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Physiology Flashcards

1
Q

What part of the ear is involved in hearing?

A

Middle Ear

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2
Q

What is the basic principle of hearing?

A

Transform acoustic energy (Air-Fluid)

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3
Q

What is the process of hearing?

A
  1. Middle ear acts as an amplifier of sound waves due to area ratio
  2. In tympanic membrane- Staples Footplate (Attached to tympanic membrane)- vibrations (sound)-acts on oval window- moves perilymph in cochlea
  3. Travelling wave at basilar membrane
  4. Hair cells on the basilar membrane (Inner Ear)- Centre are long fibres for low pitch eg./ dog bark and Wide End- stimulated by travelling wave of perilymph
  5. Stereocilia bend against overlying structures (bony labyrinth) as the bend they open the pore channels (on tip of stereo cilia) + chemicals rush into cells= electrical signal produced- cochlear nerve-primary auditory cortex (temporal lobe)
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4
Q

What is the ratio of tympanic membrane:stapes footplate?

A

17:1

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5
Q

What is the ratio of staple footplate: malleus?

A

1.3:1

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6
Q

In what order do the bones of the ear come from outter- inner

A

Tympanic Membrane- Malleus- lncus-Stapes- Oval Window

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7
Q

How can you test hearing?

A

1.Webers (middle of head)- test of lateralisation
2.Rinnes- Compare ear/ bone conduction
3.Audiometry- Pure tone earphones, Visual Reinforcement, Play.
Tympanometry- Fluid in middle ear/ perforation/ wax detected via pushing air pressure into ear canal (measure drums motility)
4.Objective testing via otoacoustic emissions (OAE)- sounds given off by cochlea (stereo cilia). If hearing loss >25-30dB don’t produce audible sounds.
5.Auditory Brianstem Response/ Auditory Evoked Potential- Electrodes- brain activity with sound- info about inner ear.

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8
Q

What hearing tests are used as part of the newborn screening programme?

A
  1. Objective testing via acoustic emissions (OAE) + 5. Auditory Brainstem Response/ Auditory Evoked Potential.
    Detects blockage of outer ear/ damage of hair cells + middle ear fluid
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9
Q

What is the vestibular system?

A

3 canals- superior, posterior + horizontal that end in swellings called the ampulla.
Ampulla contain cristae (hairs, sensory) at bases

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10
Q

What do the 3 canals of the vestibular system detect?

A

Superior, Posterior + Horizontal canals detect rotational acceleration and filter into the otolith

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11
Q

What is the otolith?

A

Detect Linar acceleration of movement

Utricle (horizontal movement, hair cells) + Saccule (vertical movement, hair cells)

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12
Q

What is the cristae?

A

In the ampulla (ending of the 3 canals of the vestibular system) contains a gelatinous structure called the cupla which stretch across the width go the ampulla and responds to movement of endolymph (within membranous labyrinth). Contains cilia.

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13
Q

How is movement detected by the ear?

A

Skull rotates left/ right- ampulla moves- endolymph has a high degree of inertia (slower to move)so creates a drag- drag bends cupla and cilia in it- hair cells (cupla) get moved in opposite direction (shearing forces)- impulses sent via CN8 (hyper polarisation)
Endolymph catches up + keeps moving (even when movement stops)- cilia moved in opposite direction (depolarisation)
= dizziness as ear says you are moving but proprioceptors know you’re not

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14
Q

What are the cilia? What is their arrangement and how does this fit their function?

A 
In cupla (cristae- ampulla)
One big Kinocilium surrounded by smaller steriocilia.
If move towards Kinocilia= Depolarisation (Inc AP to brain via CN8)
If move away from Kinocilia= Hyperpolarisation (Dec AP to brain via CN8)
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15
Q

What is the structure of the otolith?

A

Utricle + Saccule (+maccule- sensory apparatus) have kinocilia + sterocilum + gelatinous mass (otolith membrane) + CaCO3 (cal.carb) crystals in membrane

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16
Q

What is the function of the otolith during head tilt + lift movements?

A
  1. Head Tilt- Horizontal- Utricle
    Detected by macula in utricle- otolith have greater density than endolymph (affected more by gravity)- otolith + membrane move- distorts jelly (otolith membrane) + stereocilia move away from kinocilium- Dec in AP firing
  2. Head Lift- Verticle- Saccule
    Detected by macula in saccule- otoliths moved in direction of kinocilium- depolarisation + Inc AP firing to CN8
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17
Q

How is information integrated from ear- brain?

A

Cristae of semicircular canals + macula of otolith- brain via vestibularcochlear nerve (CN8)

  • Vestibular Centres of Medulla- sensory afferent terminals of CN8
  • Cerebella Centres coordinate postural muscles for balance- projections from vestibular nuclei- descending motor pathways + extraoccular muscles- + thalamus- cerebral cortex (perception of movement and body position)
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18
Q

What kind of symptoms are associated with ear pathology?

A 
Hearing Loss
Vertigo- Movement sensation
Otalgia- Pain
TInnitus- Hearing sounds (unilateral, pulsatile-if vascular problem, ring/buzz/whoosh
Otorrhea- Discharge
Facial Pain
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19
Q

What is Rinnes Test and what do the results show?

A

Sensory/ Conduction hearing loss
Normal- Air> Bone = +ve test
Conductive HL- Bone>Air= -ve (outter/middle loss)
Sensoryneural HL- Air>Bone= +ve (inner ear loss- reduced by the same amount)

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20
Q

What is Webers hearing test and what do the results show?

A 
On forehead
Normal left=right
Conductive HL(1 ear) loss ear>normal ear (sound travelling through bone)
Senerineural HL(1 ear) normal>loss (sound equal but won't conduct in lost)
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21
Q

What are the 3 types of hearing loss?

A

Conductive HL- problems with the ear canal, ear drum, or middle ear(the malleus, incus, and stapes).
Sensorineural HL - problems of the inner ear, (nerve-related hearing loss)
Mixed HL -combination of conductive and sensorineural hearing loss- damage in the outer or middle ear and in the inner ear (cochlea) or auditory nerve.

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22
Q

What common conditions are found in the outter ear?

A
  1. Auricular Haemotoma- irregular shape, need to drain (cauliflower ear)
  2. Foreign Body- remove with microscope (careful not to damage structures)
  3. Ottitis Externa- Commonest, Inflamation (canal)= itch, pain + ottorhea- degree + hearing loss.
  4. Malignant Ottitis- Aggressive form of Ottitis Externa- Osteomalleritis of temporal bone= granulation tissue in ear canal.
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23
Q

How do you treat Ottitis Externa + Malignant Ottitis?

A

Conditions of the outter ear

  1. Ottitis Externa (can be due to foreign body) Discharge, Pain. Aural Microsuction, topical Steroids + Antibiotics drops (+remove debree)
  2. Malignant Ottitis (more aggressive form)- Treat with systemic antibiotics (month long course) NOTE: more at risk if elderly + diabetic
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24
Q

What common conditions are found in the middle ear?

A
  1. Ottitis Media + Effusion (glue ear)- Fluid under tympanic membrane- blocks euschian tube- cant equailise drum- air in- pressure in ear drops= vacuum- ear secreted fluid to deal with vacuum- grommet
  2. Acute Ottitis Media- Infection (h.fluenza, strep pneumonia) of the tympanic membrane- Inc pain- perforate- better- tympanosclerosis (watch it doesn’t turn into mastoditis)
  3. Chronic Suppurative Ottitis Media
    - Perforated tympanic membrane- hearing loss, repeated infection
    - Cholesteatoma- Tube dysfunction- vacum- skin cant migrate out so lump builds- erodes mastoid- facial nerve (repeated, smelly discharge) Treat via mastoidectomy.
  4. Tympanosclerosis- Calcium deposits in tympanic membrane (after acute OM- no symtoms)
  5. Otosclerosis- extra bone around stapes (conductive hearing loss)
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25
Q

How do you treat otitis media + effusion?

A 
Common in kids as eustachian tube is straighter so more prone to dysfunction
Glue ear (middle ear)- fluid level
Treat via grommet to equalise pressure/ autoinflation (pressure to open tube via blowing)
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26
Q

What is the function of the euschain tube?

A

Canal that connects the middle ear to the nasopharynx- controls the pressure within the middle ear (equalises with the air pressure outside the body)

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27
Q

What common conditions are found in the inner ear?

A
  1. Presbyacusis- Natural, Elderly, loose high pitch sounds
  2. Noise Induced Hearing Loss- Damage to hair cells (damage to cochlea)
  3. Ototoxic medications eg./ gentamicin (high frequency loss)
  4. Menieres Loss- Inc pressure- low frequency loss, vertigo , tinnitus.
  5. head Injury
  6. Infection eg./ Meningitis
  7. Vestibular Schwannoma (acoustic neuroma)- benign tumours of vestibular nerve gives sensorineural loss of 1 ear
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28
Q

What is vertigo? What kind of conditions is it associated with?

A

Perception of movement in the absence of movement (+/- nystagmus)
Migrane
Menieres Disease
Kinetosis (motion sickness)
Benign Paroxysmal Positional Vertigo- In semicircular canals, fixed via epley manouver

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29
Q

What is vestibular neuritis/ Labyrinthisits? How do you treat this?

A

No associated symtoms aside from unilateral hearing loss
Is a reactivation of HSV infection
Actue- Vestibular sedatives 9train brian to new signals
Chronic- Vestibular Rehabilitation (compensation)

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30
Q

What can cause facial palsy?

A
  1. LMN= facial weakness
  2. Infratemporal via cholesteatoma- erodes facial nerve
  3. Extratemporal via parotid gland tumour (press on facial nerve)
    eg. / Bells Palsy- Acute, Idiopathic (LMN) treat via steroids eg./predinsolone NOT antivirals
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31
Q 
A Pt presents with-
vertigo
low pitched tinnitus
hearing loss
What is your clinical diagnosis? How has this occurred?
A

Meniere’s Disease
Excessive accumulation of endolymph in the membranous labyrinth- distension of ducts. This pressure damages the tympanic membrane

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32
Q

How do you treat Meniere’s Disease?

A

Give Betahistamine (improve BS), Bendroluazine (diuretic), Intralymphatic Dexamethasone + Gentamicin

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33
Q

What parts of the body are involved in postural control?

A 
Vestibulo-occular Reflexes
Afferents from semi-circular canals
Visual System
Afferents from extra-ocular muscles
= postural control
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34
Q

What do the vestibulospinal + vestibulocortical tracts control in terms of posture?

A
  1. Tonic Labyrinthine Reflexes- Info from maculae + neck proprioreceptros to keep neck in balance with rest of the body.
  2. Dynamic Rightening Reflexes- Rapid postural adjustments to stop you falling when you trip eg./ extension of limbs
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35
Q

What is a static reflex? What clinical sign occurs when it is not functioning?

A

Visual + vestibular integration (when head tilts eyes introit/extort to compensate so image stays right way up.
When this fails (cerebral pathology)= nystagmus- rapid flick- saccadic eye movements rotating eye against movement/ direction of rotation

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36
Q

How do you test vestibular function?

A
  1. Post-rotatory Nystagmus- Accelerated on chair (left rotation= left nystagmus)
  2. Caloric Stimulation- wash outter ear with
    -Cold= Nystagmus away from affected side
    -Hot= Nystagmus towards affected side
    Temp diffference from core travels through thin bone- acts on endolymph
    C(old) O(opposite beating nystagmus) W(arm) S(ame)
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37
Q

How does Kinetosis occur?

A

Motion Sickness
Via maintained stimulation of vestibular system in absence of movement
= nausea, vomiting, dizziness, BP drop, sweating (autonomic symptoms as visual + vestibular system saying different things)

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38
Q

What are the layers of the cornea? (from the layers that touches the air to touching the iris)

A
  1. Stratified squamous non-keratinised epithelium
  2. Bowmans Membrane (cant regenerate past here)
  3. Stroma- regularly arranged collagen NO BV- lets light through
  4. Descemets Layer- basement membrane of endothelium
  5. Endothelium- simple squamous
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39
Q

At what point in the eye, if damage occurs after here, is regeneration no longer possible?

A

After Bowmans Capsulr

Damage- Scar tissue (harder for light to ge through)

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40
Q

Why is there no BV in the stroma?

A

Let light through

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41
Q

What is the job of the endothelial cells in the innermost (5th) layer of the eye)

A

Has a pump that actively pumps aqueous humour out (as if gets into stroma will destroy the arrangement)

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42
Q

How does the cornea receive nutrition?

A

-Tear fluid (outside)
- Aqeuous Humour (inside)
- Sclera
Doesn’t have it’s own nutrition

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43
Q

Where is aqueous humour produced? How does it circulate?

A

Produced by ciliary body(posterior chamber)- angle- (anterior chamber) meshwork of trabecular- schemes canal- out via aqueous- episcleral veins
Out-take is balanced by rate of secretion= maintainable of intra-ocular pressure

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44
Q

What is the function of aqueous humour?

A

Gives nutrients and O2 to lens (no direct BS) + cornea

Pressure (21mmHg) keeps eyeball shape

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45
Q

Why is a corneal transplant considered ‘less risky’ than others? Why is the eye considered an ‘immune privileged’ organ?

A

Corneal is avascular so there is less chance of foreign bodies (other peoples cells) being detected by immune cells= no immune response so immune privileged

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46
Q

What is the lens?

A

Transparent crystalline biconvex structure suspended by zonules (suspensory ligaments) from a ciliary body- ability to change the eyes shape.
NOTE: Any new fibres formed will compact old= opaque= cataracts

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47
Q

What is the tear film made up of? What’s its job?

A
  1. Oily- Tarsal Plate (stops aqueous evaporating too quickly)
  2. Aqueous- Lacrimal Glands
  3. Mucinous- Conjunctiva
    When Aqueous layer evaporates (7s) then oil layer touches the conjunctiva- blink- more from lacrimal gland
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48
Q

What is the path and function of tear film?

A

Lacrimal gland (top left of eye)- across eye when blink- out via lacrimal sac- lacrimal canal (nose)
Functions-
1. Cornea moist, prevents drying
2. wash away foreign bodies
3. Antibodies + lysosomes to kill bacteria
4. Smooth surface for refraction
Can see surface via fluroscene dye (goes green in light refraction)

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49
Q

Where is the vitreous humour located?

A

Space between lens and retina (vitreous chamber)

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50
Q

Where is the aqueous humour located?

A

Space between lens and cornea (anterior chamber)

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51
Q

How many layers does the retina have? What are the important ones?

A

10 layers

  1. Nerve Fibre Layer
  2. Rods + Cones layer
  3. Pigment epithelial layer
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52
Q

What is the purpose of the choroid + how is it vascularised?

A

Supply outter layers of the retina with blood.
Vascularised by-
1. Central Retinal Artery (internally)
2. Fenestrated BV (externally)

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53
Q

What is the foeva centralis?

A

Cone cells concentrated, no rod cells (histologically different from rest of retina) + dendrites fro maximum visual acuity.
Centre of macula

54
Q

What is phototransduction?

A

Turning light energy-photoreceptors (rods +cones)- electrochemical response (via AP generation)

55
Q

What do the cones do?

A

Respond to different wavelengths of light via Small, Medium and large opsins

56
Q

How is light produced?

A

Light falls on 11-cis-retinal (chromophore of opsin in outer segment of rod cones)- isomerisation- All-trans-retinal (straight so can’t fit in opsin) splits rhobopsin- retina bleaches- closes sodium channel- relative hyper polarisation- spread by Ca- AP formed- optic nerve

57
Q

How are photoreceptor cells kept in a depolarised state?

A

At rest (in the dark) due to Na/Ca channels

58
Q

What is rhodopsin?

A

Integral transmembrane helical protein with chromophore of opsin (rhodopsin) from dietary Vit A= 11cis-retinal

59
Q

How is the pigment regenerated after the retina bleaches (as a result of the phototransduction cascade)?

A

Dietary Vit A- AT ROI- 11cisral(retinal)-rhodopsin
This process produces Retinyl Esters (unrecoverable so need constant Vit A supply).
If deficient in Vit A (malnutrition, malabsorption, coeliac) vision will be affected (night blindness)

60
Q

What are the signs of Vit A deficiency?

A
  1. Bitots Spots (in conjunctiva)- white
  2. Corneal Ulceration
  3. Corneal Melting (opacification of cornea)
61
Q

What is the area of crossing over of optic fields called?

A

Optic Chiasma

62
Q

Where does sensory information from the eye go once it crosses at the optic chiasma?

A

Optic Tracts- Synapses at lateral geniculate body of thalamus

63
Q

What does the right visual cortex see?

A

Left half of field and vice versa

64
Q

What happens when right optic nerve is damaged?

A

Blind in right eye

65
Q

What happens when optic chiasma is disrupted in the middle?

A

No crossing over= bitemporal hemianopia

66
Q

What happens when R optic tract is damaged?

A

Left visual field loss= contralateral homonymous hemianopia

67
Q

What happens when the optic radiation is damaged?

A

(synapse)
1 sided visual field loss (info not getting to lateral geniculate body of the thalamus)
= contralateral homonymous hemianopia

68
Q

What is trachoma and what can it cause?

A

Bacterial infection due to facewashing with dirty water, flies + sharing bed linen.
Vit A deficency (malnutrition) predisposes
Eyelid turns inwards scratching cornea- corneal opacity

69
Q

What is the threshold for hearing loss? What are the common congenital and acquired reasons?

A

> 40db (adults)
Congenital- birth asphyxia, maternal infection eg./ rubella, syphilis
Acquired- Infection, trauma, excessive noise

70
Q

What are the movements of the eye?

A 
Abduction- away from nose
Adduction- into nose
Elevate- upwards
Depress- downwards
Dextroelevation/depression- up/down to right
Levoelevation/depression- up/down to left
Extortion- Top away from nose
Intortion- Top towards nose
71
Q

What is a strabismus? What kinds exist?

A

Squint-misalignment of the eyes

  1. Esotropia- Convergent Squint (Adductus)
  2. Extropia- Divergent Squint (Abducts)
  3. Amblyopia (lazy eye)- brain surpasses image in 1 eye so poor vision. No pathology so correctable with patch in youth
  4. Diplopia (double vision)- as a result of nerve palsy
72
Q

What are the intrinsic eye muscles? What is their function and how are they innervated?

A

Cilliaris + Constrictor Pupillae
Contract via parasympathetic CN3 (oculomotor) causing the eye to dilate.
Dilator Pupillae- sympathetic via plexus around BVs, thoracic-lumbar constrict causing the eye to dilate

73
Q

How can Ms affect vision?

A

Causes optic neuritis of the optic nerve= detachment, dystrophy , degeneration of retina

74
Q

What is Horners Disease?

A

Anisocria (pupils different size) due to damage of sympathetic innervation + ptosis (droop) + anhidrosis (loss of sweating on one side of face).
Disruption can be anywhere eg./ pan coast tumour of the lungs

75
Q

A diabetic comes to your clinic with a suspected cranial nerve palsy affecting their eyes. What test must you do urgently? Why?

A

Shine torch in eyes and look for constriction/ dilation to light- usually no damage to parasympathetic fibres in palsy so check papillary reflex. If absent EMERGENCY as cerebral arterial aneurysm is possible.

76
Q

How do the eyes focus on close objects?

A
  1. Ciliary muscle contracts (parasympathetic, CN3)
  2. Suspensory ligaments become lax + lens is no longer stretched
    = lens thicker and can bend light rays more (see closer objects)
    + convergence via medial rectus muscles
77
Q

What is refraction?

A

Bending of light as it passes from one optical medium to another (depends on refractive index).
In the eye light rays bend via cornea(most powerful) + lens (can change bending power) to form image on retina

78
Q

How are light rays bent in an emmetrope (normal) for close and far objects?

A

Close (<6m)- Divergent light rays from an object reach- bend more (as in all directions) + focus on the retina
Far (>6m)- Parallel light rays- bend light rays inwards to focus on light

79
Q

How are light rays bent in myopia (short signtedness) for near and far objects?

A

Eyeball too long
Far- Focus infant of retina= hazy vision
Close- Divergent rays seen without an Inc in curvature= headaches (loss of interest) give biconcave lenses as will spread light so it focuses on retina/ laser eye surgery- remove top of cornea and reshape lens

80
Q

How are light rays bent in hyperopia (far sightedness) for near and far objects?

A

Eye ball too short
Far- can use accommodative power to make sense thicker
Close- not enough space to bend light= eyestrain, give biconcave glasses/lenses/surgery

81
Q

What is astigmatism?

A

Non-spherical curvature of the lens- surface has different curvature at different medians so picture never matches= hazy vision
Treat via cylinders glasses/ laser eye surgery/toric contact lenses (weighed so tilt on plane)

82
Q

What is presbyopia?

A

Far sightedness in the elderly as lens gets less mobile/ elastic so less able to change shape= less accommodation. Struggle to see up close so need biconcave lenses to correct

83
Q

What equipment can be used to view the eye?

A
  1. Direct ophthalmoscope- see important parts of retina
  2. Slit Lamp= see anterior section of the eye + back of retina
  3. Biometry- calculate lens power
  4. Fundus Camera- picture of back of eye
  5. Optical Coherence Tomography (OCT)- Ct to see all 10 layers
84
Q

What tests can be done on the eye?

A
  1. Fluroscein Angiography- Inject Dye (hand) + take photo of back of eye- pass light with blue filter- when light comes back green take another photo of back of eye. Capillaries in eye are impermeable to leaks so if see dye out of them= pathology eg./ macular degeneration/ diabetic retinopathy
  2. Optic Coherence Tomography (OCT)
  3. Electrophysiology- electrical signals from eye-optic nerve-brain in response to visual stimuli.
    - Electroretinogram (ERG)- measure retinal layer function
    - Electro-oculogram (EOG)- Retinal Pigment Epithelium + photoreceptors (dark and light)
    - Visually Evoked Potentials (VEP)- Optic Nerve Function (optic nerve function)
85
Q

A Pt presents with sudden, painless loss of vision. What are your differentials? How are these caused?

A
  1. Central Retinal Vein Occlusion- vein taking blood from retina blocked= hypertension, glaucoma- Inc pressure- haemorrhage. OCT- Fluid in retinal layers
  2. Central Retinal Artery Occlusion- main artery supplying retina blocked= ischaemic/pale retina on fundoscopy
  3. Ischaemic Optic Neuropathy- Optic nerve doesn’t get blood supply (acute) arthritic(due to arterial inf- optic disk swells + oedema) or non-arthritic (unknown, better prognosis)
  4. Giant Cell Arteritis (most common)= headache, scalp tension, jaw claudication, neck pain, Inc in inflammatory biomarkers
  5. Optic Neuritis- Inf of optic nerve (MS), pain on movement
86
Q

A Pt presents with gradual loss of vision. What are your differentials? How are they caused?

A
  1. Age related macular degeneration- +smoking+antioxidants. Progressive loss of central vision. Dry Type (no treatment) + Wet Type (blood+fluid- sudden vision loss)
  2. Diabetic Retinopathy- Background, preproliferative, proliferative, maculopathy/rubious iris (retinal detachment) need to laser quadrants
  3. Hypertensive Retinopathy- Arteries no supply (flame like haemorrhages), ischamic (no new vessel formation)
87
Q

What are the 2 types of retinal dystrophies (retinal conditions affecting photoreceptor function)? What are their subtypes?

A

ERG Decreased
1. Retinitis Pigmentosa- Rod layer thinner out
2. Cone Dystrophy (difficulty reading + writing)
EOG Decreased
1. Bests Vitelliform Macular Dystrophy
2. Sorsby Macular Dystrophy- night blindness
3. Stargait Macular Dystrophy- bad vision
4. North Carolina Macular Dystrophy- congenital, blurred central vision (doesn’t deteriorate further after birth)

88
Q

A Pt presents with an acute onset of a red eye. What are your differentials?

A 
Uveitis
Conjunctivitis
Episcleritis + Scleritis
Keratitis/ Corneal Ulcer
Acute Glucoma
Orbital/ Preseptal Cellulitis
89
Q

What is Uveitis?

A

Inflammation of the urea (iris, choroid + ciliary body)
Visual Axis + IAnterior(iris + CB- red pain +vision loss) Intermediate8 (CB- leaks= floaters)/ Posterior (retina/choroid/BV)/Panuveitis (all layers)
=Visual Problems/Pain/Diplopia
Cause: sarcoidosis, lupus, wegners, TB, syphilis, herpes, lymes
Treat:Topical anti-inflammatory, steroid, systemic immunosupressants

90
Q

What is conjunctivitis?

A

Infection/ Inflammation of outter part of eye
=Discharge- Bacterial (yellow), Viral(watery), Allergic(mucous)
Vision normal as only outer coat affected

91
Q

What is Keratitis/Corneal Ulcer?

A

Inflammation of cornea eg./ via corneal abrasion

Pain is severe/ eye closing (do visual test)

92
Q

What is Episcleritis + Scleritis?

A

Episcleral Tissue + conjunctival layers cover the sclera
No discharge/ vision loss if doesn’t go towards posterior pole. Severe pain
Nectrosing Scleritis- ischemia of sclera (white/yellow)

93
Q

What is orbital/ preseptal cellulitis?

A

Dental/ Lid Cysts/Insect Bites etc
Pain, Redness, Lid swelling, systemically unwell, conjunctivitis
NOTE: In kids septum isn’t well developed so swelling around the eye can progress to the orbit and brain

94
Q

What is the urea?

A

Choroid Plexus, Ciliary Body + Iris

95
Q

What areas of the eye does adnexal oncology cover?

A

Orbit, eyelid + lacrimal drainage system

96
Q

What is the pathology of benign eyelid tumours?

A

Normal cells in abnormal number +/- location

Cells lack the ability to invade local tissue/ metabolise so slow growing.

97
Q

What 2 types of benign papillomas exist in the eyelid?

A
  1. Squamous cell papilloma- pedunculate (attached via stalk) + sessile (broad based), raspberry texture. Treat via excision or laser abrasion.
  2. Basal Cell papilloma- seborrhoea keratosis (greasy, brown, flat and oval)
    Both look like they have been stuck on
98
Q

What presentation can usual melanocytes give on the eyelid?

A 
Melanocytic Naevus (atypical melanocytes)
Benign
Early signs of malignancy-
A-atypical
B-order (irregular)
C-olour (variegated)
D-iamete (>6mm)
E-volving
Malignant Potential- 
Elevated, firm to touch, growing
99
Q

What oncological affects can occur on the eyelid as a result of sun exposure?

A
  1. Actinic Keratosis- flat, scaly, hyperkertanoic skin (premalignant) excise/ ablation
  2. Keratoacanthoma- pink papule, hyperkeratonic crater
100
Q

What are the 2 types of haemangioma found on eyelids?

A
  1. Capillary Haemangioma (infancy) eyes close from back= amblyopia, astigmatism. Treat with B-Blockers, intralesion steroids + surgery
  2. Cavernous Haemangioma- pink patch darkening with age
101
Q

What is the pathology of malignant eyelid tumours?

A

Anaplastic cells (lost function)- rapid growing, invasive

102
Q

What is Basal Cell Carcinoma of the eyelid?

A

Slow Growth
Non pigmented, elevated, irregular border, nodular (pearly)
Progresses to ulcerative/ crusty + bleeding
Treat: Excision, Mohn Surgery, Chemo/Radiotherapy

103
Q

What is Squamous Cell Carcinoma of the eyelid?

A

Sun damage over pre-existing sites (eg./Actinic Keratosis, Keratocanthoma)
Mets risk (MRI + US)
Treat: Excision (Mohns) 4mm margin

104
Q

What kind of malignant tumour can be found in sebaceous glands?

A

Sebaccous Gland Carcinoma- Nodular, yellowish discolouration (lipid)
Treat: excision 5-10mm

105
Q

Describe the process of an orbital fracture

A

Orbit is closely related to the air sinuses (thin walls easily fractured
Contents of orbit herniate out to maxillary sinus (+/- sensory branch of the maxillary caught)= diplopia
CT- tear drop sign (on lower orbital crest)
Usually heals itself

106
Q

Describe the process of a ‘blow out’ fracture

A

Eye ball hits off- herniation of fat into ethmoid air space

107
Q

How does infection spread to the brain?

A

Valveless emissary veins to cavernous sinus= Canvernous Venous Thrombosis
Via fundoscopy can see veins engorged(high back flow)- venous drainage compromised- swelling + paralysis of nerves= death

108
Q

What happens to eye movements is paralysis of CN6 happens?

A

CN6= Abducents- Innervates lateral rectus

= inability to abduct

109
Q

What happens to eye movements in paralysis of CN3?

A

CN3- Oculomotor- Superior Rectus, Inferior Rectus, Medial Rectus, Inferior Oblique= very limited eye movement, drooping lid (LPS)

110
Q

What happens to eye movement in a 4th nerve palsy?

A

CN4=Trochlear- Superior Oblique

Inferior Oblique overcompensates, eyeball turns up as no force to push down

111
Q

Congentially the chorioid fissure can sometimes not fuse. What kind of problems can this cause?

A

Coloboma (keyhole shape) retina and choroid and thin and under-developed

112
Q

What is the conjunctiva?

What happens if this area comes infected?

A

Thin, vascular membrane covering the inner surface of eyelids (+loops back over sclera)
Conjunctivitis- self limiting bacterial/ viral, can give antibiotic drops if bacterial)= red discharge, watery. If blurring/ vision loss then has spread to cornea.

113
Q

What is a stye/ Hordeslum?

A

Blockage of Meibomian gland (oil)- external/ internal treat with heat, hygiene and surgical excision if needed

114
Q

How do cataracts occur?

A

Older fibres are never shed but absorb harmful UV rays (prevent retina damage) get damaged- opaque= blurry vision
Treat: Surgery (lens removed by emulsification and posterior chamber intraocular lens inserted)

115
Q

What is Glucoma?

A

Raised intra ocular pressure (>23mmHg)

116
Q

What is Primary Open Angle Glucoma? How do you treat it?

A

Blockage of drainage through trabecular meshwork
Bilateral + slow rising
TRIAD- Raised IOP, Visual Field Defect, Optic Disk Change
Pressure on nerve fibres= visual field defect
Pressure on optic nerve head= optic disk unhealthy, pale, cupped
Treat: Prostyglandin drops, B blockers, carbonic anhydrase inhibitors, laser trabeculopathy/Trabeculotomy

117
Q

What is Angle Closure Glucoma? How do you treat it?

A

Unilateral sudden onset of pain/ blurred vision/ headache
Red, opaque cornea, pupil mid-dilated
Cause: Functional Block; Mid-Dilated Pupil (iris around angle); Synechia (iris sticks to pupillary border)
Long sighted, short eye
Treat: Carbonic Anhydrase Inhibitors eg./ Acetazolamide, Steriods eg./ dexamethasone, B blockers, Iridotomy (laser hole in iris to pass block)

118
Q

What is allergic rhinitis? How do you treat it?

A

Hayfever (Exaggerated immune reaction via IgE)- skin test for allergens
Get in inferior turbinate/conchae.
Can be Acute- vasocdilation, mucous secretions, nerve stimulation, smooth muscle contraction. OR Late (2-4 hrs after exposure)
Test: Allergen test, IgE in serum/ against specific antigens
Treat via anti-histamines or steriods if severe

119
Q

What is Rhinosinitus?

A

Concurrent inflammatory infective process
Acute (bacterial) <12 weeks
Chronic (allergic/ non-allergic-polyps/non-polps)

120
Q

What is littles area?

A

Front of nose very vascular (anastomoses of vessels) area nose bleed (epistaxis) via- trauma, anticoagulant/ hypertension, iatrogenic, idiopathic.
Give anterior/ posterior nasal packs to cortorise bleeding, embolism + laser ablation

121
Q

What is tonsillitis?

A

Bacterial Infection- Quinsy (peritonsillar abscess)

If 6-7 attacks in a year= tonsillectomy

122
Q

What is sinusitis?

A

Overlap with rhinitis + large adenoids(sleep apnoea)
Associated with CF
If crosses to eye get ptosis + vision loss

123
Q

How is tonsillitis linked to nephropathy?

A

IgA nephropathy presents after upper upper airway/ gastric infection

124
Q

How can you determine a thyroglossal duct cyst? How do you treat this?

A

Moves if stick tongue out
Give US to make sure thyroid is functioning elsewhere
Treat: Antibiotics, incision, drainage

125
Q

What is a septal haemotoma and what can happen?

A

Trauma- blood collection-abscess- perforate= saddle nose

126
Q

What are nasal polyps? How do you investigate + treat them?

A

Must rule out CF (sweat test)
RAST- skin test
Coronal CT
Treat: polypectomy, immunotherapy (steriods/ anti-histamines if allergic rhinitis)

127
Q

What is a potts puffy tumour?

A

Fever, Frontal Headache + Nasal Discharge

128
Q

How many pairs of somites are there? What do they go onto form?

A

33 pairs= limbs

129
Q

What do each of the brachial arches go onto form?

A

1st- mandibular branch of trigeminal- muscles of mastication
2nd- Facial Nerve- Muscles of facial expression
3rd- Glossopharyngeal- stylopharyngess
4th- Superior Laryngeal branch of vagus-cricothyroid muscle
5th- gone
6th- recurrent laryngeal (vagus)

130
Q

What is stridor? What types indicate the placement of airway obstruction?

A

Clinical sign of airway obstruction

  1. On inspiration= laryngeal
  2. On expiration= trachobronchial
  3. Biphasic- glottic
131
Q

What is a pharyngeal pouch?

A

UOS doesn’t relax well - herniation of pharyngeal muscosa= hoarseness, dysphagia, aspiration pneumonia, weight loss
Diagnose via barium swallow

132
Q

How can you asses function of swallowing?

A

Videofluroscopy (stroke, NG tube, PEG Tube, Blom-singer valve for Pst that can’t speak)

ENT (2 decks)

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