Ophthalmology Flashcards

1
Q

What is glaucoma?

A

Optic nerve damage caused by rise in intraocular pressure caused by blockage in aqueous humour

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2
Q

Where would you find vitreous humour?

A

In vitreous chamber of eye

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3
Q

Where would you find aqueous humour?

A

In the anterior chamber (between cornea and iris) and posterior chamber (between lens and iris) of eye

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4
Q

What is the role of the aqueous humour, where is it produced, and where does it drain?

A

Supplies nutrients to cornea
Produced by ciliary body
Drains through trabecular mesh work to canal of Schlemm at angle between cornea and iris

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5
Q

What is normal intraocular pressure?

A

10-21mmHg
Created by resistance to flow through trabecular meshwork

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6
Q

What is the pathophysiology of open angle glaucoma?

A

Gradual increased in resistance to flow through trabecular moshwork

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7
Q

What is the pathophysiology of acute angle closure glaucoma?

A

Iris bulges forwards and seals off trabecular mesh work from anterior chamber preventing aqueous humour from draining
Continual build up of pressure and acute onset of symptoms
EMERGENCY

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8
Q

What happens to the optic disc with raised intraocular pressure?

A

Cupping of optic disc

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9
Q

What are the risk factors for open angle glaucoma?

A

Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)

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10
Q

Outline presentation of open angle glaucoma

A

Affects peripheral vision first, resulting in gradual onset tunnel vision
Fluctuating pain
Headaches
Blurred vision
Halos around lights (particularly at night)

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11
Q

How do you measure intraocular pressure?

A

Non-contact tonometry- Puff of air at cornea and measures response
Goldmann applanation tonometry (gold standard)- Lamp applies pressure to cornea

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12
Q

How is open angle glaucoma diagnosed?

A

Goldmann applanation tonometry
Slit lamp to assess cup-disc ratio and optic nerve health
Visual field assessment
Gonioscopy (assess angle between iris and cornea)
Central corneal thickness

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13
Q

Outline management of open angle glaucoma

A

Started at IO pressure >24mmHg
360 degree selective trabeculoplasty
Prostaglandin analogue eye drops (latanoprost)- Increase uveoscleral outflow
BB eye drops (timolol)- Reduce production of aqueous humour
Carbonic anhydride inhibitors (dorzolamide)- Reduce production of aqueous humour
Sympathomimetics (brimonidine)- Reduce production of aqueous fluid and increase uveoscleral outflow
Trabeculectomy- If other treatment ineffective- Creates bleb

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14
Q

What are the side effects of prostaglandin analogue eye drops (latanoprost)?

A

Eyelash growth
Eyelid pigmentation
Iris pigmentation (browning)

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15
Q

What is acute angle closure glaucoma?

A

Iris bulges forward and seals off trabecular mesh work from anterior chamber, preventing aqueous humour draining, leading to continual increase in IO pressure
Pressure builds in posterior chamber, pushing iris forward and exacerbating angle closure
EMERGENCY

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16
Q

What are the risk factors for acute angle closure glaucoma?

A

Increasing age
Family history
Female (4x more likely)
Chinese and East Asian ethnic origin
Shallow anterior chamber

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17
Q

Which medications can precipitate acute angle closure glaucoma?

A

Adrenergic meds (noradrenaline)
Anticholinergic meds (oxybutynin and solifenacin)
TCAs (amitriptyline)

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18
Q

How does acute angle closure glaucoma present?

A

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

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19
Q

List signs on examination of acute angle closure glaucoma

A

Red eye
Hazy cornea
Decreased visual acuity
Mid dilated pupil
Fixed size pupil
Hard eyeball on gentle palpation

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20
Q

What is the initial management of acute angle closure glaucoma?

A

Lie patient on back without pillow
Pilocarpine eye drops (2% for blue, 4% for brown)
Acetazolamide 500mg orally
Analgesia and antiemetic if required

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21
Q

How does pilocarpine work?

A

Acts on Muscarinic receptors in sphincter muscles in iris and causes pupil constriction (miosis) and ciliary muscle contraction
Opens pathway for flow of aqueous humour from ciliary body around iris and into trabecular meshwork

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22
Q

How does Acetazolamide work?

A

Carbonic anhydride inhibitor
Reduces production of aqueous humour

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23
Q

What is the definitive treatment of acute angle closure glaucoma?

A

Laser iridotomy
Hole in iris with laser

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24
Q

What is age-related macular degeneration?

A

Progressive condition affecting macula
Most common cause of blindness
2 types- Wet and dry

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25
Q

What is the most common type of age related macular degeneration?

A

Dry

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26
Q

What is the difference between wet and dry AMD?

A

Dry- No Neovascularisation (90%)
Wet- Neovascularisation (10%)

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27
Q

What is the function of the macula?

A

Found in centre of retina
Generates high definition colour vision in central visual field

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28
Q

What are the 4 layers of the macula?

A

Choroid- Base layer, contains blood vessels that supply the macula
Bruch’s membrane
Retinal pigment epithelium
Photoreceptors

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29
Q

Which condition are Drusen associated with?

A

AMD
Deposits of proteins and lipids between retinal pigment epithelium and Bruchs membrane

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30
Q

What are frequent and large Drusen a sign of?

A

Early sign of AMD

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31
Q

What features are common on ophthalmoscope of AMD?

A

Atrophy of retinal pigment epithelium
Degeneration of photoreceptors
Drusen

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32
Q

What is the chemical that stimulates development of new vessels?

A

Vascular endothelial growth factor (VEGF)

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33
Q

What are the risk factors for AMD?

A

Old age
Smoking
FHx
CVD (eg: HTN)
Obesity
Poor diet (low in vitamins, high in fat)

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34
Q

Outline presentation of AMD

A

Unilateral
Gradual loss of central vision
Reduced visual acuity
Crooked or wavy appearance to straight lines (metamorphosia)
Gradually worsening ability to read small text

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35
Q

What is the difference in presentation of wet and dry AMD?

A

Wet- More acute presentation- Vision loss can develop within days and progress to complete vision loss in 2-3y- Often progresses to bilateral disease

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36
Q

What are the examination findings in AMD?

A

Reduced visual acuity on snellen chart
Scotoma (enlarged central area of vision loss)
Amsler grid test (assesses distortion on straight lines)
Drusen on fundoscopy

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37
Q

What is used to diagnose AMD?

A

Slit lamp- Detailed view of retina and macula
Optical coherence tomography- Cross section of layers of retina- Used for diagnosis and monitoring
Fluorescein angiography- Photographs retina to assess blood supply- Shows oedema and Neovascularisation in wet AMD

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38
Q

Outline management of dry AMD

A

Avoid smoking
Control BP
Vit supplements

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39
Q

Outline management of wet AMD

A

Anti-VEGF meds- Ranibizumab, aflibercept, bevacizumab- Block VEGF and slow development of new vessels
Inject directly into vitreous chamber once a month

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40
Q

What is diabetic retinopathy?

A

Damage to retinal blood vessels due to prolonged high blood sugar levels

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41
Q

Outline the management of non-proliferative diabetic retinopathy

A

Close monitoring
Diabetic control

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42
Q

Outline management of proliferative diabetic retinopathy

A

Pan-retinal photocoagulation- Extensive laser treatment to suppress new vessels
Anti-VEGF
Virectomy

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43
Q

What is a treatment option for macular oedema?

A

Intravitreal implant containing dexamethasone

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44
Q

List complications of diabetic retinopathy

A

Vision loss
Retinal detachment
Vitreous haemorrhage
Rubeosis iridis (new blood vessel formation in iris)- Can lead to Neovascular glaucoma
Optic neuropathy
Cataracts

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45
Q

What is diabetic maculopathy?

A

Exudates within macula
Macular oedema

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46
Q

Outline grading of diabetic retinopathy

A

Background- Microaneurysms, retinal haemorrhages, hard exudates, cotton wool spots
Pre-proliferative- Venous bleeding, multiple blot haemorrhages, intraretinal micro vascular abnormality (IMRA)
Proliferative- Neovascularisation and vitrous haemorrhage

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47
Q

Outline pathophysiology of diabetic retinopathy

A

Hyperglycaemia damages retina, small vessels and endothelial cells
Increased vascular permeability = Leaky blood vessels, blot haemorrhages and hard exudates (yellow/white deposits of lipids and proteins in retina)
Damage to blood vessels leads to Microaneurysms and venous beading
Damage to nerve fibres in retina= Cotton wool spots
IMRA- Dilated and tortuous capillaries in retina- Act as shunt between arterial and venous vessels in retina
Neovascularisation- Release of growth factors into retina, new blood vessel development

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48
Q

What is management of hypertensive retinopathy?

A

Control BP and manage risk factors

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49
Q

Outline classification of hypertensive retinopathy

A

1- Mild narrowing of arterioles
2- Focal constriction of blood vessels and AV nicking
3- Cotton wool spots, exudates, haemorrhages
4- Papilloedema

50
Q

List features of hypertensive retinopathy

A

Silver/copper wiring- Arterioles thickened and scleroses
AV nipping- Arterioles cause compression of veins due to sclerosis and hardening
Cotton wool spots- Damaged nerve fibres caused by ischaemia and infarction in retina
Hard exudates- Damaged vessels leak lipids onto retina
Retinal haemorrhages
Papilloedema- Ischaemia of optic nerve results in optic nerve swelling

51
Q

What is hypertensive retinopathy?

A

Damage to small blood vessels in retina relating to HTN
Change happens slow (chronic) or quickly (malignant HTN)

52
Q

What is a cataract?

A

Progressively opaque lens– Reduces light entering eye and visual acuity

53
Q

What is the role of the lens?

A

Focus light on the retina
Held in place by suspensory ligaments attached to ciliary body
Ciliary body contracts and relaxes to change shape of lens

54
Q

How does the ciliary body work?

A

Contracts and relaxes to change shape of lens
Contracts– Releases tension on suspensory ligaments = Lens thickens
Relaxes– Suspensory ligaments tension = Lens narrows

55
Q

What is special about the blood supply to the lens?

A

No blood supply
Nourished by aqueous humour

56
Q

How do you test for congenital cataracts?

A

Red reflex

57
Q

What are the risk factors for cataracts?

A

Increasing age
Smoking
Alcohol
Diabetes
Steroids
Hypocalcaemia

58
Q

Outline presentation of cataracts

A

Asymmetrical
Slow reduction in visual acuity
Progressive blurring of vision
Colours more faded– Brown/yellow
Starbursts at night
Loss of red reflex

59
Q

Outline management of cataracts

A

Cataract surgery– Artificial lens
Cataract can hide presence of macular degeneration and diabetic retinopathy– May still have reduced visual acuity

60
Q

What is a key complication of cataracts?

A

Endophthalmitis– Inflammation of inner contents of eye– Rare but serious complication of cataract surgery– Can lead to vision loss

61
Q

How is endophthalmitis treated?

A

Intravitreal antibiotics

62
Q

What is an Argyll-Robertson Pupil?

A

Neurosyphilis
Constricted pupil
Accommodates but does not react to light
Often irregularly shaped

63
Q

What is a Holmes-Adie Pupil?

A

Damage to post-ganglionic parasympathetic fibres
Dilated
Sluggish to react to light
Accommodates
Slow to dilate following constriction

64
Q

What is Holmes-Adie syndrome?

A

Holmes-Adie pupil
Absent ankle and knee reflexes

65
Q

Which muscles are responsible for pupil constriction?

A

Circular muscles in iris
Stimulated by PNS using acetylcholine as a neurotransmitter
Travels along CN III

66
Q

Which muscles are responsible for pupil dilation?

A

Dilator muscles
Stimulated by SNS using adrenaline as a neurotransmitter

67
Q

List possible causes of a tadpole pupil

A

Migraines
Horner syndrome

68
Q

What is a coloboma?

A

Congenital malformation
Causes hole in iris and irregular pupil shape

69
Q

What is rubeosis iridis?

A

Neovascularisation in iris
Associated with poorly controlled diabetes and diabetic retinopathy

70
Q

Which condition can cause a vertical oval pupil shape?

A

Acute angle closure glaucoma

71
Q

List causes of mydriasis (dilated pupil)

A

Congenital
Stimulants (cocaine)
Anticholinergic (oxybutynin)
Trauma
Third nerve palsy
Holmes-Adie syndrome
Raised ICP
Acute angle-closure glaucoma

72
Q

List causes of mitosis (Constricted pupil)

A

Horner syndrome
Cluster headaches
Argyll-Robertson pupil
Opiates
Nicotine
Pilocarpine

73
Q

What are the features of occulomotor nerve palsy?

A

Ptosis
Dilated non-reactive pupil
Divergent strabismus (squint) in affected eye– With down and out position

74
Q

What is the function of the occulomotor nerve?

A

Supplies all extraocular muscles except lateral rectus and superior oblique
Supplies elevator palpebral superioris (lifts upper eyelid)
Carries parasympathetic fibres that innervate circular muscle of iris

75
Q

What does a 3rd nerve palsy with sparing of the pupil suggest?

A

Micro vascular cause– Parasympathetic fibres are spared
= Diabetes, HTN, ischaemia

76
Q

What are the causes of a full 3rd nerve palsy?

A

Tumour
Trauma
Cavernous sinus thrombosis
Posterior communicating artery aneurysm
Raised ICP
Idiopathic

77
Q

What is the triad of Horner syndrome?

A

Ptosis
Miosis
Anhidrosis (lack of sweating)

78
Q

Outline the journey of the occulomotor nerve

A

Brainstem through cavernous sinus, close to posterior communicating artery

79
Q

List other features of Horner Syndrome

A

Enophthalmos

80
Q

What is the mechanism of Horner Syndrome?

A

Damage to sympathetic nervous system supplying face
Sympathetic nerves arise from spinal cord in chest– Preganglionic nerves– Enter sympathetic ganglion at Base of neck and exit as post-ganglionic nerves– Travel to head alongside internal carotid artery

81
Q

How is the location of Horner syndrome identified?

A

Central lesion (before nerves exit spinal cord) - - Anhidrosis of arm, trunk, and face
Preganglionic lesion– Anhidrosis of face
Post-ganglionic lesion– Don’t cause Anhidrosis

82
Q

What are the causes of central Horner Syndrome?

A

Stroke
Multiple Sclerosis
Swelling (tumour)
Syringomyelia (cyst in spinal cord)

83
Q

What are the causes of Preganglionic lesions?

A

Tumour (pancoast)
Trauma
Thyroidectomy
Top rib

84
Q

What are the causes of post-ganglionic Horner Syndrome?

A

Carotid aneurysm
Carotid artery dissection
Cavernous sinus thrombosis
Cluster headache

85
Q

What is associated with congenital Horner Syndrome?

A

Heterochromia (different iris colour on affected side)

86
Q

What is the effect of cocaine eye drops on Horner syndrome?

A

Stop noradrenaline re-uptake at NMJ
Causes normal eye to dilate as noradrenalin stimulates dilator muscles of iris
In Horner eye- Nerves not releasing noradrenalin = No pupil reaction

87
Q

What is the effect of adrenaline eye drops in Horner Syndrome?

A

Dilate Horner pupil
Not dilate normal pupil

88
Q

What is the cause of a Holmes-Adie Pupil?

A

Caused by damage to post-ganglionic parasympathetic fibres

89
Q

How does a Holmes-Adie Pupil present?

A

Dilated
Sluggish to react to light
Responsive to accommodation (pupils constrict well when focusing on near object)
Slow to dilate following constriction (tonic pupil)

90
Q

What is Holmes-Adie Syndrome?

A

Holmes-Adie pupil
Absent ankle and knee reflexes

91
Q

What is an Argyll-Robertson Pupil?

A

Specific finding in neurosyphilis
Constricted pupil that accommodates but doesn’t react to light

92
Q

What is blepharitis?

A

Inflammation of eyelid margins
Causes gritty, itchy, dry sensation in eyes
Associated with dysfunction of Meibomian glands (responsible for secreting meibum (oil) onto surface of eye)
Can lead to styes and chalazions

93
Q

What is the management of blepharitis?

A

Warm compress
Gentle cleaning of eyelid margin to remove debris (cotton bud and baby shampoo)

94
Q

What is a stye?

A

Hordeolum externum- Infection of glands of Zeis or glands of Moll (sweat glands at base of eyelashes)- Tender red lump along eyelid, may contain pus
Hordeolum internum- Infection of Meibomian glands- Deeper, more painful, may pont in towards eyeball under eyelid

95
Q

How are styes managed?

A

Hot compress and analgesia
Topical antibiotics (chloramphenicol) if associated with conjunctivitis/symptoms persistent

96
Q

What is a chalazion?

A

Meibomian gland becomes blocked and swells
Swelling in eyelid, typically not tender

97
Q

How is a chalazion treated?

A

Warm compresses and gentle massage towards eyelashes
Rarely surgical drainage required

98
Q

What is an entropion?

A

Eyelid turns inwards with lashes pressed against the eye
Pain and can result in corneal damage and ulceration

99
Q

How are entropions managed?

A

Taping eyelid down to prevent it from turning inwards
Definitive management- Surgical
Lubricating eye drops

100
Q

What is an ectropion?

A

Eyelid turns outwards
Usually affects bottom lid

101
Q

What is a complication of an ectropion?

A

Exposure keratopathy

102
Q

Outline the management of an ectropion?

A

Regular lubricating eye drops
More significant cases may require surgery

103
Q

What is trichiasis?

A

Inward growth of eyelashes
Results in pain

104
Q

What is a complication of trichiasis?

A

Corneal damage
Ulceration

105
Q

What is the management of trichiasis?

A

Remove affected eyelashes
Recurrent cases- Electrolysis/cryotherapy/laser treatment

106
Q

What is periorbital cellulitis?

A

Eyelid and skin infection in front of orbital septum

107
Q

Outline presentation of periorbital cellulitis

A

Swollen, red, hot skin around eyelid and eye

108
Q

How is periorbital cellulitis distinguished from orbital cellulitis?

A

CT scan

109
Q

How is periorbital cellulitis treated?

A

Systemic antibiotics
Can develop into orbital cellulitis- If vulnerable patient- Admit for monitoring

110
Q

What is orbital cellulitis?

A

Infection around eyeball- Involves tissues behind orbital septum

111
Q

What are the symptoms of orbital cellulitis?

A

Pain with eye movement
Reduced eye movements
Vision changes
Abnormal pupil reactions
Proptosis

112
Q

What is the management of orbital cellulitis?

A

Emergency admission
IV antibiotics
Surgical drainage if abscess forms

113
Q

What is conjunctivitis?

A

Inflammation of conjunctiva (thin layer of tissue that covers the eyelids and sclera
Can be bacterial/viral/allergic

114
Q

Outline presentation of bacterial conjunctivitis

A

Purulent discharge
Worse in morning, eyes may be struck together
Starts in one eye, spreads to other- Highly contagious
Red, bloodshot eye
Itchy/gritty sensation
No pain/photophobia/reduced visual acuity

115
Q

Outline presentation of viral conjunctivitis

A

Clear discharge
Dry cough/sore throat/blocked nose
Tender pre-auricular lymph nodes
Very contagious
Red, bloodshot eye
Itchy/gritty sensation
No photophobia/pain/reduced visual acuity

116
Q

List causes of acute painful red eye

A

Acute angle-closure glaucoma
Anterior uveitis
Scleritis
Corneal abrasions/ulceration
Keratitis
Foreign body
Traumatic/chemical injury

117
Q

List causes of acute painless red eye

A

Conjunctivitis
Episcleritis
Subconjunctival haemorrhage

118
Q

Outline management of conjunctivitis

A

Usually resolves in 1-2wks w/o treatment
Hygiene measures to reduce spread
Cooled boiled water and cotton wool to clear discharge
Bacterial- Chloramphenicol/fusidic acid eye drops
Neonates- Urgent assessment (may be caused by gonococcal infection)

119
Q

What is the management of neonatal conjunctivitis?

A

Urgent ophthalmology assessment
May be caused by gonococcal infection- Can cause permanent vision loss

120
Q

Outline presentation of allergic conjunctivitis

A

Contact with allergens
Swelling of conjunctival sac and eyelid
Itching and watery discharge

121
Q

Outline management of allergic conjunctivitis

A

Antihistamines
Topical mast-cell stabilisers- If chronic seasonal symptoms- Prevent mast cells releasing histamine

122
Q
A