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Conjoint > Midterm 2 (Rachael's Contribution) > Flashcards

Midterm 2 (Rachael's Contribution) Flashcards

1
Q

Structure of the Eye: Cornea (Myopia)

A
  • Light goes through first
  • Most powerful focusing lens of eye
  • Lots of layers
    • Outside is thin, stratified epithelium
    • Layer of collagen
    • Layer of glycoproteins, get lots of water, makes it clear
  • Myopia, make the cornea less curved, use laser to burn the glycoproteins
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2
Q

Structure of the Eye: Aqeous Humor

A
  • Behind the cornea
  • Made in ciliary body and flows through pupil
  • Slowly made and removed
  • Source of nutrition and support of cornea
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3
Q

To make pupil larger…

A
  • Pull iris back using **sympathetic **nerves
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4
Q

Structure of the Eye: Lens

A
  • Clear, made up of cells
  • Held in place by zonular fibers
    • Are the black threads on lens
  • Ciliary body is the dark spot lateral to zonular fiber
  • Parasympathetic make it contract
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5
Q

Structure of the Eye: Vitreous Body (what can be in it)

A
  • Almost perfectly clear
  • Some floaters
    • from development or cells. Cast shadows on the retina. ​
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6
Q

Structure of the Eye: Retina (and a feature of the retina)

A
  • Orange part in back of eye
  • Optic disk, where the axons leave through the optic nerve.
    • No photoreceptors there
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7
Q

Flow of aqueous humor

A
  • From the ciliary body to the pupil, to the angle between the iris and the cornea in the aqueous humor chamber
  • Trabecular network, fibrous proteins that form mesh. Aqueous humor can go through it.
  • Schlemm’s canal is where the aqueous humor drains.
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8
Q

Glaucoma: Definition

A
  • Degeneration of axons near the optic nerve
  • Only afferent neurons
  • Too much pressure building in eye
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9
Q

Glaucoma: Diagnosis (3)

A
  • Tonometry, figure out the tone in the eye
  • Optic disk: look at blood vessels, look for hypertension
  • Retina imaging
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10
Q

Glaucoma: Open Angle

A
  • Age is a real risk factor, 90% old
  • Slow, painless
  • Aqueous humor not draining out properly
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11
Q

Glaucoma: Closed Angle

A
  • Age less of a factor
  • Sudden, attack, painful
  • The iris pushed against cornea and closing the angle.
  • Happens when pupil dilate, treatment, constrict the pupil
    • Hard for the aqueous humor to drain out of Schlemm’s Canal.
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12
Q

Drugs for Glaucoma: Alpha Agonists

A
  • Decrease aqyeous humor production
  • Increase outflow
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13
Q

Drugs for Glaucoma: Beta antagonists

A
  • Ex: timolol
  • Decrease aqeuos humor production
  • Prostaglandin analog
  • Increase outflow
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14
Q

Drugs for Glaucoma: Cholinergic agonist

A
  • Closed angle Glaucoma
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15
Q

Drugs for Glaucoma: List (5)

A
  • Alpha Agonist
  • Beta Agonist
  • Cholinergic Agonist
  • Carbonic Anhydrase Inhibitor
  • Canabis
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16
Q

Lens: Structure

A
  • Around the edge is the ciliary body.
    • zonular fibers that keep the ciliary body taught.
      • Think of a trampoline with springs
      • Ciliary muscle in the ciliary body.
  • Lens cut in half. Made of cells that are “living.
    • Long thin cells shaped like layers on an onion.
    • Have 6 sides to them.
    • Shaped like prism.
    • Clear, so no nucleus.
    • No mitochondria, etc.
  • Have 3 crystalline proteins that are clear. Highly hydrated, so needs to be maintained but can’t have any blood vessels, or else the lens becomes cloudy. Get’s its nutrition from the aqueous humor
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17
Q

Cataracts

A
  • Parts of lens becomes cloudy
  • Will start seeing cloudiness, glare, two images shifted from each other.
  • Very common
  • Caused by age/genetics, diabetes, UV, heavy glucocorticoid use.
  • Treatment: cut in sclera, probe into lens, emulsifies lens, lens is sucked out. So the lens in gone. Then artificial lens. Old lens has inherent yellow coloration. Artificial is superior to natural lens. Can’t accommodate for close up vision because lens can’t change shape, already usually have to use reading glasses.
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18
Q

Focusing Light

A
  • Light diverges, need to converge light
    • Do this with a convex lens
    • Do this with cornea and lens
  • Measure focusing power with diopters.
    • 1 diopter, takes 1 meter to converge light
    • 2 diopter, takes 0.5 meter to converge light.
  • Eye needs 60 diopters in converging power. Strongly curved lens.
    • Cornea is most precise lens, 40 diopters
    • Lens is about 20 diopters
  • As objects gets close, need more diopters
    • Do this by contracting ciliary muscle.
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19
Q

Myopia

A
  • Eyeball is too long
  • Image fall in front of retina
  • Want to move image back, so want negative diopters.
  • Want a concave lens to diverge light.
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20
Q

Hyperopia

A
  • eyeball too short
  • Image fall behind retina
  • Puts strain on eye because contract ciliary body
  • Want positive diopters to move the image up.
  • Convex lens.
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21
Q

Astigmatism

A
  • cornea different curvature on different axes
  • Cornea is not symmetric on all axes
  • If wearing glasses, need different curvatures on different axes
  • In contact lens, sticks to cornea to give the correct curvature
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22
Q

Presbyopia

A
  • lens stiff from age so little accommodation for close up vision
  • Late 40’s to early 50’s
  • Loss of ability of lens to bulge when ciliary muscle contracts
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23
Q

Transduction in Rods and Cones

A
  • Light on center 1 mm falls on the fovea
    • High density of cones. Detailed vision (fine vision), Colored vision. Color from cones.
  • Peripheral
    • Rods, extra sensitive to light, black and white, night vision.
  • Macula lutea
    • 5 mm in diameter
  • Cones
    • 3: Red (559nm), Green (53nm) and Blue (419nm) absorbers
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24
Q

Diabetic Retinopathy

A
  • Leading cause of blindness
  • Later in diabetes
  • Boils down to problems of small blood vessels in eyes that get leaky and then grow abnormally
  • The prevalence of this has been going down because there has been better control. 4-5% diabetics have severe retinopathy
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25
Q

Diabetic Retinopathy: Non-proliferative Phase

A
  • Rods and cones, supportive layer called retinal pigment epithelium, choroid layer (black, has blood vessels), sclera (white of eye)
  • Focus on choroid layer (highly vascularized)
    • Leakage and blockage (clots) from blood vessel damage
      • Vessel break, clot, get a floater
    • Macular edema, lipid accumulation
    • Neuropathies, axonal damage
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26
Q

Diabetic Retinopathy: Proliferative Phase

A
  • Angiogenesis, blood vessels begin to grow abnormally and fragility
  • Tufts of highly permeably blood vessels
    • Bleeding into the vitreous body and get hemorrhage
  • Responding to abnormal growth factor release
    • Vascular Endothelial Growth Factor (VEGF)
    • Normal growth factor that is released abnormally
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27
Q

Diabetic Retinopathy: Treatments (5)

A
  • Reduce risk factor, hyperglycemia (control the diabetes)
  • If angiogenesis, then antibody (anti-VEGF), injected directly into the eye
  • Anti-inflammatory (glucocorticoid) injection…webpage patient
  • Laser photocoagulation
    • (1) “pan” laser, over a wide area of retina, not as intense of laser, cuts down on oxygen in retina
    • (2) spots that are intensely laser to destroy blood vessels
  • Vitrectomy, chopping up vitreous body and suck it out, put other fluid in there.
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28
Q

Retinal Detachment: Causes

A
  • May happen in diabetes
  • Also myopia, puts tension on the edge
    • Ophthalmologist may see “lattice degeneration”
      • Edges of retina break loose and peel back
  • Cataract surgery (small risk)
  • Trauma
  • Macular Degeneration (small risk)
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29
Q

Retinal Detachment: Symptoms

A
  • Variable
  • All of a sudden, new floaters/big floaters
  • Flashes of light because abnormal stimulation of retina
    • Vitreous pulling at retina (shriveling up)
    • As retina pulls away
  • Black edge like a curtain is falling. Retina is peeling from the side. EMERGENCY.
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30
Q

Retinal Detachment: Treatment (3)

A
  • Photocoagulation: cooking retina and sticking back
  • Remove vitreous
  • Bubble of gas into eyeball, pushes the retina back into place
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31
Q

Macular Degeneration

A
  • Shows up in the 60-80 year old
  • Drusen, protein deposits in retinal pigment epithelium
    • Not diagnostic
  • Damages retinal pigment epithelium (the support that keeps rods and cones healthy)
  • Dry form (90%), Wet form (10%), dry can become advanced to wet form
    • Wet form has angiogenesis, treatment similar to diabetic retinopathy. Distorting retina, uniform grid will see curved lines, leak fluid
    • Dry form, gradual thinning, atrophy, lose rods and cones, vision starts to become blurred.
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32
Q

Macular Degeneration: Treatments

A
  • AREDS formulation (wet or dry), supplements that slow down macular degeneration
  • Lifestyle (wet or dry); stop smoking, obesity, dietary fat/cholesterol
  • Wet: anti-VEGF
  • Wet: Laser photocoagulation
  • Wet: Verteporfin, molecule that is injected into general circulation, adheres to injured blood vessels. Activated by light. Then destroy the injured endothelial. Way to preferentially destroy damaged blood vessels
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33
Q

Structure of the Ear (3 parts)

A
  • Outer, middle, innter
    • Outer: tympanic membrane
    • Inside external auditory canal: cerumen (can get impacted)
    • Middle: Eustacian tube (air filled, goes to pharynx), short is children and they can get otitis media (fills with fluid and puss)
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34
Q

Role of Ossicles

A
  • Small bones
  • Form lever system that picks up vibration from tympanic membrane and transfers to the oval window
  • Delicate system
  • NOT an amplification
  • When sound hit medium of a different density, the sound energy bounces off…problem, 99% of sound energy bounces off
  • Need to ease the sudden transition of density
    • Tympanic membrane has 25% more surface area and then applied to smaller membrane, therefore sound energy enters fluid more efficiently. This is what middle ear is all about
  • Can have conduction deafness (middle ear problem)
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35
Q

Bone Conduction

A
  • Sound energy to bone, can conduct sound energy through bone
  • If middle ear not working, still have sound conduction through bone conduction
  • It just can’t be accessed as easily
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36
Q

Otosclerosis

A
  • Deafness
  • Excess bone growth (dominant gene), one of most common cause of deafness
  • Freezes stapes in place so that can’t move against oval window effectively
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37
Q

Sensory Transduction at Hair Cells

A
  • Transforming sound energy into action potentials
  • Oval window has sensory cells that detect sound vibrations.
  • Basilar membrane is narrower and stiffer near the oval window
    • Wider further away
    • High pitch vibrates near oval window
    • Low pitch vibrates further away from oval window
  • Hair cells are stuck on the basilar membrane
    • Glutamate as NT
    • Basilar membrane bounces, then the hair cells bounce
    • Finger-like projections called stereocilia
      • Mechanically gated ion channels
      • Causes glutamate release
  • Tectorial membrane not move up and down with basilar membrane
    • Hair cells bounce up and down against the tectorial membrane
    • Potassium through Mechanically gated ion channels
      • Ionic concentration in fluid above hair cells is very weird, K equilibrium potential is not -90mV (actually higher)
  • Molecular movements of sterocilia can be detected (highly sensitive)
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38
Q

Sensorineural Deafness

A
  • Degeneration of hair cells
    • Noise can cause hair cell damage
      • Hearing loss might be pitch dependent depending on where the hair cells were damaged
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39
Q

Presbycusis

A
  • Atrophy of hair cells with age
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40
Q

Drugs that damage hair cells

A
  • Aminoglycosides and other antibiotics
  • Diuretics
  • Antimalarials
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41
Q

Viruses causing damage to hair cells

A
  • Cytomegalo virus
  • Rubella, mumps
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42
Q

Vestibular System

A
  • Senses accelerations
    • Rotational acceleration
    • Linear acceleration
  • Best sense of acceleration is the head and neck movement
  • Linear acceleration from gravity can be felt in limbs
  • So, vestibular system is not the most sophisticated
  • Motion sickness when vestibular system not matches visual input
  • Important for controlling eyes
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43
Q

Nystagmus

A
  • Info into inferior colliculis that has eye reflexes that compensate for body movements
  • Activated if rotating slow enough of the scenery move by slow enough, info about moving to occipital cortex and coded as moving image and then cause optically nystagmus
  • Vestibular nystagmus is much faster because not all the way to the cerebral cortex (move head fast and can still see hand, but not move hand fast and still see)
  • Paralyzed eyes and move head, would just see a blurr
  • When rotating, eyes track back and then jump ahead (slow, fast, slow, fast)
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44
Q

Meniere’s “Endolymphatic hydrops”

A
  • Symptoms: Vertigo, sensoineural deafness, tinnitus
  • Shows up in 30’s or 40’s
  • Too much fluid in vestibular system and pressure on hair cells
  • Usually goes away without hearing loss
  • Treat with getting rid of sodium in body
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45
Q

Semicircular canals

A
  • 3 of them, cover three spatial places (forward and 2 diagnoal cartwheels)
  • Inertia of fluid lags behind of causes hair cells in the cupula to bend
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46
Q

Utricle and Saccule

A
  • Sense linear acceleration
  • Carpet of hair cells
  • Otoconia: stones, inertia of stones causes hair cells to move
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47
Q

Benign Paroxysmal

A
  • Positional vertigo, common
  • Couple of otoconia break off and get into posterior semicircular canal and sit there, when person leans back in bed, room rotates because otoconia move and starts fluid moving.
    • Cured by moving bee-bee out of semicircular canal
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48
Q

Auditory Information in the CNS

A
  • 8th cranial nerve into the medulla, then to the inferior colliculus, then the thalamus, then the temporal cerebral cortex.
  • Temporal cerebral cortex is tonotopic (lined like keys of keyboard)
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49
Q

Grey Matter; cerebral coretex; Collection of anatomically defined cell bodies

A
  • neuronal cell bodies
  • Cerebral cortex
    • Highly layered structure, usually 6 layers
    • Patterns of cellular architecture
    • Brodmann’s areas, regions defined by cellular architecture; match up with functional regions (visual, auditory, somatosensory, motor, etc.)
  • Collection of anatomically defined cell bodies: nucleus
    • May be defined functionally or by common neurotransmitters
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50
Q

White Matter

A
  • Axons
  • White because of myelin, full of lipids, basically cell membrane
  • Tract: bundle of axons
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51
Q

anatomical methods to studying higher brain function

A

Links of one region of brain to the other by mapping connections with dyes

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52
Q

lesion studies for studying brain higher function

A
  • There is localization of complicated function
  • Shows that there is lateralization. Cerebral hemispheres appear symmetric, but functionally, they are specialized. Language is found on the left side
  • Can do lesion studies in animal brains to see more precisely where the areas are
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53
Q

Broca’s area

A
  • damaged in Broca’s aphasia, aka: expressive aphasia
  • Difficulty producing speech. A lot of effort, only use single words. No fluency in speech, no problems in articulations
  • Difficulty in finding the words, they understand meaning
  • Troubled by speech because understand the meaning
  • Area of brain that produces language
    *
54
Q

Wernicke’s aphasia

A
  • receptive aphasia
  • No trouble producing words, speaking fluidly
  • No content to speech, nonsensical speaking
  • Defect in speech comprehension, can’t understand a command
  • Hearing intact, problem in decoding sounds as language
  • Area in brain that decodes sound into language
55
Q

Broca’s and Wernicke’s area damage can cause aphasia in sign language “speakers”

A

Similar localization to areas for vocal language

56
Q

Global aphasia

A
  • Difficulty in both production and comprehension of speech
  • Usually have motor problems on the right side
    • Right sided paralysis
  • Due to large left hemisphere lesion, includes motor areas
57
Q

Plasticity

A
  • change in brain
  • More so in younger people, more plasticity in developing brain
  • Can recover somewhat after a stroke
58
Q

methods to record brain activity: overview

A
  • Maps obtained in patients undergoing brain surgery
  • Patients were conscious (awake) with local anesthesia
  • Surface stimulated and patients were asked to report sensation
59
Q

electroencephalography (EEG)

A
  • changes in electrically potential difference at the scalp
    • non-invasive
    • Low spatial resolution
    • Different patterns of activity represent levels of consciousness
  • Beta Rhythm:
    • Eyes open and alert
    • High frequency, low amplitude
    • Due to desynchronized activity
  • Alpha Rhythm:
    • Relaxed with eyes closed, awake
    • All depolarize at the same time
    • Rhythmic activity between thalamus and cortex
    • High amplitude and 10-12 Hz
    • Synchronized activity
60
Q

functional imaging

A
  • Increased activity in a region caused increased blood flow
  • fMRI: functional magnetic resonance imaging
    • Measures brain activity indirectly by measuring changes in blood flow between different regions
    • Shows where regions are active during an activity
    • Small signals
    • Hard for patients to do only the activity asked
      • Hard to pick out relevant signals
    • Not reached level of diagnostics yet
61
Q

Role of the hippocampus in human memory: HM

A
  • Located in medial temporal lobe
  • Lesions here can lead to amnesia (memory deficit)
  • Patient H.M.: bilateral removal of hippocampus
    • Seizure activity was under control
  • Severe anterograde amnesia (going forward)
    • Could not learn anything new
    • But still had memory and long-term memory
  • Working memory: short term memory
    • What use to take in information
    • Hold in brain for a little bit to be able to write it down
    • Keeping phone number in mind in order to dial it
    • Depends upon ongoing activity
    • HM had this
    • Working memory involves the prefrontal cortex
      • Focuses attention
  • Process of transferring things to long term memory is the hippocampus
    • Depends upon stable changes in the brain
    • Hippocampus: consolidation of long-term memory
      • Consolidation: transfer information to long-term memory
    • Hippocampus is NOT a site of storage for memory
  • H.M. had affected declarative memory (explicit memory)
    • Form of long term memory
    • Conscious memory for facts, places, events
  • Procedural memory
    • Form of long term memory
    • Unconscious
    • For skills and habits
    • H.M. had this
    • Doesn’t involve the hippocampus
62
Q

Animal models of learning and memory: test spatial memory

A
  • Morris Water Maze
  • Opaque water hiding platform, animal finds platform and then can navigate to space.
  • Video tape and quantify how much time/territory until find platform
  • Requires the hippocampus
63
Q

Electrophysiological studies of the hippocampus

A
  • Shown that the hippocampus is good at developing synaptic plasticity
  • Needs to happen for learning to occur
    • Long term potentiation (LTP)
    • On course website
    • Cell inputs onto another cell by excitatory synapse. Stimulate A and record B, see an EPSP.
    • Initiation LTP with train of action potentials. Strongly depolarize B
      • Wait and excite A and the EPSP is MUCH larger
      • Long term, because it will last for hours or days
64
Q

LTP and cellular models of memory formation

A
  • Involves the activity of NMDA receptors
  • NMDA is a coincidence detector.
    • Glu needs to bind but also need strong depolarization
    • Strong depolarization causes Mg plug to move
    • Causes Ca++ to flow in
      • 2nd messenger, activates variety of changes in cell
      • Influences the number of glutamate receptors at the synapse.
      • More likely that when A is active, B is active, forming a network
  • Can disrupt LTP and learning is disrupted (also when disrupt NMDA)
65
Q

Alzheimer’s disease: Symptoms and Diagnosis

A
  • Most common form of dementia (cognitive impairment)
  • Problems with memory, problem solving, working memory, etc.
  • Definitive diagnosis: post-mortem examination of brain tissue
66
Q

Cell biology of neurodegeneration in Alzheimer’s: amyloid hypothesis

A
  • Pathological feature of Alzheimer’s disease observed in postmortem examination of brain tissue
    • Amyloid plaques: extracellular accumulations of A-beta peptide
    • Neurofibrillary tangles: intracellular accumulations of hyper phosphorylated tau
  • Amyloid hypothesis
    • Accumulations of A beta in abherrant way (too much made, or not enough cleared away)
    • Over time causes neuro-degeneration
    • Amyloid precursor protein (APP) is cleaved by two proteases to generate A-beta (ABeta)
      • Is a normal membrane protein
    • Plaques might be a way to prevent ABeta from hurting the brain as much. Insoluable
    • Most toxic: soluble oligomers of A-beta
      • Lots of hypothesis about why harmful…not exactly sure
    • Early onset, genetically linked, mutations in APP protein that make it more likely to be cleaved
      • Could also be mutation in enzymes that cleave APP
    • Also on chromosome 21, plaques form in Down-Syndrome
67
Q

Alzheimer’s: Treatments

A
  • Cholinesterase inhibitors: increase Ach at synapses
  • Memantine: NMDA receptor antagonist
    • Reduces excitotoxicty
      • When neurons are degenerating, get abnormal release in glutamate, activates NMDA channels and end up with a lot of calcium in cell, causes cell to die
  • In development: therapies to block amyloid or tau accumulation
  • Hard to determine early Alzheimers, when there is mild cognitive impairment, they are already pretty progressed in the disease
68
Q

Alzheimers: Future directions

A
  • Trying to find biomarkers so that detect earlier to treat earlier
69
Q

Sleep

A
  • Sleep state and waking state
  • Memory consolidation?
  • Sleep homeostasis
    • When deprived up sleep make up for lost sleep later on
70
Q

EEG patterns associated with states of consciousness

A
  • Someone will progress through stages of sleep architecture
  • Progress down stages (1-4) to slow wave sleep and then back up stages to REM
  • Awake and eyes open, beta rhythm
  • Close eyes and drift, alpha rhythm
  • Get to high amplitude and low frequency wave, called delta rhythm
    • 4 Hz frequency
    • Also referred to as slow wave sleep
71
Q

Sleep stages: REM sleep vs. NREM sleep

A
  • REM: rapid eye movement
    • Desynchronized EEG (see with beta rhythm)
    • Lack of skeletal muscle tone, as though body is paralyzed during REM sleep
    • Vivid dreaming
  • NREM sleep: non-REM sleep that include all other sleep stages
72
Q

Regions of the brain controlling arousal (arousal promoting area)

A
  • Nuclei, color-coded, important in different process
  • Defined by interconnections to other parts of the brains and also by neurotransmitters they release
  • Projections of arousal-promoting nuclei
    • Make vast projects throughout the cerebral cortex, diffuse projections
    • Release NT that involved in slow synaptic transmission
      • Binding to receptors that are coupled to G-proteins (7TMD)
      • Direct inhibitory connection to VLPO
73
Q

VLPO

A
  • Sleep Promoting
  • Releases sleep transmitter GABA
    • Inhibitory NT
  • Turns of arousal-promoting nuclei
74
Q

Orexins neurons

A
  • help maintain activity during arousal by exciting the arousal-promoting nuclei
  • Direct excitatory connections to all arousal-promoting nuclei
  • LHA–>Releases orexin (peptide NT)
  • Maintain wakefulness and prevent unwanted transitions into sleep.
    • Maintaining “on” state for arousal-promoting nuclei
  • Mutual inhibition between arousal-promoting and sleep-promoting nuclei ensure rapid, efficient transitions between sleep and arousal
  • VLPO inhibits arousal promoting and removes inhibitions on itself
    • Flip flop switch
75
Q

Glaucoma

A
  • progressive degeneration at the optic disc
  • rim of the optic disc becomes thinner and the optic disc cups inward
  • retinal ganglion cell axons degenerate, followed by their cell bodies
  • increased intraocular pressure
    • from excessive accumulation of aqueous humor
    • aqueous humor is formed in the ciliary body
    • flows through the pupil, and exits through the trabecular network, which is found in the angle between the cornea and iris
76
Q

Open-Angle Glaucoma

A
  • does not cause overt symptoms until permanent damage has occurred
  • “angle” in the term refers to the angle between the cornea and iris where the trabecular network drains the aqueous humor.
    • this space is open so that there is no anatomical obstruction preventing the fluid reaching the trabecular network.
77
Q

Closed-Angle Glaucoma

A
  • angle between the edge of the cornea and pupil is narrowed to the extent that the aqueous humor has difficulty reaching the trabecular network
    • especially if pupil is dialated
  • painful, halo of light, dilated conjunctival blood vessels
78
Q

Drugs for Glaucoma

A
  • Alpha2 adrenergic agonists
  • Beta adrenergic antagonists
  • Prostaglandin analogs
  • Cholinergic agonists
  • Carbonic anhydrase inhibitors
79
Q

Alpha2 adrenergic agonists

A

both decrease the rate of formation at the ciliary body and increase the the drainage.

80
Q

Beta adrenergic antagonists

A

decrease the rate of formation at the ciliary body. (Note, importantly, the alpha and beta receptors produce quite different actions in this case. While often true, don’t draw any firm rules. Each system has its own characteristics.)

81
Q

Prostaglandin analogs

A

increase the drainage of the aqueous humor.

82
Q

Cholinergic agonists

A

decrease the production of aqueous humor and constrict the pupil, the latter effect being useful in closed-angle glaucoma.

83
Q

Carbonic anhydrase inhibitors

A

inhibitors act to reduce the formation of HCO3-, which in turn reduces solute and thus fluid secretion at the ciliary body. (In the kidney these are diuretics.)

84
Q

Drugs for Glaucoma: Overview

A

Drugs used in glaucoma increase the drainage of the aqueous humor and/or reduce its rate of formation at the ciliary body. They are used mainly as eye drops. But enough of the drugs enter the circulation so some of side effects are systemic.

85
Q

Surgery for Glaucoma

A

Laser surgery is used to open up the trabecular network. The effect is not permanent. Conventional surgery can be used to create a opening through which the aqueous humor can drain out of the eye. There are a variety of techniques.

86
Q

Risk factors in open-angle glaucoma

A
  • older age, black race, family history of glaucoma, myopia and especially elevated intraocular pressure.
  • People with significant risk are usually urged to have a dilated pupil eye examination each year.
87
Q

Macula and Fovea

A
  • macula lutea is an area of the retina about five millimeters in diameter. It is centered on the optical axis of the eye, so that light falls on the macula from something small you look at directly.
  • At the center at the macula is the fovea centralis (or just “fovea”). The fovea is about one millimeter in diameter and contains a very high concentration of cones. Indeed, about one-half of the axons in the optic nerve carry visual information from the fovea.
  • Thus, most sharp visual accuity and most all of color vision comes from the fovea
88
Q

Age-Related Macular Degeneration

A
  • Areas outside the macula provide much less accuity, and since the photoreceptors are almost all rods, only provide black and white vision.
  • If there is degeneration of the macula, the sharp visual accuity is lost in the center of the field of vision, and the lower visual accuity of the peripheral vision is retained. Reading, for example, becomes difficult, while the patient can usually navigate around larger objects.
89
Q

Dry macular degeneration

A
  • Most Common
  • yellow deposits called drusen appear in the retina
    • a combination of protein and lipid​
  • Photoreceptors atrophy
  • fundamental problem is the retinal pigment epithelium, which provides a crucial supportive role for the photoreceptors
90
Q

Wet macular degeneration

A
  • More serious, more rare
  • Develops from the dry form
  • retinal pigment epithelium is abnormal, but here it leads to abnormal growth of blood vessels occurs under the macula
    • leaky​
91
Q

Macular Degeneration Risk Factors

A
  • Old age
  • smoking, family history, white race, obesity, female gender.
92
Q

Macular Degeneration Treatments

A
  • wet form, injected directly into eye
  • These substance bind to and inactivate vacular endothelial growth factor (VEGF)
  • ranibizumab (Lucentis) is an antibody
  • injecting a substance into the circulation that binds to new blood vessels. This substance is then activated by light striking it, leading to destruction of the new blood vessels.
93
Q

Otosclerosis

A
  • excess formation of spongy bone about the oval window, leading to reduced mobility of the stapes
  • teenagers/early adulthood
  • genetic
  • hearing aid/surgery
94
Q

Meniere’s Disease

A
  • a disorder of the inner ear
  • incapacitating episodes of vertigo leading to nausea and vomiting
  • Tinnitus and hearing loss are often present
  • Unknown cause
  • involves excess accumulation of endolymph in the cochlear duct and vestibular system.
95
Q

Circadian regulation of sleep

A
  • Jet lag: disruption between circadian clock and actual clock
  • Circadian: hormones, sleep, apetite, temperature
  • Suprachiasmatic nucleus
    • Regulates circadian adjustment of the sleep/wake cycle
    • Pacemaker for circadian rhythms
    • Found in hypothalamus
    • Can be reset from light-dark cues.
      • Input from retinaàentrains circadian rhythm
  • Light/dark has direct affect on SCN. Then SCN has indirect effect on sleep/wake control
  • SCN influences the pineal body
    • Releases hormone melatonin
96
Q

Melatonin

A
  • Increased secretion in the dark
  • Promotes sleepiness
  • Action back on SCN and influence sleep/wake control
97
Q

Drugs affecting arousal: Stimulants

A
  • Ampethetamines and related compounds:
    • Increases NE, DA, serotonin
  • Modafinil (Provigil); armodafinil (Nuvigil)
    • Increases NE, DA (maybe also histamine, serotonin)
  • Caffeine:
    • Adenosine antagonist
    • Inhibit neural activity, sleep drive?
98
Q

Drugs affect arousal: Hypnotics (5)

A
  • Benodiazepines and Z-drugs:
    • GABA potentiators
    • GABA receptor: ligand-gated cl- channels
    • Gaba potentiator increase GABA effect
    • Z-drugs, zolpidem (etc)
    • More widespread
  • GHB (Xyrem):
    • Works via GABA or maybe its own receptor specifically used in treatment of narcolepsy
  • Suvorexant (Belsomra)
    • Orexin antagonist
    • Released in specific nucleus
    • Only recently approved
  • Antihistimines
    • Block action of histamine
    • More widespread
  • Ramelteon (Rozerem)
    • Melatonin agonist
    • Not have next day “hang-over” grogginess
    • Elderly though to be more deficient in melatonin
99
Q

Insomnia

A
  • increased sleep latency
  • decreased sleep efficiency
  • poor sleep quality
  • Causes
    • Hyperarousal
      • Increased activation of arousal promoting nuclei (LC, Raphe, TMN, LHA)
  • Treatments
    • Behavioral therapy
    • Hypnotic drugs
100
Q

Narcolepsy

A
  • Excessive daytime sleepiniess
  • Disturbed sleep
  • Sleep paralysis
  • Dream-like hallucinations while awake
  • Rapid transition into REM sleep
  • Cataplexy
    • Loss of skeletal muscle tone while awake
    • NOT a sleep attack
  • Narcoleptic dogs: mutation in orexin receptor
  • In human narcoplesy: deficiency of orexin
    • Lack of stability in awake and sleep states
    • Unwanted transition between states
  • Cataplexy: REM atonia controller is turned on inappropriately
101
Q

Narcolepsy Treatments

A
  • Excessive daytime sleepiness
    • Treated with stimulants (modafinil)
  • Disturbed sleep
    • Treated with Xyrem (GHB)
    • Consolidates sleep, hleps with daytime sleepiness also reduces cataplexy
  • Cataplexy
    • Treated with antidepressants
    • Increase NE and serotonin
102
Q

REM sleep behavior disorder, NREM, Diagnosis, Why occurs, other risks

A
  • Vigorous movement during REM sleep
  • REM sleep without atonia
  • Violent dreams where being attacked
  • Might attack sleeping partner
  • “Parasomina” abnormal behavior during sleep
  • Children usually have NREM parasominas
    • Occur earlier in sleep cycle
  • Diagnosiss:
    • Ploysomnography: EEG to show that person in REM and EMG and show that atonia isn’t occurring
  • Defect in the control of the REM atonia controller. Not being turned on appropriately (or it is defective)
    • Big red X through REM atonia controller
  • Patients with RBD have increased risk of going on to develop neurodegenerative diseases involving accumulation of alpha-synuclein (e.g. Parkinson’s disease)
  • Affects men more (80%)
103
Q

Components of the limbic system:Cingulate cortex

A
  • right above corpus collosum and prefrontal cortex
    • Prefrontal cortex, ahead of motor areas, concerned with working memory
      • Executive function: Selection, planning and performance of appropriate behavior
      • Concious experience of emotion
104
Q

Components of the limbic system: amygdala

A
  • Most central structure in emotional processing
  • ­­­Related to fear and aggression
  • Has sensory inputs, close to olfactory input, inputs from association cortex (drawing info from variety of areas), inputs form other limbic areas
  • Output to regions associated with emotional expression
    • Hypothalamus connected to autonomic nervous system
    • Brainstem to motor units
105
Q

Components of limbic system: Basal Ganglia

A
  • Involved in motor control and cognitive processing
  • Knowing whether something is rewarding or important
    • Nucleus accumbens and prefrontal cortex
  • Mesocorticolimbic dopamine pathway: “reward circuitry”
    • Cell bodies located in the VTA (midbrain)
    • Synaptic terminals (releasing dopamine) in the nucleus accumbens and prefrontal cortexa
106
Q

Addiction Definition

A

loss of control over drug-taking behavior

107
Q

Tolerance Definition

A

adaptation to drug, needs to take more to achieve te same effect

108
Q

Dependence Definition

A

need to take drug to avoid withdrawal

109
Q

Withdrawal definition

A

set of negative symptoms that occur when drug is discontinued

110
Q
  • Drug–>Action
    • Heroin
    • Nictotine
    • Alcohol
    • Cocaine
    • Amphetimine
A
  • Heroin, opioid agonist
  • Nicotine, cholinergic agonist
  • Alcohol, increases GABA effects
  • Cocaine, blocks dopamine reuptake
  • Amphetamine, increases norepinephrine and dopamine release
111
Q

Mesocorticolimbic pathway

A
  • Addictive drugs activate the mesocorticolimbic dopamine pathway, increases DA release in nucleus accumbens and pre-frontal cortex
    • Reinforces drug usage
  • Long term effects: Changes that underlie dependency, craving, withdrawls etc.
  • Effects on decision making
  • Decreases natural ability to stimulate this pathway
112
Q

Opioid addiction

A
  • Opioid addiction has increased with the increased use of prescription opioid analgesics
  • High risk of overdose…makes dangerous
    • Causes respiratory depression
  • Push to expand use of naloxone: opioid antagonist, knock of opioid agonists
    • Used for emergency treatment
113
Q

Agonist therapys for opioid addicition

A
  • Methadone
  • Buprenorphine
114
Q

Methadone treatment for opioid addiction

A
  • Full opioid agonist
  • Administered in treatment centers requiring daily visits
  • Not get high because administered slowly and so gets absorbed slowly
115
Q

Buprenorphine treatment for opioid addicition

A
  • Partial opioid agonist, when fully occupy receptor still doesn’t have 100% of biologic effect
  • Available by prescription
116
Q

Naltrexone treatment for opioid addiction

A
  • Opioid antagonist
  • Used to prevent reinforcing effects of opioids
  • Deterrent to relapse, prevents feelings of euphoria
117
Q

expressive aphasia

A
  • Broca’s aphasia
  • normal comprehension for simple speech, but has great difficulty producing speech
  • need to search for words, and will speak in a halting and non-fluent manner.
  • have damage in a region of the left inferior frontal lobe
118
Q

receptive aphasia

A
  • also known as Wernicke’s aphasia
  • due to damage in a region of the posterior temporal lobe near to the auditory cortex (Wernicke’s area)
  • fluent but meaningless speech, and will have great difficulty with speech comprehension
  • may be remarkably unaware of their condition
119
Q

variability between individuals as to the precise location of Wernicke’s and Broca’s areas

A
  • language function is localized to the left side of the brain, but in about 5%, language function may be bilateral or localized to the right side (most commonly in left-handers).
120
Q

Dementia

A
  • severe loss of general cognitive ability
  • most common cause of dementia is Alzheimer’s disease, a neurodegenerative disease characterized by the accumulation of amyloid plaques and neurofibrillary tangles
121
Q

Alzheimer’s disease

A
  • early stages: memory impairment, suggesting degeneration in the hippocampus and medial temporal lobes
  • and can eventually affect any area of the brain
  • death in 3-8 years of diagnosis
  • while alive diagnosed by tests that can show impaired cognitive ability
  • neurons show cytoskeletal abnormalities called neurofibrillary tangles, and there are amyloid plaques, which are large extracellular accumulations of protein
  • aberrant processing of a particular neuronal membrane protein (amyloid protein precursor, or APP) leads to the accumulation of a peptide fragment (b-amyloid) that forms toxic aggregates.
  • Therapeutics measures in development:
    • inhibit the enzymes involved in cleaving APP (b-secretase and g-secretase)
    • try and prevent plaque formation through vaccination with b-amyloid.
122
Q

Chronic Traumatic Encephalopathy (CTE)

A
  • long-term consequence of repeated concussions that occur in contact sports such as American football and boxing
  • formerly known as “dementia pugilistica”
123
Q

Concussion

A
  • alteration in neurologic function following head injury
    • may or may not lose conciousness
  • dizziness, headache, confusion, temporary amnesia along with signs such as slurred speech and disorientation
  • concussion probably causes brain contusions and axonal damage.
124
Q

Repeated concussions

A
  • concussions set in motion cumulative pathological changes that after some time lead to the development of CTE
  • cognitive impairment along with psychiatric symptoms such as depression and bizarre behavioral change
  • deposits of tau, the protein found in neurofibrillary tangles
    • Tau is normally associated with microtubules, but under pathological conditions, it becomes hyperphosphorylated and forms aggregates
  • A disorder characterized by deposits of tau is called a “tauopathy”
    • CTE and Alzheimer’s disease are both tauopathies
  • In CTE, no tau deposits are found in the hippocampus, a typical site of lesions in Alzheimer’s disease. Instead, tau deposits are mainly found in the outer layers of the cerebral cortex.
125
Q

four criteria to diagnose and classify mental illnesses

A
  1. Symptoms: these are behavioral changes that the patient reports to the doctor.
  2. Signs: these are behavioral changes that the doctor observes in examining the patient.
  3. Natural history: this includes the time of first onset of the disease, and whether it is progressive, or whether it is episodic.
  4. Response to treatment: this last criterion became more significant in the 1950’s with the development of drugs to treat mental illness.
126
Q

Schizophrenia

A
  • a dissociation of thought processes from emotions
  • often show inappropriate affect (emotional response)
  • psychotic episodes, periods in which the individual has hallucinations and delusions, and shows an inability to test reality
  • signs such as social withdrawal, poor attention span, neglect of personal hygiene, and flattened affect
  • worsens with time
127
Q

Treatments for Schizophrenia

A
  • Antipsychotic drugs block specific subtypes of dopamine receptors
    • ​suggests that schizophrenia involves excess activity of the dopaminergic neurons of the midbrain that project to structures in the limbic system
  • ​Side Effects: they interfere with regulation of activity in the basal ganglia, and thus cause motor symptoms
    • Tardive dyskinesia
      • ​Parkinson’s-like motor symptoms that occur in long-term users of antipsychotic drugs
128
Q

Mood disorders

A
  • are sustained changes in emotional response that are significant enough to alter an individual’s perception of the world, and interfere with normal function
  • major depressive disorder and bipolar disorder
129
Q

Major depressive disorder

A
  • profound sadness, loss of energy, and lack of joy or ability to experience pleasure (anhedonia)
  • Treatment: prolong or enhance the action of monoamine neurotransmitters (mainly serotonin and norepinephrine)
    • First Line: a selective serotonin reuptake inhibitor (SSRI) because these drugs have fewer side effects
    • serotonin and norepinephrine reuptake inhibitor (SNRI).
130
Q

Bipolar disorder

A
  • episodes of depression will alternate with episodes of mania
    • excessive euphoria, overactivity, overconfidence, and an exaggerated sense of well-being. A manic individual may also be irritable.​
    • lithium is an effective treatment for bipolar disorder
      • ​​altering the production of second messengers in certain neurons
131
Q

Optical Coherence Tomography

A
  • Interference Technology
  • UV light reflects off and gives a picture of what it would look like if sliced through retina
  • Can see the layers, see the relative thickness.
  • Big dipty doo is the fovea
    • Bipolar and ganglion cells are pulled apart so that the light hits the cones directly. Used for reading/fine detail

Conjoint (9 decks)

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