
movements of lateral pterygoid muscle
bilateral:
- protrusion
- depression
unilateral
1. contralateral excursion
medial pterygoid muscle movements
bilateral
- protrusion
- elevation
unilateral
1. contralateral excursion
which pterygoid muscle is superior
lateral
what are the 2 terminal branches of external carotid
maxillary artery
superficial temporal artery
what are the sections of the maxillary artery
- deep to neck of mandible
- laterl pterygoid (anterior)
- pterygopalatine fossa
branches of maxillary artery first portion (what is supplied)
- middle meningeal (goes up to dura)
2. inferior alveolar (dives down, supplies teeth exits mental foramen)
branches of maxillary artery second portion (what is supplied)
- deep temporal (goes up to muscles of mastication)
2. buccal artery (down to buccinator)
branches of maxillary artery third part (what is supplied)
infra orbital artery (floor of orbit)
venous drainage of infratemporal fossa (3)
- retromandibular vein (side of face/neck)
- facial (front of face)
- inferior ophthalmic vein (to cavernous sinus)
what foramen does V3 exit from skull
foramen ovale
what is special about auriculotemporal nerve
acts as a highway for postganglionic parasympathetic (from otic ganglion) to parotid gland
sensory info to anterior 2/3 of tongue supplied by what
lingual nerve of V3
what is special about lingual nerve
highway for chorda tympani (branch of facial) that carries BOTH taste and preganglionic parasympthatetic fibers of submandibular and sublingual glands
what does parasymp of CN7 do
innervates submandibular and sublingual glands
what does parasymp of CN9 do
innervates parotid gland
what is the ganglion that parasymp of CN7 go to
submandibular ganglion
what are the SENSORY nuclei of trigeminal from superior to inferior
mesencephalic
main
spinal trigeminal
where are first order neurons of sensory trigeminal nerve
in trigeminal ganglion (analagous to dorsal root ganglion)
where are the second order neurons of sensory trigeminal nerve
EITHER main sensory or spinal trigeminal nuclei
where are the 3rd order neurons of sensory trigeminal nerve
ventral posteroMEDIAL nucleus (VPM) of thalamus
when do sensory trigeminal nerves deccusate
between 2nd and 3rd order neurons
what info is carried in main sensory nucleus
discriminative touch and pressure - like dorsal column, meets up with medial lemniscus
where is main sensory nucleus
PONS
where does info go after main sensory nucleus
ascends in medial lemniscus - most contralaterally, but some from ORAL CAVITY are ipsilateral as trigeminothalamic tract
where is face on homunculous
laterally, right above lateral fissure
what info is carried in spinal trigeminal nucleus (2)
- pain and temp from face
2. sensory info from CN 7, 9, 10
where is spinal trigeminal nucleus located
pons, medulla and spinal cord C1-C3
what is the pathway of trigeminal trigeminal tract neurons
enter from trigeminal ganglion and DESCEND in spinal trigeminal tract (lateral) to reach spinal trigeminal nculeus
what info does mesencephalic nucleus contain?
prprioception from head (how to regulate force of bite)
what is different about mesencephalic nucleus compared to the other trigeminal sensory nuclei
it contains first order neurons (the other first order neurons are in the trigeminal ganglion)
what is path of neurons in mesencephalic nucleus
from mesencephalic to trigeminal motor nucleus (below and medial) and then back out through V3
what is input to motor trigeminal nucleus
- mesencephalic for force of bite
2. bilateral corticobulbar
how to test motor of CN5
jaw jerk test - USUALLY DOES NOT CAUSE RESPONSE. if there’s an upper motor neuron lesion, there will be a reflex
what can cause someone to have violent bursts of pain sensation coming from all 3 branches of CN5
trigeminal neuralgia caused by arterial compression from superior cerebellar artery (SCA)
nuclei of CN7 and location in mid-pons
- motor nucleus (middle and medial, tract loops up and around abducens nucleus)
- spinal trigeminal (middle and lateral)
- nucleus solitarus (up/dorsal, between abducens and spinal trigeminal)
- superior salivatory nucleus (medial and up to motor nucleus)
where are 1st order neurons for CN7
geniculate ganglion
what info does nucleus solitaris carry for CN7
taste from anterior 2/3rd of tongue
what info does spinal trigeminal nucleus carry for CN7
somatic sensory from external ear
what info does superior salivatory nucleus carry
parasymp neurons to lacrimal, nasal, palatal, submandibular and sublingual glands
where does CN7 exit skull
with vestibular cochlear through INTERNAL ACOUSTIC MEATUS
what does geniculate ganglion contain
CN7 taste and sensory neurons
what is the “hay fever” ganglion
pterygopalatine galgnion (pregang parasymp from CN7)
where does CN7 exit face
stylomastoid foramen
what nerve branch of 7 is parasymp
petrosal nerve
which part of face recieves bilateral innervation
upper face
what kind of innervation does lower face recieve
ONLY contralateral innervation
what kind of facial paralysis will you see with upper motor neuron lesions
partial paralysis of upper, full paralysis of lower
what kind of facial paralysis will you see with lower motor neuron lesions
paralysis to both upper and lower face (bell’s palsy)
what carries taste from hard palate
greater petrosal
what nerve does pterygopalatine postganglionic neruons hitchhike on to get to lacrimal
V2
componentes of blink reflex
afferent via V1 of CN5
motor via CN7 to blink
tearing via parasymp of CN7
is high or low cortisol protective against PTSD
high (fast cortisol response shuts down the stress response)
what areas of brain are hypoactive in PTSD (3)
prefrontal cortex
dorsal cingulate cortex
hippocampus (can become damaged/ atrophied)
what area of brain is hyperactive in PTSD
amygdala
medicine in PTSD (3 to use, 1 not to)
firstline = SSRIs
Prazosin for nightmares
Topiramate for nightmares
avoid prolonged use of benzos - could cause more risk
gender risk for PTSD
female:male is 2:1
what percentage of PTSD risk is genetic
30%
how to test CN8 in comatose patient
caloric reflex
warm water into ear - eyes deviate toward contralateral ear, fast nystagmus towards ipsilateral
cold water into ear - eyes deviate toward ipsilateral ear and fast phase is in opposite direction
dizziness in diabetic patient when standing, what could the cause be
orthostatic hypertension due to dysautonomia - disruption of autonomic nervous system
or position sense
or medication
definition of orthostatic hypotension
drop in systolic BP of 20 or diastolic BP of 10 within 3 min of standing
what does pulse do in neurogenic orthostatic hypertension
doesn’t change
what phase of nystagmus do you define it by
fast phase
in peripheral vertigo, what direction is fast phase of nystagmus
away from the affected ear
if you see vertical nystagmus, what could it be
Brainstem disease
which type of nystagmus is fatiguable
peripheral (inner ear)
which pole of eye determines direction of nystagmus in rotatory nystagmus
upper
what is head impulse thrust test
move head to left and to right, look at eyes. if eyes are able to stay fixed forward, that’s normal. if you turn the head to the right and it takes some time before the eyes turn back forward, there’s a vestibular lesion on the right
3 maini causes of peripheral vertigo
- benign postural vertigo
- meniere’s
- vestibular neuronitis
what is hallpike maneuver
patient sits down, turn head 45 degrees, keep eyes open, tell them to lie down with head over edge - you will see delayed nystagmus that will eventually disappear (if inner ear vertigo)
what to do for benign paroxismal postural vertigo
ekley maneuver to try to move crystals away
tx for meneiers
salt and volume reduction
kinocilium structure and function
nonmotile cilium (no central core)- only one per array of stereocilia in vestibules that bend towards kinocilium to cause calcium flux via pulling on tip-links between stereocilia
what is source of endolymp
stria vascularis in cochlear duct, drains through endolymphatic sac
NCC and ear development
NCC stimulate differentiation of hair cells
emmetropic means what
normal eye
normal length from lens to retina
17mm
diopters of cornea and lens
40 and 20
myopia - where do rays converge and what kind of lens do you need
before the retina - too much converging power - need concave (-) lens
hyperopia - where do rays converge and what kind of lens do you need
behind the retina - not enough converging power, need convex (+) lens
what does lens have to do when you’re trying to read
has to get more round - ciliary muscles have to contract so that the zonule fibers relax
types of blepharatis
anterior (ulcerative or sebhorreic)
posterior
what is a stye
AKA external Hordeolum
staph abcess of lash follicle
what is chalazion
chronic blockage of meibomian gland - PAINLESS
sx for acute lacrymal sac infection/inflammation
dacryocystorhinostomy - connect sac with nasal mucosa
what is the discharge like in viral conjunctivitis
watery
what is pingueculum
whitish deposit on bulbar conjuctiva (does not involve cornea) usually due to UV exposure - deveneration of conjunctiva. lubricate for tx
what is pterygium
can extend over cornea - can happen in hot climates
how to test between episcleritis or scleritis
episcleritis will blanch with phenlephrine and is mobile
causes of scleritis
usually connected to connective tissue disorders, can also be (rarely) infectious like syphilis. rule out infection betfore treating with immunosuppression or steroids
risk factors for infectious keratitis (2)
contact wearing herpes simplex (see dendritic keratitis)
when to check eye with herpes zoster
when tip of nose is involved
3 components of uvea
iris
ciliary body
choroid
symptoms of uveitis (4)
- diffuse injection
- keratic percipitates
- hypopyon
- inflammation of blood vessels if posterior is involved
what does traumatic cataract look like
rosette shaped
sx of choice for catarats
phacoemulsification
what is dreaded complication of cataract sugery
endophthalmitis (1:1,000) - inflamation of cavities caused by infection - 50% of eyes will become blind
when you do peripheral iridotomy, where are you maing a hole
between anterior and posterior chambers
which is worse for the eye, acids or bases
bases - can result in liquefaction necrosis - can penetrate tissues faster
older one day of vision loss, shadow at bottom of vision, now middle too, flashing lights and floaters, hx of cataract surgery
retinal detachment (shadow) (retina tear caused floaters/flashers)
what kind of retinal detachment do you see in DM
tractional
older woman, decreased vision for 2 weeks, black spot in center of vision, hx of smoking and HTN
macular degeneration (see hemorhage in one eye, drusen in the other)
which are better, soft or hard drusen
hard. soft will more likely become wet macular degeneration
hx of blurriness for a year, getting worse. last week noticed new floaters. decreased red reflex. hx of DM, HTN and smoking
diabetic retinopathy - proliferative
decreased vision, progressively worse, feels “darker”, hx: HTN, PE, smoking, lots of infarcts and bleeding on fundoscope “blood and thunder”
central retinal vein occlusion
older man, 1 day of dark vision in R eye, last week, vision became blurry, then black, then normal. hx of HTN, high cholesterol and smoking. see “cherry red spot” on fundoscope
central retinal artery occlusion
older man, dark vision, blurry then black then normal, headache, jaw claudication, scalp tenderness, joint aches
giant cell arteritis
tx for GCA
steroids
older woman, pain redness photophobia and decreased vision. had cataract sx 1 week ago
post op endophthalmitis due to staph
tx for post op endophthalmitis
aspirate vitreous (or sx if really bad vision), inject broad spectrum antibiotics
what are the “order” neurons for the vestibular reflexes
1 = vestibular ganglion cells 2 = vestibular nuclei 3 = motor nucleus
which vestibular nuclei are involved in vestibuloocular reflex
all 4
which vestibular nuclei are involved in vesteibulocolic reflex
medial vestibular nucleus
which vestibular nuclei are involved in vestibulospinal reflex
lasteral vestibular nucleus only
what is the range of hearing for intensity/loudness of sound (in decibels)
0 dB = threshold of hearing
20 dB = whisper
60 dB = convo
120 dB = thunder
which middle ear bones have muscles attached to them and what are they innervated by
malleus = tensor tympani muscle innervated by CN5
stapes = stapedius muscle innervated by CN7
what ions and neurotransmitters cause transduction at inner hair cells
potassium at tip links, calcium at base, glutamate to auditory nerve cell
pathway from orgain of corti to auditory cortex
auditory ganglion cell to dorsal and ventral cochlear nuclei, then most cross over, synapse in superior olive or just straight ascend to inferior colliculus, then to MGN, then to auditory cortex
describe the vetsibuloocular reflex as you turn your head left
left vestibular nerve excites neurons in left vestibular nuclei. neurons then cross over and excite the RIGHT ABDUCENS nucleus to excite RIGHT LATERAL RECTUS. the abducens nucleus also contains INTERNUCLEAR NEUROS which cross back over, ascend in MEDIAL LONGITUDINAL FASCULIS and excite LEFT OCULOMOTOR and thus LEFT MEDIAL RECTUS
if you have on left sided internuclear opthalmoplegia, what would happen when you move your head to the left
right eye lateral rectus would work, but medial rectus on left eye wouldn’t
woman with colors looking pink in one eye, with bluriness and dark spot in superior visual field, got worse with hot bath
MS - clinically isolated syndrome
papilledema
patient with white matter lesions that is NOT MS, what is it?
migraine
what will you find more of in CSF in MS
IgG
what are dawson’s fingers and what are they characteristic of
lesions at 90 degree angles to ventricles - characteristic of MS
if you find aquaporin 4 in blood, why dont you think it’s MS
because it’s Devic’s disease/neuromyelitis optica - also the lesion will travel for multiple spinal cord segments
what is a big risk for biologics used for MS (underlying issue)
PML (Progressive multifocal leukoencephalopathy) due to JC virus
first medication with defined benefit in primary progressive MS
ocrelizumab (very similar to rituximab)
most common reason for relapse in MS
non compliance with meds
DSM criteria (2+) for personality disroder
deviation from cultural norms in 2+ ways:
- cognition
- affectivity
- interpersonal functioning
- impulse control
these traits are inflexibile and maladaptive
how old do you have to be to be dx with personality disorders
can be less than 18 if you have symptoms for more than a year, however, antisocial personality disorder needs you to be 18y/o for dx
what are cluster A personality disorders (3)
“odd, eccentric, weird”
- paranoid personality disorder (no psychosis)
- schizoid personality
- schizotypal personality
what are cluster B personality disorders (4)
“dramatic, emotional, wild”
- antisocial personality disroder (need conduct disorder in adolescence)
- borderline personality
- histrionic personality disorder
- narcissistic personality
what are the cluster C personality disorders
“anxious”
- avoidant personality disorder
- dependent personality disorder
- obsessive compulsive personality disorder
schizoid personality traits (and tx)
does not enjoy relationships, detachment, emotional coldness, hard to tx with therapy
schizotypal personality traits (and tx)
odd beliefs, magical thinking, social anxiety, peculiar speech, tx with social skills training
antisocial personality traits (and tx)
breaks the law, lies, cons people, impulsivity, recklessness, irresponsibility, lack of remorse, violence, use of weapons and drugs, low risk preventional benefit with group parenting training
borderline personality disorder traits (and tx)
associated with hx of abuse, very sensitive to stress and interpersonal slights, suicidal behavior, or non-suicidal self-harm, impulsivity that are self-damaging, feeling of emtpiness. tx dialectical behavioral therapy, transferance focus, mentalization-based.
histrionic personality diroder traits
excessive emotionality and attention seeking, provocative, need to be center of attention, rapidly shifting and shallow emotional expression, speech is impressionistic and lacking in detail, is suggestible
narcissistic personality disorder traits
grandiose sense of self, needs to be liked, lack of empathy, thinks they are special and can only be understood by high-status people, fantasies of power, success, brilliance, is arrogance, interpersonal exploitative.
avoidant personality disorder traits
avoids interpersonal contact, shows restraint within intimate relationships for fear of being ridiculed, very low self esteem, preoccupied with criticism and rejection, reluctant to take personal risks
dependent personality disorder traits
needs a lot of reaassurance from others, needs other to assume responsibility, difficulty expressing disagreement with others for fear of loss of support, difficulty initiating project or doing things on their own, will volunteer to do things that are unpleasant to obtain support from others, feels uncomfortable when alone, seeks relationships as source of care
obsessive compulsive personality disorder traits
preoccupation with orderliness, perfectionism, control, at the expense of efficiency, can’t meet deadlines, excludes leisure activities, can’t delegate, shows rigidity, ego-syntonic (doesn’t see it as an issue),
somatic symptom disorder traits
excesive thoughts, feelings or behaviors related to symptoms (disproportionate thoughts about severity, energy devoted to symptoms, high anxiety) for 6months
illness anxiety diroder traits
hypochondria - preoccupation with having or acquiring a serious illness for more than 6 months, with mild or absent somatic symptoms. equally common in men and women (somatic symptom and conversion more common in women)
conversion disorder traits
symptoms of altered voluntary motor or sensory function incompatible with known conditions - diplopia, blindness, deafness, numbness, dysphasia, seizures, tremor (sometimes with indifference to these symptoms). usually just an acute response to an acute stressor
pseudocyesis
false belief of pregnancy - amenhhoreah, fat distribution, breast enlargement
primary gain
something rewarding about being in sick role - i.e. when people were sick in abusive childhood, they were taken care of
secondary gain
external rewards - bed, drugs, benefits
factitious disorder AKA
munchausens
