week 13 Flashcards
parison and Lewy body dementia have
Alpha synuclein + lewy bodies
alzheimers compoennts
b amyloid plaque and tau tangle
frontotemporal dementia contains
tau tangles
what causes dementia pathophysoiology
[arteriosclerotic cerebrovascular disease] vascular occlusion (arteriosclerosis) and multiple infarcts/ strokes
[severe cerebral trauma lesions] diffuse axonal injury/ shearing or chronic hydrocephalus (increase pressure)
inflammation (i.e. HIV, herpes)
prion disease
leukodystrophy
disrupt proteostasis (protein not folded, and aggregate and dont degrade etc)
Alzheimer disease has 2 proteins
b amyloid plaques (extracellular)
neurofibrillary tau tangles (intracellular)
most common dementia
alzheimers
brain changes in alzheimers
cortical atrophy,
gyro narrow, sulci widen and ventricular enlargement and reduction in brain weight
plaques in alzheimers
sensile plaques (of beta amyloid)
plaques are encircled by reactive astrocytes and microglia
neurofibrillary tau tangles in AD
hyperphosphorylates tau
dementia: beta amyloid peptide are derived from? this protein gets hydrolyzed at 3 sites and 2 are toxic?
amyloid precursor protein (APP)
alpha secretase= non toxic
beta and gamma secretase= toxic
pathology of alzhimers
toxic polypeptides aggregate extracellularly, adhere to AMPA receptors and cause Ca2+ influx
causing intracellular tangles
alzheimers clinical feithers
cognitive, memory, languages, behaviour
3 stages of alzheimers
- pre symptomatic (accumulate b amyloid)
- MCI
- AD
frontotemporal dementia is accumulation of
tau
(NO B amyloid)
how does frontotemporal dementia differ from AD
Alzheimer’s Disease, which usually starts with memory difficulties, FTLD initiates with disruptive and inappropriate behavior
2 subtypes of frontotemporal dementia (3 types total)
behavioral variant (bvFTD)
and
primary progressive aphasia (PPA) [semantic and nonflucent/ agrammatic]
frontotemporal dementia findings
astrogliosis and neuron loss in frontotemporal
picks bodies= inclusions of tau
variants of frontotemporal dementia
- behavioural variant: personality, depression, compulsive
- primary progressive aphasia semantic variant: cant comprehend
- primary progressive aphasia nonfluent/ agrammatic varient: impaired motor speech
2 types of lewy body dementia
parkinson
and Lewy body
lewy body dementia contains
Lewy body inclusion (alpha synuclein aggregates)
absence of neurofibrillary tangles and amyloid plaques
3 stages of Lewy body dementia
- brainstem predominant
- transitional limbic
- diffuse neocortical
how does Parkinson symptoms usually begin
non motor i.e. constipation and hyposmia
what neurotransmitter deficit in Lewy body disease causing inattention, character fluctuations and visual hallucinations
acetylcholine
what is well preserved in Lewy body dementias
episodic memory
lewy body dementia early symptoms
hallucinate, cognition, REM sleep disorder, anosmia (lose smell)
vascular dementia from
1+ asymptomatic strokes
- large cerebral strokes (ischemic of hemorrhagic, symptomatic)
- cerebral small vessel disease (lacks symptoms, arteriosclerosis and cerebral amyloid antipathy- bet amyloid)
dementia and sensorineural hearing loss
increase cognitive load, change brain structure, social disengage
degenerate stria vascularis, lose hair cells
traumatic brain injury and dementia
ok
gut microbiome and dementia
gut microbiota in AD pathogenesis is realized through diverse pathways, including abnormalities in Aβ, tau phosphorylation, neuroinflammation, neurotransmitter dysregulation, and oxidative stress
Which of the following neurodegenerative diseases is characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain?
A) Vascular dementia
B) Lewy body dementia
C) Frontotemporal dementia
D) Alzheimer’s disease
D) Alzheimer’s disease
Which type of dementia is associated with motor symptoms such as tremors, rigidity, and bradykinesia?
A) Alzheimer’s disease
B) Vascular dementia
C) Lewy body dementia
D) Parkinson’s dementia
D) Parkinson’s dementia
Which type of dementia is associated with a gradual decline in cognitive function due to multiple small strokes or impaired blood flow to the brain?
A) Alzheimer’s disease
B) Vascular dementia
C) Lewy body dementia
D) Frontotemporal dementia E) Parkinson’s dementia
B) Vascular dementia
what is opening between nasal cavity and nasophayrnx (for airflow)
choanae
upper and lower boundary of nose
upper- cribriform plate and ethmoid bone
lower- hard palate
nasal conchae AKA turbinates
superior, middle and inferior bony projections on lateral walls
vascularize mucosa for inhaling air (humidify, filter, olfactory, SA)
meatus in nose
superior - below superior concha; drain posterior ethmoidal air cells, aifrlow and odor detection
middle
inferior (beneath inferior conchae) = contains nasolacrimal duct, drain tear from lacrimal sac to nasal cavity = cry and nose runs
sensory innervation of nsoe
olfactory nerve (CN I) - for smell
ophthalmic (V1) and maxillary (V2) division of trigeminal nerve (CN V) - sensory fibers
tongue muscles
*Genioglossus Muscle: functions to extend and lower the tongue.
*Hyoglossus Muscle: functions to lower and pull back the rear part of the tongue.
*Styloglossus Muscle: functions to lift and retract the tongue.
*Palatoglossus Muscle: acts on the tongue but is categorized as a muscle associated with the palate
sensory innervation of oral cavity
general sensation:
mandibular branch (V3) of trigeminal nerve (CN V) for anterior 2/3
glossopharyngeal nerve (CN IX) for posterior 1/3
taste sensation:
facial nerve (VII): anterior 2/3 of tongue
glossopharyngeal (IX) for posterior 1/3
boundaries of oral cavity
- The upper boundary of the mouth is formed by the palate, while the mylohyoid muscle defines its lower limit. The cheeks are framed by the buccinator muscles on either side, and the posterior boundary is marked by the palatoglossal arches.
motor innervation of oral cavity
vagus nerve (X) for all muscles of palate (except tensor deli palatine is via V3 mandibular branch of CN V)
hypoglossal nerve (XII) for all muscle of tongue
(except palatoglossus muscle via vagus nerve)
mylohyoid muscle via V3 of CN V
facial nerve VII for posterior belly of digastric and stylohyoid muscle
light focusing of the eye
change shape of lens (refraction)
change size of pupil
eye movement - extra ocular
transparency of the eye
cornea and lens and aqueous and vitreous humour
transduction (action potential) of eye
retina takes photons and turns into electrical signals to send to brain
3 layers/ tunics of the eye
fibrous tunic (sclera and cornea)
–> protect eye, EOM, refraction
vascular tunic (choroid, ciliary body, iris)
–> nutrients, absorb stray light, pupil consist, lens shape
neurosensory layer (retina)
–> signal transduction (AP), process visual info, absorb stray light
sclera vs cornea (both in fibrous tunic)
sclera- opaque, vascularized, EOMs insert,
cornea- transparent, avascular , 5 layers (i.e. bowman membrane and descement membrane)
choroid (in vascular tunic)
vascularized, lots of melanocytes, Bruch’s membrane
ciliary body (in vascular tunic)
ciliary muscles:
ciliary processes: vascular, melanin
ciliary zonule: suspensory ligament
ciliary muscles and zonular ligaments for what function
accomodation
accomodation what happens to muscles and ligaments
muscles contract when object is near and ligaments relax
lens more convex
where is aqeusou humor
Aqueous humour circulates from the posterior chamber to the anterior chamber of the anterior compartment
if drainage of aqueous humor impaired what happens
increase intra ocular pressure
push back and damage retina behind it
steps in production of aqeusou humor
- secreted by ciliary processes in posterior chamber
- travel to pupil then anterior chamber (all of anterior compartment)
3.excess aqueous humor is resorbed via scleral venous sinus
what secretes and what absorbs aqueous humor
secreted by ciliary process
absorbed by scleral venous sinus
what is the filter that overlies the scleral venous sinus which drains aqeiosus humor
trabecular meshwork
what can block sceral venous sinus and drainage of aqeusous humor
- The iris can “flop over” the scleral venous sinus and block it
- The angle between the the iris and the lens can also become blocked
these cause glaucoma
iris (part of vascular layer)
2 muscles
covers part of the lens, doesnt cover the pupil
dilator pupillae muscle- SNS
sphincter pupillae muscle- PNS
location of vitreous humor vs aqueous humor
vitreous- posterior cavity
aqeusou- anterior cavity
what is vitreous body/ humor made of
99% water, collagen fibrils and hyaluronate also present
when embryo makes the retina
out pouching of diencephalon
what attaches to the inner limiting membrane of retina surface
and what is outer layer of retina
vitreous humor
choroid
rods and cones
transducer light info via NT
Bipolar cells, ganglion cells, axons of ganglion cells
“line of communication” from rods and cones to the optic nerve
what are the interneurons in the retina
Horizontal cells, amacrine cells
what membrane is pigment epithelium of the retina on
Bruch’s membrane
where in the retina are cones and rods most concentrated
▪ Most cones are concentrated in the fovea
▪ The rest of the retina mostly contains rods
blind spot (optic disc)
no photoreceptors over optic nerve
lens abnormalities
▪ Loss of elasticity with age= presbyopia
▪ Opacities = cataracts
where are the viable cells in the lens
periphery
the center has mature lens fibers which loss nuclei and full of crystallins
accomodation and the lens for near vs far
(a) The lens flattens for distant vision when the ciliary muscles are relaxed, and the shape of the ciliary body holds the ciliary zonule taut
far= ligaments taught and muscle relax
(b) To see closer objects the ciliary muscle fibers contract, changing the shape of the ciliary body, relaxing tension on the ciliary zonule, and allowing the lens to assume the more rounded shape
near= ligaments relaxed and muscle contract
Light passes through cornea and enters the eye through the _______. The size of this structure is mediated by the _________.
* Light is bent as it passes through the various structures of the eye, but it is the ______ that can change its shape to focus the beams on the ________.
* Bending of light is called “refraction”
Light passes through cornea and enters the eye through the pupil. The size of this structure is mediated by the iris.
- Light is bent as it passes through the various structures of the eye, but it is the lens that can change its shape to focus the beams on the retina.
- Bending of light is called “refraction”
refraction is
via which eye part
the bending of light (so see 1 image)
lens
how does image of object in visual field change to get projected onto retina
upside down and inverted on retina then brain flips it correct way
i.e. top is bottom, left is right
what changes shape to refract light
lens
convex= more rounded when objected are closer
need more refraction when closer
accomodation
rounding of lens to focus on nearby object
3 parts to accomodation
- increase convexity of lens
2.convergence of eyes via muscles (i.e. medial rectus muscle)
- constrict pupils (miosis)
what is need to increase convexity/ round the lens
PNS
oculomotor nerve
ciliary muscles contract and suspensory ligaments (ciliary zonule) relax
distant vision vs near vision
muscle relaxed, ligaments tight, lens flat
Near vision: muscle contracted, ligaments loose, lens rounded up
miosis
constrict pupils in bright light and accomodation (close)
under PNS
mydriasis
dilate pupils in dim light and fight/flight
SNS
myopia
near sighted
eyeball too long
beams converge before retina
hyperopia
far sighted
eyeball too short
beams converge after retina
20/20 vision
first # is furthest patient can do
send # is person with normal vision
20/18= better
20/30= worse
convex vs concave glass lens
convex cause beam to converge so for hyperopia
concave cause beams to diverge so for myopia
depth perception
-moving parallax (i.e. observe changes viewpoint)
-access to previous knowledge
-stereopsis (eyes are offset and have slightly different overlapping view causing retinal disparity then brain puts back together)
stenosis (both eyes have slightly different view) needs
Stereopsis requires both eyes to fix on same point
▪ Fixed focus point projects to fovea of both eyes (no disparity)
▪ Closer object projects to different places on each retina (retinal disparity)
uses the retinal disparity of two objects to contribute to depth perception
in the pigment layer of the retina what is in it
melanin
vitamin A for helping rods and cones with photoreception
outer segment of cones and rods contain
photopigments and vitamin A
synaptic terminal of rods and cones release
glutamate
rods vs cones
cones are low convergence (good acuity), highly concentrated in fovea and have colour photopigments
rods are highly convergent circuits (poor acuity), not in the fovea, high photopigment for night vision, no colour
what does the fovea only contain
cones
rods in periphery
colour via
short wavelengths- blue
medium- green
long- red
anopia and anomaly
anomia- missing a type of cone (dichromy)
anomaly- defective type of cone (trichromy)
Protanopia and protanomaly: red cone issue
Red-green colour blindness
Deuteranopia and deuteranomaly: green cone issue
Red-green colour blindness
Tritanopia and tritanomaly: blue cone issue
Blue-yellow colour blindness
red green colour blindness
x linked recessive more in males
chromophore component = retinal/ vitamin A in rods and cones to
pigment
Captures light and induces a conformational change in the opsin component
opsonin component in rods and cones is
a GPCR and used for signal transduction
rhodopsin vs iodopsin
rhodospsin- rod photopigment for light
iodopsin- cone photopigment for colour wavelengths (red, blue, green)
when rods response to light what happens
rhodopsin captures light and is activated (meta-rhodopsin)
convert cis to trans retinal
meta-rhodopsin activated GPCR transducin
close Na+ channels and hyper polarize and depolarize the on center
decrease glutamate
**in the dark rod depolarize, increase glutamate and then hyper polarize and inhibit on centers **
