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NSS Flashcards

Ophthal ✔ Neuro - ENT - derm -

1
Q

What two blood tests will support a diagnosis of a seizure after a fall?seizure

A

Serum lactate
Serum prolactin

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2
Q

How can red eye be divided into categories, and what are the causes?

A

Painless- conjunctivitis, episcleritis, subconjunctival haemorrhage
Painful- acute glaucoma, anterior uveitis, scleritis, corneal ulcer or abrasion, keratitis, foreign body, trauma/chemicals

Vision loss- Corneal ulceration, glaucoma

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3
Q

What are the causes of painful vision loss?

A

Acute closed angle glaucoma
Corneal abrasion

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4
Q

What are the causes of painless vision loss?

A

Cataracts
AMD
Retinal detachment
Retinal vein occlusion
Central retinal artery occlusion
Retinitis pigmentosa

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5
Q

Vision loss is described as a painless shadow/ curtain coming across vision. What are the likely dx? How can you tell the difference o/e?

A

Retinal detachment or Central retinal artery occlusion (will have RAPD)

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6
Q

Vision loss is described as painless gradual loss of central vision. What is the likely dx?

A

AMD

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7
Q

What conditions are associated with anterior uveitits?

A

Autoimmune conditions:
-Seronegative spondyloarthropathies, e.g. ankylosing spondylitis, psoriatic arthritis and reactive arthritis
-Inflammatory bowel disease
-Sarcoidosis
-Behçet’s disease

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8
Q

What is the first line management for anterior uveitis?

A

Steroids
Cycloplegics e.g. cyclopentolate or atropine

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9
Q

How do cycloplegics work?

A

They dilate the pupil and reduce pain associated with ciliary spasm by paralysing the ciliary muscles. They reduce the action of the iris sphincter muscles and ciliary muscles.

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10
Q

Symptoms:
Painful red eye
Reduced visual acuity
Photophobia
Excessive lacrimation

What is the diagnosis?

A

Scleritis or Anterior uveitis

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11
Q

What are the signs of anterior uveitis?

A

Ciliary flush
Miosis
Abnormal shape pupil - due to synechiae
Hypopyon

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12
Q

What is the definitive management of cataracts?

A

Phacoemulsification

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13
Q

What is the main complication of phacoemulsification?

A

Endophthalmitis

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14
Q

Symptoms:
Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting

What is the likely diagnosis?

A

Acute closed angle glaucoma

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15
Q

What can be done to manage acute closed angle glaucoma, before reaching hospital?

A

Lying the pt on their back
Pilocarpine eye drops
Acetazolamide
Analgesia and anti emetic

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16
Q

What is the definitive management of acute closed angle glaucoma?

A

Laser iridotomy

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17
Q

What examination is done to diagnose keratitis, and what does it show?

A

Slit lamp examination with fluorescein staining, showing a dendritic corneal ulcer

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18
Q

What are the risks with posterior vitreous detachment?

A

Retinal tears
Retinal detachments

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19
Q

What are the risk factors for retinal detachment?

A

Lattice degeneration/thinning of retina
PVD
Trauma
Diabetic retinopathy
Retinal malignancy
Family history

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20
Q

Symptoms:
Peripheral vision loss- shadow coming across vision
Blurred or distorted vision
Flashes and floaters

What is the likely diagnosis?

A

Retinal detachment

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21
Q

What are the options for reattaching the retina in retinal detachment?

A

Vitrectomy
Scleral buckling
Pneumatic

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22
Q

What are the most common causes of central retinal artery occlusion? And what are the risk factors for them?

A

GCA:
White ethnicity
Older
Female
PMR

Atherosclerosis:
Smoking
Hypertension
Diabetes
Hyperlipidaemia

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23
Q

What does a pale retina and cherry red spot suggest on fundoscopy?

A

Central retinal artery occlusion

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24
Q

What are the risk factors for retinal vein occlusion?

A

HTN
Hyperlipidaemia
DM
Smoking
High plasma viscosity e.g. myeloma
Myeloproliferative disorders
Inflammatory conditions e.g. SLE

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25
Q

What are the fundoscopy findings of retinal vein occlusion?

A

‘Blood and thunder’ appearance

Dilated tortuous retinal veins
Flame and blot haemorrhages
Retinal oedema
Cotton wool spots
Hard exudates

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26
Q

How is orbital compartment syndrome managed?

A

Urgent lateral canthotomy

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27
Q

What is the finding of dry AMD on fundoscopy?

A

Drusen

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28
Q

What can cause optic neuritis?

A

MS most common
Living at high altitude
Autoimmune disorders
Infectious conditions

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29
Q

What is the classic triad of optic neuritis?

A

Vision loss- central plus red green colour blind
Periocular pain
Dyschromatopsia

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30
Q

What is first line management of optic neuritis?

A

IV methylprednisolone

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31
Q

What is the most definitive way to diagnose optic neuritis?

A

MRI of the brain and orbits with gadolinium contrast

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32
Q

What are the risk factors for cataracts?

A

Increasing age
Smoking
Alcohol
DM
Steroids
Hypocalcaemia

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33
Q

What are the risk factors for AMD?

A

Age
Smoking
Caucasian
CVD, HTN
Light iris
Hyperopia
FMH- genetic component linked to drusen formation

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34
Q

What are the stages of dry AMD? Describe them

A

Early - few medium drusen
Intermediate- one or more large drusen, or many medium. Global atrophy not affecting macular centre.
Advanced- Drusen and global atrophy extend to the macular centre. May have gradual vision loss.

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35
Q

What is worse, soft or hard drusen? Why?

A

Soft is worse as it can lift the RPE away from Bruch’s membrane. Can result in inflammation and hypoxic state.
Soft drusen is more likely to promote progression to advanced AMD.

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36
Q

How is dry AMD managed?

A

Self monitoring using Amsler grid
Inc dietary or supplementary vit A
Protect eyes from sunlight
Avoid smoking

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37
Q

What protein plays a key role in converting dry AMD into wet AMD?

A

VEGF-A

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38
Q

How is wet AMD managed?

A

Anti VEGF medication injections, monthly:
Ranibizumab
Aflibercept
Bevacizumab

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39
Q

What treatment can be given to differentiate between scleritis and episcleritis?

A

Phenylephrine eye drops- will blanch the episcleral vessels, but will not affect episcleritis

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40
Q

What is episcleritis and what conditions is it associated with?

A

Inflammation of the episclera, the outermost layer of the sclera (just beneath the conjunctiva)
Associated with inflammatory conditions e.g. RA, IBD.

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41
Q

How can you differentiate scleritis from episcleritis from history and examination?

A

Scleritis has symptoms in addition to the red sclera and congested vessels:
Severe pain, and pain with eye movement
Photophobia
Epiphora
Reduced visual acuity
Tenderness to palpation of the eye

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42
Q

What are the causes of scleritis

A

Idiopathic
Underlying systemic condition, like:
-RA
-Vasculitis e.g. granulomatosis with polyangiits
Infection

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43
Q

How is scleritis managed?

A

Urgent assessment by ophthal
NSAIDs
Steroids
Immunosuppression for underlying condition
Antibiotics if infectious scleritis

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44
Q

What is the most severe type of scleritis?

A

Necrotising scleritis
Can lead to perforation of the sclera

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45
Q

How is episcleritis managed

A

Self limiting condition, in 1-2 weeks
Analgesia and lubricating eye drops.

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46
Q

What is the pathophysiology of diabetic retinopathy?

A

Hyperglycaemia damages small retinal vessels and endothelial cells
Inc vasc permeability= blot haemorrhages and hard exudates (lipids and proteins)
Damage to the blood vessel walls= microaneurysm and venous beading
Damage to nerve fibres causes cotton wool spots
Tortuous capillaries form AV malformations
Growth factors are released causing neovascularisation

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47
Q

What are the treatment options for proliferative diabetic retinopathy?

A

Pan retinal photocoagulation
Anti VEGF intravitreal injections
Surgery e.g. vitrectomy

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48
Q

What are the grades of diabetic retinopathy, based on the findings on fundus examination?

A

Background- microaneurysms, retinal haemorrhages, hard exudates and cotton wool spots
Pre-proliferative – venous beading, multiple blot haemorrhages, AV malformation
Proliferative- neovascularisation and vitreous haemorrhage

Also, can be classified depending on if there is macular oedema/involvement or not.

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49
Q

What are the features on fundoscopy of hypertensive retinopathy?

A

Silver wiring
AV nipping
Cotton wool spots
Hard exudates
Retinal haemorrhages
Papilloedema - ischaemia to the optic nerve

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50
Q

What is the Keith Wagener classification?

A

HTN retinopathy:
1- mild arteriole narrowing
2- AV nipping
3- cotton wool patches, exudates, haemorrhages
4- papilloedema

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51
Q

What can cause painless peripheral vision loss?

A

Open angle glaucoma
Retinitis pigmentosa

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52
Q

What is the name of the condition whereby visual hallucinations occur due to significant vision loss?

A

Charles Bonnet syndrome

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53
Q

What are the risk factors for open angle glaucoma?

A

Myopia- short sightedness
Increasing age
Black ethnic origin
FMHx

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54
Q

What are the ways in which we can measure intraocular pressures?

A

Non contact tonometry
Goldmann applanation tonometry

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55
Q

What is the normal intraocular pressure, and at what pressure is treatment needed for glaucoma?

A

Normal is 10-21
Treatment at 24mmHg or above

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56
Q

What is the key finding on fundoscopy in open angle glaucoma?

A

Disk cupping:
The optic cup is more than 50% of the optic disk

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57
Q

What is the most common cause of normal pressure glaucoma, and how is it investigated?

A

Over treating HTN causes hypotension and optic nerve ischaemia at night
24 hour BP is done

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58
Q

What are the side effects of latanoprost?

A

Eyelash growth
Eyelid pigmentation
Iris pigmentation

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59
Q

What are the medical management options for open angle glaucoma? What is their MoA? Which is first line?

A

Prostaglandin eye drops increase the uveoscleral outflow, and are first line. E.g. Latanoprost.
B-blocker timolol reduces aqueous humour production.
Carbonic anhydrase inhibitor dorzolamide reduced aqueous humour production.
Sympathomimetic brimonidine reduces aqueous humour production and increases uveoscleral outflow

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60
Q

What are the surgical management options for open angle glaucoma?

A

Trabeculotomy- creates a channel from the anterior chamber through the sclera to just under the conjunctiva. Forms a bleb under the conjunctiva.
Laser iridotomy- more for emergencies

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61
Q

What is the normal route and physiology of aqueous humour?

A

Provides nutrients to the cornea.
Produced in the ciliary body. Flows through the posterior chamber and around the iris to the anterior chamber. Drains through the trabecular meshwork to the canal of Schlemm. Re-enters circulation.

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62
Q

What symptoms can be caused by closed angle glaucoma?

A

Peripheral vision is affected first. Gradual tunnel vision develops.
Intermittent pain
Headaches
Blurred vision
Halos around lights

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63
Q

What are the risk factors for closed angle glaucoma?

A

Increasing age
FMH
Female
Chinese or east asian
Hyperopia
Medications- adrenergic, anticholinergic, tricyclic antidepressants

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64
Q

What is the outermost layer of the eye and what does it consist of? What is it’s function?

A

Fibrous outer layer consists of the cornea and sclera
Provides the shape of the eye

65
Q

What layer is beneath the sclera in the eye? What is the function?

A

Vascular layer:
Choroid- provides blood vessels to outer layers
Ciliary body- muscle and processes to control shape of the lens and forms aqueous humour
Iris- smooth muscle fibres alter the diameter of the pupil

66
Q

What is the inner layer of the eye called and what does it consist of? What is the function?

A

Retina: light detecting
Pigmented outer layer- assists choroid in scattering light
Neural inner layer- photoreceptors detect light. Posterior and does not continue anteriorly.
Macula is the centre of the retina- contains fovea centralis with high concentration of photoreceptors for visual acuity
Optic disc- area optic nerve enters retina

67
Q

What layers are separated in retinal detachment?

A

The neural layer of the retina comes away from the pigmented layer

68
Q

What are the risk factors for a corneal ulcer?

A

Contact lens use
Vit A deficiency

69
Q

What is can cause a third nerve palsy

A

DM
Vasculitis
HTN
Posterior communicating artery aneurysm
Cavernous sinus thrombosis
Weber’s syndrome
Raised ICP- late sign
Brain tumour
Amyloid
MS

70
Q

What are the features of a third nerve palsy? And surgical

A

Down and out eye
Ptosis
Dilated, fixed pupil (mydriasis)- surgical

71
Q

Third nerve palsy, why is there a difference in presentation?

A

If microvascular cause, the parasympathetic n fibres are external on the third nerve so are spared. Pupil is normal.
If compression, parasympathetic n is compressed and pupil is unable to constrict

72
Q

What features indicate the location of Horner’s syndrome?

A

Anhidrosis of the arm, trunk and face is caused by central lesion.
Pre ganglionic lesions cause anhidrosis of the face.
Post ganglionic lesions do not cause anhidrosis

73
Q

What are the causes of Horner’s syndrome (by location)

A

Remember Sentral, T for torso (pre ganglion), C for cervical (post ganglion)
Central- Stroke, MS, Swelling/tumour, syringomyelia
Pre ganglion- pancoast tumour, trauma, thyroidectomy, top rib
Post ganglion- carotid aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache

74
Q

What eye drops can be used to investigate, if horner’s syndrome is suspected?

A

Cocaine eye drops- normal eye will dilate, horners won’t
Adrenaline 0.1% eye drops- will dilate horner’s pupil, but not a normal pupil

75
Q

What is the most common cause of a surgical third nerve palsy?

A

Posterior communicating artery aneurysm- in the circle of Willis

76
Q

How does an abducens nerve palsy present, and why?

A

Inward deviation (esotropia)
-unopposed medial rectus muscle action
Causes diplopia, worse looking at distance. Worse in direction of palsied muscle(abduction), and better in contralateral gaze.
Patients likely to hold head towards the affected eye to correct this.

77
Q

How does a trochlear nerve palsy present?

A

Eye may appear to be rotated up and out.
Vertical AND horizontal diplopia.
Head tilted down and towards the unaffected side to eliminate the diplopia.
Diplopia worse in down gaze e.g. difficulty reading.

78
Q

What is RAPD and what causes it?

A

Relative afferent pupillary defect
Swinging light test compares the constriction of the pupil. Occurs in conditions where the optic nerve afferents are affected, or retina.
-central retinal artery occlusion
-optic neuritis
-optic nerve compression

79
Q

What does keratitis mean?

A

Inflammation of the cornea

80
Q

How does HSV keratitis present?

A

Primary infection can be mild blepharoconjunctivitis
Recurrent:
Painful red eye
Vesicles and foreign body sensation
Watery discharge
Reduced visual acuity
Photophobia

81
Q

How is herpes keratitis managed?

A

Urgent ophthal referral
Topical or oral aciclovir
Corneal transplant if scarring and vision loss afterwards

82
Q

What nerve does HSV lie dormant in to cause keratitis?

A

Trigeminal nerve

83
Q

What are the complications of HSV keratitis?

A

Stromal keratitis
-stromal necrosis
-vascularisation
-scarring
-corneal blindness

84
Q

What is a stye?

A

Infection of the glands of Zeis or Moll

85
Q

What is a chalazion?

A

Meibomian cyst:
Meibomian gland is blocked and wells

86
Q

How are chalazion and styes treated?

A

Warm compress and gentle massage

87
Q

What is the MoA of Latanoprost?

A

Increased uveoscleral outflow

88
Q

How does presbycusis present?

A

Gradual sensorineural hearing loss. Symmetrical loss most commonly at higher freq.

89
Q

What are the risk factors for presbycusis?

A

Age
Male
FMH
Loud noise exposure
DM
HTN
Ototoxic medications
Smoking

90
Q

How is presbycusis managed?

A

Hearing aids or cochlear implants.

91
Q

What is the pathophysiology of presbycusis?

A

Loss of hair cells and neurons in the cochlea

92
Q

What is the pathophysiology of BPPV?

A

Calcium carbonate crystals (otoconia) are displaced in the semicircular canals in the inner ear (post. canal mos common)
This disrupts the flow of endolymph in the canals, confusing the vestibular system

93
Q

What are the causes of BPPV?

A

Idiopathic
Trauma
Infection
Aging

94
Q

How does BPPV present?

A

Vertigo only.
Triggered by head movement and lasts 20-60 seconds

95
Q

How is BPPV diagnosed and treated?

A

Diagnosis- Dix-hallpike manoeuvre
Management- Epley manoeuvre

96
Q

Labrynthitis vs vestibular neuronitis?

A

Labrynthitis causes hearing loss as well as vertigo

97
Q

What examination can be done to exclude central causes of vertigo?

A

HiNTS
(Head impulse test, nystagmus, test of skew)
?+ve means peripheral cause?
Head impulse- Eyes move with head and then fix back on the point

98
Q

How is vestibular neuronitis and labrynthitis managed?

A

Supportive
Short term (3 days) prochlorperazine or antihistamines
Vestibular rehabilitation therapy if no improvement after 1 wk, or no resolution by 6 weeks

99
Q

What is a potential complication of labrynthitis?

A

Rare:
Permanent hearing loss if bacterial cause, esp if meningitis

100
Q

What is the complication of vestibular neuronitis?

A

BPPV

101
Q

What are bilateral acoutic neuromas asscoaited with?

A

Neurofibromatosis type 2

102
Q

What is the pathophysiology of acoustic neuromas and where do they occur?

A

AKA vestibular schwannoma:
Benign tumour of the schwann cells surrounding the vestibulocochear nerve.
Occurs at the cerebellopontine angle

103
Q

What is the gold standard investigation for acoustic neuroma?

A

MRI head

104
Q

How are vestibular schwannomas managed? what are the risks?

A

Watch and wait
Surgical removal if symptomatic or over 40mm
- risk to facial nerve and vestibular nerve

105
Q

What are the most common causative organisms of otitis media?

A

Strep pneumoniae - most common
H influenzae
Moraxella catarrhalis
Staph aureus

106
Q

How is a cholesteatoma formed?

A

Abnormal collection of squamous epithelial cells
Negative pressure in the middle ear is caused by ET dysfunction, resulting in TM retraction trapping squamous cells

107
Q

Where are you most likely to see a cholesteatoma?

A

In the ear, at the attic of the TM

108
Q

What are the main symptoms of cholesteatoma?

A

Unilateral conductive hearing loss
Foul discharge from the ear

109
Q

How is a cholesteatoma managed?

A

Surgery into the mastoid cavity, to remove cholesteatoma

110
Q

What is the pathophysiology of otosclerosis?

A

Bone remodelling and formation of the auditory ossicles, mainly to the stapes
Affects vibrations transmitted from the incus to the oval window of the cochlea

111
Q

Describe the pattern of hearing loss in otosclerosis

A

Conductive hearing loss. May be unilateral or bilateral.
Lower pitched sounds affected more.

112
Q

Who gets otosclerosis and why?

A

Under 40 at presentation usually
Mix of environmental, and genetic- inherited in autosomal dominant pattern

113
Q

How is otosclerosis managed?

A

Conservative- hearing aids
Surgical- Stapedectomy or stapedotomy

114
Q

What is the function of the eustachian tube?

A

Pressure equalisation
Mucociliary clearance of secretions

115
Q

What can cause ET dysfunction?

A

Infection- URTI or otitis media
Allergies
Enlarged adenoids

116
Q

How is ET dysfunction managed?

A

Conservative- valsalva manoeuvre or otovent
Med- decongestant nasal spray, antihistamines/steroid nasal spray
Surgery- adenoidectomy. Grommets. Balloon dilatation of ET.

117
Q

What are the possible complications of otitis media?

A

Otitis media with effusion
Hearing loss- temporary
Perforated TM
Labrynthitis
Mastoiditis
Abscess
Facial N palsy
Meningitis

(in order of most to least likely)

118
Q

What are the Parkinson’s plus syndromes?

A

Progressive supranuclear palsy
Cortico-basal degeneration
Dementia with Lewy Bodies
Multisystem atrophy

119
Q

What are the two types of MS?

A

Relapsing remitting
Primary progressive

120
Q

How is an acute attack of MS managed?

A

Glucocorticoids
1g IV methylprednisolone BD for 3 days

121
Q

What is MS and what is the pathophysiology?

A

Chronic, inflammatory, autoimmune disease of the central nervous system, characterised by the demyelination and axonal loss of neurons.
Patho: Caused by CD4 mediated destruction of oligodendroglial cells, and humoral response to myelin binding protein

122
Q

What is found in the CSF of MS pts?

A

Oligoclonal bands

123
Q

What are the most common signs and symptoms of MS?

A

Sensory disease
Spastic paraparesis
Optic neuritis
Internuclear ophthalmoplegia
Subacute cerebellar ataxia
UMN signs

124
Q

What is the pathophysiology of myasthenia gravis?

A

Autoimmune disease
Antibodies against acetylcholine receptors on muscle fibres

125
Q

What is a bedside test used specifically for MG?

A

Ice pack test (over eyes)

126
Q

What is a blood test specifically for MG?

A

Serum acetylcholine receptor antibody

127
Q

How is MG managed?

A

Immunosuppressive therapy (steroids, given acutely)
Anticholinesterase inhibitors (pyridostigmine or neostigmine)
IV IG
Thymectomy

128
Q

What is Cushing’s triad?

A

Widening pulse pressure
Bradycardia
Hypertension

129
Q

What causes target lesions?

A

Erythema multiforme
-reaction to viral infection

130
Q

What causes wheals?

A

Urticaria/hives
Hypersensitivity type 1 reaction (IgE mediated)

131
Q

What are the possible complications of erythema multiforme?

A

Ocular involvement
-keratitis
-uveitis

132
Q

What can aggravate rosacea?

A

Tea and coffee
Alcohol
Spicy foods
Excessive heat
Direct sunshine
Topical steroids

133
Q

How is rosacea managed medically?

A

Papules and pustules:
Abx creams- ivermectin first line
Systemic abx- doxy first line

Flushing/telangiectasia:
B blocker
Topical alpha adrenergic agonist e.g. brimonidine

134
Q

When does aciclovir have to be started to affect Shingles, and what does it do?

A

Within 3 days of onset
Can reduce the pain and duration of symptoms

135
Q

What is the most common causative organism of impetigo?

A

Staph aureus

136
Q

What is the most common causative organism of cellulitis?

A

Group A strep- strep pyogenes

137
Q

What is the most common causative organism of orbital cellulitis?

A

Strep pneumoniae

138
Q

What are the possible complications of cellulitis?

A

Septicaemia
Lymphangitis
Necrotising fasciitis
Nephritis

139
Q

What condition typically has a herald patch?

A

Pityriasis rosea

140
Q

What is the causative organism of molluscum contagiosum?

A

Poxvirus

141
Q

How is molluscum contagiosum managed?

A

Will self resolve but may take up to 4 years
If >2y/o: potassium hydroxide for up to 14 days, stop when lesions become inflamed
Cryotherapy- will leave scarring

142
Q

What are the risk factors for SCC?

A

Sunlight/UV
Actinic keratoses and Bowens
Immunosuppression
Smoking
Long standing leg ulcers
Genetic conditions e.g. xeroderma pigmentosum

143
Q

Is SCC or BCC faster growing?

A

SCC

144
Q

What conditions are associated with seborrhoeic dermatitis?

A

HIV
Parkinson’s disease

145
Q

What is pyoderma gangrenosum?

A

Non infectious, inflammatory disorder
Causes very painful skin ulceration
‘pathergy’

146
Q

What is the most common causative organism of GBS?

A

Campylobacter jejuni

147
Q

What blood vessels are affected in posterior circulation stroke (POCS), and what do they supply?

A

Vertebrobasilar, supplying the cerebellum and brainstem

148
Q

What are the possible complications of epistaxis?

A

Septal haematoma
Sinusitis
Deformity
Vasovagal episode
Aspiration

149
Q

What are the possible complications of a non resolving otitis media with effusion in a child?

A

Poor speech development
Delay in learning
Social problems
Behavioural problems

150
Q

What are the possible complications of acute otitis media?

A

Meningitis
Mastoiditis
Hearing loss
TM perf
Intracranial abscess
Facial n. palsy

151
Q

What are the different salivary glands?

A

Parotid gland
Submandibular gland
Sublingual gland

152
Q

What is the most common type of parotid gland tumour?

A

Pleomorphic adenoma

153
Q

What are sinuses and what are the different ones called?

A

Air filled cavity in the facial bones, connected to the nasal cavity
-maxillary
-sphenoid
-frontal
-ethmoidal

154
Q

What is the most common causative organism of quinsy?

A

Strep pyogenes

155
Q

What would indicate a dx of quinsy o/e?

A

Thick voice
Uvula deviation
Swelling next to tonsil
Erythema of the arch and palate
Snoring
Trismus

156
Q

How is quinsy managed medically?

A

Steroids
Abx
Fluids
Analgesia

157
Q

What are the possible complications of quinsy?

A

Airway obstruction and death
Deep neck space infection

158
Q

What are the macroscopic and microscopic pathological changes seen in Alzheimer’s?

A

Macro:
Widespread cerebral atrophy, particularly involving the cortex and hippocampus
Micro:
Amyloid plaques
Intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein

Finals (8 decks)

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